Vitamina D ajuda a prevenir diabetes, câncer, hipertensão e infecções

Vitamina D ajuda a prevenir diabetes, câncer, hipertensão e infecções

05/11/2009 – 13h24

Publicidade

FERNANDA BASSETTE
JULLIANE SILVEIRA
da Folha de S.Paulo

Não passa uma semana sem que surja uma nova pesquisa associando a falta de vitamina D no organismo a alguma doença. Os problemas vão além da saúde óssea prejudicada –relação já estabelecida, pois o nutriente contribui para a fixação do cálcio nos ossos. Hoje, estudos mostram que a deficiência pode levar a hipertensão, diabetes, infecções e alguns tipos de câncer.

Há até pouco tempo, os especialistas acreditavam que a discussão sobre a falta da vitamina era desnecessária no Brasil, já que um país tropical recebe luz solar suficiente –a maior parte da vitamina D é sintetizada com a ajuda dos raios solares.

No entanto, pesquisas recentes já apontam problemas entre os brasileiros. Um estudo realizado com 603 funcionários do Hospital Universitário da USP (Universidade de São Paulo) mostrou deficiências da vitamina tanto no fim do inverno quanto no término do verão.

Leonardo Wen/Folha Imagem

A empresária Vera Folli, 53, trocou os remédios contra esclerose múltipla por vitamina D e não manifesta nenhum sintoma da doença

“Ninguém esperava esses resultados para São Paulo. Ainda faltam estudos em outras partes do país, mas talvez seja possível extrapolar os resultados para toda a região que vai de Belo Horizonte ao Sul, principalmente nas grandes cidades”, diz Rosa Moysés, nefrologista do Hospital das Clínicas de São Paulo e autora da pesquisa.

Um outro trabalho, feito por pesquisadores da Unifesp (Universidade Federal de São Paulo), com 177 idosos que vivem em instituições e outros 243 idosos que moram em casa. Entre os primeiros, 41% tinham níveis muito baixos de vitamina D e, entre os outros, 30%.

“Os números são assustadores. Mesmo trabalhos com mulheres no Recife encontraram grande deficiência, porque elas também se escondem do sol. É um problema das grandes cidades”, afirma a endocrinologista Marise Castro, chefe do Setor de Doenças Osteometabólicas da universidade.

O deficit também existe entre adolescentes. A nutricionista Bárbara Peters, pesquisadora da Unifesp, detectou o problema em uma pesquisa feita com 136 jovens de Indaiatuba (interior de São Paulo) –62% deles apresentavam índice insuficiente de vitamina D.

“Não esperava esse resultado, pois são adolescentes saudáveis que vivem em uma cidade bastante ensolarada.”

Trabalhos feitos em animais mostraram que a vitamina D tem um papel inibidor da renina, hormônio que contribui para elevar a pressão arterial.

Um trabalho finlandês divulgado na semana passada no “American Journal of Epidemiology” confirma o alerta. Por 27 anos, foram monitoradas 5.000 pessoas.

Houve relação entre baixos índices da vitamina e maior risco de derrame e de outras doenças cardiovasculares.

“Pessoas com níveis adequados de vitamina D têm menos risco de calcificação das artérias, pois a vitamina possui uma ação anti-inflamatória”, afirma Marcelo de Medeiros Pinheiro, reumatologista da Unifesp.

Leonardo Wen/Folha Imagem

A aposentada Suely Pedroso Riskala, 58, toma vitamina D há mais de dez anos; ela não se expunha ao sol diariamente

O nutriente também estimula a produção de insulina, melhorando o controle da glicose, e diminui a resistência ao hormônio –o que ocorre em quem tem diabetes tipo 2. Sua falta pode favorecer o desenvolvimento da doença.

Tumores de cólon, de próstata e de mama também já foram associados à deficiência de vitamina D em pesquisas. A explicação pode estar no papel da vitamina no ciclo de proliferação celular -a substância ajuda a equilibrar a divisão das células.

Quem tem deficiência da vitamina é também mais vulnerável a infecções, pois o nutriente atua na produção de proteínas antibacterianas.

“Uma das mais estudadas é a tuberculose. Um estudo em laboratório mostrou o papel da vitamina D na doença”, acrescenta Moysés.

Combate

A explicação para as baixas taxas da vitamina no sangue são a pouca exposição ao sol –já que as pessoas passam boa parte do tempo em escritórios– e o baixo consumo de alimentos com o nutriente em quantidade razoável.

Com relação ao sol, ainda existe uma grande polêmica: o uso de filtro solar. Para alguns especialistas, o protetor dificulta a absorção dos raios UVB, responsáveis por atuar na sintetização da vitamina.

Por isso, eles sugerem uma exposição de pernas e braços descobertos por cerca de 15 minutos diários sem filtro.

“O produto certamente diminui a produção da vitamina D. Mas hábitos saudáveis [como exercícios ao ar livre] também podem ajudar a diminuir a hipovitaminose D, pois aumentam a exposição solar, mesmo naqueles que irão usar o protetor”, diz Moysés.

No entanto, Marcus Maia, dermatologista e oncologista da Santa Casa de São Paulo, discorda e diz que não existe fotoproteção tão intensa capaz de impedir a síntese da vitamina.

Rafael Hupsel/Folha Imagem

Vera Magalhães, 80, teve deficiência de vitamina diagnosticada devido à osteoporose

Ele diz que sete minutos de exposição solar, três vezes por semana, são o suficiente. Maia analisou os níveis de vitamina D no sangue de 50 pessoas: 25 com melanoma (tipo mais agressivo de câncer de pele) e que usavam protetor solar diariamente nas doses recomendadas e 25 pessoas que não tinham a doença.

Ele constatou que nenhum paciente tinha níveis insuficientes da vitamina. “Nem quem precisa usa o filtro solar corretamente. Proteção solar absoluta, capaz de bloquear a síntese da vitamina D, é impossível. Por isso, outras possíveis causas do deficit da vitamina teriam de ser estudadas”, diz.

O consumo de alimentos que contêm o nutriente é indicado, mas não resolve o problema. Só de 10% a 20% do valor diário recomendado podem ser obtido por meio dos alimentos.

Segundo Marcelo Pinheiro, pesquisa feita com 2.400 pessoas constatou que o brasileiro consome cinco vezes menos vitamina D do que o recomendado internacionalmente -que é de dez a 15 microgramas.

Por esse motivos, especialistas acreditam que seja necessária uma política de fortificação de alimentos e de suplementos da vitamina. No Brasil, o nutriente só é encontrado em versão manipulada.

Roseli Sarni, presidente do Departamento de Nutrição da Sociedade Brasileira de Pediatria, diz que crianças de até 18 meses devem receber suplementação, pois o que ingerem com o leite materno não é suficiente.

Sarni afirma que a suplementação de vitamina independe do fato de a criança tomar sol. Nessa faixa etária, a recomendação semanal é de meia hora se o bebê estiver só de fraldas ou de duas horas se estiver com rosto, mãos e pés expostos ao sol.

Colaborou CLÁUDIA COLLUCCI

*

Alimentos com mais vitamina D
É indicada a ingestão de 10 a 15 microgramas por dia, além da exposição ao sol

Salmão
100 g = 7 microgramas

Sardinha
100 g = 4,5 microgramas

Atum
100 g = 3,5 microgramas

Gema de ovo
1 unidade = 0,9 micrograma

Ostra
100 g = 8 microgramas

Leite integral
1 copo (250 ml) = 0,5 micrograma

Leite de soja fortificado
1 copo (250 ml) = 2,5 microgramas

Fonte: BÁRBARA SANTA ROSA EMO PETERS, nutricionista, e MARCELO PINHEIRO, reumatologista

*

Sintetizando
A maior parte da vitamina D presente no organismo é produzida coma ajuda do sol

1 – Uma substância chamada 7-dehidrocolesterol está presente na epiderme

2 – Os raios UVB do sol entram em contato com a pele e o calor converte a substância em vitamina D3

3 – A vitamina D3 cai na corrente sanguínea e chega ao fígado

4 – No órgão, se transformaem 25-hidroxivitaminas D

5 – Nos rins, se transformam em vitamina D ativa

6 – Então, participa de processos como fixação de cálcio no osso, absorção de cálcio pelo intestino e funções neuromusculares

Fonte: MARISE CASTRO, endocrinologista

http://www1.folha.uol.com.br/folha/equilibrio/noticias/ult263u648076.shtml

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Folha de São Paulo: Terapia polêmica usa vitamina D em doses altas contra esclerose múltipla

Folha de São Paulo: Terapia polêmica usa vitamina D em doses altas contra esclerose múltipla

 

28/05/2012 — Celso Galli Coimbra

Ediçao de Domingo – 27/05/2012

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O vídeo referido na reportagem dominical da Folha está no endereço:

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)

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DÉBORA MISMETTI
EDITORA-ASSISTENTE DE “CIÊNCIA+SAÚDE”

Há quase três anos o paulistano Daniel Cunha, 26, acordou com metade de seu rosto dormente. Foi trabalhar, voltou para casa e achou que a sensação ia passar. Não só não passou como piorou.

Foi ao hospital, fez exames e, depois de algumas consultas, recebeu o diagnóstico de esclerose múltipla. O mal é autoimune, causado pelo ataque ao revestimento dos neurônios pelo sistema imunológico da própria pessoa.

Desde 2010, Cunha abandonou o tratamento convencional, com injeções de interferon, remédio que controla a ação inflamatória da esclerose, mas causa efeitos colaterais como febre e mal-estar.

Ele passou a tomar todo dia uma dose alta de vitamina D, prescrita pelo neurologista Cícero Galli Coimbra, da Unifesp (Universidade Federal de São Paulo). O tratamento não é reconhecido pela maioria dos especialistas, que o consideram experimental.

Isso não impediu Cunha de usar a vitamina. Ele ficou tão satisfeito que realizou, com meios próprios e ajuda de amigos, um documentário de 30 minutos, disponível desde abril no YouTube (http://www.youtube.com/watch?v=erAgu1XcY-U), sobre a terapia.

No vídeo, com 18 mil acessos, pacientes de Coimbra falam sobre a vida antes e depois do novo tratamento, e o médico explica a relação entre a vitamina D e a doença.

 

                     Daniel Cunha, 26, autor de documentário sobre esclerose                    

 

HORMÔNIO

Produzida pelo corpo quando a pele fica exposta ao sol, a vitamina D na verdade é um hormônio, apesar de manter o nome consagrado.

É consenso há muito tempo que ela tem papel importante na mineralização dos ossos. “Experimentos vêm mostrando que ele age em vários outros tecidos, especialmente no sistema imunológico”, afirma a endocrinologista Marise Castro.

No caso da esclerose múltipla, pesquisas mostram que a prevalência da doença é mais alta em países distantes da linha do Equador, com incidência solar mais baixa, onde a população produz menos vitamina D.

Segundo Coimbra, a suplementação com o hormônio vem sendo testada desde os anos 1980 para reduzir os surtos de esclerose, períodos em que a doença pode deixar sequelas. Para ele, já há evidência suficiente de que as pessoas com a moléstia têm deficiência da vitamina.

“Desde 2003 venho cumprindo o dever ético de corrigir o problema metabólico desses pacientes. Todo médico tem a obrigação de fazer isso”, afirma o neurologista.

Até hoje, diz Coimbra, quase 900 pacientes com esclerose múltipla foram tratados. A maioria usa de 30 mil a 70 mil UI de vitamina D ao dia, mas alguns tomam 200 mil.

A dose ideal para a suplementação ainda é motivo de debate. Segundo Marise Castro, a quantidade usual é de 400 a 2.000 UI.

Mas, segundo Coimbra, essas doses não são realistas. “As pessoas com esclerose têm uma resistência genética à vitamina e precisam de doses mais altas.”

Os pacientes dele seguem uma dieta sem laticínios e fazem exames periódicos para controlar os níveis de cálcio na urina e no sangue. A vitamina D tem relação com o cálcio, e as doses altas podem causar cálculos renais.

“A intoxicação por vitamina D pode ser grave e leva meses para curar, porque ela se deposita no tecido adiposo”, diz a endocrinologista.

Coimbra rebate, citando um estudo que acompanhou pacientes com esclerose tomando vitamina D por sete meses, em doses crescentes, até chegar a 40 mil UI por dia.

Editoria de Arte/Folhapress

 

Para Maria Fernanda Mendes, membro-titular da Academia Brasileira de Neurologia, não há provas suficientes para receitar a terapia.

“Temos feito exames para dosar a vitamina e repô-la em caso de deficiência, até por conta da demanda dos pacientes, mas não é a recomendação oficial. Como há um tratamento comprovadamente melhor, esse só pode ser usado em pesquisas.”

Coimbra diz que não concorda com a realização de estudos controlados em que parte dos pacientes recebam a vitamina e parte, placebo.

“Alguém já fez estudo controlado sobre usar insulina para crianças diabéticas? Não, porque elas iam morrer. Se você tivesse uma filha com esclerose múltipla, que poderia ficar cega em um surto, correria o risco do placebo?”

Coimbra afirma que a relutância dos médicos em aceitar o tratamento vem dos conflitos de interesse com as farmacêuticas. “Há um interesse fabuloso no tratamento tradicional, que custa até R$ 11 mil por paciente por mês.”

O conflito de interesses foi um dos motivos que levou Daniel Cunha a fazer o documentário. “O tratamento com vitamina D me custa R$ 50 por mês. É a minha saúde, não é um leilão. Não me interessa se alguém vai ganhar dinheiro com isso. As pesquisas que todo mundo pede nunca vão sair, quem pagaria isso se não as farmacêuticas? Mas as pessoas não precisam ser reféns. A internet é nossa arma.”

Editoria de Arte/Folhapress

 

Fonte: http://www1.folha.uol.com.br/equilibrioesaude/1096497-terapia-polemica-usa-vitamina-d-em-doses-altas-contra-esclerose-multipla.shtml

Vídeos e textos sobre o assunto:

1.

Vitamina D pode revolucionar o tratamento da esclerose múltipla

http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

 

2.

Vitamina D pode combater males que mais matam pessoas no mundo

http://biodireitomedicina.wordpress.com/2010/03/20/vitamina-d-pode-combater-males-que-mais-matam-pessoas-no-mundo/

 

3.

 

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, como Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão

http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/

 

4.                                       

 

Vitamina D – Por uma outra terapia

http://biodireitomedicina.wordpress.com/2012/04/12/vitamina-d-por-uma-outra-terapia/  

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-30.039254 -51.216930

 

http://biodireitomedicina.wordpress.com/2012/05/28/folha-de-sao-paulo-terapia-polemica-usa-vitamina-d-em-doses-altas-contra-esclerose-multipla/

Maior lobby no Congresso, ruralistas controlam 1/4 da Câmara

Maior lobby no Congresso, ruralistas controlam 1/4 da Câmara

João Fellet

Da BBC Brasil em Brasília

Atualizado em  24 de maio, 2012 – 14:07 (Brasília) 17:07 GMT

 

Com 120 deputados e 13 senadores, ruralistas são grupo mais poderoso do Congresso, dizem analistas

Responsáveis pelas maiores derrotas do governo no Congresso neste ano, os ruralistas cresceram desde a última legislatura, passando a controlar um quarto da Câmara.

A bancada, considerada por analistas o mais poderoso grupo de interesse no Parlamento brasileiro, vale-se de alianças com outras agremiações no Congresso para promover uma agenda que inclui, entre suas principais principais bandeiras, o perdão às dívidas de agricultores, a expansão de terras cultiváveis no país e a oposição à ampliação de Terras Indígenas.

Notícias relacionadas

Tópicos relacionados

O último grande embate do grupo com o governo ocorreu em abril, com a aprovação pela Câmara de uma versão do Código Florestal tida como favorável aos agricultores. Espera-se que a presidente Dilma Rousseff vete até o fim desta semana partes da legislação.

Segundo a Frente Parlamentar da Agropecuária (FPA), 120 deputados federais e 13 senadores integram a bancada ruralista, perfazendo 23,4% da Câmara e 16% do Senado. Os dados são próximos dos de levantamento feito em 2011 pelo Departamento Intersindical de Assessoria Parlamentar (DIAP), que apontou a existência de 120 deputados e 18 senadores ruralistas.

Na última legislatura (2007-2010), de acordo com o DIAP, 117 deputados federais pertenciam ao grupo (não há dados sobre senadores).

Embora não exista formalmente, a bancada ruralista agrega os parlamentares que, articulados, defendem no Congresso os pleitos do agronegócio. Grande parte de seus integrantes são donos de terra ou empresários dos setores alimentar e agroquímico.

Conquistas

A FPA afirma, porém, que a causa agrária conta com a simpatia de outros 77 deputados, que pertencem à frente mas não endossam todas as suas posições. Somando esses congressistas, a bancada diz influenciar ao menos 41% dos votos na Câmara.

 

Ruralistas são maior bancada do Congresso Nacional, perfazendo 23,4% da Câmara e 16% do Senado

O peso do grupo explica algumas de suas conquistas recentes: além de impor sua versão do Código Florestal, aprovou em comissão da Câmara, em março, uma PEC (Proposta de Emenda Constitucional) que transfere do Executivo ao Legislativo a prerrogativa de demarcar Terras Indígenas. Nesta terça-feira, a bancada aprovou ainda em subcomissão da Câmara a compra de terras por estrangeiros.

Nas três votações acima, o grupo se contrapôs a parlamentares ambientalistas, que integram a Frente Parlamentar Ambientalista. Ainda que seja mais numeroso que a frente agropecuária (com 247 deputados e 21 senadores) o grupo não tem conseguido fazer frente ao agrário.

Segundo especialistas, isso ocorre porque a maior parte dos congressitas que aderiu à frente o fez somente para simular interesse pelas causas ambientais, sem endossá-las na prática.

Derrota

A bancada ruralista, no entanto, foi derrotada em votação também nesta terça-feira sobre a PEC do Trabalho Escravo. Aprovada por 360 votos a 29, a medida prevê a expropriação de terras onde houver flagrante de exploração laboral. Os ruralistas tentaram esvaziar a votação, questionando a atual definição de trabalho escravo.

Segundo o historiador e assessor do Inesc (Instituto de Estudos Socioeconômicos) Edélcio Vigna, que estuda a bancada ruralista desde 2001, o resultado da votação mostra os limites da articulação do grupo.

Ele afirma que há na bancada “meia dúzia” de líderes, que definem as posições da agremiação e orientam as votações. “O êxito depende de essa meia dúzia chegar a um consenso, difundi-lo em nome da bancada e se articular com outros setores conservadores”, diz à BBC Brasil.

Na votação do Código Florestal, por exemplo, o grupo foi endossado por grande parte do PMDB, o partido mais representado na bancada ruralista e principal membro da base do governo no Congresso.

Influência e interesses

A agremiação tem ainda representantes em todas as bancadas estaduais do Congresso e em quase todos os partidos. E a influência do grupo, diz Vigna, vai além: controla a Comissão de Agricultura da Câmara e define o alto escalão do Ministério da Agricultura, hoje chefiado por Mendes Ribeiro (PMDB-RS).

“O ministro serve aos interesses da bancada dentro do Estado”, afirma.

O historiador afirma ainda que a influência do agronegócio no Congresso também se apoia no financiamento de campanhas eleitorais.

“Sabemos que há bancos, grandes empresas agroalimentares e agroquímicas financiando as campanhas de ruralistas. Queremos descobrir o que há por trás desse biombo”. Segundo Vigna, esses grupos exercem na bancada um poderoso lobby, atividade não regulamentada no país.

Já os ruralistas dizem representar interesses legítimos de um dos setores mais prósperos da economia brasileira. Eleito o próximo presidente da FPA, o deputado Homero Pereira (PR-MT) diz que o grupo busca garantir o direito de propriedade no campo, evitar a criação de parques sem indenização a donos de terra e combater a “tentativa de qualificar empregadores rurais como pessoas que exploram trabalho análogo à escravidão”.

Além disso, diz Pereira, a bancada está empenhada em garantir o uso integral das propriedades rurais. Hoje, a legislação define percentuais obrigatórios de preservação em terras privadas, que chegam a 80% para fazendas na Amazônia. “O proprietário paga impostos sobre 100% da terra e não pode mexer em 80% dela. É uma agressão”, afirma à BBC Brasil.

O deputado enaltece o desempenho do agronegócio brasileiro – “um dos poucos setores em que o Brasil consegue se inserir no mercado internacional” – e diz que o país tem “vocação e um potencial enorme para a produção de alimentos”.

Apesar do papel econômico que desempenham, afirma Pereira, os produtores rurais brasileiros não recebem o reconhecimento devido. “Como a sociedade brasileira se urbanizou rapidamente, as novas gerações perderam o ‘link’ com o meio rural. Mas o abastecimento da cidade se dá pelo campo e, diferentemente de outros países que concedem subsídios para o homem rural, aqui há um preconceito contra a atividade”.

 

http://www.bbc.co.uk/portuguese/noticias/2012/05/120524_ruralistas_abre_jf.shtml

 

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Para ONGs, Brasil perde liderança ambiental ao mudar Código Florestal

Para ONGs, Brasil perde liderança ambiental ao mudar Código Florestal

Daniel Gallas

 

Da BBC Brasil em Londres

 

Atualizado em  26 de abril, 2012 – 15:43 (Brasília) 18:43 GMT

Anistia a desmatamento do passado é uma das questões mais polêmicas do Congresso

Organizações ambientalistas internacionais afirmam que o Brasil pode estar perdendo a liderança no movimento ecológico global, depois que a Câmara dos Deputados aprovou na quarta-feira um novo texto que altera o Código Florestal brasileiro.

 

Em entrevista à BBC Brasil, representantes da WWF e do Greenpeace em Londres disseram que o Brasil sempre foi visto como um dos países mais ativos na promoção de ideias ambientais em fóruns internacionais, como as reuniões sobre mudanças climáticas da ONU. Mas, a aprovação do texto do deputado Paulo Piau (PMDB-MG) pode provocar uma mudança nessa percepção.

 

Notícias relacionadasMudança no Código Florestal ameaça liderança do Brasil, diz Marina SilvaBrasil precisará de ofensiva de comunicação para esclarecer ‘anistia’ ao desmatamentoRevisão do Código Florestal é aprovada

Tópicos relacionadosMeio Ambiente, BrasilO texto ainda precisa ser apreciado pela presidente Dilma Rousseff, que pode vetá-lo na íntegra ou parcialmente. Neste caso, a proposta volta para o Congresso, que pode fazer alterações ou derrubar o veto.

 

‘Choque’Entre os pontos mais polêmicos do parecer de Piau está a questão da anistia a produtores que desmataram florestas nas proximidades de rios.

 

O texto afeta os proprietários de terra que desmataram os 30 metros das Áreas de Preservação Permanente (APPs) nas margens de rios de até 10 metros de largura, segundo as normas estabelecidas em 1989. Eles ficam liberados da obrigação de recuperar totalmente a área degradada. De acordo com o texto aprovado por 274 votos a 189, os proprietários que infringiram tais regras terão de replantar apenas 15 metros.

 

“É um choque estarem alterando o Código Florestal que protege a floresta amazônica. Com a proximidade da Rio+20, isso bota muita pressão sobre a presidente Dilma Rousseff. Será muito difícil para ela se apresentar como defensora do ambiente”, disse à BBC Brasil Sarah Shoraka, ativista especialista em florestas do Greenpeace do Reino Unido.

 

“Durante a campanha ela [Dilma Rousseff] havia dito que não apoiaria nenhuma legislação que aumentasse o desmatamento e que desse anistia a criminosos, mas a proposta atual faz exatamente essas duas coisas. Agora é tudo uma questão da credibilidade dela, e o quanto ela está disposta a mudar”, disse.

 

“Agora é tudo uma questão da credibilidade dela [Dilma], e o quanto ela está disposta a muda.”

 

Sarah Shoraka, do Greenpeace em Londres

Para a diretora de Florestas da WWF no Reino Unido, Sandra Charity, a comunidade internacional está “perplexa” com a votação da quarta-feira no Congresso brasileiro.

 

“O Brasil tem uma trajetória de país moderno, que sempre esteve na liderança dos compromissos ambientais tendo em vista a sua posição na Conferência de Mudanças Climáticas de Copenhague [2009]. O país sempre esteve na frente e puxando os outros países. A aprovação deste texto é um retrocesso”, disse ela.

 

A representante da WWF ressalvou que o texto foi aprovado no Congresso, e não pela Presidência, mas que mesmo assim a medida tende a respingar na imagem do governo e do país como um todo.

 

‘Legado de Lula’Tanto a WWF e o Greenpeace dizem que o governo de Dilma Rousseff parece estar menos comprometido com ideias ambientalistas do que o do ex-presidente Lula.

 

“Nós estávamos acostumados com um Brasil que era líder no front ambiental. O ex-presidente Lula anunciou metas ambiciosas de redução de CO2 na em Copenhague”, disse Shoraka.

 

“Existe um descompasso entre o que a sociedade como um todo está esperando e pedindo e o que os dirigentes que fazem as leis estão decidindo.”

 

Sandra Charity, da WWF em Londres

Questionada se Dilma é menos preocupada com o ambiente do que Lula, afirmou: “Esta começando a dar essa impressão. O Código Florestal é o primeiro teste, mas se você olhar para outras tendências, como a aprovação de grandes hidrelétricas ou estradas sem os estudos de impacto ambiental corretos. É possível notar um padrão de valores ambientais se degradando no Brasil. Internacionalmente as pessoas estão de olho na Dilma agora. É o momento para ela provar que vai levar adiante o legado de Lula.”

——————-

 

Dilma vai anunciar medida provisória tratando de trechos vetados do Código Florestal

 

Dilma vai anunciar medida provisória tratando de trechos vetados do Código Florestal

 

25/05/2012 – 14h10

 

senado, dilma rousseff, código florestal, medida, desmatamento

 

 

BRASÍLIA – Informação foi dada pelo senador Jorge Viana e segundo ele, haverá obrigação de se recompor as áreas desmatadas ilegalmente…

 

Agência Brasil

 

 foto: Antonio Cruz/ABr

 

Presidente Dilma Rousseff vai editar medida provisória sobre temas que serão vetados no Código Florestal Brasileiro

BRASÍLIA – O senador Jorge Viana (PT-AC) acaba de informar no Senado, no início da tarde desta sexta-feira (25), que a presidente Dilma Rousseff vai editar medida provisória sobre temas que serão vetados no Código Florestal Brasileiro aprovado pelo Congresso, entre esses, a anistia a produtores que desmataram áreas de preservação permanente. Haverá obrigação de se recompor as áreas desmatadas ilegalmente, segundo o senador.

 

Viana, que foi um dos relatores do Código Florestal no Senado, junto com o senador Luiz Henrique (PMDB-SC), esteve no final da manhã no Palácio do Planalto, onde recebeu a informação, a ser divulgada oficialmente apenas às 14 horas desta tarde, em entrevista coletiva com os ministros do Meio Ambiente, Izabella Teixeira, da Agricultura, Mendes Ribeiro, e do Desenvolvimento Agrário, Pepe Vargas.

 

“A presidente vai tirar do texto aprovado tudo que implicar em novos desmatamentos e em anistia aos produtores rurais que desmataram [áreas de preservação permanente]. Está mais do que na hora de virarmos a página da insegurança jurídica [com relação ao tema]”, disse o senador, referindo-se à decisão de editar medida provisória para preencher as lacunas legais geradas a partir do possível veto a trechos do Código Florestal.

 

De acordo com o senador, a medida provisória dará tratamento diferenciado a pequenos produtores e agricultores familiares com propriedades até 2 módulos rurais. Deve fazer parte da nova legislação, conforme Jorge Viana, a obrigação de recomposição ambiental das reservas que foram desmatadas ilegalmente. Também deve ser incluída na medida provisória a proibição a novos desmatamentos.

 

Segundo Jorge Viana, a medida provisória texto não incluirá anistia para os produtores rurais que desmataram área de preservação a partir de 2008, inviabilizando uma das principais mudanças obtidas pela bancada ruralista na aprovação do Código Florestal. Por conta da vitória ruralista, o texto aprovado pela Câmara, no fim de abril, deixou fora pontos que haviam sido negociados pelo governo durante a tramitação no Senado.

 

http://www.dci.com.br/dilma-vai-anunciar-medida-provisoria-tratando-de-trechos-vetados-do-codigo-florestal-id295852.html

 

 

Here in the “True North,” getting enough vitamin D — the sunshine vitamin — is especially important for people with HIV

Vitamin D & HIV/AIDS

http://www.thebody.com/index/dietnut/vitamin_d.html

See also: Vitamins, Minerals & Other Supplements: Main Page

  • Daily Dose of D (Winter 2012)
    Here in the “True North,” getting enough vitamin D — the sunshine vitamin — is especially important for people with HIV.
    To read PDF, click here.

http://img.thebody.com/catie/2012/ps_v14i1.pdf#page=13
In The Positive Side, from Canadian AIDS Treatment Information Exchange

 

 

 

ADOBE

Personal Computer Software License Agreement

1. WARRANTY DISCLAIMER, BINDING AGREEMENT AND ADDITIONAL TERMS AND AGREEMENTS.

1.1 WARRANTY DISCLAIMER. THE SOFTWARE AND OTHER INFORMATION IS DELIVERED TO YOU “AS IS” AND WITH ALL FAULTS. ADOBE, ITS SUPPLIERS AND CERTIFICATION AUTHORITIES DO NOT AND CANNOT WARRANT THE PERFORMANCE OR RESULTS YOU MAY OBTAIN BY USING THE SOFTWARE, CERTIFICATE AUTHORITY SERVICES OR OTHER THIRD PARTY OFFERINGS. EXCEPT TO THE EXTENT ANY WARRANTY, CONDITION, REPRESENTATION, OR TERM CANNOT OR MAY NOT BE EXCLUDED OR LIMITED BY LAW APPLICABLE TO YOU IN YOUR JURISDICTION, ADOBE AND ITS SUPPLIERS AND CERTIFICATION AUTHORITIES MAKE NO WARRANTIES CONDITIONS, REPRESENTATIONS, OR TERMS (EXPRESS OR IMPLIED WHETHER BY STATUTE, COMMON LAW, CUSTOM, USAGE OR OTHERWISE) AS TO ANY MATTER INCLUDING WITHOUT LIMITATION NONINFRINGEMENT OF THIRD PARTY RIGHTS, MERCHANTABILITY, INTEGRATION, SATISFACTORY QUALITY, OR FITNESS FOR ANY PARTICULAR PURPOSE. THE PROVISIONS OF SECTIONS 1.1 AND 10 SHALL SURVIVE THE TERMINATION OF THIS AGREEMENT, HOWSOEVER CAUSED, BUT THIS SHALL NOT IMPLY OR CREATE ANY CONTINUED RIGHT TO USE THE SOFTWARE AFTER TERMINATION OF THIS AGREEMENT.

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Use(Section 3);
Transferability(Section 5);
Connectivity and Privacy(Section 7), including:
Updating,
Local Storage
,
Settings Manager
,
Peer Assisted Networking Technology
,
Content Protection Technology
, and
Use of Adobe Online Services
;
Warranty Disclaimer
(Section 1.1), and;
Liability Limitations (Sections 10 and 17).

Upon acceptance, this agreement is enforceable against you and any entity that obtained the Software and on whose behalf it is used. If you do not agree, do not Use the Software.

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“Personal Computer” or “PC” shall mean a hardware product which is designed and marketed with the primary purpose of operating a wide variety of productivity, entertainment, and other software applications provided by unrelated third party software vendors, which operates depending upon the use of a full function and full feature set computer operating system of the type(s) then in widespread use with hardware to operate general purpose laptop, desktop, server, and large format tablet microprocessor based computers. This definition of Personal Computer shall exclude hardware products that are designed and/or marketed to have as their primary purpose any number of the following: television, television receiver, portable media player, audio/video receiver, radio, audio headphone, audio speaker, personal digital assistant (“PDA”), telephone or similar telephony based device, game console, personal video recorder (“PVR”), player for digital versatile disc (“DVD”) or other optical media, video camera, still camera, camcorder, video editing and format conversion device, video image projection device, and shall further exclude any similar type of consumer, professional or industrial device.

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“Use” means to access, install, download, copy, or otherwise benefit from using the functionality of the Software.

3. Software License.

If you obtained the Software from Adobe or one of its authorized licensees, and subject to your compliance with the terms of this agreement, including the restrictions in Section 4, Adobe grants to you a non-exclusive license to Use the Software in the manner and for the purposes described in the Documentation as follows:

3.1 General Use. You may install and Use one copy of the Software on your Compatible Computer. See Section 4 for important restrictions on the Use of the Software.

3.2 Server Use. This agreement does not permit you to install or Use the Software on a computer file server. For information on Use of Software on a computer file server please refer to http://www.adobe.com/go/acrobat_distribute for information about Adobe Reader; or http://www.adobe.com/go/licensing for information about the Adobe Runtimes.

3.3 Distribution. This license does not grant you the right to sublicense or distribute the Software. For information about obtaining the right to distribute the Software on tangible media or through an internal network or with your product or service please refer to http://www.adobe.com/go/acrobat_distribute for information about Adobe Reader; or http://www.adobe.com/go/licensing for information about the Adobe Runtimes.

3.4 Backup Copy. You may make one backup copy of the Software, provided your backup copy is not installed or used other than for archival purposes. You may not transfer the rights to a backup copy unless you transfer all rights in the Software as provided under Section 5.

4. Obligations and Restrictions.

4.1 Adobe Runtime Restrictions. You will not Use any Adobe Runtime on any non-PC device or with any embedded or device version of any operating system. For the avoidance of doubt, and by example only, you may not Use an Adobe Runtime on any (a) mobile device, set top box (STB), handheld, phone, game console, TV, DVD player, media center (other than with Windows XP Media Center Edition and its successors), electronic billboard or other digital signage, Internet appliance or other Internet-connected device, PDA, medical device, ATM, telematic device, gaming machine, home automation system, kiosk, remote control device, or any other consumer electronics device, (b) operator-based mobile, cable, satellite, or television system or (c) other closed system device. No right or license to Use any Adobe Runtime is granted for such prohibited uses. For information on Software license terms for non-PC versions of Adobe Runtimes please visit http://www.adobe.com/go/runtime_mobile_EULA. For information on licensing Adobe Runtimes for distribution on such systems please visit http://www.adobe.com/go/licensing.

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THIS SOFTWARE IS LICENSED UNDER THE AVC PATENT PORTFOLIO LICENSE FOR THE PERSONAL AND NON-COMMERCIAL USE OF A CONSUMER TO (I) ENCODE VIDEO IN COMPLIANCE WITH THE AVC STANDARD (“AVC VIDEO”) AND/OR (II) DECODE AVC VIDEO THAT WAS ENCODED BY A CONSUMER ENGAGED IN A PERSONAL AND NON-COMMERCIAL ACTIVITY AND/OR WAS OBTAINED FROM A VIDEO PROVIDER LICENSED TO PROVIDE AVC VIDEO. NO LICENSE IS GRANTED OR SHALL BE IMPLIED FOR ANY OTHER USE. ADDITIONAL INFORMATION MAY BE OBTAINED FROM MPEG LA, L.L.C. SEE http://www.adobe.com/go/mpegla.

4.2 Adobe Flash Player Restrictions. You will not use Adobe Flash Player with any application or device that circumvents technological measures for the protection of video, audio, and/or data content, including any of Adobe’s secure RTMP measures. No right or license to use Adobe Flash Player is granted for such prohibited uses.

4.3 Adobe Reader Restrictions.

4.3.1 Conversion Restrictions. You will not integrate or use Adobe Reader with any other software, plug-in or enhancement that uses or relies upon Adobe Reader when converting or transforming PDF files into a different format (e.g., a PDF file into a TIFF, JPEG, or SVG file).

4.3.2 Plug-in Restrictions. You will not integrate or use Adobe Reader with any plug-in software not developed in accordance with the Adobe Integration Key License Agreement, more information can be found at http://www.adobe.com/go/rikla_program.

4.3.3 Disabled Features. Adobe Reader may contain features or functionalities that are hidden or appear disabled or “grayed out” (the “Disabled Features”). Disabled Features will activate only when opening a PDF document that was created using enabling technology available only from Adobe. You will not access, or attempt to access, any Disabled Features other than through the use of such enabling technologies, nor will you rely on Adobe Reader to create a feature substantially similar to any Disabled Feature or otherwise circumvent the technology that controls activation of any such feature. For more information on disabled features, please refer to http://www.adobe.com/go/readerextensions.  

4.4 Notices. You shall not alter or remove any copyright or other proprietary notice that appears on or in the Software.

4.5 No Modification or Reverse Engineering. You shall not modify, adapt, translate, or create derivative works based upon the Software. You shall not reverse engineer, decompile, disassemble, or otherwise attempt to discover the source code of the Software. If you are located in the European Union, please refer to the additional terms at the end of this agreement under the header “European Union Provisions,” in Section 16.

5. Transfer.

You may not rent, lease, sublicense, assign, or transfer your rights in the Software, or authorize all or any portion of the Software to be copied onto another user’s Computer except as may be expressly permitted by this agreement. You may, however, transfer all your rights to Use the Software to another person or legal entity provided that: (a) you also transfer (i) this agreement, and (ii) the Software and all other software or hardware bundled or pre-installed with the Software, including all copies, Updates, and prior versions, to such person or entity, (b) you retain no copies, including backups and copies stored on a Computer, and (c) the receiving party accepts the terms and conditions of this agreement and any other terms and conditions upon which you obtained a valid license to the Software. Notwithstanding the foregoing, you may not transfer education, pre-release, or not for resale copies of the Software.

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The Software and any authorized copies that you make are the intellectual property of Adobe and its suppliers. The structure, organization, and code of the Software are the valuable intellectually property (e.g. trade secrets and confidential information) of Adobe and its suppliers. The Software is protected by law, including without limitation the copyright laws of the United States and other countries, and by international treaty provisions. Except as expressly stated herein, this agreement does not grant you any intellectual property rights in the Software and all rights not expressly granted are reserved by Adobe and its suppliers.

7. Connectivity and Privacy. You acknowledge and agree to the following:

7.1 Use of PDF Files. When you Use the Software to open a PDF file that has been enabled to display ads, your Computer may connect to a website operated by Adobe, an advertiser, or other third party. Your Internet Protocol address (“IP Address”) is sent when this happens. The party hosting the site may use technology to send (or “serve”) advertising or other electronic content that appears in or near the opened PDF file. The website operator may also use JavaScript, web beacons (also known as action tags or single-pixel gifs), and other technologies to increase and measure the effectiveness of advertisements and to personalize advertising content. Your communication with Adobe websites is governed by the Adobe Online Privacy Policy found at http://www.adobe.com/go/privacy (“Adobe Online Privacy Policy”). Adobe may not have access to or control over features that a third party may use, and the information practices of third party websites are not covered by the Adobe Online Privacy Policy.

7.2 Updating. If your Computer is connected to the Internet, the Software may, without additional notice, check for Updates that are available for automatic download and installation to your Computer and let Adobe know the Software is successfully installed. For Reader, Updates may be automatically downloaded but not installed without additional notice unless you change your preferences to accept automatic installation. Only non-personally identifying information is transmitted to Adobe when this happens, except to the extent that IP Addresses may be considered personally identifiable in some jurisdictions. The use of such information, including your IP Address, as provided by the auto update process is governed by the Adobe Online Privacy Policy. Please consult the Documentation for information about changing default update settings, or online at http://www.adobe.com/go/settingsmanager for Flash Player, http://www.adobe.com/go/update_details_url (or successor website) for Reader, and http://www.adobe.com/go/air_update_details and http://airdownload.adobe.com/air/applications/SettingsManager/SettingsManager.air for Adobe AIR.

7.3 Local Storage. Flash Player and Adobe AIR may allow third parties to store certain information on your Computer in a local data file known as a local shared object. The type and amount of information that the third party application requests to be stored in a local shared object can vary by application and such requests are solely controlled by the third party. You can find more information on local shared objects at http://www.adobe.com/go/flashplayer_security. For more information on how to limit or control the storage of local shared objects on your Computer, please visit http://www.adobe.com/go/settmgr_storage_en.

7.4 Settings Manager. Flash Player and Adobe AIR may cause certain user settings to be stored on your Computer as a local shared object. These settings are associated with the instance of Flash Player or Adobe AIR on your Computer, but do not contain personally identifiable information associated with you, and allow you to configure certain settings within the Flash Player including the ability to limit third parties from storing local shared objects. You can find more information on how to configure your version of Flash Player or Adobe AIR, including how to disable local shared objects in the Settings Manager for Flash Player, at http://www.adobe.com/go/settingsmanager, or http://airdownload.adobe.com/air/applications/SettingsManager/SettingsManager.air for Adobe AIR.

7.5 Peer Assisted Networking Technology. Adobe Flash Player and Adobe AIR runtimes provide the ability for applications built by third parties to connect to an Adobe Server or Service and permit direct communication between two Adobe Runtime clients or to connect an Adobe Runtime client as part of a peer or distributed network that allows a portion of your resources, such as network bandwidth, to be made directly available to other participants. Prior to joining such peer or distributed network, you will be provided with the opportunity to accept such connectivity. To manage Peer Assisted Networking settings, please go to the Settings Manager at http://www.adobe.com/go/settmgr_networking_en. You can find more information on Peer Assisted Networking at http://www.adobe.com/go/RTMFP.

7.6 Content Protection Technology. If you Use the Adobe Runtimes to access content that has been protected with Adobe Flash Media Rights Management Server or Flash Access software (“Content Protection”), in order to let you play the protected content, the Software may automatically request media usage rights and individualization rights from a rights server on the Internet, and may download and install required components of the Software, including any available Content Protection Updates. You can find more information on Content Protection at http://www.adobe.com/go/protected_content.

7.7 Use of Adobe Online Services. If your Computer is connected to the Internet, the Software may, without additional notice and on an intermittent or regular basis, facilitate your access to content and services that are hosted on websites maintained by Adobe or its affiliates (“Adobe Online Services”). Examples of such Adobe Online Services might include, but are not limited to: Acrobat.com. In some cases an Adobe Online Service might appear as a feature or extension within the Software even though it is hosted on a website. In some cases, access to an Adobe Online Service might require a separate subscription or other fee in order to access it, and/or your assent to additional terms of use. Adobe Online Services might not be available in all languages or to residents of all countries and Adobe may, at any time and for any reason, modify or discontinue the availability of any Adobe Online Service. Adobe also reserves the right to begin charging a fee for access to or use of an Adobe Online Service that was previously offered at no charge. If your Computer is connected to the Internet, the Software may, without additional notice, update downloadable materials from these Adobe Online Services so as to provide immediate availability of these Adobe Online Services even when you are offline. When the Software connects to the Internet as a function of an Adobe Online Service, your IP Address, user name, and password may be sent to Adobe’s servers and stored by Adobe in accordance with the Additional Terms of Use or the “help” menu in the Software. This information may be used by Adobe to send you transactional messages to facilitate the Adobe Online Service. Adobe may display in-product marketing to provide information about the Software and other Adobe products and Services, including but not limited to Adobe Online Services, based on certain Software specific features including but not limited to, the version of the Software, including without limitation, platform version, version of the Software, and language. For further information about in-product marketing, please see the “help” menu in the Software. Whenever the Software makes an Internet connection and communicates with an Adobe website, whether automatically or due to explicit user request, the Adobe Online Privacy Policy shall apply. Additionally, unless you are provided with separate terms of use at that time, the Adobe.com Terms of Use (http://www.adobe.com/go/terms) shall apply. Please note that the Adobe Privacy Policy allows tracking of website visits and it addresses in detail the topic of tracking and use of cookies, web beacons, and similar devices.

8. Third Party Offerings. You acknowledge and agree to the following:

8.1 Third Party Offerings. The Software may allow you to access and interoperate with third party content, software applications, and data services, including rich Internet applications (“Third Party Offerings”). Your access to and use of any Third Party Offering, including any goods, services, or information, is governed by the terms and conditions respecting such offerings and copyright laws of the United States and other countries. Third Party Offerings are not owned or provided by Adobe. You agree that you will not use any of such Third Party Offerings in violation of copyright laws of the United States or other countries.Adobe or the third party may at any time, for any reason, modify or discontinue the availability of any Third Party Offerings. Adobe does not control, endorse, or accept responsibility for Third Party Offerings. Any dealings between you and any third party in connection with a Third Party Offerings, including such party’s privacy policies and use of your personal information, delivery of and payment for goods and services, and any other terms, conditions, warranties, or representations associated with such dealings, are solely between you and such third party. Third Party Offerings might not be available in all languages or to residents of all countries and Adobe or the third party may, at any time and for any reason, modify or discontinue the availability of any Third Party Offerings. 

8.2 EXCEPT AS EXPRESSLY AGREED BY ADOBE OR ITS AFFILIATES OR A THIRD PARTY IN A SEPARATE AGREEMENT, YOUR USE OF ADOBE AND THIRD PARTY OFFERINGS IS AT YOUR OWN RISK UNDER THE WARRANTY AND LIABILITY LIMITATIONS OF SECTIONS 1.1 AND 10.

9. Digital Certificates. You acknowledge and agree to the following:

9.1 Use. Adobe AIR uses digital certificates to help you identify the publisher of Adobe AIR applications created by third parties. Additionally, Adobe AIR uses digital certificates to establish the identity of servers accessed via the Transport Layer Security (TLS) protocol, including access via HTTPS. Adobe Reader uses digital certificates to sign and validate signatures within PDF documents and to validate certified PDF documents. Adobe Runtimes use digital certificates to secure protected content from unauthorized usage. Your Computer may connect to the Internet at the time of validation of a digital certificate in order to download current certificate revocation lists (CRLs) or to update the list of digital certificates. This access may be made both by the Software and by applications based on the Software. Digital certificates are issued by third party certificate authorities, including Adobe Certified Document Services (CDS) vendors listed at http://www.adobe.com/go/partners_cds and Adobe Approved Trust List (AATL) vendors listed at http://www.adobe.com/go/aatl, and individualization vendors found at http://www.adobe.com/go/protected_content (collectively “Certification Authorities”), or can be self-signed.

9.2 Terms and Conditions. Purchase, use and reliance upon digital certificates are the responsibility of you and a Certification Authority. Before you rely upon any certified document, digital signature, or Certification Authority services, you should review the applicable terms and conditions under which the relevant Certification Authority provides services, including, for example, any subscriber agreements, relying party agreements, certificate policies, and practice statements. See the links on http://www.adobe.com/go/partners_cds for information about Adobe’s CDS vendors and http://www.adobe.com/go/aatl for information about Adobe’s AATL vendors.

9.3 Acknowledgement. You agree that (a) a digital certificate may have been revoked prior to the time of verification, making the digital signature or certificate appear valid when in fact it is not, (b) the security or integrity of a digital certificate may be compromised due to an act or omission by the signer of the document, the applicable Certification Authority, or any other third party, and (c) a certificate may be a self-signed certificate not provided by a Certification Authority. YOU ARE SOLELY RESPONSIBLE FOR DECIDING WHETHER OR NOT TO RELY ON A CERTIFICATE. UNLESS A SEPARATE WRITTEN WARRANTY IS PROVIDED TO YOU BY A CERTIFICATION AUTHORITY, YOU USE DIGITAL CERTIFICATES AT YOUR SOLE RISK.

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10. Limitation of Liability.

IN NO EVENT WILL ADOBE, ITS SUPPLIERS, OR CERTIFICATION AUTHORITIES BE LIABLE TO YOU FOR ANY DAMAGES, CLAIMS OR COSTS WHATSOEVER INCLUDING ANY CONSEQUENTIAL, INDIRECT, INCIDENTAL DAMAGES, OR ANY LOST PROFITS OR LOST SAVINGS, EVEN IF AN ADOBE REPRESENTATIVE HAS BEEN ADVISED OF THE POSSIBILITY OF SUCH LOSS, DAMAGES, OR CLAIMS. THE FOREGOING LIMITATIONS AND EXCLUSIONS APPLY TO THE EXTENT PERMITTED BY APPLICABLE LAW IN YOUR JURISDICTION. ADOBE’S AGGREGATE LIABILITY AND THAT OF ITS SUPPLIERS AND CERTIFICATION AUTHORITIES UNDER OR IN CONNECTION WITH THIS AGREEMENT SHALL BE LIMITED TO THE AMOUNT PAID FOR THE SOFTWARE, IF ANY. Nothing contained in this agreement limits Adobe’s liability to you in the event of death or personal injury resulting from Adobe’s negligence or for the tort of deceit (fraud). Adobe is acting on behalf of its suppliers and Certification Authorities for the purpose of disclaiming, excluding, and/or limiting obligations, warranties, and liability as provided in this agreement, but in no other respects and for no other purpose. For further information, please see the jurisdiction specific information at the end of this agreement, if any, or contact Adobe’s Customer Support Department.

11. Export Rules.

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12. Governing Law.

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PlatformClients_PC_WWEULA-en_US-20100625_1419

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Vida é o maior bem e a Constituição brasileira a protege do arbítrio da estrutura política

 

Vida é o maior bem e a Constituição brasileira a protege

 

Por Cristiane Rozicki

 

Filósofos políticos analisam a sociedade segundo a ética do discurso e do agir comunicativo, dando ‘as relações entre os homens um novo ‘centro’ no pensamento humano, identificando uma nova radicalidade social. É através de toda ação comunicativa – a começar pela fala, que os seres humanos concebem a sociedade, constroem consensos e mantêm a sociedade sob permanente controle através dos mecanismos de gerenciamento, decisão e poder, usando a mídia, a moda – nas palavras e na aparencia – e o discurso da autoridade política nos meios de comunicação.

 

Porem, ainda, é preciso notar que essa ‘comunicabilidade’ garante o poder de força e coerção hoje, poder de controle e decisão, que          tem sido desenvolvido pelo absoluto uso da ilegalidade, na atuação estatal administrativa e executiva sem consideração ‘as leis, na criação de projetos de leis, manutenção de ambiente carente de informação verdadeira e atualizada, e na falta de permanente apresentação das contas públicas ‘a população. Estas são caraterísticas de um Estado politico não democrático e arbitrário.

    

Ocorre que as grandes maiorias da humanidade excluidas por essa radicalidade da nova ‘ética’ são as minorias silenciadas a quem se nega o direito de fala e de expressão, embora o conhecimento cientifico demonstre e prove a existencia da vida humana nestas condições vulneraveis – por exemplo, embriões, deficientes, anencefalos e pessoas em estado coma mesmo o severo. Isto está acontecendo no Brasil, não obstante exista Lei a garantir a vida para todos igualmente.

 

Vida é o maior bem e a Constituição brasileira a protege. A vida do homem é valor supremo que não pode ser relativizado. Vida é bem indisponivel. Esta é a inteligência imperante em todo o mundo civilizado e é o superior motivo que deve orientar o comportamento humano.A vida é valor transindividual e universal.

Oexame do espírito humano fica evidente, a partir do momento em que se observa o sentido e o alcance das atividades humanas. O sentido da vida humana reside na realizaçao dos valores. Este é o aspecto prático dos valores, que aponta sua relação direta com a vida na realidade, o que acusará a disposição que move o homem à prática de certas ações. Ou, como elucida Aristóteles, tornará evidente a disposição da alma.

 
Assim, pode-se definir VALOR como um “quid”, diz Hessen. O “quid” é um o que que satisfaz certa necessidade humana. Mas a valoração não parte apenas desse “quid”. Isso porque ainda há valores éticos, estéticos e religiosos, além dos vitais, fala-se de valores interiores e individuais. Estes são descobertos com as necessidades espirituais, morais, diferentes das necessidades vitais. Asseguram a vitalidade aquelas necessidades que são externas ao ser humano, tais como as biológicas, e das quais depende a possibilidade material de existência.

 

Daí que se diz, simplesmente, que os valores produzem determinados efeitos. O efeito é a satisfação das necessidades ou interesses.

 

O grupo das ciências dos seres pertence a das ciências naturais, que tem um ponto de vista inteiramente estranho a valores, enfatiza Hessen. Por sua vez, as ciências dos valores têm por função, precisamente, tomar posição e valorar, por exemplo, a Ética.

  

A partir da determinação de valores que se consegue extrair normas para a ação prática. Estas normas visam as ações humanas.

 

 Para que se possa ter a percepção consciente dos valores é preciso que os mesmos sejam identificados por todos e que valham para todos, para todas pessoas (POR ISSO QUE O SUBJETIVISMO INDIVIDUALISTA É ERRÔNEO, POSTO QUE SE DEVE PENSAR EM VALORES SUBJETIVOS GERAIS, QUE VALEM PARA TODOS). Estes valores reconhecidos e identificados por todas pessoas são transindividuais, superiores aos valores puramente sensíveis, são transubjetivos pertencentes a um reino de validade intemporal e dirigem o seu incondicional apelo a todos os homens, POR SEREM SIMPLESMENTE HOMENS, TENDO VALIDADE ABSOLUTA [HESSEN, 1980, 90-103].

 

Vida é o maior bem e a Constituição brasileira a protege. A categoria bem jurídico, neste texto, considerando idéias de bens e valores eleitos por uma comunidade politicamente organizada, como é o Estado Democrático de Direito brasileiro previsto na Constituição da República, compreende os interesses legítimos de cada indivíduo e de toda sociedade, firmados no reconhecimento fundamental de direitos e garantias previstos na Lei Maior. Os bens jurídicos têm assentamento expresso na Constituição. Isto quer dizer que esta mesma Lei apresenta os valores fundamentais da sociedade, e é destes que deriva o conceito de bem jurídico.

 

A vida do homem é valor supremo que não pode ser relativizado. Vida é bem indisponivel. Esta é a inteligência imperante em todo o mundo civilizado e é o superior motivo que deve orientar o comportamento humano.A vida é valor transindividual e adignidade da vida humana é interessetranscendental ao homem. Pois que a dignidade está intrínseca à existência do próprio homem, intrínseca ‘a sua vida. E isto é assim mesmo independentemente e acima das variações históricas de outros valores e interesses.


Assim, a vida é Direito inviolsavel na Constituição brasileira, direito fundamental, garantido desde o caput do 5º artigo.

Todos são iguais perante a lei, sem distinção de qualquer natureza, garantindo-se aos brasileiros e as estrangeiros residentes no pais a inviolabilidade do direito à vida, à liberdade, á igualdade, à segurança e à propriedade(…)” – art. 5º da CF/88.

 

Obvio que nada, nenhum valor ou interesse alheio ao valor supremo vida, pode conferir aos homens, sejam legisladores sejam juízes ou ministros, a liberdade de dispor da vida de outrem.

 

Vida é o maior bem jurídico que se pode ter. O bem jurídico é um valor. Em outras palavras, bem jurídico é todo valor da vida humana protegido pelo Direito. Vida é o maior bem. Vida é valor superior e, portanto, como decorrência de várias razões que estão indicadas na Constituição da República Federativa do Brasil de 1988 (CRFB/88), é oferecida garantia ao direito de viver.

A Convenção Americana sobre Direitos Humanos, Pacto de San José da Costa Rica[1], foi adotada e aberta à assinatura na Conferência Especializada Interamericana sobre Direitos Humanos, em San José de Costa Rica, em 22 de novembro de 1969. O Pacto reconheceu “que os direitos essenciais do homem não derivam do fato de ser ele nacional de determinado Estado, mas sim do fato de ter como fundamento os atributos da PESSOA HUMANA […]” preâmbulo. Ratificada pelo Brasil em 25 de setembro de 1992.

 

A validade das Convenções internacionais no âmbito territorial brasileiro é tema tratado na Carta de 1988, que indubitavelmente reconheceu de forma inédita a validade normativa constitucional dos Tratados e Convenções internacionais sobre direitos humanos ratificados, com os termos da disposição do § 2º de seu 5º artigo.

  

No caso do Direito Constitucional brasileiro, em virtude de as normas de composição da Lei Maior acolherem preceitos universais sobre direitos humanos como ordem capital de existência do Estado, a Constituição reconhece e protege direitos previstos no âmbito internacional, NORMAS QUE PASSAM A TER FORMA CONSTITUCIONAL TAIS COMO DIREITOS FUNDAMENTAIS.

 

 

Ratificada pelo Brasil em 25 de setembro de 1992, A Convenção Americana sobre Direitos Humanos, Pacto de San José protege a vida no Artigo 4º – “Direito à vida. 1. Toda pessoa tem direito de que se respeite sua vida. Esse direito deve ser protegido pela lei e, em geral, desde o momento da CONCEPÇÃO. Ninguém pode ser privado da vida arbitrariamente.”

 

São José, Serraria, 25 de maio de 2012.

Cristiane Rozicki

HESSEN, Johannes. Filosofia dos valores. Trad. por L. Cabral de Moncada. 5a ed. Colecção Stvdivm. Coimbra: Armênio Amado, 1980.

A Convenção Americana sobre Direitos Humanos, Pacto de San José
http://www.dhnet.org.br/direitos/sip/oea/oeasjose.htm

Ministro de Justiça reconhece e defende o direito de viver dos embriões.

 

Ministro de Justiça reconhece e defende o direito de viver dos embriões.  

Ministro Alberto Ruiz-Gallardón diz aos Deputados na Espanha “o mais progresista que tenho feito é defender o direito aa vida” e “muitas mulheres vêm violentado seu Direito ‘a ser mãe por Pressoes que     determinadas estruturas geram ao seu redor.”   

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Felicita al ministro de Justicia por defender el derecho a vivir

 

A Alberto Ruiz-Gallardón los abortistas le están llamando de todo por haber defendido en sede parlamentaria que el aborto no es un derecho y que el embrión también tiene derechos.

REDACCIÓN HO.- Los abortistas políticos y mediáticos están histéricos desde que el ministro de Justicia, Alberto Ruiz-Gallardón, dijera en el Congreso de los Diputados y a través de algunos medios que “lo más progresista que he hecho en mi vida política es defender el derecho a la vida” y que “muchas mujeres ven violentado su derecho a ser madres por la presión que genera a su alrededor determinadas estructuras“.

Los partidos políticos abortistas le llaman “retrógrado”, le acusan de querer encarcelar a las mujeres y dicen de él que quiere suspender sus derechos. Hasta los etarras de Amaiur han tenido la desfachatez de hablar de violencia, acusándole de “desconocer la violencia de género”.

¿Cuál ha sido el “delito” de Ruiz-Gallardón? El ministro de Justicia no ha hecho más que decir en el Congreso de los Diputados lo que tantos llevamos años proclamando: que la vida es un derecho y el aborto no, que la maternidad debe ser protegida y el extermino de seres humanos no.

Derecho a Vivir, que ultima los detalles del lanzamiento de la campaña Aborto Cero, quiere felicitar al ministro de Justicia y animarle a convertir sus declaraciones en ley.

La plataforma en defensa de la vida de HazteOir.org señala que seguirá vigilante los próximos pasos del Gobierno en relación con el aborto y llevará su movilización hasta donde sea necesario para conseguir en España el objetivo final de Aborto Cero.

Pero DAV quiere también celebrar los triunfos que va consiguiendo en ese camino y por ello anima a la ciudadanía a felicitar a Alberto Ruiz-Gallardón por sus declaraciones y por el compromiso que ha adquirido ante la sede de la soberanía nacional.

http://www.hazteoir.org/alerta/44701-felicita-ministro-justicia-defender-derecho-vivir

‘No nos resignamos’: Los ciudadanos europeos, en pie por la cultura de la vida

Enquanto a Europa luta pelo fim do aborto livre e sem restriçoes em lei, sem pena criminal, o Brasil suporta o governo Lula-PT-Dilma investir na ilegalidade para transformar o país em fornecedor de matéria-prima humana fresca, congelada e usada nas farmacias e alimentos.

‘No nos resignamos’: Los ciudadanos europeos, en pie por la cultura de la vida

 

La  European Meeting for Life, imagen de la unión de los europeos en defensa de la Vida, ha sido presentada en la Eurocámara por Mayor Oreja. Histórica sesión en la que tuvimos voz como destacado movimiento cívico provida, y que marca hitos para una cultura de la vida en Europa, comenzando con una ILP en defensa del primer derecho humano.

REDACCIÓN HO.- El vicepresidente del Grupo Popular Europeo y eurodiputado del PP Jaime Mayor Oreja presentaba en la tarde de ayer jueves en el Parlamento Europeo la iniciativa ciudadana europea ‘No nos resignamos. En defensa de los no nacidos’, para comenzar a recoger firmas de ciudadanos europeos en contra del aborto y a favor del derecho a la vida en la UE.  La iniciativa se presentó dentro de una reunión también histórica en Bruselas, la ‘European Meeting for Life.’ Mayor Oreja destacaba hoy, precisamente el carácter inédito de la reunión, entrevistado en Así son las Mañanas de la COPE:  

“Lo que tenemos, ya por lo pronto, es una reunión inédita, jamás celebrada en la historia de la Eurocámara, en la cual, durante unas tres horas, los colectivos en defensa de la vida más representativos de toda Europa, una treintena, han hecho una radiografía de lo que sucede, nos han ofrecido un brillante diagnóstico conjunto de la situación analizando lo que ocurre en los distintos países, y con esa misma unidad han propuesto soluciones conjuntas para trabajar, todos juntos, en una nueva cultura de la vida. Se marca un camino unitario en este sentido.  Dentro de ello, se trabajará  en una Iniciativa Legislativa Popular para recoger más de un millón de firmas ciudadanas, en lo que nos emplearemos a fondo, sobre todo por parte del comité organizador que vamos a crear”.

Carlota Ruiz de Dulanto, en la sesiónReconociendo su labor y carácter representativo, HO y Derecho a Vivir formaron parte de esa treintena de asociaciones en defensa del derecho a vivir invitadas que tuvieron voz en Europa.  En Bruselas estuvimos representados por Carlota Ruiz de Dulanto, que tomó voz ante los europarlamentarios en nombre de DAV para defender que la única tasa de aborto admisible para una Europa moderna, que piensa en el futuro es el “Aborto Cero“, concepto que da nombre a la última campaña de divulgación y opinión pública impulsada por Derecho a Vivir. Proporcionamos el texto de la intervención íntegra de Carlota en Bruselas (en inglés), así como una breve biografía (en inglés) y la presentación visual con que acompañó sus palabras.

DAV y VI WCF: defendemos los valoresRuiz de Dulanto aprovechó también para hacer extensiva a todos los presentes la invitación a participar en el VI Congreso Mundial de Familias, que  este año HO tiene el honor de organizar (Madrid, 25-27 de mayo), que atraerá a casi 3000 personas, y reunirá a los más importantes líderes mundiales provida y profamilia.

La sesión reflejó un diagnóstico común, todos los movimientos cívicos de los distintos países compartimos la misma inquietud: la cultura de la muerte  no puede seguir avanzando,  ¡No nos podemos rendir !  La iniciativa de este encuentro se erige como el principio del final de esta mentalidad homicida que se ha instalado en nuestra civilización.

Jaime Mayor Oreja, con CarlotaLas líneas de acción básicas definidas al final de esta sesión de casi cinco horas han sido las siguientes: 

 1) Promover, de acuerdo con el Tratado de Lisboa y  la Carta Europea de los Derechos Fundamentales, una Iniciativa Legislativa Popular (ILP) contra la financiación directa o indirecta  de cualquier tipo de cultura de la muerte en Europa. El nuevo Tratado de Lisboa autoriza a los ciudadanos de la UE a reclamar a la Comisión Europea que presente propuestas legislativas de su interés si reúnen un millón de firmas de ciudadanos de varios Estados miembros. Las iniciativas ciudadanas europeas, que deben limitarse a los ámbitos en los que la Comisión está facultada para proponer legislación como la agricultura, el medio ambiente, los transportes o la salud pública, podrán comenzar a presentarse desde este 1 de abril, cuando entra en vigor la normativa que las desarrolla.

Si la iniciativa ciudadana europea pidiera abiertamente promover la prohibición del aborto en la UE tiene pocos visos de prosperar, dado que la Comisión Europea no tiene competencias para legislar sobre esta cuestión, según han reconocido fuentes del Ejecutivo comunitario: “Hay Estados miembros que lo autorizan, hay Estados miembros que no lo autorizan. Esto es una competencia nacional”.

2) Institucionalizar el ‘European Meeting for Life ‘ con al menos una celebración anual, en Bruselas , donde las asociaciones provida podamos dar el diagnóstico de cada uno de nuestros países .

3) Reforzar el ‘networking’ entre todas las instituciones provida de Europa y compartir y trasladar nuestras iniciativas al propio Mayor Oreja, que se compromete a enviar un diputado parlamentario, como representante de la institución, a cada evento provida que se promueva en Europa.

4) Fomentar la unidad: Sumar esfuerzos, crear un eslogan común, evidenciarnos como una corriente unida y fuerte que lucha contra una sociedad acomodada que se está dejando destruir por la violación de los derechos fundamentales.

Mayor y eurodiputadosMayor Oreja asume el liderazgo del apoyo europarlamentario a esta iniciativa cívicajunto al eurodiputado italiano ‘popular’  Carlo Casini, que también es presidente de la Comisión de Asuntos Constitucionales de la Eurocámara; ambos promovieron la histórica sesión de ayer jueves, invitando a más de 30 organizaciones y asociaciones de defensa de la familia y la vida de Austria, Bélgica, República Checa, Dinamarca, Alemania, Estonia, Francia, Hungría, Irlanda, Italia, Lituania, Malta, Polonia, Portugal, Rumanía, Eslovaquia, Reino Unido, Suecia, Países Bajos, Rumanía y España, incluidos HO y Derecho a Vivir, el Instituto de Política Familiar, Crossroads, Foro español o la Fundación Madrina, con el objetivo de comenzar a recabar apoyos y firmas para su iniciativa.

La iniciativa ya ha recabado además el respaldo de otros eurodiputados, incluidos el también vicepresidente polaco del Grupo Popular Europeo, Jan Olbrycht, el italiano Mario Mauro, así como los eurodiputados eslovacos Miroslav Mikolasik y Anna Zaborska; el húngaro Laszlo Surjan, el esloveno Alojz Peterle; los alemanes Martin Kasler, Peter Liese y Bernd Posselt, el tory británico Nirj Deva y el polaco Konrad Szymanski.

Adjunto Tamaño
Adjunto Tamaño
Biographie Ruiz de Dulanto.doc 27 KB
20120329 DAV European Parliamen meeting v3.ppt 4.61 MB
28mar12_Discurso Carlota English_Eucamara_Bruselas.doc 1.17 MB

Etiquetas:

http://www.hazteoir.org/alerta/45048-no-nos-resignamos-ciudadanos-europeos-en-pie-cultura-vida—-

El aborto genera en España un negocio de 100 millones€ en diez años

O aborto na España gera um negócio de 100 milhões de Euros em dez anos de milhões de mortes. A interrupção voluntaria da gravidez, o aborto, chega a 70 e 90 por cento das gestantes.

El aborto genera en España un negocio de 100 millones€ en diez años

En Andalucía, la tercera comunidad de España con mayor número de abortos, unos 20 mil cada año, crece más rápidamente que a nivel nacional.

REDACCIÓN HO / ABC.ES.-  Las estadísticas que hace públicas cada año el Servicio Andaluz de Salud (SAS) sobre el aborto son siempre conocidas. Las cifras apenas cambian y cada año se practican en la comunidad autónoma unos veinte mil abortos, una cantidad que apenas oscila. Ni las políticas de prevención de embarazos ni tampoco la píldora del día después -como señalaban los defensores de su liberalización, que además tratan de negar sus efectos abortivos-, han provocado una disminución de abortos quirúgicos.

Sin embargo hay otros datos menos conocidos, como los del negocio que se mueve alrededor de las mal llamadas Interrupciones Voluntarias del Embarazo (IVE). Según un informe realizado por un grupo de profesores católicos de la Universidad de Córdoba, del que informa el diario ABC, en el periodo comprendido entre 1999 y 2008 el aborto ha supuesto en Andalucía un negocio que ha facturado entre 82.294.104 y 102.832.832 euros. Además, los profesores consideran que, en términos absolutos, los ingresos estimados para el último año del que tienen datos, 2008, oscilaría entre 9.323.211 y 13.041.550 euros.

En el estudio, que ha tenido en cuenta los precios de licitación pública de estas intervenciones, la estimación de gastos asociados (desplazamientos y manutención de los pacientes y acompañantes) así como otros informes, los investigadores han fijado una horquilla de precios que oscila entre 350 y 450 euros. Concretamente, los investigadores sitúan el precio de un aborto de hasta 12 semanas de gestación en esas cantidades aunque aseguran que hay algunas comunidades donde es más caro y esta intervención puede costar hasta 600 euros.

Claro que los precios suben a medida que aumentan las semanas de gestación, dada la complejidad de la operación. En este sentido, cuando el embarazo pasa de las 12 semanas, el precio del aborto puede estar entre 1.500 y 2.500 euros. De igual manera, en otras comunidades españolas estas intervenciones pueden alcanzar los 3.000 euros.

En cualquier caso el aborto en Andalucía representa en torno al 18 por ciento del total nacional. La tasa anual acumulativa de crecimiento para España se sitúa en el 7,9 por ciento, por debajo de la tasa de crecimiento para Andalucía, estimada en el 9,18 por ciento. Eso supone que el aborto en Andalucía crece más rápidamente que a nivel nacional, consecuencia posiblemente de las facilidades otorgadas por la administración pública a las mujeres para que encuentren en el aborto la salida a su embarazo no deseado o en situación de dificultad.

En relación con otras comunidades autónomas, Andalucía se encuentra situada en el top del aborto en España. A nivel nacional se encuentra en el quinto lugar (con un 0,25 de abortos sobre la población total) por detrás de Murcia (0,38), Madrid (0,35), Cataluña (0,34) y Baleares (0,32). Considerando el peso relativo de los abortos perpetrados en cada comunidad sobre el total de abortos en todo el país, se extrae la conclusión de que Andalucía es la tercera de España en número de abortos.

Algo que lógicamente tiene sus consecuencias económicas, lo que lleva a los profesores a afirmar que «una parte significativa del negocio del aborto se concentra en Andalucía».

Los expertos también han valorado el hecho de que Andalucía es la única comunidad autónoma que reconoce la prestación del aborto dentro de su sistema sanitario y garantiza el acceso a la misma a través del concierto con las clínicas acreditadas ante la mayoritaria objeción de losprofesionales de la sanidad pública. Además, Andalucía es la tercera región española con mayor peso económico en el negocio del aborto en España.

 

Casi la mitad en Sevilla y Málaga

Las cifras también revelan que casi la mitad de los abortos en Andalucía en el periodo entre 1999 y 2008, el 45 por ciento y hasta el 48 por ciento en 2008, se realizaron a mujeres residentes en Sevilla y Málaga. Son las provincias que, junto a Granada y Almería, concentran más del 70 por ciento de las interrupciones voluntarias del embarazo.

Llama la atención la escasa incidencia en la provincia de Jaén, que escasamente alcanza el 4 por ciento el año 2008. Además también es digno de destacar que la mayoría de los abortos, el 91 por ciento, se produce antes de las doce primeras semanas de vida, mientras que el 9 por ciento aproximadamente corresponde a abortos practicados a partir de la primera semana. Este dato tiene repercusiones evidentes, dada la diferencia en el tipo de asistencia para cada caso. Entre los centros acreditados concertados son dos en Sevilla los que realizan estas intervenciones a mujeres de más de doce semanas.

http://www.hazteoir.org/noticia/45551-aborto-genera-en-espana-negocio-100-millones%E2%82%AC-en-diez-anos

Health Benefits of Omega 3 fatty acids

 

Health Benefits of Omega 3 fatty acids

Os benefícios do ômega 3

 

Health Benefits of Omega 3 fatty acids

Written by Gloria Tsang, RD
Published in Jul 2005; Updated in Mar 2010

(HealthCastle.com) What are omega 3 fatty acids? They’re a nutritional element that first caught researchers’ attention about 20 years ago – and what they discovered could have health benefits for anyone worried about a healthy heart.

In the early 1980s, studies showed that the Inuit had low rates of heart disease despite their high-fat diet rich in fish. It turns out the omega 3 fatty acids in the fish may be what protects their hearts, along with other health benefits.

Benefits of Omega 3 Fatty Acids in Heart Disease and Cholesterol

Omega 3 fatty acids are poly-unsaturated fatty acids. Studies show that a diet rich in omega 3 fatty acids may help lower triglycerides and increase HDL cholesterol (the good cholesterol). Omega 3 fatty acids may also act as an anticoagulant to prevent blood from clotting. Several other studies also suggest that these fatty acids may help lower high blood pressure.

Potential Benefits of Omega 3 Fatty Acids in Alzheimer’s

Omega 3 fatty acids may protect against the accumulation in the body of a protein believed to be linked to Alzheimer’s disease, according to the results of a new animal study published in the March 2005 issue of The Journal of Neuroscience. This study specifically investigated one particular kind of omega 3 fatty acids – Docosahexaenoic acid (DHA), and the results are encouraging.

Health Benefits of Omega 3 fatty acids

Written by Gloria Tsang, RD
Published in Jul 2005; Updated in Mar 2010

(HealthCastle.com) What are omega 3 fatty acids? They’re a nutritional element that first caught researchers’ attention about 20 years ago – and what they discovered could have health benefits for anyone worried about a healthy heart.

In the early 1980s, studies showed that the Inuit had low rates of heart disease despite their high-fat diet rich in fish. It turns out the omega 3 fatty acids in the fish may be what protects their hearts, along with other health benefits.

Benefits of Omega 3 Fatty Acids in Heart Disease and Cholesterol

Omega 3 fatty acids are poly-unsaturated fatty acids. Studies show that a diet rich in omega 3 fatty acids may help lower triglycerides and increase HDL cholesterol (the good cholesterol). Omega 3 fatty acids may also act as an anticoagulant to prevent blood from clotting. Several other studies also suggest that these fatty acids may help lower high blood pressure.

Potential Benefits of Omega 3 Fatty Acids in Alzheimer’s

Omega 3 fatty acids may protect against the accumulation in the body of a protein believed to be linked to Alzheimer’s disease, according to the results of a new animal study published in the March 2005 issue of The Journal of Neuroscience. This study specifically investigated one particular kind of omega 3 fatty acids – Docosahexaenoic acid (DHA), and the results are encouraging.

Omega 3: Fish or Plant?

With the increasing popularity of vegetarian diets and mounting fears about mercury and PCBs in seafood, people often ask about using flax oil (which contains alpha-linolenic acids – or ALA) instead of fish oil.

Our bodies can convert ALA into eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – the beneficial elements of omega 3 – but the conversion process is slow. In addition, a high concentration of ALA (as present in flax oil pills) has been linked to higher risk of prostate cancer by some early research. Until more is known, men may be safest to choose fish oil for heart-healthy omega 3s instead of concentrated ALA.

http://www.healthcastle.com/omega3.shtml

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Ômega-3 é uma gordura essencial para o ser humano, diz nutricionista

Ômega-3 é uma gordura essencial para o ser humano, diz nutricionista

globo.com

 

10/09/2011 07h00 – Atualizado em 10/09/2011 07h00

Karin Honorato mostra benefícios e apresenta alimentos ricos na substância.
Segundo ela, consumo adequado ajuda a evitar doenças inflamatórias.

Do G1 MG

                                

A nutricionista Karin Honorato fala neste sábado (10) sobre o ômega-3 – um tipo de gordura. Ela apresenta os benefícios dessa substância. Segundo a nutricionista, o ômega-3 é uma exceção entre as gorduras. “É uma gordura tão importante para o organismo que é conhecida como gordura essencial, que nós não podemos viver sem ela e que o corpo não produz. Ou seja, nós precisamos consumi-la via alimentos”, diz.

Karin ressalta a importância do consumo diário de ômega-3 para gestantes. Pois, segundo ela, essa substância contribui na formação do bebê. Durante o período de amamentação, a nutricionista recomenda que a mãe continue consumindo alimentos ricos em ômega-3. Por meio do leite, o bebê vai absorver essa substância.

Com relação aos idosos, Karin afirma que o consumo de ômega-3 deve ser ainda maior. “Com o passar do tempo, os idosos vão perdendo os benefícios do organismo de produzir enzimas”, explica.

De acordo com a nutricionista, o consumo adequado dessa substância ajuda a evitar doenças inflamatórias, como doenças cardiovasculares, diabetes, atrites reumatóides e câncer. Segundo ela, “nas doenças cardiovasculares, por exemplo, o ômega-3 é excelente para diminuir o índice de triglicérides e até para evitar a agregação plaquetária, ou seja, aqueles coágulos que se formam nas artérias”.

Karin ressalta também a importância do consumo de alimentos ricos em ômega-3 para pessoas que sofrem de osteoporose, “doença onde a absorção de cálcio é pequena”. Segundo ela, o ômega-3 auxilia na absorção do cálcio pelo organismo. No caso da artrite reumatóide, ela explica que o ômega-3 favorece na redução do uso de anti-inflamatórios, “porque ele já é um anti-inflamatório natural”.

O ômega-3 também traz benefícios ao cérebro, de acordo com Karin. “Ajuda a diminuir o risco de doenças degenerativas – como alzheimer e parkinson – favorecendo a memória, a parte cognitiva e até a depressão”, explica. Ainda segundo ela, o ômega-3 melhora o humor, a ansiedade e também estimula o prazer.

Alimentos ricos em ômega-3
O primeiro alimento que a nutricionista destaca é o peixe de águas salgadas e profundas. Segundo Karin, o salmão, a sardinha e o atum possuem grande concentração da substância. “O número um em ômega-3 é o salmão. Que a pessoa deve consumir no máximo duas vezes por semana”. Sobre peixes enlatados, ela recomenda que a pessoa evite consumir o molho da conserva.

A segunda fonte mais importante de ômega-3 é a semente de linhaça, de acordo com a nutricionista. Karin cita ainda a semente de chia como outro alimento rico em ômega-3.
O óleo de canola também é citado pela nutricionista. Mas ela pede cautela no consumo, pois, esse óleo também possui ômega-6, que se consumido em excesso ajuda a aumentar o risco de doenças inflamatórias.

As nozes também são destacadas pela nutricionista. Ela ainda cita algumas verduras escuras e o azeite, que possuem pequenas doses de ômega-3. Para concluir Karin apresenta como alternativa as cápsulas de ômega-3, nesse caso, segundo ela, o consumo deve ser acompanhado por um nutricionista.

http://g1.globo.com/minas-gerais/noticia/2011/09/omega-3-e-uma-gordura-essencial-para-o-ser-humano-diz-nutricionista.html

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Vitamin D and the immune system: new perspectives on an old theme

Vitamin D and the immune system: new perspectives on an old theme

Martin Hewison, PhD

PUBMED CENTRAL Journal List – NIH Public Access – Autor Manuscript

———-

Journal List > NIHPA Author Manuscripts

Endocrinol Metab Clin North Am. Author manuscript; available in PMC 2011 June 1.

Published in final edited form as:
Endocrinol Metab Clin North Am. 2010 June; 39(2): 365–379.
doi:  10.1016/j.ecl.2010.02.010
PMCID: PMC2879394
NIHMSID: NIHMS180153
Copyright notice and Disclaimer

Vitamin D and the immune system: new perspectives on an old theme

Martin Hewison, PhD

Martin Hewison, Professor in Residence, Department of Orthopaedic Surgery and Molecular Biology Institute, David Geffen School of Medicine at UCLA, 615 Charles E. Young Drive South, Los Angeles, CA 90095, USA;
Corresponding author for proof and reprints: Martin Hewison, PhD, Department of Orthopaedic Surgery, David Geffen School of Medicine UCLA, 615 Charles E. Young Drive South, Los Angeles, CA 90095, USA, Tel: 310 206 1625, Fax: 310 825 5409, Email: mhewison@mednet.ucla.edu
The publisher’s final edited version of this article is available at Endocrinol Metab Clin North Am
See other articles in PMC that cite the published article.
Publisher’s Disclaimer
•  Other Sections▼
o Synopsis
o Introduction
o Vitamin D and innate immunity
o Vitamin D and adaptive immunity
o Vitamin D,  the immune system and human health
o Conclusions
o References

Synopsis
Interaction with the immune system is one of the most well-established non-classical effects of vitamin D. For many years this was considered to be a manifestation of granulomatous diseases such sarcoidosis, where synthesis of active 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is known to be dysregulated. However, recent reports have supported a role for 1,25(OH)2D3 in mediating normal function of both the innate and adaptive immune systems. Crucially, these effects appear to be mediated via localized autocrine or paracrine synthesis of 1,25(OH)2D3 from precursor 25-hydroxyvitamin D3 (25OHD3), the main circulating metabolite of vitamin D. As such, the ability of vitamin D to influence normal human immunity will be highly dependent on the vitamin D status of individuals, and may lead to aberrant response to infection or autoimmunity in those who are vitamin D-insufficient. The potential health significance of this has been underlined by increasing awareness of impaired vitamin D status in populations across the globe. The following review article will describe in more detail some of the recent developments with respect to vitamin D and the immune system, together with possible clinical implications.
Keywords: vitamin D, CYP27b1, toll-like receptor, macrophage, cathelicidin, regulatory T-cells
o Vitamin D,  the immune system and human health

Introduction
Historical perspective
Non-classical actions of vitamin D were first recognized thirty years ago when receptors for active 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) were detected in various neoplastic cells lines 23,59. Other studies immediately following this showed that binding of 1,25(OH)2D3 to the vitamin D receptor (VDR) promoted antiproliferative and prodifferentiation responses in cancer cells 1,18, highlighting an entirely new facet of vitamin D action. The spectrum of non-classical responses to vitamin D was then extended to include actions on cells from the immune system 2,13. This interaction was further endorsed by the observation that some patients with the granulomatous disease sarcoidosis present with elevated circulating levels of 1,25(OH)2D3 and associated hypercalcemia 11,72. In these patients the high serum 1,25(OH)2D3 is due to increased activity of the enzyme 25-hydroxyvitamin D-1α-hydrooxylase (1α-hydroxylase). However, in contrast to normal subjects where 1α-hydroxylase is classically localized in the kidney, the increased synthesis of 1,25(OH)2D3 in patients with sarcoidosis involves 1α-hydroxylase activity in disease-associated macrophages 4,6,9. Thus, it was concluded that the immune system had the potential to both synthesize 1,25(OH)2D3 and elicit autocrine or paracrine responses from immune cells expressing the vitamin D receptor 38.
Despite these early advances, the precise nature of the interaction between vitamin D and the immune system remained unresolved for many years. Some pieces of the puzzle were easier to complete than others. For example, it became evident that dysregulation of 1,25(OH)2D3 was not restricted to sarcoidosis but was a common feature of many granulomatous disorders and some forms of cancer 39. Likewise, at least in vitro, it was possible to potently regulate a range of immune cell functions using 1,25(OH)2D3 or its synthetic analogs 35,97. However, the key remaining question concerned whether or not vitamin D could act as a physiological regulator of normal immune responses. Answers to this question began to appear about five years ago and new information on the fundamental nature of vitamin D sufficiency/insufficiency has provided a fresh perspective on non-classical actions of vitamin D. As a consequence, there is now a much broader acceptance that vitamin D plays an active role in regulating specific facets of human immunity. This will be detailed in the following review together with discussion on the possible impact of vitamin D insufficiency and vitamin D supplementation on normal immune function and human disease.
•  Other Sections▼
o Synopsis
o Introduction
o Vitamin D and innate immunity
o Vitamin D and adaptive immunity
o Vitamin D,  the immune system and human health
o Conclusions
o References

Vitamin D and innate immunity
Macrophages, vitamin D and cathelicidin
Consistent with the earlier seminal observations of extra-renal 1α-hydroxylase activity in patients with sarcoidosis, the effects of vitamin D on macrophage function have been central to many of the new observations implicating vitamin D in the regulation of immune responses. In common with natural killer cells (NK) and cytotoxic T-lymphocytes (cytotoxic T-cells), macrophages and their monocyte precursors play a central role in initial non-specific immune responses to pathogenic organisms or tissue damage – so called cell-mediated immunity. Their role is to phagocytose pathogens or cell debris and then eliminate or assimilate the resulting waste material. In addition, macrophages can interface with the adaptive immune system by utilizing phagocytic material for antigen presentation to T-lymphocytes (T-cells).

For many years, the key action of vitamin D on macrophages was thought to be its ability to stimulate differentiation of precursor monocytes to more mature phagocytic macrophages 1,2,45,93. This concept was supported by observations showing differential expression of VDR and 1α-hydroxylase during the differentiation of human monocytes macrophages 49. The latter report also emphasized early studies showing that normal human macrophages were able to synthesize 1,25(OH)2D3 when stimulated with interferon gamma (IFNγ) 46. Localized activation of vitamin D, coupled with expression of endogenous VDR was strongly suggestive of an autocrine or intracrine system for vitamin D action in normal monocytes/macrophages.

However, confirmation of such a mechanism was only obtained in 2006 when Robert Modlin and colleagues carried out DNA array analyses to define innate immunity genes that were specifically modulated in monocytes by Mycobacterium tuberculosis (M. tb). In a seminal investigation both the VDR and the gene for 1α-hydroxylase (CYP27B1) were shown to be induced following activation of the principal pathogen recognition receptor for M. tb, toll-like receptor 2/1 (TLR2/1) 56. Subsequent experiments confirmed that precursor 25OHD3 was able to induce intracrine VDR responses in monocytes that had been treated with a TLR2/1 activator. In particular, the TLR2/1–25OHD3 combination stimulated expression of the antibacterial protein cathelicidin, so that vitamin D was able to promote monocyte killing of M. tb 56. Notably, the ability to promote expression of the antibacterial protein following a TLR2/1 challenge was directly influenced by the 25OHD3 status of the donor serum used for monocyte culture 56. More recently, we have shown that vitamin D supplementation in vivo can also enhance TLR2/1-induced cathelicidin expression 5. Cathelicidin was identified several years ago as a target for transcriptional regulation by 1,25(OH)2D3-liganded VDR, in that its gene promoter contains a functional vitamin D response element (VDRE) 30,100. Interestingly, this VDRE occurs within a small interchangeable nuclear element (SINE) sequence which only appears to be present in the cathelicidin gene promoter of higher primates, suggesting that vitamin D regulation of this facet of innate immunity is a relatively recent evolutionary development 30.

Recent reports have underlined the importance of cathelicidin as a target for vitamin D but also suggest that this mechanism may be more complex than initially thought. As yet, the precise signal system by which TLR activation induces expression of VDR and 1α-hydroxylase remains unclear. Promoter-reporter analysis of the events involved in transcriptional regulation of CYP27B1 suggest that TLR4-mediated induction of the enzyme involves JAK-STAT, MAP kinase and nuclear factor kappB (NF-κB) pathways, and that these synergize with IFNγ-mediated induction of CYP27B192. However, other studies have proposed that TLR2/1 induction of 1α-hydroxylase occurs indirectly as a consequence of TLR2/1 induced interleukin-15 (IL-15) which is a potent inducer of CYP27B1 and 1α-hydroxylase activity 50. In a similar fashion, interleukin 17A (IL-17A) has been shown to enhance 1,25(OH)2D3-mediated induction of cathelicidin, although this response does not appear to involve transcriptional regulation of 1α-hydroxylase or increased VDR sensitivity 77. One pathway that has been poorly studied in this regard concerns the enzyme 24-hydroxylase, which is conventionally considered to function by inactivating 1,25(OH)2D3. The gene for 24-hydroxylase (CYP24) is potently induced by 25OHD3 following TLR2/1 activation of monocytes 56 but, as yet, it is unclear whether this involves the non-metabolic splice variant form of CYP24 known to be expressed by macrophages 82.

Regulation of the antibacterial protein by 1,25(OH)2D3 has been described for a wide variety of cell types other than macrophages, including keratinocytes 84,85,100, lung epithelial cells 104, myeloid cell lines 30,85,100 and placental trophoblasts 54. In some cases 54,84, this appears to involve an intracrine response similar to that reported for monocytes. However, the mechanisms controlling local synthesis of 1,25(OH)2D3 in these cells vary considerably. In keratinocytes, low baseline expression of 1α-hydroxylase is enhanced following epidermal wounding by transforming growth factor beta (TGFβ) 84. The resulting rise in 1,25(OH)2D3 concentrations upregulates expression of TLR2 and TLR4 by keratinocytes, thereby priming these cells for further innate immune responses to pathogens or tissue damage 84. By contrast, in trophoblasts, induction of cathelicidin and subsequent bacterial killing by 25OHD3 appears to be due to constitutive 1α-hydroxylase activity, which is not further enhanced by TLR activation 54. The latter may be due to the rapid non-immune induction of 1α-hydroxylase and VDR which occurs within the placenta during early gestation 24.

Although most of the studies of vitamin D-mediated innate immunity have focused on the role of 1,25(OH)2D3-bound VDR as a pivotal transcriptional regulator of cathelicidin, it is also important to recognize that other ligands may interact with the VDR 58. For example, recent studies of bilary epithelial cells have shown that cathelicidin expression can be induced in a VDR-dependent fashion by bile salts 19. This provides a mechanism for maintaining bilary sterility, although additive effects of 1,25(OH)2D3 also highlight a novel therapeutic application for vitamin D in the treatment of primary bilary cirrhosis. Conversely, other compounds may act to disrupt normal 1,25(OH)2D3-VDR-mediated immunity. The polycyclic aromatic hydrocarbon benzo(A)pyrene, a prominent product of cigarette smoking, has been shown to attenuate vitamin D-mediated induction of macrophage cathelcidin in a VDR-dependent fashion by stimulating expression of 24-hydroxylase, and vitamin D catabolism 64. The precise mechanism by which this occurs has yet to be determined but these data suggest that some toxic compounds are actively detrimental to vitamin D-mediated immunity.

The observations detailed above show clearly that vitamin D is a potent stimulator of mechanisms associated with pathogen elimination. In subsequent sections the clinical importance of this with respect to vitamin D insufficiency and immune-related diseases is discussed in more detail. However, one key question that immediately arises from the current observations is why there is a need to involve the vitamin D system in the TLR-induction of innate immunity. As previously described, VDR-mediated transcriptional regulation of cathelicidin is a relatively recent evolutionary change and was presumably advantageous when primates (including early Homo sapiens) were exposed to abundant sunlight, thereby priming high serum levels of vitamin D. Other benefits of incorporating vitamin D into innate immune regulation include the fact that it is associated with key feedback control pathways. As already mentioned, vitamin D has its own catabolic enzyme in the form of 24-hydroxylase which sensitively attenuates responses to 1,25(OH)2D3 and, in the case of the CYP24 splice variant, may also attenuate synthesis of this vitamin D metabolite 82. However, vitamin D may also provide feedback regulation of immune activation pathways in that 1,25(OH)2D3 has been shown to potently downregulate expression of monocyte TLR2 and TLR4, thereby suppressing inflammatory responses that are normally activated by these receptors 83. Thus, by utilizing both CYP24 and TLR regulatory mechanisms, vitamin D may help to promote appropriate innate immune responses whilst preventing an over-elaboration of innate immune responses and the tissue damage frequently associated with this.

Dendritic cells and antigen presentation

In addition to the phagocytic acquisition and elimination of pathogens and cell debris, innate immunity also involves the presentation of resultant antigen to cells involved in the adaptive arm of the immune system (see Figure 1). Although several cells are able to do this, the most well-recognized group of professional antigen presenting cells (APCs) are dendritic cells (DCs). Expression of VDR by purified tissue DCs was first reported in 198715. Subsequent studies using populations of DCs isolated from skin (Langerhans cells) provided evidence that 1,25(OH)2D3 could act to attenuate antigen presentation 20. However, it was not until the later advent of in vitro monocyte-derived DC models that the effects of vitamin D metabolites on antigen presentation were fully elucidated. In 2000 parallel studies by the Adorini and Kumar groups showed that 1,25(OH)2D376 and its synthetic analogs 34 inhibited the maturation of monocyte-derived DCs, thereby suppressing their capacity to present antigen to T-cells. Based on these observations, it was proposed that vitamin D could act to promote tolerance and this was endorsed by studies of pancreatic islet transplantation in which lower rejection rates were observed in 1,25(OH)2D3-treated mice 32. Crucially this response to 1,25(OH)2D3 appeared to be due to decreased DC maturation and concomitant enhancement of suppressor or regulatory T-cells (Treg) 32. Further studies have underlined the importance of Treg generation 68 as part of the interaction between vitamin D and the immune system and this is discussed in greater detail in later sections of this review.

 

Figure 1
Effects of vitamin D on innate and adaptive immunity

Although regulation of DC maturation represents at potential target for 1,25(OH)2D3 and its synthetic analogs as treatment for autoimmune disease and host-graft rejection, another perspective was provided by the observation that DCs express 1α-hydroxylase in a similar fashion to macrophages 25,40. Data from monocyte-derived DCs showed that 1α-hydroxylase expression and activity increases as DCs differentiate towards an a mature phenotype 40. Functional analyses showed that treatment with 25OHD3 suppresses DC maturation and inhibits T-cell proliferation, confirming the existence of an intracrine pathway for vitamin D similar to that observed for macrophages 40. Interestingly, mature DCs showed lower levels of VDR than immature DCs or monocytes 40. This reciprocal organization of 1α-hydroxylase and VDR expression may be advantageous in that mature antigen-presenting DCs may be relatively insensitive to 1,25(OH)2D3, thereby allowing induction of an initial T-cell response. However, the high levels of 1,25(OH)2D3 being synthesized by these cells will be able to act on VDR-expressing immature DCs and thus prevent their further development 41. In this way, paracrine action of locally produced 1,25(OH)2D3 will allow initial presentation of antigen to T-cells whilst preventing continued maturation of DCs and over-stimulation of T-cells.

Although DCs are heterogeneous in terms of their location, phenotype and function, they are broadly divided into two groups based on their origin. Myeloid (mDCs) and plasmacytoid (pDCs) express different types of cytokines and chemokines and appear to exert complementary effects on T-cell responses, with mDCs being the most effective APCs 57 and pDCs being more closely associated with immune tolerance 91. It is therefore interesting to note that 1,25(OH)2D3 preferentially regulates mDCs, suggesting that the key effect of vitamin D in this instance is to suppress activation of naïve T-cells. Although in this study pDCs showed no apparent immune response to 1,25(OH)2D3, this does not preclude a role for vitamin D in the regulation of tolerogenic responses. One possibility is that local, intracrine, synthesis of 1,25(OH)2D3 will be more effective in achieving these responses. Alternatively, 1,25(OH)2D3 synthesized by pDCs may regulate tolerance through paracrine effects on VDR-expressing T-cells. This is discussed in further detail in the following section.

Vitamin D and adaptive immunity
Vitamin D and T-cell function

Resting T-cells express almost undetectable levels of VDR, but levels of the receptor increase as T-cells proliferate following antigenic activation 44,66,78. As a consequence, initial studies of the effects of vitamin D on T-cells focused on the ability of 1,25(OH)2D3 to suppress T-cell proliferation 44,66,78. However, the recognition that CD4+ effector T-cells were capable of considerable phenotypic plasticity, suggested that vitamin D might also influence the phenotype of T-cells. Lemire and colleagues first reported that 1,25(OH)2D3 preferentially inhibited T-helper 1 (Th1) cells which are a subset of CD4+ effector T-cells closely associated with cellular, rather than humoral, immune responses 52. Subsequent studies confirmed this observation and demonstrated that the cytokine profile of 1,25(OH)2D3-treated human T-cells was consistent with Th2 cells, a subset of CD4+ T-cells associated with humoral (antibody)-mediated immunity 14,70. The conclusion from these observations was that vitamin D promotes a T-cell shift from Th1 to Th2 and thus might help to limit the potential tissue damage associated with Th1 cellular immune responses. However, the validity of this generalization was called into question by studies using mouse T-cells in which 1,25(OH)2D3 was shown to inhibit cytokines associated with both Th1 (IFNγ) and Th2 (interleukin-4, IL-4). Subsequent analysis of immune cells from the VDR gene knockout mouse added further confusion by showing that these animals had reduced (rather than the predicted elevated) levels of Th1 cells 69. Thus, whilst in vitro vitamin D appears to broadly support a shift from Th1 to Th2 in CD4+ cells, it seems likely that in vivo its effects on T-cells are more complex.

The T-cell repertoire has continued to expand with the characterization of another effector T-cell lineage distinct from Th1 or Th2 cells, termed Th17 cells because of their capacity to synthesize interleukin-17 (IL-17) 36,101. Th17 cells play an essential role in combating certain pathogens but they have also been linked to tissue damage and inflammation 12,48. The precise role of vitamin D as a regulator of Th17 cells has yet to be fully elucidated but it is interesting to note that studies of animal models of the gastrointestinal inflammatory disease colitis have shown that treatment with 1,25(OH)2D3 reduces expression of IL-1721, whilst loss of 1,25(OH)2D3 as a result of CYP27b1 gene ablation leads to elevated levels of this cytokine 55. Thus, it possible that vitamin D exerts some of its effects on inflammation and autoimmune disease through the regulation of Th17 cells.

A fourth group of CD4+ T-cells, exert suppressor rather than effector functions and are known as regulatory T-cells or Tregs. In view of its early recognition as a suppressor of T-cell proliferation, it was anticipated that vitamin D would have effects on Tregs, and indeed in 2002 O’Garra and colleagues demonstrated that 1,25(OH)2D3, in conjunction with glucocorticoids, potently stimulated the generation of interleukin-10 (IL-10)-producing CD4+/CD25+ Tregs 10. Subsequent reports indicated that 1,25(OH)2D3 alone can induce Tregs 31, and it appears that preferential differentiation of Tregs is a pivotal mechanism linking vitamin D and adaptive immunity, with potential beneficial effects for autoimmune disease and host-graft rejection 33,62,89. This immunosuppressive mechanism is likely to be mediated by the induction of tolerogenic DCs as described in the previous section of the review 7,22,32, but direct effects on T-cells may also be important 95. In this latter study, it was notable that 1,25(OH)2D3 increased both IL-10-secretion and TLR9 expression by Tregs, suggesting a novel link between innate and adaptive immune responses 95.

Relative to the wealth of literature on CD4+ effector cells, our understanding of the effects of vitamin D on CD8+ suppressor T-cells remains somewhat limited. In contrast to CD4+ cells, CD8+ show poor antiproliferative response to 1,25(OH)2D378,98,99. However, VDR expression appears to be abundant in CD8+ cells suggesting that they are still potential targets for 1,25(OH)2D3. Indeed subsequent reports have shown that 1,25(OH)2D3 actively regulates cytokine production by CD8+ cells 103, and can also regulate the proliferation of CD8+ cells following specific immune stimuli 43. Despite this, 1,25(OH)2D3 does not appear to have a significant impact on animal disease models such as experimental autoimmune encephalomyelitis where CD8+ cells have been implicated 65.

Although many of the studies linking 1,25(OH)2D3 with adaptive immunity have focused on changes in T-cell proliferation and phenotype, it is important to recognize that other facets of T-cell function may also be affected by the hormone. In particular recent studies have shown that vitamin D can exert powerful effects on the homing of T-cells to specific tissues. Initial studies suggested that 1,25(OH)2D3 acts to inhibit migration of T-cells to lymph nodes 94. However, more recent reports have demonstrated an active role for vitamin D in promoting homing of T-cells to the skin via upregulation of chemokine receptor 10 (CCR10), the ligand for which, CCL27, is expressed by epidermal keratinocytes 87. Notably this T-cell homing response was induced by 25OHD3 as well as 1,25(OH)2D3 and the author suggested that both DCs and T-cells were possible sources of the local 1α-hydroxylase activity 87. In contrast to its positive effect on epidermal T-cell homing, vitamin D appears to exert a negative effect on chemokines and chemokine receptors associated with the GI tract 87. However, it seems likely that this is will be highly T-cell selective as newer studies using the VDR gene knockout mouse have demonstrated aberrant GI migration of a subset of CD8+ cells, and this effects appears to be closely linked to the increased risk of colitis in VDR knockout mice 105.

Vitamin D and B-cell function

Like T-cells, active but not inactive B-cells express the VDR 79. Consequently, initial studies indicated that 1,25(OH)2D3 could directly regulate B-cell proliferation 86 and immunoglobulin (Ig) production 79. Subsequent work contradicted this, suggesting instead that the ability of 1,25(OH)2D3 to suppress proliferation and immunoglobulin (Ig) production was due to indirect effects mediated via helper T-cells 51. However, more recent reports have demonstrated that 1,25(OH)2D3 does indeed exert direct effects on B cell homeostasis 17. In addition to confirming direct VDR-mediated effects on B cell proliferation and Ig production, this study also highlighted the ability of 1,25(OH)2D3 to inhibit the differentiation of plasma cells and class switched memory cells, suggesting a potential role for vitamin D in B cell-related disorders such as systemic lupus erythamtosus. Notably, expression of CYP27b1 was also detected in B-cells, indicating that B-cells may be capable of autocrine/intracrine responses to vitamin D 17. Indeed, this may be common to lymphocytes in general as CYP27b1 expression has also been detected in T-cells 87.

Vitamin D, the immune system and human health

For many years vitamin D status was defined simply by whether or not the patient in question exhibited symptoms of the bone disease rickets (osteomalacia in adults). However, an entirely new perspective on vitamin D status has arisen from the observation that serum levels of the main circulating form of vitamin D (25OHD3) as high as 75 nM correlate inversely with parathyroid hormone 16. This, has prompted the introduction of a new term – vitamin D ‘insufficiency’ – defined by serum levels of 25OHD3 that are sub-optimal (< 75 nM) but not necessarily rachitic (< 20 nM) 42. Unlike serum concentrations of 1,25(OH)2D3, which are primarily defined by the endocrine regulators of the vitamin D-activating enzyme, 1α-hydroxylase, circulating levels of 25OHD3 are a direct reflection of vitamin D status, which for any given individual will depend on access to vitamin D either through exposure to sunlight or through dietary intake. The net effect of this is that vitamin D status can vary significantly in populations depending on geographical, social or economic factors. As a result of these new parameters for vitamin D status, a consensus statement from the 13th Workshop on Vitamin D concluded that vitamin D insufficiency was a worldwide epidemic. Moreover, recent studies have shown that in the last ten years alone, serum vitamin D levels have on average fallen by 20% 28. The key question now being considered is what is the physiological and clinical impact of global vitamin D insufficiency beyond classical bone diseases such as rickets? Epidemiological studies have highlighted possible links between vitamin D insufficiency and a wide range of human diseases 42. The final section of the review will describe four of the key clinical problems which have been linked to the immunomodulatory properties of vitamin D.

Vitamin D and tuberculosis

The observation that vitamin D acts to promote innate immune responses to TLR-activation by M. tb 56, has provided a new perspective on observations made many decades ago concerning the beneficial effects of UV light exposure on the disease TB. As a consequence this has become the most well studied facet of the interaction between vitamin D and innate immunity 60. Initial studies to assess the effects of 25OHD status on ex vivo macrophage function have shown that supplementation with a single oral dose of 2.5 mg vitamin D enhances the ability of recipient macrophages to combat BCG infection in vitro 61. The potential benefits of vitamin D as treatment for tuberculosis (TB) have been further endorsed by a study which showed that adjunct vitamin D supplementation (0.25 mg vitamin D/day) of TB patients receiving conventional therapy for the disease reduced the time for sputum smear conversion from acid fast bacteria (AFB) positive to AFB-negative status 67. A recent double-blind randomized placebo-controlled trial showed that vitamin D supplementation had no effect on clinical outcomes or mortality amongst TB patients, although it should be emphasized that none of the supplemented patients in this study showed a significant rise in serum vitamin D levels 102.

Vitamin D and multiple sclerosis

Several epidemiology studies have reported association between vitamin D insufficiency and the incidence and/or severity of the autoimmune disease multiple sclerosis (MS) (reviewed in 80. These observations have been supported by analysis of animal models such as the experimental autoimmune encephalomyelitis (EAE) mouse, which shows increased disease severity under dietary vitamin D restriction 88. Conversely administration of 1,25(OH)2D3 to EAE mice confers disease protection through effects on cytokine synthesis and apoptosis of inflammatory cells 75,90. Some effects of 1,25(OH)2D3 on EAE appear to be dependent on IL-10 activity 89.

Vitamin D and type 1 diabetes

In common with MS, published reports suggest that there is a link between vitamin D deficiency and another autoimmune disease, type 1 diabetes (reviewed in 63). Low circulating levels of 25OHD3 have been reported in adolescents at the time of diagnosis of type 1 diabetes 53, and other data have documented the beneficial effects of vitamin D supplementation in protecting against type 1 diabetes 37. Another strand of evidence linking vitamin D with type 1 diabetes stems from the extensive genetic analyses that have explored the physiological impact of inherited variations in the genes for various components of the vitamin D metabolic and signaling system. Previous studies have indicated that some VDR gene haplotypes confer protection against diabetes 81 and more recently this has been expanded to show that genetic variants of the CYP27b1 gene also affect susceptibility to type 1 diabetes 8. Finally, in a similar fashion to animal model studies for MS, in vivo use of the non-obese diabetic (NOD) mouse as a model for type 1 diabetes has shown increased disease severity under conditions of dietary vitamin D restriction 29.

Vitamin D and Crohn’s disease

Several strands of evidence have linked vitamin D to the dysregulated immune responses observed with inflammatory bowel diseases such as Crohn’s disease. Firstly, epidemiology suggests that patients with Crohn’s disease have decreased serum levels of 25OHD373,74,96. Secondly, studies in vivo using various animal models indicate that 1,25(OH)2D3 plays a crucial role in the pathophysiology of experimentally-induced forms of inflammatory bowel disease 26,27,47,55. Finally, expression of 1α-hydroxylase has been detected in the human colon 106, with the vitamin D-activating enzyme being upregulated in disease-affected tissue from patients with Crohn’s disease 3. In the case of the latter, dysregulated colonic expression of 1α-hydroxylase was associated with increased circulating levels of 1,25(OH)2D3 indicating that, as with sarcoidosis, localized synthesis of this vitamin D metabolite can spill-over into the general circulation under conditions of persistent disease 3. Intriguingly, current studies have implicated aberrant innate immune handling of enteric microbiota as an initiator of the adaptive immune damage associated with Crohn’s disease 71. It is thus tempting to speculate that effects of vitamin D on this disease may involve both the activation of innate immunity, together with the suppression of adaptive immunity and associated inflammation.

Conclusions

It is almost thirty years since an interaction between vitamin D and the immune system was first documented. Although this was initially proposed as a non-classical effect of vitamin D associated with granulomatous diseases, our current view is now considerably changed. Recent studies have demonstrated a potential physiological role for vitamin D in regulating normal innate and adaptive immunity. Future studies will now need to focus on the clinical implications of vitamin D-mediated immunity and, in particular, the possible beneficial effects of supplementary vitamin D with respect to infectious and autoimmune diseases.

Acknowledgments

This work was supported by NIH grant RO1AR050626 to M.H.
Footnotes

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References

1. Abe E, Miyaura C, Sakagami H, et al. Differentiation of mouse myeloid leukemia cells induced by 1 alpha,25-dihydroxyvitamin D3. Proc Natl Acad Sci U S A. 1981;78:4990. [PMC free article] [PubMed]

2. Abe E, Miyaura C, Tanaka H, et al. 1 alpha,25-dihydroxyvitamin D3 promotes fusion of mouse alveolar macrophages both by a direct mechanism and by a spleen cell-mediated indirect mechanism. Proc Natl Acad Sci U S A. 1983;80:5583. [PMC free article] [PubMed]

3. Abreu MT, Kantorovich V, Vasiliauskas EA, et al. Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn’s disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density. Gut. 2004;53:1129. [PMC free article] [PubMed]

4. Adams JS, Gacad MA. Characterization of 1 alpha-hydroxylation of vitamin D3 sterols by cultured alveolar macrophages from patients with sarcoidosis. J Exp Med. 1985;161:755. [PMC free article] [PubMed]

5. Adams JS, Ren S, Liu PT, et al. Vitamin d-directed rheostatic regulation of monocyte antibacterial responses. J Immunol. 2009;182:4289. [PMC free article] [PubMed]

6. Adams JS, Sharma OP, Gacad MA, et al. Metabolism of 25-hydroxyvitamin D3 by cultured pulmonary alveolar macrophages in sarcoidosis. J Clin Invest. 1983;72:1856. [PMC free article] [PubMed]

7. Adorini L, Penna G, Giarratana N, et al. Dendritic cells as key targets for immunomodulation by Vitamin D receptor ligands. J Steroid Biochem Mol Biol. 2004;89–90:437.

8. Bailey R, Cooper JD, Zeitels L, et al. Association of the vitamin D metabolism gene CYP27B1 with type 1 diabetes. Diabetes. 2007

9. Barbour GL, Coburn JW, Slatopolsky E, et al. Hypercalcemia in an anephric patient with sarcoidosis: evidence for extrarenal generation of 1,25-dihydroxyvitamin D. N Engl J Med. 1981;305:440. [PubMed]

10. Barrat FJ, Cua DJ, Boonstra A, et al. In vitro generation of interleukin 10-producing regulatory CD4(+) T cells is induced by immunosuppressive drugs and inhibited by T helper type 1 (Th1)- and Th2-inducing cytokines. J Exp Med. 2002;195:603. [PMC free article] [PubMed]

11. Bell NH, Stern PH, Pantzer E, et al. Evidence that increased circulating 1 alpha, 25-dihydroxyvitamin D is the probable cause for abnormal calcium metabolism in sarcoidosis. J Clin Invest. 1979;64:218. [PMC free article] [PubMed]

12. Bettelli E, Korn T, Kuchroo VK. Th17: the third member of the effector T cell trilogy. Curr Opin Immunol. 2007;19:652. [PMC free article] [PubMed]

13. Bhalla AK, Amento EP, Serog B, et al. 1,25-Dihydroxyvitamin D3 inhibits antigen-induced T cell activation. J Immunol. 1984;133:1748. [PubMed]

14. Boonstra A, Barrat FJ, Crain C, et al. 1alpha,25-Dihydroxyvitamin d3 has a direct effect on naive CD4(+) T cells to enhance the development of Th2 cells. J Immunol. 2001;167:4974. [PubMed]

15. Brennan A, Katz DR, Nunn JD, et al. Dendritic cells from human tissues express receptors for the immunoregulatory vitamin D3 metabolite, dihydroxycholecalciferol. Immunology. 1987;61:457. [PMC free article] [PubMed]

16. Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int. 1997;7:439. [PubMed]

17. Chen S, Sims GP, Chen XX, et al. Modulatory effects of 1,25-dihydroxyvitamin d3 on human B cell differentiation. J Immunol. 2007;179:1634. [PubMed]

18. Colston K, Colston MJ, Feldman D. 1,25-dihydroxyvitamin D3 and malignant melanoma: the presence of receptors and inhibition of cell growth in culture. Endocrinology. 1981;108:1083. [PubMed]

19. D’Aldebert E, Biyeyeme Bi Mve MJ, Mergey M, et al. Bile salts control the antimicrobial peptide cathelicidin through nuclear receptors in the human biliary epithelium. Gastroenterology. 2009;136:1435. [PubMed]

20. Dam TN, Moller B, Hindkjaer J, et al. The vitamin D3 analog calcipotriol suppresses the number and antigen-presenting function of Langerhans cells in normal human skin. J Investig Dermatol Symp Proc. 1996;1:72.

21. Daniel C, Sartory NA, Zahn N, et al. Immune modulatory treatment of TNBS colitis with calcitriol is associated with a change of a Th1/Th17 to a Th2 and regulatory T cell profile. J Pharmacol Exp Ther. 2007

22. Dong X, Bachman LA, Kumar R, et al. Generation of antigen-specific, interleukin-10-producing T-cells using dendritic cell stimulation and steroid hormone conditioning. Transpl Immunol. 2003;11:323. [PubMed]

23. Eisman JA, Martin TJ, MacIntyre I, et al. 1,25-dihydroxyvitamin-D-receptor in breast cancer cells. Lancet. 1979;2:1335. [PubMed]

24. Evans KN, Bulmer JN, Kilby MD, et al. Vitamin D and placental-decidual function. J Soc Gynecol Investig. 2004;11:263.

25. Fritsche J, Mondal K, Ehrnsperger A, et al. Regulation of 25-hydroxyvitamin D3-1 alpha-hydroxylase and production of 1 alpha,25-dihydroxyvitamin D3 by human dendritic cells. Blood. 2003;102:3314. [PubMed]

26. Froicu M, Cantorna MT. Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury. BMC Immunol. 2007;8:5. [PMC free article] [PubMed]

27. Froicu M, Weaver V, Wynn TA, et al. A crucial role for the vitamin D receptor in experimental inflammatory bowel diseases. Mol Endocrinol. 2003;17:2386. [PubMed]

28. Ginde AA, Liu MC, Camargo CA., Jr Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004. Arch Intern Med. 2009;169:626. [PubMed]

29. Giulietti A, Gysemans C, Stoffels K, et al. Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice. Diabetologia. 2004;47:451. [PubMed]

30. Gombart AF, Borregaard N, Koeffler HP. Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. Faseb J. 2005;19:1067. [PubMed]

31. Gorman S, Kuritzky LA, Judge MA, et al. Topically applied 1,25-dihydroxyvitamin D3 enhances the suppressive activity of CD4+CD25+ cells in the draining lymph nodes. J Immunol. 2007;179:6273. [PubMed]

32. Gregori S, Casorati M, Amuchastegui S, et al. Regulatory T cells induced by 1 alpha,25-dihydroxyvitamin D3 and mycophenolate mofetil treatment mediate transplantation tolerance. J Immunol. 2001;167:1945. [PubMed]

33. Gregori S, Giarratana N, Smiroldo S, et al. A 1alpha,25-dihydroxyvitamin D(3) analog enhances regulatory T-cells and arrests autoimmune diabetes in NOD mice. Diabetes. 2002;51:1367. [PubMed]

34. Griffin MD, Lutz WH, Phan VA, et al. Potent inhibition of dendritic cell differentiation and maturation by vitamin D analogs. Biochem Biophys Res Commun. 2000;270:701. [PubMed]

35. Griffin MD, Xing N, Kumar R. Vitamin D and its analogs as regulators of immune activation and antigen presentation. Annu Rev Nutr. 2003;23:117. [PubMed]

36. Harrington LE, Mangan PR, Weaver CT. Expanding the effector CD4 T-cell repertoire: the Th17 lineage. Curr Opin Immunol. 2006;18:349. [PubMed]

37. Harris SS. Vitamin D in type 1 diabetes prevention. J Nutr. 2005;135:323. [PubMed]

38. Hewison M. Vitamin D and the immune system. J Endocrinol. 1992;132:173. [PubMed]

39. Hewison M, Burke F, Evans KN, et al. Extra-renal 25-hydroxyvitamin D3-1alpha-hydroxylase in human health and disease. J Steroid Biochem Mol Biol. 2007;103:316. [PubMed]

40. Hewison M, Freeman L, Hughes SV, et al. Differential regulation of vitamin D receptor and its ligand in human monocyte-derived dendritic cells. J Immunol. 2003;170:5382. [PubMed]

41. Hewison M, Zehnder D, Chakraverty R, et al. Vitamin D and barrier function: a novel role for extra-renal 1 alpha-hydroxylase. Mol Cell Endocrinol. 2004;215:31. [PubMed]

42. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357:266. [PubMed]

43. Iho S, Iwamoto K, Kura F, et al. Mechanism in 1,25(OH)2D3-induced suppression of helper/suppressor function of CD4/CD8 cells to immunoglobulin production in B cells. Cell Immunol. 1990;127:12. [PubMed]

44. Karmali R, Hewison M, Rayment N, et al. 1,25(OH)2D3 regulates c-myc mRNA levels in tonsillar T lymphocytes. Immunology. 1991;74:589. [PMC free article] [PubMed]

45. Koeffler HP, Amatruda T, Ikekawa N, et al. Induction of macrophage differentiation of human normal and leukemic myeloid stem cells by 1,25-dihydroxyvitamin D3 and its fluorinated analogues. Cancer Res. 1984;44:5624. [PubMed]

46. Koeffler HP, Reichel H, Bishop JE, et al. gamma-Interferon stimulates production of 1,25-dihydroxyvitamin D3 by normal human macrophages. Biochem Biophys Res Commun. 1985;127:596. [PubMed]

47. Kong J, Zhang Z, Musch MW, et al. Novel Role of the Vitamin D Receptor in Maintaining the Integrity of the Intestinal Mucosal Barrier. Am J Physiol Gastrointest Liver Physiol. 2007

48. Korn T, Oukka M, Kuchroo V, et al. Th17 cells: effector T cells with inflammatory properties. Semin Immunol. 2007;19:362. [PMC free article] [PubMed]

49. Kreutz M, Andreesen R, Krause SW, et al. 1,25-dihydroxyvitamin D3 production and vitamin D3 receptor expression are developmentally regulated during differentiation of human monocytes into macrophages. Blood. 1993;82:1300. [PubMed]

50. Krutzik SR, Hewison M, Liu PT, et al. IL-15 links TLR2/1-induced macrophage differentiation to the vitamin D-dependent antimicrobial pathway. J Immunol. 2008;181:7115. [PMC free article] [PubMed]

51. Lemire JM, Adams JS, Sakai R, et al. 1 alpha,25-dihydroxyvitamin D3 suppresses proliferation and immunoglobulin production by normal human peripheral blood mononuclear cells. J Clin Invest. 1984;74:657. [PMC free article] [PubMed]

52. Lemire JM, Archer DC, Beck L, et al. Immunosuppressive actions of 1,25-dihydroxyvitamin D3: preferential inhibition of Th1 functions. J Nutr. 1995;125:1704S. [PubMed]

53. Littorin B, Blom P, Scholin A, et al. Lower levels of plasma 25-hydroxyvitamin D among young adults at diagnosis of autoimmune type 1 diabetes compared with control subjects: results from the nationwide Diabetes Incidence Study in Sweden (DISS) Diabetologia. 2006;49:2847. [PubMed]

54. Liu N, Kaplan AT, Low J, et al. Vitamin D Induces Innate Antibacterial Responses in Human Trophoblasts via an Intracrine Pathway. Biol Reprod. 2009;80:398. [PMC free article] [PubMed]

55. Liu N, Nguyen L, Chun RF, et al. Altered endocrine and autocrine metabolism of vitamin D in a mouse model of gastrointestinal inflammation. Endocrinology. 2008;149:4799. [PMC free article] [PubMed]

56. Liu PT, Stenger S, Li H, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006;311:1770. [PubMed]

57. Liu YJ. IPC: professional type 1 interferon-producing cells and plasmacytoid dendritic cell precursors. Annu Rev Immunol. 2005;23:275. [PubMed]

58. Makishima M, Lu TT, Xie W, et al. Vitamin D receptor as an intestinal bile acid sensor. Science. 2002;296:1313. [PubMed]

59. Manolagas SC, Haussler MR, Deftos LJ. 1,25-dihydroxyvitamin D3 receptors in cancer. Lancet. 1980;1:828. [PubMed]

60. Martineau AR, Honecker FU, Wilkinson RJ, et al. Vitamin D in the treatment of pulmonary tuberculosis. J Steroid Biochem Mol Biol. 2007;103:793. [PubMed]

61. Martineau AR, Wilkinson RJ, Wilkinson KA, et al. A single dose of vitamin d enhances immunity to mycobacteria. Am J Respir Crit Care Med. 2007;176:208. [PubMed]

62. Mathieu C, Badenhoop K. Vitamin D and type 1 diabetes mellitus: state of the art. Trends Endocrinol Metab. 2005;16:261. [PubMed]

63. Mathieu C, Gysemans C, Giulietti A, et al. Vitamin D and diabetes. Diabetologia. 2005;48:1247. [PubMed]

64. Matsunawa M, Amano Y, Endo K, et al. The Aryl Hydrocarbon Receptor Activator Benzo[a]pyrene Enhances Vitamin D3 Catabolism in Macrophages. Toxicol Sci. 2009

65. Meehan TF, DeLuca HF. CD8(+) T cells are not necessary for 1 alpha,25-dihydroxyvitamin D(3) to suppress experimental autoimmune encephalomyelitis in mice. Proc Natl Acad Sci U S A. 2002;99:5557. [PMC free article] [PubMed]

66. Nunn JD, Katz DR, Barker S, et al. Regulation of human tonsillar T-cell proliferation by the active metabolite of vitamin D3. Immunology. 1986;59:479. [PMC free article] [PubMed]

67. Nursyam EW, Amin Z, Rumende CM. The effect of vitamin D as supplementary treatment in patients with moderately advanced pulmonary tuberculous lesion. Acta Med Indones. 2006;38:3. [PubMed]

68. O’Garra A, Barrat FJ. In vitro generation of IL-10-producing regulatory CD4+ T cells is induced by immunosuppressive drugs and inhibited by Th1- and Th2-inducing cytokines. Immunol Lett. 2003;85:135. [PubMed]

69. O’Kelly J, Hisatake J, Hisatake Y, et al. Normal myelopoiesis but abnormal T lymphocyte responses in vitamin D receptor knockout mice. J Clin Invest. 2002;109:1091. [PMC free article] [PubMed]

70. Overbergh L, Decallonne B, Waer M, et al. 1alpha,25-dihydroxyvitamin D3 induces an autoantigen-specific T-helper 1/T-helper 2 immune shift in NOD mice immunized with GAD65 (p524–543) Diabetes. 2000;49:1301. [PubMed]

71. Packey CD, Sartor RB. Commensal bacteria, traditional and opportunistic pathogens, dysbiosis and bacterial killing in inflammatory bowel diseases. Curr Opin Infect Dis. 2009;22:292. [PMC free article] [PubMed]

72. Papapoulos SE, Clemens TL, Fraher LJ, et al. 1, 25-dihydroxycholecalciferol in the pathogenesis of the hypercalcaemia of sarcoidosis. Lancet. 1979;1:627. [PubMed]

73. Pappa HM, Gordon CM, Saslowsky TM, et al. Vitamin D status in children and young adults with inflammatory bowel disease. Pediatrics. 2006;118:1950. [PMC free article] [PubMed]

74. Pappa HM, Grand RJ, Gordon CM. Report on the vitamin D status of adult and pediatric patients with inflammatory bowel disease and its significance for bone health and disease. Inflamm Bowel Dis. 2006;12:1162. [PubMed]

75. Pedersen LB, Nashold FE, Spach KM, et al. 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by inhibiting chemokine synthesis and monocyte trafficking. J Neurosci Res. 2007;85:2480. [PubMed]

76. Penna G, Adorini L. 1 Alpha,25-dihydroxyvitamin D3 inhibits differentiation, maturation, activation, and survival of dendritic cells leading to impaired alloreactive T cell activation. J Immunol. 2000;164:2405. [PubMed]

77. Peric M, Koglin S, Kim SM, et al. IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes. J Immunol. 2008;181:8504. [PMC free article] [PubMed]

78. Provvedini DM, Manolagas SC. 1 Alpha,25-dihydroxyvitamin D3 receptor distribution and effects in subpopulations of normal human T lymphocytes. J Clin Endocrinol Metab. 1989;68:774. [PubMed]

79. Provvedini DM, Tsoukas CD, Deftos LJ, et al. 1 alpha,25-Dihydroxyvitamin D3-binding macromolecules in human B lymphocytes: effects on immunoglobulin production. J Immunol. 1986;136:2734. [PubMed]

80. Raghuwanshi A, Joshi SS, Christakos S. Vitamin D and multiple sclerosis. J Cell Biochem. 2008;105:338. [PMC free article] [PubMed]

81. Ramos-Lopez E, Jansen T, Ivaskevicius V, et al. Protection from type 1 diabetes by vitamin D receptor haplotypes. Ann N Y Acad Sci. 2006;1079:327. [PubMed]

82. Ren S, Nguyen L, Wu S, et al. Alternative splicing of vitamin D-24-hydroxylase: a novel mechanism for the regulation of extrarenal 1,25-dihydroxyvitamin D synthesis. J Biol Chem. 2005;280:20604. [PubMed]

83. Sadeghi K, Wessner B, Laggner U, et al. Vitamin D3 down-regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen-associated molecular patterns. Eur J Immunol. 2006;36:361. [PubMed]

84. Schauber J, Dorschner RA, Coda AB, et al. Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism. J Clin Invest. 2007;117:803. [PMC free article] [PubMed]

85. Schauber J, Dorschner RA, Yamasaki K, et al. Control of the innate epithelial antimicrobial response is cell-type specific and dependent on relevant microenvironmental stimuli. Immunology. 2006;118:509. [PMC free article] [PubMed]

86. Shiozawa K, Shiozawa S, Shimizu S, et al. 1 alpha,25-dihydroxyvitamin D3 inhibits pokeweed mitogen-stimulated human B-cell activation: an analysis using serum-free culture conditions. Immunology. 1985;56:161. [PMC free article] [PubMed]

87. Sigmundsdottir H, Pan J, Debes GF, et al. DCs metabolize sunlight-induced vitamin D3 to ‘program’ T cell attraction to the epidermal chemokine CCL27. Nat Immunol. 2007;8:285. [PubMed]

88. Spach KM, Hayes CE. Vitamin D3 confers protection from autoimmune encephalomyelitis only in female mice. J Immunol. 2005;175:4119. [PubMed]

89. Spach KM, Nashold FE, Dittel BN, et al. IL-10 signaling is essential for 1,25-dihydroxyvitamin D3-mediated inhibition of experimental autoimmune encephalomyelitis. J Immunol. 2006;177:6030. [PubMed]

90. Spach KM, Pedersen LB, Nashold FE, et al. Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis. Physiol Genomics. 2004;18:141. [PubMed]

91. Steinman RM, Hawiger D, Nussenzweig MC. Tolerogenic dendritic cells. Annu Rev Immunol. 2003;21:685. [PubMed]

92. Stoffels K, Overbergh L, Giulietti A, et al. Immune regulation of 25-hydroxyvitamin-d(3)-1alpha-hydroxylase in human monocytes. J Bone Miner Res. 2006;21:37. [PubMed]

93. Tanaka H, Abe E, Miyaura C, et al. 1 alpha,25-dihydroxyvitamin D3 induces differentiation of human promyelocytic leukemia cells (HL-60) into monocyte-macrophages, but not into granulocytes. Biochem Biophys Res Commun. 1983;117:86. [PubMed]

94. Topilski I, Flaishon L, Naveh Y, et al. The anti-inflammatory effects of 1,25-dihydroxyvitamin D3 on Th2 cells in vivo are due in part to the control of integrin-mediated T lymphocyte homing. Eur J Immunol. 2004;34:1068. [PubMed]

95. Urry Z, Xystrakis E, Richards DF, et al. Ligation of TLR9 induced on human IL-10-secreting Tregs by 1alpha,25-dihydroxyvitamin D3 abrogates regulatory function. J Clin Invest. 2009;119:387. [PMC free article] [PubMed]

96. Vagianos K, Bector S, McConnell J, et al. Nutrition assessment of patients with inflammatory bowel disease. JPEN J Parenter Enteral Nutr. 2007;31:311. [PubMed]

97. Van Etten E, Decallonne B, Verlinden L, et al. Analogs of 1alpha,25-dihydroxyvitamin D3 as pluripotent immunomodulators. J Cell Biochem. 2003;88:223. [PubMed]

98. Vanham G, Ceuppens JL, Bouillon R. T lymphocytes and their CD4 subset are direct targets for the inhibitory effect of calcitriol. Cell Immunol. 1989;124:320. [PubMed]

99. Veldman CM, Cantorna MT, DeLuca HF. Expression of 1,25-dihydroxyvitamin D(3) receptor in the immune system. Arch Biochem Biophys. 2000;374:334. [PubMed]

100. Wang TT, Nestel FP, Bourdeau V, et al. Cutting edge: 1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression. J Immunol. 2004;173:2909. [PubMed]

101. Weaver CT, Hatton RD, Mangan PR, et al. IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu Rev Immunol. 2007;25:821. [PubMed]

102. Wejse C, Gomes VF, Rabna P, et al. Vitamin D as supplementary treatment for tuberculosis: a double-blind, randomized, placebo-controlled trial. Am J Respir Crit Care Med. 2009;179:843. [PubMed]

103. Willheim M, Thien R, Schrattbauer K, et al. Regulatory effects of 1alpha,25-dihydroxyvitamin D3 on the cytokine production of human peripheral blood lymphocytes. J Clin Endocrinol Metab. 1999;84:3739. [PubMed]

104. Yim S, Dhawan P, Ragunath C, et al. Induction of cathelicidin in normal and CF bronchial epithelial cells by 1,25-dihydroxyvitamin D(3) J Cyst Fibros. 2007;6:403. [PMC free article] [PubMed]

105. Yu S, Bruce D, Froicu M, et al. Failure of T cell homing, reduced CD4/CD8alphaalpha intraepithelial lymphocytes, and inflammation in the gut of vitamin D receptor KO mice. Proc Natl Acad Sci U S A. 2008;105:20834. [PMC free article] [PubMed]

106. Zehnder D, Bland R, Williams MC, et al. Extrarenal expression of 25-hydroxyvitamin d(3)-1 alpha-hydroxylase. J Clin Endocrinol Metab. 2001;86:888. [PubMed]
________________________________________ PubMed articles by these authors
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• 1,25-dihydroxyvitamin-D-receptor in breast cancer cells.
Lancet. 1979 Dec 22-29; 2(8156-8157):1335-6.
[Lancet. 1979]
• 1,25-dihydroxyvitamin D3 receptors in cancer.
Lancet. 1980 Apr 12; 1(8172):828.
[Lancet. 1980]
• Differentiation of mouse myeloid leukemia cells induced by 1 alpha,25-dihydroxyvitamin D3.
Proc Natl Acad Sci U S A. 1981 Aug; 78(8):4990-4.
[Proc Natl Acad Sci U S A. 1981]
• 1,25-dihydroxyvitamin D3 and malignant melanoma: the presence of receptors and inhibition of cell growth in culture.
Endocrinology. 1981 Mar; 108(3):1083-6.
[Endocrinology. 1981]
• 1 alpha,25-dihydroxyvitamin D3 promotes fusion of mouse alveolar macrophages both by a direct mechanism and by a spleen cell-mediated indirect mechanism.
Proc Natl Acad Sci U S A. 1983 Sep; 80(18):5583-7.
[Proc Natl Acad Sci U S A. 1983]
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• Extra-renal 25-hydroxyvitamin D3-1alpha-hydroxylase in human health and disease.
J Steroid Biochem Mol Biol. 2007 Mar; 103(3-5):316-21.
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• ReviewVitamin D and its analogs as regulators of immune activation and antigen presentation.
Annu Rev Nutr. 2003; 23():117-45.
[Annu Rev Nutr. 2003]
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J Cell Biochem. 2003 Feb 1; 88(2):223-6.
[J Cell Biochem. 2003]

• Differentiation of mouse myeloid leukemia cells induced by 1 alpha,25-dihydroxyvitamin D3.
Proc Natl Acad Sci U S A. 1981 Aug; 78(8):4990-4.
[Proc Natl Acad Sci U S A. 1981]
• 1 alpha,25-dihydroxyvitamin D3 promotes fusion of mouse alveolar macrophages both by a direct mechanism and by a spleen cell-mediated indirect mechanism.
Proc Natl Acad Sci U S A. 1983 Sep; 80(18):5583-7.
[Proc Natl Acad Sci U S A. 1983]
• Induction of macrophage differentiation of human normal and leukemic myeloid stem cells by 1,25-dihydroxyvitamin D3 and its fluorinated analogues.
Cancer Res. 1984 Dec; 44(12 Pt 1):5624-8.
[Cancer Res. 1984]
• 1 alpha,25-dihydroxyvitamin D3 induces differentiation of human promyelocytic leukemia cells (HL-60) into monocyte-macrophages, but not into granulocytes.
Biochem Biophys Res Commun. 1983 Nov 30; 117(1):86-92.
[Biochem Biophys Res Commun. 1983]
• 1,25-dihydroxyvitamin D3 production and vitamin D3 receptor expression are developmentally regulated during differentiation of human monocytes into macrophages.
Blood. 1993 Aug 15; 82(4):1300-7.
[Blood. 1993]
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• Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response.
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J Immunol. 2009 Apr 1; 182(7):4289-95.
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• Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3.
FASEB J. 2005 Jul; 19(9):1067-77.
[FASEB J. 2005]
• Cutting edge: 1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression.
J Immunol. 2004 Sep 1; 173(5):2909-12.
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• Immune regulation of 25-hydroxyvitamin-D3-1alpha-hydroxylase in human monocytes.
J Bone Miner Res. 2006 Jan; 21(1):37-47.
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• IL-15 links TLR2/1-induced macrophage differentiation to the vitamin D-dependent antimicrobial pathway.
J Immunol. 2008 Nov 15; 181(10):7115-20.
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• IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes.
J Immunol. 2008 Dec 15; 181(12):8504-12.
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• Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response.
Science. 2006 Mar 24; 311(5768):1770-3.
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• Alternative splicing of vitamin D-24-hydroxylase: a novel mechanism for the regulation of extrarenal 1,25-dihydroxyvitamin D synthesis.
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[J Biol Chem. 2005]

• Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism.
J Clin Invest. 2007 Mar; 117(3):803-11.
[J Clin Invest. 2007]
• Control of the innate epithelial antimicrobial response is cell-type specific and dependent on relevant microenvironmental stimuli.
Immunology. 2006 Aug; 118(4):509-19.
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• Cutting edge: 1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression.
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• Induction of cathelicidin in normal and CF bronchial epithelial cells by 1,25-dihydroxyvitamin D(3).
J Cyst Fibros. 2007 Nov 30; 6(6):403-10.
[J Cyst Fibros. 2007]
• Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3.
FASEB J. 2005 Jul; 19(9):1067-77.
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• Vitamin D receptor as an intestinal bile acid sensor.
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• Alternative splicing of vitamin D-24-hydroxylase: a novel mechanism for the regulation of extrarenal 1,25-dihydroxyvitamin D synthesis.
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• Vitamin D3 down-regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen-associated molecular patterns.
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• Dendritic cells from human tissues express receptors for the immunoregulatory vitamin D3 metabolite, dihydroxycholecalciferol.
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[Immunology. 1987]
• 1 Alpha,25-dihydroxyvitamin D3 inhibits differentiation, maturation, activation, and survival of dendritic cells leading to impaired alloreactive T cell activation.
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• Regulation of 25-hydroxyvitamin D3-1 alpha-hydroxylase and production of 1 alpha,25-dihydroxyvitamin D3 by human dendritic cells.
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• 1,25(OH)2D3 regulates c-myc mRNA levels in tonsillar T lymphocytes.
Immunology. 1991 Dec; 74(4):589-93.
[Immunology. 1991]
• Regulation of human tonsillar T-cell proliferation by the active metabolite of vitamin D3.
Immunology. 1986 Dec; 59(4):479-84.
[Immunology. 1986]
• 1 Alpha,25-dihydroxyvitamin D3 receptor distribution and effects in subpopulations of normal human T lymphocytes.
J Clin Endocrinol Metab. 1989 Apr; 68(4):774-9.
[J Clin Endocrinol Metab. 1989]
• ReviewImmunosuppressive actions of 1,25-dihydroxyvitamin D3: preferential inhibition of Th1 functions.
J Nutr. 1995 Jun; 125(6 Suppl):1704S-1708S.
[J Nutr. 1995]
• 1alpha,25-Dihydroxyvitamin d3 has a direct effect on naive CD4(+) T cells to enhance the development of Th2 cells.
J Immunol. 2001 Nov 1; 167(9):4974-80.
[J Immunol. 2001]
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• ReviewExpanding the effector CD4 T-cell repertoire: the Th17 lineage.
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• ReviewIL-17 family cytokines and the expanding diversity of effector T cell lineages.
Annu Rev Immunol. 2007; 25():821-52.
[Annu Rev Immunol. 2007]
• ReviewTh17: the third member of the effector T cell trilogy.
Curr Opin Immunol. 2007 Dec; 19(6):652-7.
[Curr Opin Immunol. 2007]
• ReviewTh17 cells: effector T cells with inflammatory properties.
Semin Immunol. 2007 Dec; 19(6):362-71.
[Semin Immunol. 2007]
• Altered endocrine and autocrine metabolism of vitamin D in a mouse model of gastrointestinal inflammation.
Endocrinology. 2008 Oct; 149(10):4799-808.
[Endocrinology. 2008]

• In vitro generation of interleukin 10-producing regulatory CD4(+) T cells is induced by immunosuppressive drugs and inhibited by T helper type 1 (Th1)- and Th2-inducing cytokines.
J Exp Med. 2002 Mar 4; 195(5):603-16.
[J Exp Med. 2002]
• Topically applied 1,25-dihydroxyvitamin D3 enhances the suppressive activity of CD4+CD25+ cells in the draining lymph nodes.
J Immunol. 2007 Nov 1; 179(9):6273-83.
[J Immunol. 2007]
• A 1alpha,25-dihydroxyvitamin D(3) analog enhances regulatory T-cells and arrests autoimmune diabetes in NOD mice.
Diabetes. 2002 May; 51(5):1367-74.
[Diabetes. 2002]
• ReviewVitamin D and type 1 diabetes mellitus: state of the art.
Trends Endocrinol Metab. 2005 Aug; 16(6):261-6.
[Trends Endocrinol Metab. 2005]
• IL-10 signaling is essential for 1,25-dihydroxyvitamin D3-mediated inhibition of experimental autoimmune encephalomyelitis.
J Immunol. 2006 Nov 1; 177(9):6030-7.
[J Immunol. 2006]
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• 1 Alpha,25-dihydroxyvitamin D3 receptor distribution and effects in subpopulations of normal human T lymphocytes.
J Clin Endocrinol Metab. 1989 Apr; 68(4):774-9.
[J Clin Endocrinol Metab. 1989]
• T lymphocytes and their CD4 subset are direct targets for the inhibitory effect of calcitriol.
Cell Immunol. 1989 Dec; 124(2):320-33.
[Cell Immunol. 1989]
• Expression of 1,25-dihydroxyvitamin D(3) receptor in the immune system.
Arch Biochem Biophys. 2000 Feb 15; 374(2):334-8.
[Arch Biochem Biophys. 2000]
• Regulatory effects of 1alpha,25-dihydroxyvitamin D3 on the cytokine production of human peripheral blood lymphocytes.
J Clin Endocrinol Metab. 1999 Oct; 84(10):3739-44.
[J Clin Endocrinol Metab. 1999]
• Mechanism in 1,25(OH)2D3-induced suppression of helper/suppressor function of CD4/CD8 cells to immunoglobulin production in B cells.
Cell Immunol. 1990 Apr 15; 127(1):12-25.
[Cell Immunol. 1990]
See more articles cited in this paragraph
• The anti-inflammatory effects of 1,25-dihydroxyvitamin D3 on Th2 cells in vivo are due in part to the control of integrin-mediated T lymphocyte homing.
Eur J Immunol. 2004 Apr; 34(4):1068-76.
[Eur J Immunol. 2004]
• DCs metabolize sunlight-induced vitamin D3 to ‘program’ T cell attraction to the epidermal chemokine CCL27.
Nat Immunol. 2007 Mar; 8(3):285-93.
[Nat Immunol. 2007]
• Failure of T cell homing, reduced CD4/CD8alphaalpha intraepithelial lymphocytes, and inflammation in the gut of vitamin D receptor KO mice.
Proc Natl Acad Sci U S A. 2008 Dec 30; 105(52):20834-9.
[Proc Natl Acad Sci U S A. 2008]

• 1 alpha,25-Dihydroxyvitamin D3-binding macromolecules in human B lymphocytes: effects on immunoglobulin production.
J Immunol. 1986 Apr 15; 136(8):2734-40.
[J Immunol. 1986]
• 1 alpha,25-dihydroxyvitamin D3 inhibits pokeweed mitogen-stimulated human B-cell activation: an analysis using serum-free culture conditions.
Immunology. 1985 Sep; 56(1):161-7.
[Immunology. 1985]
• 1 alpha,25-dihydroxyvitamin D3 suppresses proliferation and immunoglobulin production by normal human peripheral blood mononuclear cells.
J Clin Invest. 1984 Aug; 74(2):657-61.
[J Clin Invest. 1984]
• Modulatory effects of 1,25-dihydroxyvitamin D3 on human B cell differentiation.
J Immunol. 2007 Aug 1; 179(3):1634-47.
[J Immunol. 2007]
• DCs metabolize sunlight-induced vitamin D3 to ‘program’ T cell attraction to the epidermal chemokine CCL27.
Nat Immunol. 2007 Mar; 8(3):285-93.
[Nat Immunol. 2007]

• Prevalence of vitamin D insufficiency in an adult normal population.
Osteoporos Int. 1997; 7(5):439-43.
[Osteoporos Int. 1997]
• ReviewVitamin D deficiency.
N Engl J Med. 2007 Jul 19; 357(3):266-81.
[N Engl J Med. 2007]
• Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004.
Arch Intern Med. 2009 Mar 23; 169(6):626-32.
[Arch Intern Med. 2009]

• Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response.
Science. 2006 Mar 24; 311(5768):1770-3.
[Science. 2006]
• ReviewVitamin D in the treatment of pulmonary tuberculosis.
J Steroid Biochem Mol Biol. 2007 Mar; 103(3-5):793-8.
[J Steroid Biochem Mol Biol. 2007]
• A single dose of vitamin D enhances immunity to mycobacteria.
Am J Respir Crit Care Med. 2007 Jul 15; 176(2):208-13.
[Am J Respir Crit Care Med. 2007]
• The effect of vitamin D as supplementary treatment in patients with moderately advanced pulmonary tuberculous lesion.
Acta Med Indones. 2006 Jan-Mar; 38(1):3-5.
[Acta Med Indones. 2006]
• Vitamin D as supplementary treatment for tuberculosis: a double-blind, randomized, placebo-controlled trial.
Am J Respir Crit Care Med. 2009 May 1; 179(9):843-50.
[Am J Respir Crit Care Med. 2009]

• ReviewVitamin D and multiple sclerosis.
J Cell Biochem. 2008 Oct 1; 105(2):338-43.
[J Cell Biochem. 2008]
• Vitamin D3 confers protection from autoimmune encephalomyelitis only in female mice.
J Immunol. 2005 Sep 15; 175(6):4119-26.
[J Immunol. 2005]
• 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by inhibiting chemokine synthesis and monocyte trafficking.
J Neurosci Res. 2007 Aug 15; 85(11):2480-90.
[J Neurosci Res. 2007]
• Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis.
Physiol Genomics. 2004 Jul 8; 18(2):141-51.
[Physiol Genomics. 2004]
• IL-10 signaling is essential for 1,25-dihydroxyvitamin D3-mediated inhibition of experimental autoimmune encephalomyelitis.
J Immunol. 2006 Nov 1; 177(9):6030-7.
[J Immunol. 2006]

• ReviewVitamin D and diabetes.
Diabetologia. 2005 Jul; 48(7):1247-57.
[Diabetologia. 2005]
• Lower levels of plasma 25-hydroxyvitamin D among young adults at diagnosis of autoimmune type 1 diabetes compared with control subjects: results from the nationwide Diabetes Incidence Study in Sweden (DISS).
Diabetologia. 2006 Dec; 49(12):2847-52.
[Diabetologia. 2006]
• ReviewVitamin D in type 1 diabetes prevention.
J Nutr. 2005 Feb; 135(2):323-5.
[J Nutr. 2005]
• Protection from type 1 diabetes by vitamin D receptor haplotypes.
Ann N Y Acad Sci. 2006 Oct; 1079():327-34.
[Ann N Y Acad Sci. 2006]
• Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice.
Diabetologia. 2004 Mar; 47(3):451-62.
[Diabetologia. 2004]

• Vitamin D status in children and young adults with inflammatory bowel disease.
Pediatrics. 2006 Nov; 118(5):1950-61.
[Pediatrics. 2006]
• ReviewReport on the vitamin D status of adult and pediatric patients with inflammatory bowel disease and its significance for bone health and disease.
Inflamm Bowel Dis. 2006 Dec; 12(12):1162-74.
[Inflamm Bowel Dis. 2006]
• Nutrition assessment of patients with inflammatory bowel disease.
JPEN J Parenter Enteral Nutr. 2007 Jul-Aug; 31(4):311-9.
[JPEN J Parenter Enteral Nutr. 2007]
• Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury.
BMC Immunol. 2007 Mar 30; 8():5.
[BMC Immunol. 2007]
• A crucial role for the vitamin D receptor in experimental inflammatory bowel diseases.
Mol Endocrinol. 2003 Dec; 17(12):2386-92.
[Mol Endocrinol. 2003]
See more articles cited in this paragraph
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——–

Cães cobaias: Experimentos com animais revoltam alunos da Universidade Federal de Santa Maria

Cães cobaias: Experimentos com animais revoltam alunos da Universidade Federal de Santa Maria

 

 

Zero Hora

Cães cobaias

10/05/2012 | 03h54

 

Experimentos com animais revoltam alunos da Universidade Federal de Santa Maria

http://zerohora.clicrbs.com.br/rs/geral/noticia/2012/05/experimentos-com-animais-revoltam-alunos-da-universidade-federal-de-santa-maria-3753990.html

 

Projeto na UFSM removia parte de mandíbulas e maxilares para colocação de placas de titânio

 

Denúncias mostraram cachorros em situação precária, mas doutorando nega maus-tratos aos animais

 

Foto: Jean Pimentel / Agencia RBSÉ

 

 

 

inquestionável o avanço que as pesquisas científicas têm proporcionado no desenvolvimento da medicina humana e veterinária.

 

Mas muitos desses estudos, que utilizam experimentação animal, são polêmicos e deixam indignados quem simpatiza com os bichos.

 

Em Santa Maria, o projeto de um doutorando da Pós-Graduação de Medicina Veterinária da Universidade Federal de Santa Maria (UFSM) revoltou alunos, funcionários e professores do curso.

 

O experimento consistiu em criar e testar uma placa de titânio para recomposição de mandíbulas e maxilares de cães que, por causa de um câncer na boca, tenham passado por cirurgia de remoção de parte ou de toda a mandíbula.

 

O projeto testou o desempenho de próteses humanas e de uma placa específica desenvolvida pelo doutorando com ajuda de engenheiros para a anatomia dos cães.

 

O estudante usou cães cobaias que tiveram parte ou toda a mandíbula retirada para a colocação e teste das placas. O doutorando Cristiano Gomes e o orientador dele, professor Ney Luis Pippi, negaram os maus-tratos.

 

Imagens enviadas ao jornal Diário de Santa Maria – as pessoas que mandaram pediram suas identidades preservadas – mostraram os animais magros, trancados em gaiolas, deitados em meio à própria urina, com pratos de ração virados e vazios, em um ambiente sem condições de higiene.

 

— O problema foi que houve descaso no cuidado com os animais. O Cristiano praticamente não acompanhou o pós-operatório, deixando tudo para estagiários que, muitas vezes, não sabiam nem o que fazer — disse uma estudante, que preferiu não se identificar.

 

Gomes diz que os cães estavam sob os cuidados de 12 pessoas – além dele, quatro doutorandos, três mestrandos e quatro bolsistas da graduação. O estudante teria ficado na cidade até março, acompanhando os animais e, depois, teria mudado para Tubarão (SC), onde passou em um concurso. Segundo ele, depois do seu afastamento, os demais membros do projeto permaneceram cuidando dos bichos.

 

Ainda segundo Gomes, no pós-operatório, os animais teriam ficado cerca de uma semana, recebendo medicação (anti-inflamatórios e antibióticos), diariamente, de manhã, à tarde e à noite. Conforme o doutorando, todos eram alimentados por sonda com ração umedecida e batida no liquidificador.

 

UFSM diz que não sabia dos desdobramentos da pesquisa

 

Tanto a coordenação da pós-graduação em Medicina Veterinária quanto a direção do Hospital Veterinário e a reitoria da UFSM não tinham conhecimento dos desdobramentos da pesquisa sobre câncer de boca em cães.

 

— Fiquei sabendo da história na última sexta-feira. A coordenação (da pós) não tem ingerência sobre os experimentos dos pós-graduandos. A coordenação não tem como sair e inspecionar os cento e poucos alunos que temos — disse a coordenadora da pós-graduação em Medicina Veterinária, professora Sonia Terezinha dos Anjos Lopes.

 

A coordenadora comentou que iria se informar com o doutorando Cristiano Gomes e com seu orientador, Ney Luis Pippi, sobre o ocorrido no projeto.

 

— A área física é a do hospital, mas o hospital não interfere nem nas aulas nem nas pesquisas da pós — disse Luiz Sérgio Segala de Oliveira, diretor do Hospital Veterinário da UFSM.

 

A reitoria disse que só se manifestará sobre o assunto depois do pronunciamento do Comitê de Ética.

 

ZERO HORA

Animais, Santa Maria universidade

Mirella Pacheco

  

Espero uma ação efetiva do Ministerio Publico, CRMS-RS, MEC e da própria UFSM. Saibam que uma cadela prenha foi tb utilizada no “experimento”, conforme a reportagem do Diario de Santa Maria. Leiam a reportagem ATÉ ONDE IR EM NOME DA CIENCIA? Tudo tem limite! Qual a etica deste profissional??

 

11/05/2012 | 11h26

Michele Cunha Lima

 ————

Projeto do Novo Código Penal: aborto, desinformação e impedimentos legislativos

“1) Tem GRAVES INCONSTITUCIONALIDADES e não se tem suscitado este assunto como necessário.

2) Tem normas penais em branco que tornam impossível fazer uma tipificação de conduta, senão com alto grau de subjepúblicas simuladas para aparentar consulta à sociedade.

3) Foi feito às pressas com consultas a indispensável qualificação técnica.

4) Foi elaborado por uma Comissão que é SUBORDINADA à IDEOLOGIA PARTIDÁRIA do Governo Federal [PT] e sem tividades – o que permite perseguição aos desafetos do Poder.

5) Insere-se dentro de um procedimento golpista com a atual constituição do Congresso Nacional.”

Por Celso Galli Coimbra

Projeto do Novo Código Penal: aborto, desinformação e impedimentos legislativos

http://biodireitomedicina.wordpress.com/2012/05/09/projeto-do-novo-codigo-penal-aborto-desinformacao-e-impedimentos-legislativos/

“Norma específica da Convenção Americana de Direitos Humanos (CADH), firmada pelo Brasil em 1992 e, por isso integrada como norma de direitos humanos da Constituição Federal como cláusula pétrea por força do disposto no art. 5º, § 2º (“Os direitos e garantias expressos nesta Constituição não excluem outros decorrentes do regime e dos princípios por ela adotados, ou dos tratados internacionais em que a República do Brasil seja parte.”) e § 3º (“Os tratados e convenções internacionais sobre direitos humanos […] serão equivalentes às emendas constitucionais.”), assegura a proteção à vida humana desde a concepção, no seu art. 4º: “Toda pessoa tem direito de que se respeite sua vida. Esse direito deve ser protegido pela lei e, em geral, desde o momento da concepção. Ninguém pode ser privado da vida arbitrariamente.”

“Diante destes mandamentos constitucionais, acrescidos pela integração da CADH ao constitucionalismo brasileiro, em 1992, verifica-se: (1) o nascituro, desde a concepção, passa a ser considerado pessoa para o direito, não mais apenas vida humana que já seria protegida por ele; e (2) seu direito à vida está protegido desde o momento da concepção sob o status de cláusula pétrea constitucional por ser preceito de direitos humanos; (3) o que significa que a vida do nascituro, desde a concepção, não pode ser desrespeitada sequer por emenda à Constituição, diante do art. 60, § 4º, IV, da CF: “Não será objeto de DELIBERAÇÃO a proposta de emenda tendente a abolir os direitos e garantias individuais.” (grifos nossos)”

Projeto do Novo Código Penal: aborto, desinformação e impedimentos legislativos

09/05/2012 — Celso Galli Coimbra

 

Por Celso Galli Coimbra

 

Em 09 de março de 2012, foi publicada a notícia de que a Comissão de Juristas nomeada pelo Senado para elaborar o anteprojeto de lei do novo Código Penal estaria ampliando as regras para o aborto legal.  Se formos examinar o conteúdo desta suposta “ampliação” veremos que é mais uma pegadinha jurídica em torno desta questão, pois o que está de fato sendo proposto é a total liberação do aborto [1].

 

É  induzir a erro a sociedade brasileira dizer que existe mera “ampliação” das hipóteses de aborto, mas que ele “continua sendo crime”, pois o texto em que está exarada confere norma em branco à administração da subjetividade de profissionais da medicina e da psicologia para autorizar o amplo abortamento, quando preceitua que abortar é possível sem punibilidade  “Por vontade da gestante até a 12ª semana de gravidez, se o médico ou o psicólogo atestar que a mulher não apresenta condições de arcar com a maternidade”

 

Se qualquer médico ou psicólogo puder atestar que a mulher pode abortar até a 12a. semana de gravidez por não ter “condições de arcar com a maternidade”, então o aborto pode ser objeto de mera concessão em aberto de médicos e psicólogos e ainda sob o indefinido pretexto de “não poder arcar com a maternidade”.  Para resumir o assunto: é suficiente uma mulher dizer para médico ou psicólogo que não quer continuar a gestação, que isto pode, sem dúvida alguma, ser aceito como “falta de condições para arcar com a maternidade”.

 

Porém, antes deste estratagema, é notória a falta de competência legislativa para o Congresso Nacional aprovar a alteração do momento de proteção ao início da vida humana estabelecido no momento da concepção ou sequer exceções ao mesmo, que por disposição constitucional – a seguir demonstrada – sequer por Emenda Constitucional pode ser objeto de tramitação no Poder Legislativo. Um Código Penal é apenas legislação ordinária federal.

 

LEI COM CONTEÚDO ABORTISTA SEQUER PODE TER TRAMITAÇÃO NO LEGISLATIVO ou LEI INCONSTITUCIONAL É DIFERENTE DE TRAMITAÇÃO INCONSTITUCIONAL

 

Dizer que uma lei é inconstitucional é diferente de dizer que a tramitação de projetos de lei que têm por objeto a alteração do momento de proteção à vida humana, ou abertura de exceções ao mesmo, não podem ter andamento para votação pelos parlamentares.

 

Uma lei pode ser inconstitucional e mesmo assim pode ter andamento nas casas legislativas, seguida da sanção dos Executivos e entrar em vigor no Brasil, de tal forma que sua inconstitucionalidade somente possa vir a ser declarada para todos ou para alguns mediante ação judicial própria.

 

Ao contrário, quando o valor maior protegido pela Constituição é de caráter pétreo por dizer respeito a tratados de direitos humanos firmados pelo Brasil e que seguiram a ratificação interna e formal prevista na época dentro do país, SEQUER a tramitação de Emendas Constitucionais – que já é o exercício de Poder Constituinte derivado – são permitidas na vigência da atual Constituição.

 

Isto é assim determinado para não haver risco de uma lei inconstitucional – que altere o momento de proteção da vida humana – possa entrar em vigor para ter – e somente depois deste momento – a sua inconstitucionalidade levada a julgamento.

 

Nestes casos especiais, o legislador constitucional impede, então, é a própria tramitação no Congresso Nacional.

 

Esta diferença vital entre lei inconstitucional e projeto de lei cuja a tramitação legislativa está proibida passa normalmente despercebida. No último caso, em situações excepcionais, como a alteração do momento de proteção à vida humana ou exceções a este momento, o que é inconstitucional é desde logo a tramitação de um PL ou emenda constitucional com este conteúdo.

 

Isto significa que apenas com uma nova Constituição seria cogitável esse encaminhamento, não com a que está em vigor.

 

A CONVENÇÃO AMERICANA DE DIREITOS HUMANOS NA CONSTITUIÇÃO FEDERAL

 

Norma específica da Convenção Americana de Direitos Humanos (CADH), firmada pelo Brasil em 1992 e, por isso integrada como norma de direitos humanos da Constituição Federal como cláusula pétrea por força do disposto no art. 5º, § 2º (“Os direitos e garantias expressos nesta Constituição não excluem outros decorrentes do regime e dos princípios por ela adotados, ou dos tratados internacionais em que a República do Brasil seja parte.”) e § 3º (“Os tratados e convenções internacionais sobre direitos humanos […] serão equivalentes às emendas constitucionais.”), assegura a proteção à vida humana desde a concepção, no seu art. 4º: “Toda pessoa tem direito de que se respeite sua vida. Esse direito deve ser protegido pela lei e, em geral, desde o momento da concepção. Ninguém pode ser privado da vida arbitrariamente.”

 

Diante destes mandamentos constitucionais, acrescidos pela integração da CADH ao constitucionalismo brasileiro, em 1992, verifica-se: (1) o nascituro, desde a concepção, passa a ser considerado pessoa para o direito, não mais apenas vida humana que já seria protegida por ele; e (2) seu direito à vida está protegido desde o momento da concepção sob o status de cláusula pétrea constitucional por ser preceito de direitos humanos; (3) o que significa que a vida do nascituro, desde a concepção, não pode ser desrespeitada sequer por emenda à Constituição, diante do art. 60, § 4º, IV, da CF: “Não será objeto de DELIBERAÇÃO a proposta de emenda tendente a abolir os direitos e garantias individuais.” (grifos nossos)

 

A Constituição está proibindo que projetos de lei e emendas de conteúdo abortista possam seguir para deliberação do Poder Legislativo: a própria tramitação destes projetos, sejam de leis, sejam de emendas, não podem ir além da Comissão de Constituição e Justiça do Poder Legislativo, onde constatada esta inconstitucionalidade de conteúdo, eles terão que ser obrigatoriamente vetados e excluídos de encaminhamento para deliberação do Poder Legislativo Federal, por força do citado acima.

 

É um direito pétreo de proteção da vida humana, desde a sua concepção, a proibição de deliberação de leis ou emendas que comprometam a sua existência. Como a todo direito sempre corresponde uma ação judicial em sua defesa, caso aquele não seja respeitado, desde esta fase proibitiva de deliberação, cabe acionar o Poder Judiciário, que tem por última instância nesta hipótese a Corte Interamericana de Direitos Humanos, sem que isto represente interferência alguma em outro poder, se a CCJ aprovar para deliberação do Poder Legislativo emenda ou projeto de lei que conflite com o art. 60, § 4º, IV, da CF.

 

Celso Galli Coimbra

OABRS 11.352

cgcoimbra@gmail.com

 

1. Comissão do novo Código Penal amplia regras para aborto legal e eutanásia

http://www.estadao.com.br/noticias/vidae,comissao-do-novo-codigo-penal-amplia-regras-para-aborto-legal-e-eutanasia,846404,0.htm

 

2. Impossibilidade de legalização do aborto no Brasil desde sua proibição constitucional de ir à deliberação pelo Poder Legislativo

http://biodireitomedicina.wordpress.com/2008/11/22/impossibilidade-de-legalizacao-do-aborto-no-brasil-desde-sua-proibicao-constitucional-de-ir-a-deliberacao-pelo-poder-legislativo/

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disponivel em

http://biodireitomedicina.wordpress.com/2012/05/09/projeto-do-novo-codigo-penal-aborto-desinformacao-e-impedimentos-legislativos/

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