Potential biomarker to detect SCID (severe combined immunodeficiency)

 

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Xin M. Luo (right), an assistant professor of immunology in the Virginia-Maryland College of Veterinary Medicine, and Husen Zhang, a research assistant professor of Civil and Environmental Engineering, work to discover ways to detect a deadly childhood illness.

A genetic disease called SCID, short for severe combined immunodeficiency, forces patients to breathe filtered air and avoid human contact because their bodies' natural defenses are too weak to fight germs.

Although it affects fewer than 2,000 new births each year worldwide, SCID is a cousin to acquired immune deficiency syndrome triggered by a human immunodeficiency virus -- HIV/AIDS.

Now, using a mouse model, Virginia Tech researchers in the September issue of The ISME Journal describe a potential biomarker to detect SCID by analyzing for a microbe in the fecal matter of infants.

"If SCID is not detected, children cannot live past their first year," said Xin M. Luo, an assistant professor of immunology Virginia-Maryland College of Veterinary Medicine. "Now, we may have a noninvasive way to screen for this disease because this microbe may be present only in negligible amounts in healthy, young children. If larger populations of the microbe are present, quick examination is needed to prevent a potentially deadly emergency."

Luo, a faculty member in the Department of Biomedical Sciences and Pathobiology, worked with Husen Zhang, a research assistant professor in the Department of Civil and Environmental Engineering in the College of Engineering, to compare the gut microbes in healthy mice with those in mice with a defective immune system, both before and after weaning. They found that the defective mice had a greater supply of a particular microbe called Akkermansia muciniphila.

"This is also a human intestinal microbe," said Zhang, a microbial ecologist who performed the gene sequencing in partnership with the Virginia Bioinformatics Institute. "Although it is rather newly discovered, it has been there for a long time. Previous reports found that the microbe increases with antibiotic use, indicating that it might thrive when other gut microbes don't survive a round of antibiotics."

When Luo performed bone marrow transplants on the defective mice to give them an adaptive immune system, the researchers found that this particular microbe returned to normal levels. The difference only occurs in younger mice and gradually subsides with age.

"This is an interesting finding because it means we can potentially screen for this microbe at an early age to find defects in the immune system," Luo said.

Although SCID affects less than 0.1 percent of the human population, the disease is typically fatal to children without diagnosis and treatment within their first year. Physicians have found success in treating the genetic disorder with bone marrow transplants.

The researchers are collaborating with a pediatrician to test samples from human infants and have filed a provisional patent for the biomarker screening. Joshua Sparks, a third-year medical student at the Virginia Tech Carilion School of Medicine, also assisted with the research as a part of his degree program.

Many researchers have looked into the impact of gut microbes on the immune system -- with recent studies investigating the unintended effects of antibiotics on helpful bacteria or the use of probiotics to boost the immune system. But Luo and Zhang are among only a handful of researchers who have turned their attention in the opposite direction.

"There have been many studies recently on how gut microbes modulate the immune response, but we wanted to do the opposite" Luo said. "We are asking the question, 'How does our immune system affect bacteria in the gut?' "

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Story Source:

The above story is based on materials provided by Virginia Tech. Note: Materials may be edited for content and length.

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Journal Reference:

1. Husen Zhang, Joshua B Sparks, Saikumar V Karyala, Robert Settlage, Xin M Luo. Host adaptive immunity alters gut microbiota. The ISME Journal, 2014; DOI: 10.1038/ismej.2014.165

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Depression increasing in many countries including in the USA.

 

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Analyzing data from 6.9 million adolescents and adults from all over the country, Twenge found that the US people now report more psychosomatic symptoms of depression, such as trouble sleeping and trouble concentrating, than their counterparts in the 1980s.

"Previous studies found that more people have been treated for depression in recent years, but that could be due to more awareness and less stigma," said Twenge, the author of "Generation Me: Why Today's Young people from the USA are More Confident, Assertive, Entitled -- and More Miserable than Ever Before." "This study shows an increase in symptoms most people don't even know are connected to depression, which suggests adolescents and adults really are suffering more."

Compared to their 1980s counterparts, teens in the 2010s are 38 percent more likely to have trouble remembering, 74 percent more likely to have trouble sleeping and twice as likely to have seen a professional for mental health issues. College students surveyed were 50 percent more likely to say they feel overwhelmed, and adults were more likely to say their sleep was restless, they had poor appetite and everything was an effort -- all classic psychosomatic symptoms of depression.

"Despite all of these symptoms, people are not any more likely to say they are depressed when asked directly, again suggesting that the rise is not based on people being more willing to admit depression," said Twenge.

The study also found that the suicide rate for teens decreased, though the decline was small compared to the increase in symptoms of depression. With the use of anti-depressant medications doubling over this time period, Twenge speculates that medication may have helped those with the most severe problems but has not reduced increases in other symptoms that, she says, can still cause significant issues.

Twenge's findings were published in the journal Social Indicators Research, and an updated and revised edition of "Generation Me" is being released today.

 

Nota do blog – Depressão e outras doenças relacionadas são observadas em quase todos os paises, emergentes e desenvolvidos, e podem estar ligadas à fatores climáticos, econômicos, sociais, comportamentais, e outros. Nos Estados Unidos que é o país-alvo do artigo acima, hábitos prejudiciais, como privação de sono, uso de estimulantes ou medicamentos controlados, excesso ou falta de alguns tipos de alimentos, como por exemplo, excesso de açúcares e falta de verduras de folhas verde-escuras, podem estar contribuindo para essa onda de estados depressivos, e tantos outros fatores mais. Os adolescentes e os adultos jovens, na maior parte, ficam muito tempo ligados em jogos, celulares, computadores, televisão, e esquecem-se dos exercícios, e não se preocupam em obterem informações ligadas à um estilo de vida saudável. O resultado será então um progressivo cansaço físico e mental, que será traduzido por um estado depressivo.

Mas vários outros paises desenvolvidos também sofrem com esses mesmos problemas, não sendo portanto uma “epidemia de depressão” somente dos Estadunidenses. Mas um país tão importante para o mundo em geral deve incrementar seus esforços no sentido de determinar as causas desse aumento nas condições depressivas.

Quando os Estados Unidos esfria, o resto da humanidade bate os dentes.

 

 

 

 

 

 

Failed cancer vaccines might live again with new immune drugs

Health

 

Reuters September 28, 2014 , 2 : 04 pm GST

 

Using vaccines to fight cancer is a field littered with failures but experts believe it is possible the approach could get a new lease of life if such shots are combined with a new class of drugs called checkpoint inhibitors.
Unlike traditional preventative vaccines, therapeutic cancer vaccines are designed for people with established disease and are supposed to boost the patient's immune system to keep tumours at bay.
Unfortunately, the theory has not worked out in practice because, while the vaccines are successful at triggering a response from the "foot soldiers" of the immune system, cancer cells still manage to escape detection.
The result has been a series of failures with high-profile experimental cancer vaccines such as Merck KGaA's Stimuvax and GlaxoSmithKline's MAGE-A3.

GSK threw in the towel on its vaccine in April, dashing hopes for a project that was once seen as a potential multibillion-dollar sales opportunity in lung cancer and melanoma.
Johan Vansteenkiste of Belgium's University Hospitals Leuven, who led research into use of MAGE-A3 in lung cancer, reported full results of the failure at a medical meeting on Sunday and said the setback was a clear disappointment.
But he thinks the new checkpoint inhibitors, which are designed to stop the molecular trickery that is used by tumour cells to escape detection by the immune system, could finally unlock the value of such vaccines.
"For future progress, I think a combination of vaccination and checkpoint inhibition may be of major interest," he told the European Society of Medical Oncology annual congress in Madrid.
Advances with checkpoint inhibitors - particularly so-called PD-1 and PD-L1 drugs being developed by Bristol-Myers Squibb , Merck & Co, Roche and AstraZeneca - is dominating discussion at this year's ESMO meeting.
The new drugs are generating promising results in a growing range of tumour types and scientists are now casting around for novel ways to combine them with other therapies to get even better outcomes.
Therapeutic vaccines could be one such promising avenue, since they have very few side effects compared to many harsh cancer treatments.
Roche Chief Executive Severin Schwan said earlier this month that the Swiss drugmaker - the world's largest maker of cancer drugs - was already exploring ways of combining its checkpoint inhibitors with vaccines that had failed in tests when given on their own.

SAP compra desenvolvedora de softwares Concur por US$7,3 bi

 

Empresa fortaleceu sua posição em computação em nuvem, mas levou suas ações a cairem quase 3 por cento por preocupações sobre o preço

Krisztian Bocsi/Bloomberg

SAP: negócio acelera crescimento na nuvem e protege posição em administração de despesas

Frankfurt - A alemã SAP acertou a aquisição da desenvolvedora norte-americana de softwares Concur por 7,3 bilhões de dólares em caixa, fortalecendo sua posição em computação em nuvem mas levando suas ações a cairem quase 3 por cento por preocupações sobre o preço.

A SAP tem sido lenta em abraçar a computação em nuvem, que permite que negócios cortem custos ao descartar grandes servidores para sistemas baseados em rede, mas o negócio com a Concur anunciado no final da quinta-feira acelera seu crescimento na nuvem ao mesmo tempo que protege sua posição em administração de despesas e viagens.

A companhia alemã de softwares empresarias disse que vai oferecer 129 dólares por ação pela Concur, um prêmio de 20 por cento sobre o preço de fechamento em 17 de setembro e pouco abaixo da máxima recorde de 130,36 dólares alcançada pelo papel em janeiro, após dois anos de avanços.

"Parece caro. Porém, acreditamos que a Concur é líder em seu mercado e as potenciais sinergias serão um acréscimo valioso", disseram analistas da Bernstein em nota.

A SAP, que compete em computação em nuvem com rivais globais incluindo a Oracle, IBM e Salesforce, vai financiar a aquisição da Concur através de um acordo de linha de crédito de até 7 bilhões de euros (9 bilhões de dólares).

Com a aquisição da Concur, a SAP ampliará seus usuários de nuvem para 50 milhões, antes 38 milhões.

O papel da SAP recuava 3,6 por cento, às 8h25 (horário de Brasília), uma das quedas mais fortes dentre o índice europeu de tecnologia que caía nesta sexta-feira, em meio ao mercado mais amplo sustentado por alívio pela Escócia ter votado por continuar parte do Reino Unido.

Guia de smartphones: confira os lançamentos de setembro de 2014

 

Setembro foi um mês bastante movimentado no Brasil e no mundo para quem deseja comprar um novo telefone. Por aqui, a Motorola lançou novas versões para os seus populares Moto X e Moto G, acompanhada da LG com variantes do G3. Lá fora, a Apple roubou a cena ao apresentar os novos iPhone 6 e iPhone 6 Plus, assim como a Samsung, Sony e Microsoft com mais modelos. Confira os destaques do mês.

Veja também: Conheça os smartphones top de linha do mercado brasileiro

Lançamentos no Brasil

Motorola Moto X (2014)

O Moto X, top de linha da Motorola, ganhou uma nova e mais poderosa versão neste mês. O modelo 2014 do aparelho conta agora com uma tela de 5,2 polegadas Full HD (1080p), Android 4.4.4 (KitKat) e uma câmera de 13 megapixels com flash Dual LED e gravação em 4K, enquanto na parte frontal o sensor possui 2 megapixels. O aparelho traz ainda algumas funções exclusiva da Motorola, como o recurso de controle por voz, o display inteligente e outros.

Novo Moto X da Motorola recebeu melhorias na tela, câmera e especificações (Isadora Díaz/TechTudo)

Na parte interna, o Moto X traz um processador quad-core Snapdragon 801 de 2,5 GHz, 2 GB de RAM e 32 GB de memória interna, sem entrada para cartão de memória. Estão presentes ainda a bateria de 2.300 mAh e as conectividades 4G, 3G, Wi-Fi, NFC e Bluetooth. O Moto X (2014) pode ser encontrado pelo preço sugerido de R$ 1499.

- Motorola Moto G (2014)

O Novo Moto G conta com opção com TV integrada (Foto: Isadora Díaz/TechTudo)

O Moto G também ganhou uma atualização da Motorola. A nova versão do modelo possui 5 polegadas com resolução HD, Android 4.4.4 (KitKat) e câmera traseira de 8 megapixels com gravação HD, além de frontal de 2 MP. O processador é um Snapdragon 400 quad-core de 1,4 GHz, a memória RAM tem 1 GB e o armazenamento interno possui 8 ou 16 GB, expansíveis em até 32 GB por microSD. O aparelho pode ser encontrado na versão com um só chip por R$ 699 ou na versão dual-chip com TV Digital por R$ 799.

- LG G3 Stylus

LG G3 Stylus tem tela de 5,5 polegadas, Android KitKat e canetinha (Foto: Divulgação/LG)

O G3 Stylus é uma versão mais simples do top de linha da LG, equipado com Android 4.4.2 (KitKat) e uma caneta Stylus. O aparelho traz ainda uma tela de 5,5 polegadas com resolução de 960 x 540 pixels, câmera traseira de 13 megapixels e frontal de 1,3 MP. Nas configurações há um processador quad-core MediaTek de 1,3 GHz, 1 GB de RAM e 8 GB de memória interna, expansível em até 32 GB. A bateria possui 3.000 mAh e as conectividades 3G, Wi-Fi e Bluetooth completam as configurações. O preço sugerido é de R$ 1.199.

- LG G3 Beat

LG G3 Beat é uma versão mais simples do LG G3 com tela de 5 polegadas (Foto: Divulgação/LG)

O LG G3 Beat é outra versão mais simples do LG G3, equipado com uma tela de 5 polegadas HD (720p), Android 4.4.2 (KitKat) e câmera traseira de 8 megapixels, além de frontal de 1,3 MP. O processador é um quad-core Snapdragon 400 de 1,2 GHz, 1 GB de RAM e 8 GB de armazenamento interno, expansíveis em até 64 GB. A bateria possui 2.540 mAh e as conectividades são 3G, Wi-Fi e Bluetooth. O preço de lançamento sugerido é de R$ 999.

- LG G2 Lite

LG G2 Lite tem tela 4,5 polegadas, Android KitKat e processador quad-core (Foto: Divulgação/LG)

O G2 Lite é um aparelho de entrada da LG, equipado com uma tela de 4,5 polegadas com resolução de 800 x 480 pixels, Android 4.4.2 (KitKAt) e câmera traseira de 8 megapixels, além de frontal. Nas configurações, há um processador quad-core 1,2 Ghz, 1 GB de RAM e 4 GB de armazenamento interno, expansíveis em até 32 GB. A bateria do modelo possui 1.820 mAh e as conectividades são 3G, Wi-Fi e Bluetooth.

Destaques internacionais

- iPhone 6

O iPhone 6 é o novo top de linha da Apple que chegou com a aguardada tela Retina de 4,7 polegadas e o iOS 8. Equipado com um display com resolução de 1334 x 750 pixels e densidade de 326 ppi, o aparelho traz ainda uma câmera traseira com 8 megapixels com flash dual-LED e gravação em câmera lenta HD a 240 frames por segundo. Outras novidades são o leitor TouchID e o sistema de pagamento Apple Pay.

iPhone 6 ganhou tela Retina de 4,7 polegadas HD, iOS 8 e processador Apple A8 (Foto: Elson de Souza/ TechTudo)

Nas configurações, o iPhone 6 traz um processador 64 bits dual-core Apple A8 de 1,4 Ghz, 1 GB de RAM e opções de 16, 64 e 128 GB de armazenamento interno, sem espaço para cartão de memória. Completam as especificações a bateria de 1.810 mAh as conectividades 4G, 3G, Wi-Fi, Bluetooth e NFC. Ainda não há previsão de chegada do iPhone 6 e nem preços confirmados para o Brasil.

- iPhone 6 Plus

O iPhone 6 Plus é o primeiro foblet da Apple, equipado com uma tela Retina de 5,5 polegadas Full HD com densidade de 401 ppi. Lançado com o novo iOS 8, o telefone traz ainda câmera traseira com 8 megapixels com flash dual-LED, gravação em câmera lenta HD a 240 frames por segundo e estabilizador óptico de imagens (OIS), gerando vídeos menos tremidos.

iPhone 6 Plus tem tela gigante de 5,5 polegadas e configurações poderosas (Foto: Elson de Souza/TechTudo)

O foblet traz ainda um chip 64 bits dual-core Apple A8 de 1,4 Ghz, 1 GB de RAM e opções de 16, 64 e 128 GB de armazenamento interno, sem espaço para cartão microSD. Há ainda o leitor de digitais TouchID, a função Apple Pay, a bateria de 2.915 mAh e as conectividades 4G, 3G, Wi-Fi, Bluetooth e NFC. O iPhone 6 Plus ainda não tem data de lançamento e nem preços divulgados no Brasil.

- Samsung Galaxy Note 4

Galaxy Note 4 é a nova versão do foblet da Samsung, equipado com a caneta S Pen e o Android 4.4 (KitKat). Entre os destaques do aparelho estão a nova tela de 5,7 polegadas com resolução 2K (1440p) e a câmera traseira com 16 megapixels, estabilização óptica (OIS) e gravação em 4K (2180p). Na parte frontal, há ainda um sensor de 3,7 MP com a função Wide Selfie, que tira autorretratos em até 120 graus.

Galaxy Note 4 tem uma tela com resolução QHD, Android KitKat e caneta S Pen (Foto: Fabricio Vitorino/TechTudo)

Nas configurações, o smartphone da Samsung inclui ainda um processador quad-core Snapdragon 805 de 2,7 GHz, 3 GB de RAM e 32 GB de armazenamento, expansíveis em até 64 GB. Há ainda o leitor de impressões digitais, de batimentos cardíacos, bateria de 3.220 mAh e as conectividades 4G, 3G, Wi-Fi, Bluetooth, NFC e Infravermelho. Não há informações sobre a chegada do Note 4 ao mercado brasileiro e nem seu preço no país.

- Galaxy Note Edge

O Galaxy Note Edge é um novo foblet top da Samsung, que tem como diferencial uma pequena tela auxiliar na lateral do aparelho. Com ela, o usuário pode checar diversas informações, consultar atualizações e outros sem sair do app principal. Assim como o Note 4, o aparelho tem uma tela de 5,7 polegadas com resolução 2K (1440p), câmera traseira com 16 megapixels, estabilização óptica (OIS) e gravação em 4K (2180p), além do sensor frontal de 3,7 megapixels com o Wide Selfie.

Galaxy Note Edge tem tela auxiliar que pode ser usada para acessar informações adicionais ou abrir apps (Foto: Fabrício Vitorino/TechTudo)

As demais configurações também são idênticas: processador quad-core Snapdragon 805 de 2,7 GHz, 3 GB de RAM e 32 GB de armazenamento, expansíveis em até 64 GB. Outras funções presentes são o leitor de impressões digitais, de batimentos cardíacos, a bateria de 3.000 mAh e as conectividades 4G, 3G, Wi-Fi, Bluetooth, NFC e Infravermelho. O Galaxy Note Edge ainda não tem previsão para chegar ao Brasil.

- Sony Xperia Z3

O Xperia Z3 é o novo top de linha da Sony, equipado com uma tela de Full HD de 5,2 polegadas e o Android 4.4.4 (KitKat). O aparelho tem como grande destaque a sua câmera de 20,7 megapixels com função HDR, gravação em 4K e vídeos em câmera lenta a 120 fps, além de alguns truques divertidos. Além disso, o Z3 traz também uma sensor frontal de 2,2 megapixel, capaz de gravar em Full HD.

Xperia Z3 tem câmera de 20,7 megapixels, Android KitKat e tela Full HD (Foto: Fabrício Vitorino/TechTudo)

Nas especificações, o top de linha tem um processador quad-core Snapdragon 801 de 2,5 GHz, 3 GB de RAM e 16 ou 32 GB de armazenamento interno, expansíveis em até 128 GB. O Xperia Z3 é a prova d’água e poeira, tem bateria de 3.100 mAh e traz ainda as conectividades 4G, 3G, Wi-Fi, NFC e Bluetooth. Ainda não há preço ou informações sobre lançamento no Brasil.

- Xperia Z3 Compact

Z3 Compact tem tela menor, câmera de 20,7 megapixels e configurações poderosas (Foto: Fabricio Vitorino/TechTudo)

O Xperia Z3 Compact é uma versão menor do top da Sony, equipada com uma tela de 4,6 polegadas HD (720p) e Android 4.4 (KitKat). O aparelho vem equipado com uma câmera de 20,7 megapixels com gravação 4K (2160p), processador quad-core Snapdragon 801 de 2,5 GHz, 2 GB de RAM e 16 GB de espaço interno, expansível em até 128 GB. Há ainda a bateria de 2.600 mAh e as conectividades 4G, 3G, Wi-Fi, NFC e Bluetooth. A Sony não divulgou nenhuma informação sobre lançamento no Brasil.

- Nokia Lumia 830

O Lumia 830 é, segundo a Microsoft, um novo top de linha “mais acessível” dos que os demais. O aparelho traz uma tela de 5 polegadas HD (720p) e o Windows Phone 8.1 já com a nova atualização Denim, exclusiva da Nokia. Além disso, ele tem uma câmera traseira de 10 megapixels com tecnologia PureView, lentes Zeiss e estabilização óptica de imagem (OIS), além de uma câmera frontal de 0,9 MP.

Lumia 830 tem Windows Phone 8.1 Denim, câmera de 10 megapixels e processador quad-core (Foto: Fabrício Vitorino/TechTudo)

Nas configurações internas, o aparelho da Microsoft possui um processador quad-core Snapdragon 400 de 1,2 GHz, 1 GB de RAM e armazenamento interno de 16 GB, expansíveis em ate 128 GB. Há ainda a bateria de 2.200 mAh e as conectividades 4G, 3G, Wi-Fi, NFC e Bluetooth. O aparelho ainda não foi oficialmente lançado no Brasil.

- Nokia Lumia 735

Lumia 735 tem conectividade 4G e câmera frontal de 5 megapixels para selfies (Foto: Fabrício Vitorino/TechTudo)

O Lumia 735 é um novo intermediário da Microsoft com foco nos Selfies e na Internet de alta velocidade com o 4G. Ele traz uma tela de 4,7 polegadas HD, Windows Phone 8.1 Denim, câmera traseira 6,7 megapixels com gravação em Full HD e um sensor frontal de 5 megapixels especialmente desenvolvido para autorretratos. Há ainda um processador quad-core Snapdragon 400 de 1,2 Ghz, 1 GB de RAM e 8 GB de armazenamento interno, expansíveis em até 128 GB. Completam as especificações a bateria de 2.200 mAh e as conectividades 4G, 3G, Wi-Fi, Bluetooth e NFC. Ainda não há previsão de chegada ao Brasil.

- Nokia Lumia 730 Dual SIM

Lumia 730 tem função dual-chip, processador quad-core e câmera frontal para selfies (Foto: Divulgação/Microsoft)

O que mais falta nos celulares modernos? Comente no Fórum do TechTudo

O Lumia 730 é praticamente idêntico ao 735, exceto pelo suporte a dois chips de operadoras. Equipado com uma tela de 4,7 polegadas HD, o aparelho possui Windows Phone 8.1 Denim, câmera traseira 6,7 megapixels Full HD e um sensor frontal de 5 megapixels com resultados superiores em selfies. O processador é quad-core Snapdragon 400 de 1,2 Ghz, 1 GB de RAM e o armazenamento interno tem 8 GB, expansíveis em até 128 GB. Já a bateria possui 2.200 mAh e as conectividades são 3G, Wi-Fi, Bluetooth e NFC. Não há detalhes sobre lançamento no Brasil.

Asus revela as novas motherboards X99 e ROG Rampage V Extreme

 

por Luis Vedor

A Asus X99-Deluxe, X99-S e X99-A, são três novas motherboards ATX baseadas no chipset Intel X99. Estas motherboards incluem tecnologias como o OC Socket, Optimização em cinco vias, Crystal Sound 2, Turbo LAN, e o UEFI BIOS da Asus.

A X99-E WS é uma motherboard baseada no chipset Intel X99 que suporta multi-GPU até quatro placas e 16 vias PCI Express 3.0. A X99-E WS inclui um circuito integrado MOSFET (Dr. MOS), Beat Thermal Chokes II, condensadores sólidos 12K e um conector de alimentação ProCool. Esta motherboard suporta placas de expansão Asus PIKE II (Proprietary I/O Kit Expansion) e ThunderboltEX II. Além disso, a X99-E WS traz ainda ferramentas como a Q-Code Logger e o Dr. Power.

A Rampage V Extreme inclui o OC Socket, OC Panel, Safe Boot e botões ReTry. A Rampage V Extreme conta ainda com o VRM Extreme Engine Digi+ IV, DirectCU, tecnologias X-Socket II e Fan Xpert 3. A nova motherboard X99 tem também duas portas SATA Express, e slot PCI Express 3.0 x4 M.2.

ESPECIFICAÇÕES – ASUS X99-Deluxe

CPU
LGA 2011-v3 para Processadores Intel Core i7

Chipset
Intel X99 Express

Memória
Arquitetura Quad-channel; 8 x DIMMs até um máximo de 64GB, DDR4 3200MHz (OC)

Intel Extreme Memory Profile (XMP)

Slots de expansão
40-lane CPU:

5 x PCI Express 3.0/2.0 x16 slots (single x16, dual x16/x16, triple x16/x16/x8, quad x8/x8/x16/x8 ou quintuple x8/x8/x8/x8/x8 mode)

1 x PCI Express 2.0 x4 slot (compatível com PCI Express x1 e x4)

28-lane CPU:

3 x PCI Express 3.0/2.0 x16 slots (x16, dual x16/x8 ou triplo x8/x8/x8)

2 x PCI Express 2.0 x16 slots (máximo x1 mode, compatível com PCI Express x1)

1 x PCI Express 2.0 x4 slot (compatível com PCI Express x1 e x4)

Suporte de Multi-GPU
Até 3-way NVIDIA SLI e AMD CrossFireX

Armazenamento
2 x SATA Express

8 x SATA 6Gbit/s

1 x M.2 Socket 3 com M Key, equipamentos de armazenamento suportados do tipo 2242/2260/2280 (apenas PCI Express SSDs)

Rede/LAN
Intel I218-V & I211-AT Gigabit LAN

ASUS Turbo LAN Utility

3×3 (3T3R) 802.11ac Wi-Fi com ASUS Wi-Fi GO!

USB
14 x USB 3.0/2.0 (10 no painel traseiro, 4 na placa)

6 x USB 2.0/1.1 (2 no painel traseiro, 4 na placa)

Acessórios incluídos
ASUS Fan Extension Card

ASUS Hyper M.2 X4

Características-chave
OC Socket

5-Way Optimization by Dual Intelligent Processors 5

5X Protection

UEFI BIOS, Turbo App

Turbo LAN

Crystal Sound 2

Dimensões físicas
ATX, 12-inch x 9.6-inch (30.5cm x 24.4cm)

ESPECIFICAÇÕES – ASUS X99-A

CPU
LGA 2011-v3 para o novo processador Intel Core i7

Chipset
Intel X99 Express

Memória
Arquitetura Quad-channel; 8 x DIMMs até um máximo de 64GB, DDR4 3200MHz (OC)

Intel Extreme Memory Profile (XMP)

Slots de expansão
40-lane CPU:

3 x PCI Express 3.0/2.0 x16 slots (x16, dual x16/x16 ou tripla x16/x16/x8)

1 x PCI Express 2.0 x16 slot (máximo x4 mode, compatível com PCI Express x1 e x4)

2 x PCI Express 2.0 x1 slot (compatível com PCI Express x1)

28-lane CPU:

3 x PCI Express 3.0/2.0 x16 slots (x16, dual x16/x8 ou tripla x16/x8/x4)

1 x PCI Express 2.0 x16 slot (máximo x4 mode, compatível com PCI Express x1 e x4)

2 x PCI Express 2.0 x1 slot (compatível com PCI Express x1)

Suporte de Multi-GPU
Até 3-way NVIDIA SLI e AMD CrossFireX

Armazenamento
1 x SATA Express

8 x SATA 6Gbit/s

1 x M.2 Socket 3 com M Key, equipamentos de armazenamento suportados do tipo 2242/2260/2280/22110 (apenas PCI Express SSDs)

Rede/LAN
Intel I218-V Gigabit LAN

ASUS Turbo LAN Utility

USB
10 x USB 3.0/2.0 ports (6 no painel traseiro, 4 na placa)

8 x USB 2.0/1.1 ports (4 no painel traseiro, 4 na placa)

Características-chave
OC Socket

5-Way Optimization by Dual Intelligent Processors 5

5X Protection

UEFI BIOS

Turbo App

Turbo LAN

Crystal Sound 2

Dimensões físicas
ATX, 12-inch x 9.6-inch (30.5cm x 24.4cm)

ESPECIFICAÇÕES – ASUS X99-E WS

CPU
LGA 2011-3 para Processadores da próxima geração Intel Core i7 / Xeon® E5-1600 v3

Chipset
Intel X99 Express

Memória
Arquitetura Quad-channel; 8 x DIMMs, DDR4 2133MHz

Intel Extreme Memory Profile (XMP)

Slots de expansão
7 x PCI Express 3.0/2.0 x16 slots (single x16, dual x16/x16,

quad x16/x16/x16/x16, ou seven x8/x8/x8/x8)

Suporte de Multi-GPU
Suporta tecnologia Quad-GPU NVIDIA SLI e CrossFireX

Armazenamento
Intel X99 Express chipset com RAID 0, 1, 5, 10 (controller 1 e controller 2):

- 8 x SATA 6.0Gbit/s

- Suporta Tecnologia Intel Smart Response, Rapid Start e Smart Connect

ASMedia SATA Express controller

- 1 x SATA Express (compatível com 2 x SATA 6.0Gbit/s)

- 1 x SATA Express (compatível com 2 x SATA 6.0Gbit/s)

1 x M.2 Socket 3 com M Key, equipamentos de armazenamento suportados do tipo 2260/2280

Rede/LAN
1 x Intel I210-AT Gigabit LAN

1 x Intel  I218-LM Gigabit LAN de interconexão entre LAN e PHY

USB
Intel X99 Express chipset — suporta ASUS USB 3.0 Boost

- 4 x USB 3.0/2.0 na placa para suporte do painel frontal

- 4 x USB 2.0/1.1 (4 na placa, 2 no painel traseiro)

ASMedia USB 3.0 — suporta ASUS USB 3.0 Boost

- 8 x USB 3.0/2.0 (no painel traseiro)

Dimensões físicas
Compact Electronics Bay (CEB), 12-inch x 10.5-inch (30.5cm x 26.7cm)

ESPECIFICAÇÕES – ASUS ROG Rampage V Extreme

CPU
LGA 2011-v3 para o novo processador Intel Core i7

Chipset
Intel X99 Express

Memória
Arquitetura Quad-channel; 8 x DIMMs até um máximo de 64GB, DDR4 3300MHz (OC)

Intel Extreme Memory Profile (XMP)

Slots de expansão
4 x PCIe 3.0/2.0 x16 slots (x16, x16/x16, x16/x8/x8 ou x16/x8/x8/x8 mode com 40-lane CPU; x16, x16/x8, x8/x8/x8 mode com 28-lane CPU)

1 x PCIe 2.0 x16 slot (máximo x4 mode)

1 x PCIe 2.0 x1 slot

Suporte de Multi-GPU
4-way, 3-way e 2-way NVIDIA SLI e AMD CrossFireX

Armazenamento
2 x SATA Express

8 x SATA 6Gbit/s

1 x M.2 Socket 3 com M Key, equipamentos de armazenamento suportados do tipo 2260/2280/22110 (apenas PCI Express SSDs)

Rede/LAN
Intel I218-V Gigabit LAN com GameFirst III e ASUS LANGuard

USB
14 x USB 3.0 ports (10 no painel traseiro, 4 na placa)

6 x USB 2.0 ports (2 no painel traseiro, 4 na placa)

Áudio
ROG SupremeFX 2014 com 8 canais áudio de alta definição

- SupremeFX Shielding Technology

- Condensadores ELNA premium

- Jack-detection, multi-streaming, mic jack-retasking no painel frontal

- saída ótica no painel traseiro Optical S/PDIF out port

Sonic SoundStage / Sonic SenseAmp / Sonic Studio / Sonic Radar II / DTS Connect

Dimensões físicas
EATX, 12-inch x 10.7-inch (30.5cm x 27.2cm)

Medications are main culprit of allergic deaths in U.S., comprehensive study finds

 

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Medications are the leading cause of allergy-related sudden deaths in the U.S., according to an analysis of death certificates from 1999 to 2010, conducted by researchers at Montefiore Medical Center and Albert Einstein College of Medicine of Yeshiva University. The study, published online today in the Journal of Allergy and Clinical Immunology, also found that the risk of fatal drug-induced allergic reactions was particularly high among older people and African-Americans and that such deaths increased significantly in the U.S. in recent years.

Anaphylaxis is the term used for a severe, potentially life-threatening allergic reaction that can occur within seconds or minutes following exposure to an allergen. Until now, data on trends in anaphylactic deaths -- or even the number of yearly deaths from anaphylactic shock -- has not been well-defined. One reason: unlike countries such as the UK, the U.S. doesn't maintain a national registry for anaphylaxis deaths.

"Anaphylaxis-related deaths in the U.S. have not been well understood in recent years," said Elina Jerschow, M.D., M.Sc. director, Drug Allergy Center, Allergy and Immunology Division of Medicine, Montefiore Medical Center, and assistant professor of medicine, Albert Einstein College, the lead author of the study. "We hope these findings will help in identifying specific risk factors and allow physicians to formulate preventative approaches."

Dr. Jerschow and colleagues analyzed death certificates from the U.S. National Mortality Database and found that medication-related anaphylaxis was the most common cause of death (58.8 percent). Additional causes identified included unspecified anaphylaxis (19.3 percent), venom (15.2 percent) and food (6.7 percent). Further analyses revealed fatal anaphylaxis due to medications, food and unspecified allergens was significantly associated with African American race and older age; and fatal anaphylaxis rates due to venom was more common in white, older men.

Of the 2,458 deaths identified between 1999-2010, culprit drugs were not specified in most of the cases (approximately 74 percent). However, among those with an identified culprit drug, nearly half were antibiotics, followed by radiocontrast agents used during diagnostic imaging procedures and chemotherapeutics that are used in treatment of cancer.

During the years studied, there was a significant increase in fatal drug anaphylaxis, from 0.27 per million in 1999-2001 to 0.51 per million in 2008-2010. The increase in medication-related anaphylaxis deaths likely relates to increased medication and radiocontrast use, enhanced diagnosis and coding changes.

"Anaphylaxis has been dubbed 'the latest allergy epidemic,'" said Dr. Jerschow. "The U.S. and Australia have some of the highest rates of severe anaphylaxis among developed countries. We hope these results bring increased awareness of the need for a better understanding of anaphylaxis deaths."

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Story Source:

The above story is based on materials provided by Montefiore Medical Center. Note: Materials may be edited for content and length.

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Journal Reference:

1. Elina Jerschow et al. Fatal anaphylaxis in the United States, 1999-2010: Temporal patterns and demographic associations. Journal of Allergy and Clinical Immunology, September 2014 DOI: 10.1016/j.jaci.2014.08.018

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High-speed drug screen developed

 

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Mehmet Fatih Yanik.

MIT engineers have devised a way to rapidly test hundreds of different drug-delivery vehicles in living animals, making it easier to discover promising new ways to deliver a class of drugs called biologics, which includes antibodies, peptides, RNA, and DNA, to human patients.

In a study appearing in the journal Integrative Biology, the researchers used this technology to identify materials that can efficiently deliver RNA to zebrafish and also to rodents. This type of high-speed screen could help overcome one of the major bottlenecks in developing disease treatments based on biologics: It is challenging to find safe and effective ways to deliver them.

"Biologics is the fastest growing field in biotech, because it gives you the ability to do highly predictive designs with unique targeting capabilities," says senior author Mehmet Fatih Yanik, an associate professor of electrical engineering and computer science and biological engineering. "However, delivery of biologics to diseased tissues is challenging, because they are significantly larger and more complex than conventional drugs."

"By combining this work with our previously published high-throughput screening system, we are able to create a drug-discovery pipeline with efficiency we had never imagined before," adds Tsung-Yao Chang, a recent MIT PhD recipient and one of the paper's lead authors.

Peng Shi, a former MIT postdoc who is now an assistant professor at the University of Hong Kong, is the paper's other lead author.

Fish on the fly

Zebrafish are commonly used to model human diseases, in part because their larvae are transparent, making it easy to see the effects of genetic mutations or drugs.

In 2010, Yanik's team developed a technology for rapidly moving zebrafish larvae to an imaging platform, orienting them correctly, and imaging them. This kind of automated system makes it possible to do large-scale studies because analyzing each larva takes less than 20 seconds, compared with the several minutes it would take for a scientist to evaluate the larvae by hand.

For this study, Yanik's team developed a new technology to inject RNA carried by nanoparticles called lipidoids, previously designed by Daniel Anderson, an associate professor of chemical engineering, member of the Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science, and an author of the new paper. These fatty molecules have shown promise as delivery vehicles for RNA interference, a process that allows disease-causing genes to be turned off with small strands of RNA.

Yanik's group tested about 100 lipidoids that had not performed well in tests of RNA delivery in cells grown in a lab dish. They designed each lipidoid to carry RNA expressing a fluorescent protein, allowing them to easily track RNA delivery, and injected the lipidoids into the spinal fluid of the zebrafish.

To automate that process, the zebrafish were oriented either laterally or dorsally once they arrived on the viewing platform. Once the larvae were properly aligned, they were immobilized by a hydrogel. Then, the lipidoid-RNA complex was automatically injected, guided by a computer vision algorithm. The system can be adapted to target any organ, and the process takes about 14 seconds per fish.

A few hours after injection, the researchers imaged the zebrafish to see if they displayed any fluorescent protein in the brain, indicating whether the RNA successfully entered the brain tissue, was taken up by the cells, and expressed the desired protein.

The researchers found that several lipidoids that had not performed well in cultured cells did deliver RNA efficiently in the zebrafish model. They next tested six randomly selected best- and worst-performing lipidoids in rats and found that the correlation between performance in rats and in zebrafish was 97 percent, suggesting that zebrafish are a good model for predicting drug-delivery success in mammals.

"The ability to identify useful drug delivery nanoparticles using this miniaturized system holds great potential for accelerating our discovery process," Anderson says.

"The lipidoid material screen is just an example demonstrated in this article; a similar strategy can be readily extended to other libraries or other organ systems," Peng adds.

Jeff Karp, an associate professor of medicine at Harvard Medical School who was not part of the research team, says this work is "an excellent example of harnessing a multidisciplinary team to partner complementary technologies for the purpose of solving a unified problem. Yanik and colleagues, who have extensive expertise with high-throughput screening in zebrafish and other small animals, have teamed up with Anderson et al., who are leading experts in RNA delivery, to create a new platform for rapidly screening biologics and methods to deliver them. This approach should have utility across multiple disease areas."

New leads

The researchers are now using what they learned about the most successful lipidoids identified in this study to try to design even better possibilities. "If we can pick up certain design features from the screens, it can guide us to design larger combinatorial libraries based on these leads," Yanik says.

Yanik's lab is currently using this technology to find delivery vehicles that can carry biologics across the blood-brain barrier -- a very selective barrier that makes it difficult for drugs or other large molecules to enter the brain through the bloodstream.

The research was funded by the National Institutes of Health, the Packard Award in Science and Engineering, Sanofi Pharmaceuticals, Foxconn Technology Group, and the Hertz Foundation.

Story Source:

The above story is based on materials provided by Massachusetts Institute of Technology. The original article was written by Anne Trafton. Note: Materials may be edited for content and length.

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Journal Reference:

1. Tsung-Yao Chang, Peng Shi, Joseph D. Steinmeyer, Itthi Chatnuntawech, Paul Tillberg, Kevin T. Love, Peter M. Eimon, Daniel G. Anderson, Mehmet Fatih Yanik. Organ-targeted high-throughput in vivo biologics screen identifies materials for RNA delivery. Integr. Biol., 2014; 6 (10): 926 DOI: 10.1039/C4IB00150H

4 Natural Ways to Lose Water Weight Safely

 

There’s the right way and the wrong way to lose water weight, and here we’ll be focusing on how to do it safely. The key is identifying why you’re storing excess water, and then taking steps to fix the underlying problem, rather than simply focusing on the symptoms.

1. Cut Out Sodium

If you’re carrying around excess water there’s a high likelihood that you have too much sodium in your diet. Processed food such as the kind you find in bags and boxes in stores, as well as fast food, often comes with a high sodium content. Sprinkling table salt onto your meals can also be a contributing factor.

You should make the distinction between sodium and natural salt sources like sea salt and Himalayan pink salt. These natural salts are not the same as the table salt you find everywhere, or the salt used in processed foods and cold cuts.

Why It Works: Less sodium in means less sodium you have to get out through sweating and proper hydration. Start at the source of the problem and you’ll be able to avoid many of the negative effects of storing too much water.

2. Increase Water Intake

It may sound counterintuitive but staying hydrated is key to losing excess water weight. Dehydration is actually a cause of storing water weight, not a way to get rid of it. If you’ve been going through an extended period of dehydration from not getting enough water, make sure to take things slowly. Don’t go from little water to a lot of water in just one day.

Instead of following the one-size-fits-all mantra of 8-10 glasses of water a day, take your body weight and drink half of that number in ounces of water each day. If you weigh 150 pounds you need 75 ounces of water. If you weigh 200 pounds you need 100 ounces, and so on.

Why It Works: Staying properly hydrated reduces the chance of storing too much water in the first place. When you combine the right amount of water with less sodium intake and working up a daily sweat, excess water weight will no longer be a concern for you.

3. Consume Natural Diuretics

There are foods and drinks that will naturally induce more urination from you, which will help purge your system of excess water weight. These are highly preferable over drugs that have the same effect.

Note: The three methods above, sweating more, eating less sodium, and drinking enough water, should be enough to normalize your water weight. Diuretics may be used in an effort to speed things up, or help in severe situations, but in most cases will not be necessary. Also, eating enough fresh fruits and vegetables in a balanced diet will give you enough diuretic effect to regulate your water weight without direct effort on your part.

Why It Works: Diuretics get you to go to the bathroom more frequently and will speed the process along. Just be sure that you’re also drinking enough water as described above, or you can speed along the dehydration process as well, only exacerbating your water weight problem.

4. Sweat It Off

Seating is one major helpful thing you can do to help shed any water weight that doesn’t belong. The key is not to try to sweat it out all at once, but to use the power of accumulated days to do the trick. Make it your priority to build up a sweat daily. You’ll be amazed at the additional health benefits you receive on top of losing excessive water weight.

Surely you’ve tasted some of your own sweat before, and you’re familiar with its salty nature. This is excess sodium that is no longer in your body and will help with the total water weight you’re carrying.

Why It Works: Sweat not only helps you get rid of any extra sodium you may be carrying in the body, it releases toxins as well.

A New Idea for Treating Alzheimer’s

 

By Gary Stix | September 28, 2014

The views expressed are those of the author and are not necessarily those of Scientific American.

 

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If it’s good for the heart, it could also be good for the neurons, astrocytes and oligodendrocytes, cells that make up the main items on the brain’s parts list.

The heart-brain adage comes from epidemiological studies that show that people with cardiovascular risk factors such as high-blood pressure and elevated cholesterol levels, may be more at risk for Alzheimer’s and other dementias.

This connection between heart and brain has also led to some disappointments: clinical trials of lipid-lowering statins have not helped patients diagnosed with Alzheimer’s, although epidemiological studies suggest that long-term use of the drugs may help prevent Alzheimer’s and other dementias.

The link between head and heart is still being pursued because new Alzheimer’s drugs have failed time and again. One  approach that is now drawing some interest looks at the set of proteins that carry around fats in the brain. These lipoproteins could potentially act as molecular sponges that mop up the amyloid-beta peptide that clogs up connections among brain cells in Alzheimer’s.

One of these proteins—Apolipoprotein J, also known as clusterin—intrigues researchers because of the way it interacts with amyloid-beta and the status of its gene as a risk factor for Alzheimer’s.

A researcher from the University of Minnesota, Ling Li, recently presented preliminary work at the Alzheimer’s Drug Discovery Foundation annual meeting that showed that, at least in a lab dish, a molecule made up of a group of amino acids from APOJ is capable of protecting against the toxicity of the amyloid-beta peptide. It also quelled inflammation and promoted the health of synapses—the junctions where one brain cell encounters another. Earlier work by another group showed that the  peptide prevented the development of  lesions in the blood vessels of animals.

Li’s research will still require crossing a number of conceptual barriers to prove that an APOJ-derived drug can actually work in humans.  APOJ plays different roles in Alzheimer’s. In the healthy brain, it may help preserve the normal workings of brain cells, but it may also promote the Alzheimer’s disease process under other conditions.

From the preliminary results, Li hopes that the APOJ-derived peptide will  harness the beneficial effects of the protein. The work is still in early stages and Li and her team now plan to go on to test the peptide in mice. “The long term goal would be to find something that prevents or treats Alzheimer’s,” she says. An APOJ protein fragment—or a variety of other new ideas for drug candidates—are badly needed for a disease that affects tens of millions of people worldwide yet lacks any good treatment.

Image Source: Eliza Fitzhugh/Flickr-Creative Commons

Disease decoded: Gene mutation may lead to development of new cancer drugs

 

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The discovery of a gene mutation that causes a rare premature aging disease could lead to the development of drugs that block the rapid, unstoppable cell division that makes cancer so deadly.

Scientists at the University of Michigan and the U-M Health System recently discovered a protein mutation that causes the devastating disease dyskeratosis congenita, in which precious hematopoietic stem cells can't regenerate and make new blood. People with DC age prematurely and are prone to cancer and bone marrow failure.

But the study findings reach far beyond the roughly one in 1 million known DC patients, and could ultimately lead to developing new drugs that prevent cancer from spreading, said Jayakrishnan Nandakumar, assistant professor in the U-M Department of Molecular, Cellular, and Developmental Biology.

The DC-causing mutation occurs in a protein called TPP1. The mutation inhibits TPP1's ability to bind the enzyme telomerase to the ends of chromosomes, which ultimately results in reduced hematopoietic stem cell division. While telomerase is underproduced in DC patients, the opposite is true for cells in cancer patients.

"Telomerase overproduction in cancer cells helps them divide uncontrollably, which is a hallmark of all cancers," Nandakumar said. "Inhibiting telomerase will be an effective way to kill cancer cells."

The findings could lead to the development of gene therapies to repair the mutation and start cell division in DC patients, or drugs to inhibit telomerase and cell division in cancer patients. Both would amount to huge treatment breakthroughs for DC and cancer patients, Nandakumar said.

Nandakumar said that a major step moving forward is to culture DC patient-derived cells and try to repair the TPP1 mutation to see if telomerase function can be restored. Ultimately, the U-M scientist hopes that fixing the TPP1 mutation repairs telomerase function and fuels cell division in the stem cells of DC patients.

"It's conceivable that with the recent advancement in human genome-editing technology, we could, in the not-so-distant future, repair the mutation in hematopoietic stem cells in the bone marrow of DC patients," Nandakumar said.

The findings also reinforce how one tiny change in an amino acid chain can cause devastating health consequences.

"It was surprising to us that just deleting one single amino acid in a protein chain that is 544 amino acids long can result in such a severe disease," Nandakumar said.

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Story Source:

The above story is based on materials provided by University of Michigan. The original article was written by Laura Bailey. Note: Materials may be edited for content and length.

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Journal Reference:

1. H. Kocak, B. J. Ballew, K. Bisht, R. Eggebeen, B. D. Hicks, S. Suman, A. O'Neil, N. Giri, I. Maillard, B. P. Alter, C. E. Keegan, J. Nandakumar, S. A. Savage. Hoyeraal-Hreidarsson syndrome caused by a germline mutation in the TEL patch of the telomere protein TPP1. Genes & Development, 2014; DOI: 10.1101/gad.248567.114

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