When — or if — NASA finds life on Mars, the world may not be ready for the discovery, the agency chief says @ The most important lesson from 83,000 brain scans | Daniel Amen | TEDxOrangeCoast – Video – Vídeo @ Alzheimer’s Disease: Experimental Models and Reality & A mouse model for the most common form of heart failure & It’s Alive: Cautious Excitement Meets Claims of First Effective Alzheimer’s Drug @ Do gut bacteria make a second home in our brains? @ CRISPR Co-Inventor Calls for Increased Regulation of Gene Altering – Jennifer Doudna raises alarms in new article

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When — or if — NASA finds life on Mars, the world may not be ready for the discovery, the agency chief says

By Scottie Andrew, CNN

Updated 2122 GMT (0522 HKT) September 30, 2019

This is what life on Mars could be like

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(CNN)NASA’s next mission to Mars will be its most advanced yet. But if scientists discover there was once life — or there is life –on the Red Planet, will the public be able to handle such an extraterrestrial concept?NASA chief scientist Jim Green doesn’t think so.”It will be revolutionary,” Green told the Telegraph. “It will start a whole new line of thinking. I don’t think we’re prepared for the results. We’re not.”

NASA Chief Scientist Jim Green thinks news of life on Mars is coming soon, and the public isn't prepared to hear it.

NASA Chief Scientist Jim Green thinks news of life on Mars is coming soon, and the public isn’t prepared to hear it.The agency’s Mars 2020 rover, set to launch next summer, will be the first to collect samples of Martian material to send back to Earth. But if scientists discover biosignatures of life in Mars’ crust, the findings could majorly rock astrobiology, said Green, the director of the Planetary Science Division at NASA.”What happens next is a whole new set of scientific questions,” he said. “Is that life like us? How are we related?”The Mars 2020 rover, along with the European Space Agency’s ExoMars rover, will drill into the Martian crust. The surface of the Red Planet is believed to be radioactive, soif there is life on Mars, it likely livesbelow ground.”We’ve never drilled that deep,” he told the Telegraph. “When environments get extreme, life moves into the rocks.”The principle’s been proven on our home planet: After drilling miles into the Earth, researchers found more life in the Earth’s crust than on its surface, he said.”The bottom line is, where there is water there is life.”And if the agencies’ new rovers find proof that water once flowed on Mars, he said, the confirmation could come weeks or months of landing — so buckle up, space lovers. The realm of possibility might get much wider very soon.

The next mission to Mars

NASA’s Mars 2020 rover will launch in July 2020 and land at the Red Planet’s Jezero Crater in February 2021 (Mars is 140 million miles from Earth, after all). It’s equipped with two high-definition cameras and a detachable helicopter to take aerial images of the planet’s cliffs, caves and craters.The mission’s main aim is to search for signs of life. The rover will look for past habitable environments, find biosignatures in rock and will test those samples back on Earth.But if scientists fail to find evidence of life, that won’t end the hope for human exploration. Mars 2020 will test oxygen production on the planet and monitor Martian weather to evaluate how potential human colonies could fare on Mars.

Clarification: The headline of this piece has been changed to more accurately reflect NASA’s chief scientist’s comments regarding efforts to finding life on Mars.

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SubscribeSearchLoginNEWS AND VIEWS  10 APRIL 2019

A mouse model for the most common form of heart failure

A mouse model that replicates the clinical features of the most common form of heart failure opens a window on the mechanisms underlying this disease, and could help scientists to explore future therapies.

Dulguun Amgalan &

Richard N. Kitsis

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Heart failure is a lethal condition that affects at least 26 million people worldwide1. A preclinical model that faithfully recapitulates the most common form of this syndrome, known as heart failure with preserved ejection fraction (HFpEF), has been lacking. Writing in Nature, Schiattarella et al.2 report the development of a mouse model of HFpEF, and its use to identify a molecular pathway not previously known to have a role in this disease.Read the paper: Nitrosative stress drives heart failure with preserved ejection fraction

Heart failure has generally been seen as an inability of the heart to pump sufficient blood to meet the metabolic needs of the body. The weakening of the heart muscle is quantified by measuring the reduction in the percentage of blood in the heart expelled with each heartbeat, which is called the ejection fraction. This syndrome is referred to as heart failure with reduced ejection fraction (HFrEF)3. But in more than half of cases of heart failure, ejection fraction remains normal, although abnormalities in heart-muscle contraction can be detected with more sensitive tests. This form of heart failure is called HFpEF and is defined by impaired filling of the heart with blood4. Dysfunction in other organs, including the lungs, kidneys and skeletal muscles, is also likely to contribute to the symptoms of the disease.

Although the two forms of heart failure have similar symptoms, including shortness of breath, reduced ability to exercise, and fatigue, their mechanisms differ markedly. HFrEF is characterized by persistent activation of stress-associated molecular pathways in heart muscle cells (cardiomyocytes), leading to a decrease in the ability of these cells to contract, or to cell death. By contrast, HFpEF is driven by ageing, high blood pressure, metabolic changes associated with obesity and diabetes, and generalized chronic inflammation. These factors induce alterations in several cell types in the heart.

In HFpEF, the endothelial cells that line small blood vessels in the heart become dysfunctional and fail to synthesize adequate amounts of nitric oxide (NO), a substance involved in the relaxation of blood vessels. Connective-tissue cells called fibroblasts generate scarring. And the cardiomyocytes themselves become stiffer because of changes related to proteins involved in molecular signalling pathways and cellular contraction5. The end result is sluggish filling of the heart.

None of the existing therapies for HFrEF helps in HFpEF, and a good animal model for HFpEF has been lacking. Modelling HFpEF is challenging because of the complex interplay of many contributing factors and the plethora of clinical manifestations of the disease. Rather than recreating all the stimuli that lead to HFpEF, Schiattarella et al. combined two major risk factors — obesity linked with glucose intolerance (an inability to transport sugar efficiently from the blood into cells, which can lead to diabetes) and high blood pressure — in mice. The authors’ reasoning was that each of these factors activates several disease-associated pathways.

Mice were rendered obese and glucose-intolerant with a high-fat diet. High blood pressure was induced by administration of a drug called Nω-nitro-L-arginine methyl ester (L-NAME), which inhibits the enzymes that are normally expressed at constant levels to catalyse the production of NO (called constitutive NO synthases). Mice treated in this way had several characteristics of HFpEF, including impaired filling of the heart, inability to exercise, lung congestion and increased levels of molecular markers of inflammation in the heart and blood (Fig. 1). Notably, ejection fraction in these mice remained normal up to at least 12 months of age, which is half the lifespan of a mouse.

Figure 1 | Inhibition of the unfolded protein response contributes to heart failure with preserved ejection fraction. Schiattarella et al.2 fed mice a high-fat diet to produce obesity and glucose intolerance (an inability to transport sugar efficiently from the blood into cells, which can lead to diabetes), and gave the animals the drug Nω-nitro-L-arginine methyl ester (L-NAME) to cause high blood pressure. These treatments induced some of the hallmarks of heart failure with preserved ejection fraction (HFpEF), including impaired filling of the heart with blood, inability to exercise, lung congestion and increased levels of molecular markers associated with inflammation. The authors also observed increased expression of the enzyme inducible nitric oxide synthase (iNOS), which increases the production of nitric oxide (NO). The addition of NO to sulfur atoms (S-nitrosylation) of inositol-requiring enzyme 1α (IRE1α) decreases this protein’s activity. IRE1α is a component of the unfolded protein response (UPR), a mechanism that protects cells against abnormal levels of misfolded proteins. Decreased IRE1α activity leads to reduced conversion (splicing) of messenger RNA encoding X-box binding protein 1 (XBP1) to the mRNA that encodes XBP1 spliced (XBP1s), a transcription factor that activates UPR genes. The authors observed that IREα splicing activity and XBP1s levels were reduced in their mouse model of HFpEF.

The authors then used their model to investigate the role of misfolded proteins in HFpEF. These proteins accumulate in several disorders in which cardiac stress is present6, including HFpEF, and they activate a molecular program known as the unfolded protein response (UPR)7. Schiattarella et al. focused on inositol-requiring enzyme 1α (IRE1α), which is activated in response to cellular stress caused by an excess of misfolded proteins. IRE1α cuts the messenger RNA that encodes X-box binding protein 1 (XBP1) and transforms it into a shorter mRNA that encodes a protein called XBP1 spliced (XBP1s). XBP1s is a transcription factor that activates genes involved in the UPR.

Schiattarella and colleagues found that IRE1α activation and XBP1s levels were reduced in the hearts of HFpEF model mice, as well as in heart-tissue samples from people with HFpEF, when compared with those from healthy individuals (Fig. 1). By contrast, cardiac XBP1s levels were increased or unchanged in mice and humans with HFrEF. The decrease in XBP1s levels in the hearts of HFpEF mice was due to IRE1α modification by S-nitrosylation. This process, in which an NO molecule is attached to specific sulfur atoms on proteins, is known to decrease IRE1α activity8.

Although Schiattarella et al. did not identify the cells that produce NO, they observed that inducible NO synthase (iNOS), an enzyme that was highly expressed in their HFpEF model, promoted IRE1α S-nitrosylation. They went on to show that pharmacological or genetic inhibition of iNOS or cardiomyocyte-specific overexpression of XBP1s attenuated cardiac filling defects, the inability to exercise, and lung congestion in mice induced to develop features of HFpEF. These findings highlight the role of XBP1s loss in the mechanisms underlying this disease.

This work demonstrates that two common risk factors for HFpEF are sufficient to reproduce many of the manifestations of this disease. The authors’ mouse model will be useful for dissecting disease mechanisms and developing new treatments. Although large-animal models are often valuable in studying complex physiological processes and testing therapeutics, the mouse has the advantage of being easy to manipulate genetically and having a short lifespan9. The latter factor will also facilitate the study of the influence of ageing, another key risk factor for HFpEF.

Some questions remain unanswered. The less-than-complete reversal of HFpEF disease manifestations observed in response to iNOS inhibition suggests that other molecular pathways are also involved in the reduction of XBP1s levels. More generally, the study explored a single candidate mechanism for this disease. It is likely that other mechanisms also contribute, and the new HFpEF mouse model provides an in vivo platform with which to define them.

Nature 568, 324-325 (2019)doi: 10.1038/d41586-019-00983-4

References

  1. 1.Savarese, G. & Lund, L. H. Card. Fail. Rev. 3, 7–11 (2017).
  2. 2.Schiattarella, G. G. et al. Nature 568, 351–356 (2019).
  3. 3.Bloom, M. W. et al. Nature Rev. Dis. Primers 3, 17058 (2017).
  4. 4.Dunlay, S. M., Roger, V. L. & Redfield, M. M. Nature Rev. Cardiol. 14, 591–602 (2017).
  5. 5.Shah, S. J. et al. Circulation 134, 73–90 (2016).
  6. 6.Wang, Z. V. & Hill, J. A. Cell Metab. 21, 215–226 (2015).
  7. 7.Walter, P. & Ron, D. Science 334, 1081–1086 (2011).
  8. 8.Yang, L. et al. Science 349, 500–506 (2015).
  9. 9.Valero-Muñoz, M., Backman, W. & Sam, F. J. Am. Coll. Cardiol. Basic Transl. Sci. 2, 770–789 (2017).

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It’s Alive: Cautious Excitement Meets Claims of First Effective Alzheimer’s Drug

ARTICLE   Oct 23, 2019 | by Ruairi J Mackenzie, Science Writer for Technology Networks

It’s Alive: Cautious Excitement Meets Claims of First Effective Alzheimer’s Drug

Ruairi J MacKenzie

Science Writer

 @rjmsci Read Time: 3 min

American pharma giant Biogen has announced that its therapeutic compound for Alzheimer’s disease (AD), aducanumab, is to be taken to the FDA for approval. Despite being seemingly killed off after a study in March produced disappointing results, new analysis suggests that aducanumab met its target endpoints. If confirmed, this would make aducanumab the first therapy able to slow cognitive decline in AD.

An unexpected reversal

After a series of high-profile failures, aducanumab was considered the last roll of the dice for pharmacological interventions targeting the pathological protein beta-amyloid, which is thought to have a central role in AD pathology.

In a Biogen press release, study lead Dr. Anton Porsteinsson said, “This large dataset represents the first time a Phase 3 study has demonstrated that clearance of aggregated amyloid beta can reduce the clinical decline of Alzheimer’s disease, providing new hope for the medical community, the patients, and their families.”

More measured praise was also forthcoming from leaders in the field not associated with the study: Professor Bart De Strooper, Director of the UK Dementia Research Institute, University College London, commented, “It is fantastic to hear of these new positive results emerging from the aducanumab trials. We currently have no effective treatments to slow or halt the progression of Alzheimer’s disease and I hope this signifies a turning point.”

Bigger dose, better results?

Aducanamab, a monoclonal antibody, targets both soluble and insoluble forms of beta-amyloid, clearing it from the brain. Biogen said that the study results published in March, which had raised fears around side effects such as brain swelling, had been based upon an “incorrect” futility analysis.

According to Biogen, the new analysis suggests that the now-positive result (it is incredibly rare for clinical trial results to be reversed in this way) was due to increased exposure to a higher dose of aducanumab.

Delving into the datasets released by Biogen will take some time, although some in-depth analysis can be found here. In summary, the drug was tested in two trials, one of which (named EMERGE) has proved to have statistically positive results in the new, larger analysis, whilst the other (ENGAGE) trended towards significance in a subset of patients who received the higher dose (but was still insignificant). Patients were assessed on both their amyloid burden, and their performance on a battery of standardized cognitive tests. On one test, the CDR-SB, a higher dose group showed a decline in their performance that was 23% slower than patients on a placebo. But the performance of participants in other tests was not significantly different, and any significance was only found in the EMERGE group. Why patients would perform worse in these different tests is currently unclear.

Contradictions need to be cleared

The data released by Biogen also contained some strange results, such as a worse performance in some tests by patients on a higher dose of aducanumab in ENGAGE, the exact opposite of the results from EMERGE. Whilst these concerns would normally move the FDA to order another trial using the conditions that proved positive in EMERGE, one might expect immense pressure to be put on the regulator to approve the drug, given the complete lack of other effective treatments.

A “shot in the arm” for AD research

One might desperately hope that an unusually cold winter signals a reversal of rising global temperatures, even if the great majority of data suggests otherwise. In the same way, researchers across the field will desperately hope that Biogen have got things right second time around, but they will be waiting with bated breath.

At the Society for Neuroscience’s 2019 conference, Alzheimer’s researcher Li-Huei Tsai told Technology Networks, “The news today this morning that Biogen put out is exciting. For Alzheimer’s disease, in the last 15 years, there has not been a successful trial. So, if they succeed this time, I will say it’s a very strong shot in the arm. I think we need some positive results.”

Tsai went on to temper her praise with some words of caution, “But with aducanumab, when they halted the trial, they said there was no hope that this drug would ever succeed. I think right now this new information, even though it’s exciting, I think when they designed the trial, they didn’t really know what patient population to go into. It seems that it’s not that everybody responded, only a very small population of people responded. I think there is still a need for something that can be beneficial to the many, many people who suffer from memory loss and dementia.”

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* Virtual Induction Into The Human Mind = Indução Virtual Na Mente Humana - Virtual Induction Of The Human Mind = Indução Virtual Da Mente Humana I N T E R N E T #Intenções #Imaginations #Thoughts #Pensamento(s) #Imaginações #Influences #Influência(s) - Nem sempre o que fazemos na Internet com seus vários tipos de influências, faremos no ´´Mundo Real´´, obviamente. - Not always what we do on the Internet with its various types of influences, we will do in the ´´Real World´´, obviously. - “The true logic of this world is in the calculus of probabilities.” —James Clerk Maxwell * Nothing is better than reading and gaining more and more knowledge.” — Stephen Hawking #time #data #messages #information #knowledge #intentions #reading #probability #people #mind #photo #name #image #video #influences #actions #health #person #life #speak #write #researches #reference #type #listen #InternetHistory #objectives #improvement #longevity #imaginations #thinking #reality #Internet #ScientificDiscoveries #books #journals #importance #websites #analysis #SocialNetworks #links #blogs #countries #innovations #graphics #feedbacks #facts #science #technologies #ScienceEvents #poster #abstract #methodology #article #publications #team #DirectInvitations #speaker #Delegate #cities #feelings #energy #pionner #lives #work #contribuitions #pionners #minds #WorldHistory #ranking #economy ´´The world people need to have very efficient researches and projects resulting in very innovative drugs, vaccines, therapeutical substances, medical devices and other technologies according to the age, the genetics and medical records of the person. So, the treatment, diagnosis and prognosis will be very efficient and better, of course´´. Rodrigo Nunes Cal ´´O mundo precisa ter pesquisas e projetos muito eficientes que resultem em medicamentos, vacinas, substâncias terapêuticas, dispositivos médicos e outras tecnologias muito inovadoras de acordo com a idade, a genética e o prontuário da pessoa. Assim, o tratamento, o diagnóstico e o prognóstico serão bem mais eficientes e melhores, é claro´´. Rodrigo Nunes Cal ´´As you know, the world needs to have very efficient researches resulting new therapeutical substances, medical devices, prevention, diagnostic and prognostic methods, drugs and vaccines, for example. Very detailed researches are fundamental in this process. 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As you know, humanity urgently needs new scientific discoveries, highlighting the acquisition of highly effective medicines and vaccines against a large number of diseases, including unknown and silent diseases, obtaining very efficient medical devices for diagnosis, prognosis and treatment of diseases, among others. Certainly, we need to have hope and motivation to do great work and for a much better quality of life and an ever-increasing life expectancy´´. Rodrigo Nunes Cal - Note: The statistics on the number of people who visited this blog in 2018 were not entirely based on real visitors. As estatísticas sobre número de pessoas que acessaram este blog no ano de 2018 não foram totalmente baseadas em visitantes reais. ´´Great difficulties may have come, but it is of great importance to have in mind the possibility of great victories in the future, bringing happiness and health for a long time´´. Rodrigo Nunes Cal ´´O caminho muito desconhecido pode ser o melhor caminho a seguir na vida´´. Rodrigo Nunes Cal ´´Understanding the great difficulties of a given subject can be a very long process, however, of great value for the progress of Science in all aspects´´. Rodrigo Nunes Cal ´´Entender as grandes dificuldades de um determinado assunto pode ser um processo muito longo, mas de grande valor para o progresso da Ciência em todos os seus aspectos´´. Rodrigo Nunes Cal My Curriculum Lattes: http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4240145A2 My Facebook Page: www.facebook.com/scientificblog IT´S A VERY EASY, FAST AND PRACTICAL WAY TO KNOW EXCELLENT INFORMATION ABOUT SCIENCE, TECHNOLOGY AND INNOVATION, AS AN EXAMPLE, APPLYING THE SEARCH MECHANISM Ctrl + F IN THIS BLOG FOR A WORD OR WORDS. SO, THIS BLOG SHARING IS VERY IMPORTANT TO THE WORLD SOCIETY! I hope in some way with this blog to help significantly in the socio-economic and technical-scientific development of the countries. E-mails: rodrigoncal1984@gmail.com rodrigonunescal@yahoo.com calrodrigonunes@gmail.com rodrigoncal1984@yahoo.com ´´NÃO VÁ PARA ONDE O CAMINHO PODE TE LEVAR. VÁ ONDE NÃO HÁ CAMINHO E DEIXE UMA TRILHA. ´´ ´´DON'T GO WHERE THE PATH CAN TAKE YOU. GO WHERE THERE IS NO PATH AND LEAVE A TRAIL. ´´ @ KNOWING THE UNKNOWN.. CONHECENDO O DESCONHECIDO.. The world needs very innovative ideas to people live better and longer more and more. I have been invited as a Speaker/Delegate in numerous International Conferences and Congresses. * DISCOVERING HOW THE INITIAL STAGES OF A CERTAIN DISEASES WORK, SUCH AS A FATAL DISEASES, IS OF HUGE IMPORTANCE FOR SCIENCE, FOR SURE. THERE ARE SEVERAL BIOLOGICAL FACTORS CONNECTED IN THE HUMAN BODY THAT ACTING IN A VERY COMPLEX FORM. THEREFORE, IT IS OF GREAT NECESSITY TO CARRY OUT NEW SCIENTIFIC RESEARCHES MUCH MORE DETAILED AND MODERN, WITH A HIGH DEGREE OF PRECISION, EVEN IF THERE IS NO SIGNIFICANT STATISTICAL DIFFERENCE BETWEEN CERTAIN FACTORS. * DESCOBRIR COMO FUNCIONA OS ESTÁGIOS INICIAIS DE DETERMINADAS DOENÇAS, TAIS COMO AS DOENÇAS FATAIS, É DE ENORME IMPORTÂNCIA PARA A CIÊNCIA , COM CERTEZA. HÁ VÁRIOS FATORES BIOLÓGICOS INTERLIGADOS NO CORPO HUMANO QUE ATUAM DE FORMA MUITO COMPLEXA. PORTANTO, É DE GRANDE NECESSIDADE A REALIZAÇÃO DE NOVAS PESQUISAS CIENTÍFICAS MUITO MAIS MINUCIOSAS E MODERNAS, COM ALTO GRAU DE PRECISÃO, MESMO QUE NÃO HAJA DIFERENÇA ESTATÍSTICA SIGNIFICATIVA ENTRE DETERMINADOS FATORES. * The discussion of certain facts in science envolving stastistics is fundamental to the scientific community, for example, the analysis and interpretation of very important, innovative and interesting graphics with no statistical difference between them can have a big value to the researches and to the future researches. So, the quality and efficiency of researches can increase so much in a little time, increasing the possiblities of excellent references and new scientific discoveries. The facts veracity and the disclosure of them are essential for the scientific community, of course. Reconhecer o(s) erro(s) cometido(s) e não praticá-lo(s) novamente é um ato de grande sabedoria e importância para si mesmo e para a(s) outra(s) pessoa(s). Acknowledging mistakes and not doing them again is an act of great wisdom and importance for yourself and to the other person or people. ´´O IMPOSSÍVEL PODE SER POSSÍVEL´´. ´´THE IMPOSSIBLE CAN BE POSSIBLE´´. I have received positive feedbacks about this blog by LinkedIn, Twitter, Facebook, E-mails and Instagram. ´´EVERYONE DIES. THE GOAL IS NOT TO LIVE FOREVER. THE GOAL S TO CREATE SOMETHING THAT WILL´´ # time #time #internet #technologies #HighTechnologies #Cell Phones #Computer #Notebook  # Television #radio #communication #tempo  #InternetSociety # Society #person # people # age #ages #genetics #longevity #investigations #researches #efficiency #projects #ideas #reference #references #article #articles #journal # journals #magazines #websites #blogs #sites #links #SocialNetworks #energy #graphics #dissertation #monograph #citations #ImpactFactor #pesquisa #pesquisas #tecnologias #DiferentesPercepções #DifferentPerceptions #mind #mente #minds #MentesHumanas #emails #email e-mails reading #MenteHumana leitura mensagem mensagens probabilidade(s) probabilities messages message importance importância relevância assunto(s) subject subjects issue tema reflexão reflections vision visão pioneirismo pionners prêmio(s) prizes awards innovations inovações Grupos de Estudo Grupos Controle saúde doença(s) nome(s) tempo(s) Início da doença - Momento inicial da doença - Momento(s) inicial(ais) da(s) doença(s) humana(s) - Semelhança genética com camundongos - Mice researches - vaccines - drugs - eficiência - medicamento(s) - vacina(s) - High efficiency - Fatal diseases - Doenças fatais - Investments - investimentos - laboratórios - industries - indústrias - laboratories - Centros de Pesquisa - Países - cidades - cities - longevidade - desafio(s) - challenges - gráficos detalhados - interações biológicas - fatores biológicas - análise minuciosa - Very detailed analysis @ Initial moment of disease - Initial moments of human diseases - No Name @ discussion - discussão científica - science facts - detailed graphics - fatos científicos - publicação de trabalhos científicos - publications - hard work - better results - better science - diagnóstico - prognósticos - Diferença Estatística Significativa 100 Diferença Estatística Significativa @ Significant Statistical Difference - V X I Interpretations interpretações intenções intenions countries EU 100 gene Sem genes Cem genes 1 0 0 gene(s) time(s) times 100 limites limite(s) limits 1 0 0 limit NO LIMIT 10 0 @ 100 genes @ 100 gene & NO GENE NO TEMPO NOS TEMPOS NO(S) TEMPO(S) NOS TIMES NO TIME 100 GENE No Time # no time @ nos genes no(s) gene(s) * no(s) limite(s) - words- palavra(s) - listen - write - type - fala - escuta - ler - virtualidade - virtuality - reality - realidade - mundo real - mundo virtual - vida real - virtual life - real life - vida virtual - imaginations - thoughts - pensamento(s) - imaginações - melhoria - improvement - respect - respeito - speak - nome(s) - trabalho(s) - dinheiro - money - team - equipe - objetivo(s) - Best Universities of the World - Scientific Discoveries - Brazil - World - RNA - Cell - DNA - Idade biológica - biological age - pessoas - idade - idade(s) - pessoa - História da Computação Mundial - Harvard - Names - Places - City - researches - scientists - professors - pesquisador(es) - cientistas - professores - professor(es) - Produção científica - Fatores de Impacto - feelings - logic - sentimento(s) - lógica - história - world history - difficulties - dificuldades - Scientific community - comunidade científica mundial - vidas humanas - vida(s) humana(s) - trabalho(s) - human lives - life - human life - única - one life - person people @ momentos - moments memories memory memória longevidade energias energia(s) Many people liked my Twitter and Facebook comments that I informed this blog like great professors, scientists and researchers around the world who work in human health area! Many data about it aren´t in this blog. #database #system #time #data #search #information #InternetHistory #contribuitions #improvement #analysis #intentions Intenções @ #person #people #age #longevity #work #reading #probabilities #energy #money #price #clicks #jobs #country #city #countries #cities #knowledge #HumanInterdependence #WorldHistory #communication #HumanRelations #websites #e-mails #SocialNetworks #ranking #links #images #photos #texts #messages #videos #writing #typing #speak #listen #think #feelings #ideas #ScientificDiscoveries #investigations #researches #articles #ImpactFactors #journals #citations #influence #dissertations #monographs #ScientificWorks #Inventions #graphics #subjects #books #references #blogs ´´Compreender as grandes dificuldades de um determinado assunto pode ser um processo muito demorado, porém, de grande valia para o progresso da Ciência em todos os aspectos´´ Rodrigo Nunes Cal Observação/Note: I won a scholarship by FAPEMIG during the period of ´´my´´ monograph in Uberaba. Ganhei bolsa de estudo pela FAPEMIG durante o período da ´´minha´´ monografia em Uberaba. During the period that I participated of ´´my´´ dissertation at FAMERP, I didn't win a scholarship. Já durante o mestrado que fiz na FAMERP, não ganhei bolsa de estudo. ´´Os gráficos baseados em dados da ´´minha´´ dissertação que fiz podem ser uma excelente referência para muitos tipos de pesquisas e projetos, é claro !! Por exemplo, para pesquisas e projetos que tenham como objetivo analisar os tipos de influências das idades em camundongos e humanos (estudos genéticos, por exemplo) em relação a diferentes estágios de determinadas doenças, como aquelas em que a comunidade científica desconhece (doenças desconhecidas) e que poderão surgir no mundo. Outros tipos de pesquisas e projetos que podem ser feitos são aqueles que analisam a eficácia de diversos tipos de substâncias terapêuticas em camundongos e humanos nos diversos tipos de doenças com o objetivo de saber qual a melhor substância terapêutica para cada doença, levando em consideração a idade e genética, com certeza. Contudo, realizar pesquisas com o objetivo de avaliar qual é a influência da idade e da genética na eficiência terapêutica em animais de experimentação e em humanos, consequentemente, possui um grande valor, já que muitas pessoas adoecem e acabam falecendo mesmo sendo submetidas à ótimos sistemas de diagnóstico, tratamento e prognóstico, dependendo da doença que possui e do estágio da mesma´´. ´´A partir daí, ao comprovar que há influência significativa da idade e da genética, consequentemente, no processo de patogênese de doenças nos animais de experimentação e nos humanos, seria muito mais conveniente e lógico um grupo de indivíduos de certa faixa etária e histórico familiar e individual de doenças adquiridas e possíveis de serem adquiridas no decorrer do tempo serem tratados com outros tipos de medicamentos, substâncias terapêuticas, vacinas, dentre outros. Com certeza, para a realização destes tipos de pesquisa deve haver grande investimento financeiro nos laboratórios a fim de aquisição de aparelhos científicos altamente eficientes. Com certeza, pesquisas à nível genético e com relação à influência da idade do ser vivo na patogênese de doenças, até das doenças desconhecidas pelo mundo científico. O fato é que este tipo de pesquisa é muito importante porque como todos sabem, há muitas doenças que voltam a se manifestar nas pessoas mesmo depois de excelentes tratamentos, dos mais variados tipos. E outro ponto a ser refletido é a permanência de doenças fatais´´. ´´Assim, este tipo de influência da idade e consequentemente da genética na fisiopatologia das doenças hereditárias ou não hereditárias, um indivíduo de uma determinada idade será submetido a um tratamento terapêutico diferente de outro com a mesma doença mas com idade diferente da de até a pesquisa mostrou uma influência significativa na patogênese da doença, portanto, utilizará outro tipo de substância terapêutica, medicamentos, entre outros. Isso certamente acontecerá se a comunidade científica mundial comprovar cientificamente essas hipóteses por meio de várias pesquisas e projetos científicos. As pessoas precisam ter excelentes inovações para a expectativa de vida humana aumentar muito rapidamente cada vez mais. Portanto, quanto mais a medicina personalizada for, melhor será para cada um de nós´´. Rodrigo Nunes Cal ´´The graphics based on data from ´´my´´ dissertation I did can be an excellent reference for many types of researches and projects, of course!! For example, for researches and projects that the goals are analyse the type of influences of ages in mice and human (genetic studies, for example) in relation to different stages of determined diseases, like those that the scientific community do not know about them (unknown diseases). Other types of researches and projects that can be done is those that analyse the efficiency of many types of therapeutical substances in mice and human in many types of diseases with the objective of knowing which is the best therapeutic substance for each disease, taking into account age and genetics, for sure. For example, to carry out research with the objective of evaluating the influence of age and genetics on therapeutic efficiency in experimental animals and in humans´´. ´´Thus, by proving that there is a significant influence of age and genetics, consequently, in the process of pathogenesis of diseases in experimental animals and in humans, it would be much more convenient and logical to have a group of individuals of a certain age group and family and individual history of acquired diseases and possible to be acquired over time being treated with other types of drugs, therapeutic substances, vaccines, among others. Certainly, to carry out these types of research there must be a large financial investment in laboratories in order to acquire highly efficient scientific devices. Certainly, research at the genetic level and regarding the influence of the age of the living being on the pathogenesis of diseases, even diseases unknown to the scientific world. The fact is that this type of research is very important because as everyone knows, there are many diseases that come back to manifest in people even after excellent treatments, of the most varied types. And another point to be reflected on is the permanence of fatal diseases´´. ´´Taking into account this type of influence of age and consequently genetics on the pathophysiology of inherited or not inherited diseases, an individual of a certain age will be submitted to a different therapeutic treatment from another with the same disease but who has a different age than through the research has shown a significant influence on the pathogenesis of the disease, therefore, will use another type of therapeutic substance, medicine, among others. This will certainly happen if the world scientific community scientifically proves these hypotheses through various research and scientific projects. So, the people need to have excellent innovation to the human expectancy  of life increase so much faster more and more´´. Rodrigo Nunes Cal Note/Obs: I thought each person could do their own friend request permission setting since Facebook's technology is so big, for example. Eu achava que cada pessoa poderia fazer sua própria configuração de permissão de solicitação de amizade já que a tecnologia do Facebook é muito grande, por exemplo.

11 Comments

  8. I have experienced the precise very same issue. It’s currently so bad the hair around the crown of the mind is so short.
    For a thirty something female it’s quite embarrassing.

    My esteem has fallen into an all time low as well. My
    spouse and children say I invest too much time facing the mirror…ButI CAN’T help it
    to. This is driving me nuts. Ive noticed that
    it really is worse throughout noon, yet again at the early day,
    then during the night right before bed. I live in Oklahoma.
    . Assess our post on Hair Loss

    Like

    Reply

  9. Hmm is anyone else encountering problems with the pictures on this blog loading? I’m trying to figure out if its a problem on my end or if it’s the blog. Any feedback would be greatly appreciated.

    Like

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