Scientists Identify Gene That Doubles Schizophrenia Risk

by Sheela Philomena on? August 07, 2013 at 11:46 AM Genetics & Stem Cells News Wellcome Trust Sanger Institute scientists have identified a new gene that doubles the risk of schizophrenia.
A team of researchers from the Wellcome Trust Sanger Institute, the Broad Institute of MIT and Harvard and the Institute for Molecular Medicine Finland, found that a disruption of the gene TOP3B, an exceedingly rare occurrence in most parts of the world, is fairly common in a uniquely genetically distinct founder population from North-eastern Finland.

Furthermore, the biochemical investigation of the protein encoded by the TOP3B gene allowed the researchers to gain first insight into the cellular processes that might be disturbed in the affected individuals.

The team identified a rare genetic deletion affecting TOP3B in the North-eastern Finnish population that increases a person's susceptibility to schizophrenia two-fold and that also is associated with an increased frequency of other disorders of brain development such as intellectual impairment. They speculate that this deletion directly disrupts the TOP3B gene to cause its effects on the brain.

Having identified the link between TOP3B and schizophrenia, the researchers sought to understand why disrupting this gene might increase susceptibility to disease, and for this purpose they investigated the function of the protein that it encodes.

TOP3B encodes a type of protein that typically helps the cell to unwind and wind DNA helices - essential to normal cell function. Quite unexpectedly for an enzyme of this class, however, TOP3B was found to act on messenger-RNA rather than DNA.

In their further biochemical investigation into TOP3B, the team found that the TOP3B protein interacts with a protein known as FMRP. The deactivation or disruption of this protein is responsible for Fragile X syndrome, a disorder associated with autism and learning difficulties, primarily in men.

Source-ANI

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Scientists Identify Gene That Doubles Schizophrenia Risk

by Sheela Philomena on? August 07, 2013 at 11:46 AM Genetics & Stem Cells News Wellcome Trust Sanger Institute scientists have identified a new gene that doubles the risk of schizophrenia.
A team of researchers from the Wellcome Trust Sanger Institute, the Broad Institute of MIT and Harvard and the Institute for Molecular Medicine Finland, found that a disruption of the gene TOP3B, an exceedingly rare occurrence in most parts of the world, is fairly common in a uniquely genetically distinct founder population from North-eastern Finland.

Furthermore, the biochemical investigation of the protein encoded by the TOP3B gene allowed the researchers to gain first insight into the cellular processes that might be disturbed in the affected individuals.

The team identified a rare genetic deletion affecting TOP3B in the North-eastern Finnish population that increases a person's susceptibility to schizophrenia two-fold and that also is associated with an increased frequency of other disorders of brain development such as intellectual impairment. They speculate that this deletion directly disrupts the TOP3B gene to cause its effects on the brain.

Having identified the link between TOP3B and schizophrenia, the researchers sought to understand why disrupting this gene might increase susceptibility to disease, and for this purpose they investigated the function of the protein that it encodes.

TOP3B encodes a type of protein that typically helps the cell to unwind and wind DNA helices - essential to normal cell function. Quite unexpectedly for an enzyme of this class, however, TOP3B was found to act on messenger-RNA rather than DNA.

In their further biochemical investigation into TOP3B, the team found that the TOP3B protein interacts with a protein known as FMRP. The deactivation or disruption of this protein is responsible for Fragile X syndrome, a disorder associated with autism and learning difficulties, primarily in men.

Source-ANI

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Scientists: Sleeping Stem Cells Could Hold Key to Treatment of Aggressive Blood Cancer

by Rukmani Krishna on? August 02, 2013 at 12:02 AM Cancer News Rather than displacing healthy stem cells in the bone marrow as previously believed, the cancer is putting them to sleep to prevent them forming new blood cells, discovers scientists studying an aggressive form of leukaemia.
The finding offers the potential that these stem cells could somehow be turned back on, offering a new form of treatment for the condition, called Acute Myeloid Leukaemia (AML). The work was led by scientists at Queen Mary, University of London with the support of Cancer Research UK's London Research Institute.

Around 2,500* people are diagnosed with AML in the UK each year, both young and old. Although AML is curable in some the majority die from this disease.

Normally, the bone marrow produces haematopoietic stem cells which mature into "adult" blood cells. In people with AML the bone marrow is invaded by leukaemic myeloid cells which aren't able to develop into normal functioning blood cells.

The result is that the body does not have enough red blood cells or platelet cells, which can cause symptoms of anaemia, such as tiredness, and increase the risk of excessive bleeding. Patients are also more vulnerable to infection as the white blood cells, which fight bacteria and viruses, are not properly formed.

Dr David Taussig, from the Barts Cancer Institute at Queen Mary, University of London, who led the research, said: "The widely accepted explanation has held that AML causes bone marrow failure by depleting the bone marrow of normal haematopoietic stem cells by killing or displacing them.

"However, we have found that samples of bone marrow in both mice models and patients with AML contain the same, or more, of these normal stem cells than usual. So the cancer isn't getting rid of them, instead it appears to be turning them off so they aren't going on to form healthy blood cells.

"If we can find out how the cancer cells are doing this, we can look at exploiting it to find ways to wake these stem cells up. This is very important as, while the cure rate for younger patients can be around 40 per cent, in older patients it is much lower. The treatments we have, such as chemotherapy and bone marrow transplants, just aren't very successful in this older patient group."

The scientists studied the levels of haematopoietic stem cells (HSC) in the bone marrow of mice transplanted with human AML. They found the numbers of normal mouse HSCs stayed the same, however what did change was that the HSCs were no longer going through the stages of development which finally results in the formation of new blood cells.

The findings were confirmed by the analysis of bone marrow from 16 patients with AML.

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "Although major progress has been made in treating AML over the years, there's still an urgent need for more effective treatments to improve long-term survival. This study takes us an important step forwards in our understanding of what's going on in the bone marrow of people with AML, an area that we have not known enough about previously, and the challenge now is to turn this understanding into new treatments for patients."

Dr Taussig added: "Usually when the body is stressed, the stem cells become very active. For example, if you have a haemorrhage, they will jump into action to produce more new blood cells. The cancer cells are somehow over-riding this and our next phase of work will concentrate on how they are doing this."

Source-Eurekalert

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Scientists Urge Major Changes for Cancer Screening and Treatment

The "Viewpoint" article will be published online Monday, July 29, in the Journal of the American Medical Association.

When cancer screening programs were widely initiated three decades ago, medical knowledge of the disease was more simplistic. The intent was to detect cancer at its earliest stages to reduce illness and mortality, but in fact early diagnosis has not led to a proportional decline in serious disease and death, the scientists write in the JAMA commentary.

Instead, screening programs are identifying not only malignant cancers, but also slow-growing, low-risk lesions, and sweeping them into the same treatment process. As a result, patients are being diagnosed and treated for forms of cancer that might never actually harm them - a phenomenon that''s been termed overdiagnosis, which translates to "too much medicine."

Now, with the advancement of scientific understanding of the biology of cancer, the authors say it is time for significant changes in practice and policy.

"By recognizing that cancer is not one disease, but a number of different diseases, we can individualize our treatment based on biology and avoid overtreatment," said panel chair Laura J. Esserman, MD, MBA, director of the Carol Franc Buck Breast Care Center at the UCSF Helen Diller Family Comprehensive Cancer Center. "The goal going forward is to personalize screening strategies, and focus screening policies on the conditions that are most likely to result in aggressive illness and death."

The authors recommend creation of a new classification for tumors that are indolent (unlikely to cause patients harm). For example, ductal carcinoma of the breast -- currently considered the earliest form of breast cancer -- would no longer be called cancer. The authors also call for the formation of registries for lesions with low potential for malignancy, and for a multidisciplinary approach across pathology, imaging, surgery and other medical specialties "to revise the taxonomy of lesions now called cancer."

The key, they say, is to improve screening strategies to avoid overtreating tumors that would not be lethal, or that would not even have come to medical attention.

"Although our understanding of the biology of cancer has changed dramatically, perceptions on the part of the public, and among many physicians, have not yet changed," Esserman said. "Cancer is still widely perceived as a diagnosis with lethal consequences if left untreated."

The JAMA article is comprised of recommendations from a working group formed last year during a meeting convened by the National Cancer Institute. The group was charged with developing a strategy to improve current approaches to cancer screening and prevention.?

The commentary was co-written by Ian M. Thompson, MD, professor at the University of Texas Health Science Center at San Antonio; and Brian Reid, MD, PhD, director of the Seattle Barrett''s Esophagus Program and member of the Human Biology Division at the Fred Hutchison Cancer Research Center in Seattle.

The three authors served as chairs of the NCI working group.

Overdiagnosis is occurring across many medical conditions, but is particularly common in breast cancer, lung cancer, prostate, thyroid cancer and melanoma, said the authors.

They cite DCIS, or ductal carcinoma of the breast, and Barrett''s esophagus as illustrations of how the detection and surgical removal of what have been called precancerous lesions have failed to lead to lower rates of invasive cancer.

By contrast, the authors said, colon and cervical cancer serve as examples of "effective screening programs in which early detection and removal of precancerous lesions have reduced incidence as well as late-stage disease."?

Cancer screening should have three important missions, the authors write: To detect disease that would ultimately harm the patient; to uncover tumors that benefit from intervention; and to detect disease that is more likely to be cured or better treated when spotted early.

Optimal screening frequency depends on a cancer''s growth rate. If a cancer is fast growing, screening is less likely to be effective. "If a cancer is slow growing but progressive, with a long latency and a precancerous lesion, screening is ideal and less frequent screening (eg.10 years for colonoscopy) may be effective," the authors said.

Source-Newswise

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Scientists: Sleeping Stem Cells Could Hold Key to Treatment of Aggressive Blood Cancer

by Rukmani Krishna on? August 02, 2013 at 12:02 AM Cancer News Rather than displacing healthy stem cells in the bone marrow as previously believed, the cancer is putting them to sleep to prevent them forming new blood cells, discovers scientists studying an aggressive form of leukaemia.
The finding offers the potential that these stem cells could somehow be turned back on, offering a new form of treatment for the condition, called Acute Myeloid Leukaemia (AML). The work was led by scientists at Queen Mary, University of London with the support of Cancer Research UK's London Research Institute.

Around 2,500* people are diagnosed with AML in the UK each year, both young and old. Although AML is curable in some the majority die from this disease.

Normally, the bone marrow produces haematopoietic stem cells which mature into "adult" blood cells. In people with AML the bone marrow is invaded by leukaemic myeloid cells which aren't able to develop into normal functioning blood cells.

The result is that the body does not have enough red blood cells or platelet cells, which can cause symptoms of anaemia, such as tiredness, and increase the risk of excessive bleeding. Patients are also more vulnerable to infection as the white blood cells, which fight bacteria and viruses, are not properly formed.

Dr David Taussig, from the Barts Cancer Institute at Queen Mary, University of London, who led the research, said: "The widely accepted explanation has held that AML causes bone marrow failure by depleting the bone marrow of normal haematopoietic stem cells by killing or displacing them.

"However, we have found that samples of bone marrow in both mice models and patients with AML contain the same, or more, of these normal stem cells than usual. So the cancer isn't getting rid of them, instead it appears to be turning them off so they aren't going on to form healthy blood cells.

"If we can find out how the cancer cells are doing this, we can look at exploiting it to find ways to wake these stem cells up. This is very important as, while the cure rate for younger patients can be around 40 per cent, in older patients it is much lower. The treatments we have, such as chemotherapy and bone marrow transplants, just aren't very successful in this older patient group."

The scientists studied the levels of haematopoietic stem cells (HSC) in the bone marrow of mice transplanted with human AML. They found the numbers of normal mouse HSCs stayed the same, however what did change was that the HSCs were no longer going through the stages of development which finally results in the formation of new blood cells.

The findings were confirmed by the analysis of bone marrow from 16 patients with AML.

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "Although major progress has been made in treating AML over the years, there's still an urgent need for more effective treatments to improve long-term survival. This study takes us an important step forwards in our understanding of what's going on in the bone marrow of people with AML, an area that we have not known enough about previously, and the challenge now is to turn this understanding into new treatments for patients."

Dr Taussig added: "Usually when the body is stressed, the stem cells become very active. For example, if you have a haemorrhage, they will jump into action to produce more new blood cells. The cancer cells are somehow over-riding this and our next phase of work will concentrate on how they are doing this."

Source-Eurekalert

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Key Signaling Pathway That Makes Young Neurons Connect Discovered By Scientists

In the new study, the researchers identified a molecular program that controls an essential step in the fast-growing brains of young mammals. The researchers found that this signaling pathway spurs the growth of neuronal output connections by a mechanism called "mitochondrial capture," which has never been described before.

"Mutations that may affect this signaling pathway already have been found in some autism cases," said TSRI Professor Franck Polleux, who led the research, published June 20, 2013 in the journal Cell.

Branching Out

Polleux's laboratory is focused on identifying the signaling pathways that drive neural development, with special attention to the neocortex?a recently evolved structure that handles the "higher" cognitive functions in the mammalian brain and is highly developed in humans.

In a widely cited study published in 2007, Polleux's team identified a trigger of an early step in the development of the most important class of neocortical neurons. As these neurons develop following asymmetric division of neural stem cells, they migrate to their proper place in the developing brain. Meanwhile they start to sprout a root-like mesh of input branches called dendrites from one end, and, from the other end, a long output stalk called an axon. Polleux and his colleagues found that the kinase LKB1 provides a key signal for the initiation of axon growth in these immature cortical neurons.

In the new study, Polleux's team followed up this discovery and found that LKB1 also is crucially important for a later stage of these neurons' development: the branching of the end of the axon onto the dendrites of other neurons.

"In experiments with mice, we knocked the LKB1 gene out of immature cortical neurons that had already begun growing an axon, and the most striking effect was a drastic reduction in terminal branching," said Julien Courchet, a research associate in the Polleux laboratory who was a lead co-author of the study. "We saw this also in lab dish experiments, and when we overexpressed the LKB1 gene, the result was a dramatic increase in axon branching."

Further experiments by Courchet showed that LKB1 drives axonal branching by activating another kinase, NUAK1. The next step was to try to understand how this newly identified LKB1-NUAK1 signaling pathway induced the growth of new axon branches.

Stopping the Train in Its Tracks

Following a thin trail of clues, the researchers decided to look at the dynamics of microtubules. These tiny railway-like tracks are laid down within axons for the efficient transport of molecular cargoes and are altered and extended during axonal branching. Although they could find no major change in microtubule dynamics within immature axons lacking LKB1 or NUAK1, the team did discover one striking abnormality in the transport of cargoes along these microtubules. Tiny oxygen-reactors called mitochondria, which are the principal sources of chemical energy in cells, were transported along axons much more actively?and by contrast, became almost immobile when LKB1 and NUAK1 were overexpressed.

But the LKB1-NUAK1 signals weren't just immobilizing mitochondria randomly. They were effectively inducing their capture at points on the axons where axons form synaptic connections with other neurons.

"When we removed LKB1 or NUAK1 in cortical neurons, the mitochondria were no longer captured at these points," said Tommy Lewis, Jr., a research associate in the Polleux Laboratory who was co-lead author of the study.

"We argue that there must be an active 'homing factor' that specifies where these mitochondria stop moving," said Polleux. "And we think that this is essentially what the LKB1-NAUK1 signaling pathway does here."Looking Ahead

Precisely how the capture of mitochondria at nascent synapses promotes axonal branching is the object of a further line of investigation in the Polleux laboratory. "We think that we have uncovered something very interesting about mitochondrial function at synapses," Polleux said.

In addition to its basic scientific importance, the work is likely to be highly relevant medically. Developmentally related brain disorders such as epilepsy, autism and schizophrenia typically involve abnormalities in neuronal connectivity. Recent genetic surveys have found NUAK1-related gene mutations in some children with autism, for example. "Our study is the first one to identify that NUAK1 plays a crucial role during the establishment of cortical connectivity and therefore suggests why this gene might play a role in autistic disorder," Polleux says.

He notes, too, that declines in normal mitochondrial transport within axons have been observed in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. "In the light of our findings, we wonder if the decreased mitochondrial mobility observed in these cases might be due not to a transport defect, but instead to a defect in mitochondrial capture in aging neurons," he said. "We're eager to start doing experiments to test such possibilities."

Source-Eurekalert

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Scientists Find New Way to Improve Antibiotic Production

Scientists Dr Emma Sherwood and Professor Mervyn Bibb from the John Innes Centre were able to use their discovery of how the antibiotic is naturally produced to markedly increase the level of production.

"We have shown for the first time that an antibiotic with clinical potential can act as signalling molecule to trigger its own synthesis," said Professor Bibb.

The antibiotic called planosporicin is produced by a soil bacterium called Planomonospora alba. When nutrients become limited, a small amount of the antibiotic is produced. The antibiotic is then able to trigger a mechanism which coordinates its own production throughout the bacterial population resulting in high levels.

"A frequent stumbling block in developing a natural product for commercialisation is being able to provide enough material for clinical trials," said Professor Bibb.

"Our work shows with the right understanding it is possible to increase productivity very dramatically in a targeted and knowledge-based manner."

With knowledge of this signalling mechanism in hand, the scientists were able to increase production by overexpressing two positively acting regulatory genes and deleting one that acts negatively. Planosporicin is similar to the antibiotic NAI-107 that is about to enter clinical trials for Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE) infections. The knowledge gained from this study is being used to increase NAI-107 production.

Commercial manufacturers of antibiotics may be able to use the results to reduce production times and therefore reduce costs. Bacteria often have to be grown for days and sometimes weeks before they start to make effective amounts of an antibiotic. Sherwood and Bibb were able to trigger production essentially from the beginning of growth.

Source-Eurekalert

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Scientists Map Ultra-high 3-D Resolution of Human Brain

It shows the human brain at a spatial resolution of 20 microns, smaller than the size of one fine strand of hair-exceeding that of existing reference brains presently in the public domain.

The new tool is made freely available to the broader scientific community to advance the field of neuroscience.

Researchers from Germany and Canada collaborated on the ultra-high resolution brain model.

The sophisticated modern image processing methods reveal an unprecedented look at the very fine details of the human brain's microstructure, or cellular level.

The anatomical tool will allow for three-dimensional cytoarchitectonic mapping of the human brain and serve as an atlas for small cellular circuit data, or single layers or sublayers of the cerebral cortex, explained the researchers.

Until recently, reference brains did not probe further than the macroscopic, or visible, components of the brain.

Now, the BigBrain provides a resolution much finer than the typical 1 mm resolution from MRI studies.

The findings are published in the journal Science, which is published by AAAS, the international non-profit science society.

Source-ANI

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Scientists Have Found Possible Cure for Gray Hair and Vitiligo

by Mita Majumdar on? June 15, 2013 at 2:49 PM Health Watch A team of European researchers developed a topical, UVB-activated compound called PC-KUS, which they claim can reverse oxidative stress responsible for causing gray hair and vitiligo.
The pigment melanin determines the color of our skin, hair and eyes. Loss of melanin in the skin and hair causes vitiligo (white patches on the skin) and graying of hair.

Our hair goes gray due to massive oxidative stress caused by accumulation of hydrogen peroxide in the hair follicle. This causes our hair to bleach itself from the inside out. Karin Schallreuter and colleagues, from the Institute for Pigmentary Disorders, E.M. Arndt University, Greifswald, Germany; and Centre of Skin Sciences, School of Life Sciences, University of Bradford, U.K, developed a photo-activated compound (PC-KUS) that could reverse this build up of hydrogen peroxide. This proprietary treatment works for vitiligo as well.

'To date, it is beyond any doubt that the sudden loss of the inherited skin and localized hair color can affect those individuals in many fundamental ways,' said Schallreuter, the lead researcher of the study. 'The improvement of quality of life after total and even partial successful repigmentation has been documented.'

This study analyzed the effects of the medication on an international group of 2,411 patients with vitiligo, where 2.4 percent were diagnosed with strictly segmental vitiligo (SSV), and 3.2 percent were diagnosed with mixed vitiligo (SSV plus non-segmental vitiligo NSV).

Non-segmental vitiligo is the most common type of vitiligo in which the patches often become visible equally on both sides of the body, with some kind of symmetry. These symmetrical patches generally appear on skin that is exposed daily to the sun.

Segmental vitiligo, on the other hand, is rare, non-symmetrical, and usually tends to affect dorsal roots of the spine. It is more stable, less erratic, and responds well to topical treatments.

The researchers of this study found that patients who have SSV within a certain nerve distribution involving skin and eyelashes show the same oxidative stress as observed in the NSV, which is associated with decreased antioxidant capacities of enzymes like catalase and other antioxidants.

The researchers treated the patients with PC-KUS (a modified pseudocatalase) and found that the treatment led to successful re-pigmentation in their skin and eyelashes, that is, the original color was restored.

'For generations, numerous remedies have been concocted to hide gray hair, but now, for the first time, an actual treatment that gets to the root of the problem has been developed. While this is exciting news, what's even more exciting is that this also works for vitiligo. This condition, while technically cosmetic, can have serious socio-emotional effects of people. Developing an effective treatment for this condition has the potential to radically improve many people's lives,' said Gerald Weissmann, Editor-in-Chief of The FASEB Journal.

This study is a follow up on a 2009 study published in the journal FASEB which described the cause of age-related graying of hair. According to the study findings, low levels of enzyme that breaks up hydrogen peroxide into water and oxygen (catalase) cause the build up of hydrogen peroxide. These hair follicles also have low levels of enzymes MSR A and B, which are used to repair the damage. Further complicating matters, the high levels of hydrogen peroxide and low levels of these enzymes, disrupt the formation of an enzyme tyrosinase (which produces melanin in hair follicles), thus causing graying of hair.

References:

http://www.fasebj.org/content/early/2013/04/29/fj.12-226779.abstract
http://www.eurekalert.org/pub_releases/2013-05/foas-gha050313.php

Source-Medindia

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Thank Fish for Human Hand Gestures: Scientists

Scientists have found that the evolution of the control of speech and hand movements can be traced back to the same place in the brain, which could explain why we use hand gestures when we are speaking.

"We have traced the evolutionary origins of the behavioural coupling between speech and hand movement back to a developmental compartment in the brain of fishes," Professor Andrew Bass of Cornell University said.

"Pectoral appendages (fins and forelimbs) are mainly used for locomotion. However, pectoral appendages also function in social communication for the purposes of making sounds that we simply refer to as non-vocal sonic signals, and for gestural signalling."

Studies of early development in fishes show that neural networks in the brain controlling the more complex vocal and pectoral mechanisms of social signalling among birds and mammals have their ancestral origins in a single compartment of the hindbrain in fishes.

This begins to explain the ancestral origins of the neural basis for the close coupling between vocal and pectoral/gestural signalling that is observed among many vertebrate groups, including humans.

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British Scientists Develop New Screening Test to Identify Postnatal Depression Risk

Changes in estrogen levels during pregnancy make women more sensitive to the stress hormone cortisol. Soon after the baby is born, the estrogen levels return to normal. However, women with these genetic variations are unable to do so, leading to postnatal depression.

Postnatal depression is a type of depression some women experience after they have had a baby. It usually develops in the first four to six weeks after childbirth, but in some cases, it may take months to develop.

Postnatal depression is not the same as 'baby blues' which is a mild type of depression that occurs after childbirth and lasting from a few hours to a few days. During this time, the new mother may feel tearful and irritable, but no medical treatment is needed since in milder forms it is considered normal. However, if it is more prolonged and severe, it can develop into postnatal depression.

Symptoms of postnatal depression include low mood, feeling unable to cope and difficulty with sleeping. Unfortunately, many women are not aware they have the condition. Sometimes, the new mother may feel very agitated or alternatively very apathetic or have feelings of guilt and self-blame. She may even be thinking about?harming self or the baby.

In view of this, the research is very important. 'There is evidence that if you can identify women at risk early, you could treat early or introduce measures to prevent or stop the process of the disease,' Grammatopoulos said.

Based on this research, Grammatopoulos and his team have developed the first ever blood test for postnatal depression which would allow women found to be at risk to receive treatment for the disease before they give birth.

Prof Grammatopoulos said he could test women for the genetic changes for between ?30 and ?40. But automating the test so that robots could screen large numbers of samples would bring the cost down to just ?10.

'Usually we focus on the mother, but the negative impact on the child is also immense,' Prof Grammatopoulos said. He is now looking for further genetic changes to increase the predictive power of the test.

Reference: http://www.journalofpsychiatricresearch.com/article
/S0022-3956%2813%2900143-X/abstract

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How DHA Resolves Inflammation Explained By Harvard and USC Scientists

by Rukmani Krishna on? July 05, 2013 at 10:52 PM General Health News Bethesda, MD?Chronic inflammation is a major factor in a wide range of problems from arthritis to cardiovascular disease. DHA (found in fish oil) is known to temper this problem. A new research report helps explain why DHA is important in reducing inflammation, and provides an important lead to finding new drugs that will help bring people back to optimal health. The report can be found in the July 2013 issue of The FASEB Journal. Specifically, researchers found that macrophages (a type of white blood cell) use DHA to produce "maresins," which serve as the "switch" that turns inflammation off and switches on resolution.
"We hope that the results from this study will enable investigators to test the relevance of the maresin pathway in human disease," said Charles N. Serhan, Ph.D., a researcher involved in the work from the Brigham & Women's Hospital and Harvard Medical School in Boston, Mass. "Moreover, we hope to better understand resolution biology and its potential pharmacology so that we can enhance our ability to control unwanted inflammation and improve the quality of life."

To make this discovery, Serhan and colleagues deconstructed the biosynthetic pathway for maresin biosynthesis and found that human macrophages are responsible for converting DHA to the novel epoxide intermediate "13S, 14S-epoxy-maresin." Then, they learned how to synthesize the molecule and found that maresins caused macrophages to change their "type" so they no longer caused inflammation (switching them from M1 to M2 phenotypes).

"We've known for a long time that DHA tames inflammation, now, we learn exactly how DHA works: via new substances called maresins," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "We encounter inflammation almost daily, but our body has ways of turning it off. This is an important step toward understanding exactly this happens. You're likely to be hearing a lot more about maresins if, or when, new therapies arise from this discovery."

Source-Eurekalert

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Scientists Set Guidelines for Stem Cell Transplants in Older Patients With MDS

MDS is the most common blood disorders in people over 60 years of age, and frequently a precursor for leukemia.

The new study was led by an international team of Dana-Farber Cancer Institute.

Using mathematical models to analyze hundreds of MDS cases from around the world, the researchers found reduced intensity transplants of donor stem cells are advisable for patients aged 60-70 who have higher-risk forms of MDS that are likely to turn into leukemia in the near future. For patients with lower-risk MDS, non-transplant treatments are preferable, the model indicates.

The research was reported online today in the Journal of Clinical Oncology.

"Our study helps inform older MDS patients and their doctors whether a stem cell transplant is preferred or whether it makes more sense to pursue other options," says John Koreth, MBBS, DPhil, medical oncologist in the Division of Hematologic Malignancies at Dana-Farber, who is the study's lead author and co-principal investigator (with Joseph Pidala, MD, MS, of the H. Lee Moffitt Cancer & Research Institute, and senior author Corey Cutler, MD, MPH, of the Division of Hematologic Malignancies at Dana-Farber). "Until now, there haven't been statistically-quantified guidelines for making these decisions for older patients, who are most impacted by the disease."

MDS arises in the blood-forming cells of the bone marrow, causing a drop in the number of healthy white and red blood cells and of platelets needed for blood clotting. Depending on which type of cells are in short supply, the result can be fatigue, shortness of breath, easy bruising and bleeding, or infection and fever. An estimated 12,000 people in the United States are diagnosed with MDS each year, and more than 80 percent of whom are over age 60. (Some researchers believe MDS to be widely under-diagnosed, so the number of people affected may be much larger.)

In some cases, MDS produces only mild symptoms that don't worsen for years. In others, the symptoms can be severe, leading to the development of a fast-growing form of leukemia. The most common tool for predicting the course of MDS is the International Prognostic Scoring System (IPSS), which is based on a patient''s blood counts, percentage of immature "blast" cells in the blood or bone marrow, and occurrence of chromosomal abnormalities in these cells. Based on IPSS scores, the disease is classified as low risk, intermediate-1 or -2 risk, or high risk.

Patients in the first two categories, with lower-risk disease, usually receive treatments such as antibiotics, transfusions, blood cell growth-promoting agents, or other supportive therapies to alleviate their specific symptoms. Patients in the latter two categories, with higher-risk disease, often receive chemotherapy.

While these treatments are often helpful, they cannot cure the disease. The only potentially curative treatment is a donor stem cell transplant, which can, in principle, be used for patients with any stage of MDS. But because even reduced-intensity transplants are fatal in a significant minority of cases, there has been some uncertainty over the use of transplantation for older patients with MDS.

"It hasn't been clear for which older patient groups the benefits of transplant outweigh the risks," Koreth says. To find out, researchers collected data on 514 patients, age 60-70, who were newly diagnosed with MDS. For both lower- and higher-risk groups, they built separate mathematical models to compare treatment outcomes in patients who received reduced-intensity donor stem cell transplants with outcomes in patients who received non-transplant therapies. They analyzed not only length of survival but also the quality of life of patients in those groups.

Patients in the lower-risk groups who underwent transplant lived an average of 38 months after treatment, less than the 77 months for those who were treated without transplant. For patients in the higher-risk groups, by contrast, average life expectancy was 36 months for those receiving transplants, better than the 28 months for those receiving non-transplant therapies. Adjusting for patients' quality of life did not change the conclusions regarding the relative merits of the treatments.

"The clear result is that, on balance, reduced-intensity stem cell transplantation offers a survival benefit for patients with higher-risk MDS, but not for those with lower-risk disease," Koreth says. "The findings should offer useful guidance for older patients with MDS on deciding the best course of treatment."

Study co-authors include Waleska Perez, MPH, and Mary Horowitz, MD, CIBMTR Statistical Center; H. Joachim Deeg, MD, and Stephanie Lee, MD, Fred Hutchinson Cancer Research Center; Guillermo Garcia-Manero, MD, M.D. Anderson Cancer Center; Luca Malcovati, MD, and Mario Cazzola, MD, University of Pavia Medical School, Italy; Sophie Park, MD, PhD, Universite Paris V, France; Raphael Itzykson, MD, Lionel Ades, MD, and Pierre Fenaux, MD, Universite Paris 13, France; Martin Jadersten, MD, PhD, and Eva Hellstrom-Lindberg, MD, PhD, Karolinska Institutet, Sweden; C. L. Beach, PharmD, Celgene Corp.; Robert Peter Gale, MD, PhD, Celgene Corp. and Imperial College, London, U.K.; Peter Greenberg, MD, Stanford University School of Medicine; Martin Tallman, MD, Memorial Sloan-Kettering Cancer Center; John DiPersio, MD, PhD, Washington University School of Medicine, St. Louis; Donald Bunjes, MD, of University Hospital Ulm, Germany; and Daniel Weisdorf, MD, University of Minnesota.

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Scientists Discover Promising Path to Prevent Epilepsy

Epilepsy is a serious neurological disorder marked by recurring seizures. Temporal lobe epilepsy - where seizures occur in the region of the brain where memories are stored and language, emotions and senses are processed - is the most common form, and can be devastating. Because afflicted individuals have seizures that impair their awareness and may have associated behavioral problems, they may have difficulty with everyday activities, including holding a job or obtaining a driver's license.

Conventional therapies to treat epilepsy address the disease's symptoms by trying to reduce the likelihood of having a seizure. However, many people with temporal lobe epilepsy still have seizures despite taking these drugs.

Retrospective studies of people with severe temporal lobe epilepsy reveal that many of them initially have an episode of prolonged seizures, known as status epilepticus. Status epilepticus is often followed by a period of seizure-free recovery before people start to experience recurring temporal lobe seizures.

In animal studies, inducing status epilepticus in an otherwise healthy animal can cause them to become epileptic. The prolonged seizures in status epilepticus are therefore thought to cause or importantly contribute to the development of epilepsy in humans.

"An important goal of this field has been to identify the molecular mechanism by which status epilepticus transforms a brain from normal to epileptic," said study author James O. McNamara, M.D., professor of neurobiology at Duke Medicine.

"Understanding that mechanism in molecular terms would provide a target with which one could intervene pharmacologically, perhaps to prevent an individual from becoming epileptic."

Earlier research in epilepsy flagged a receptor in the nervous system called TrkB as a key player in transforming the brain from normal to epileptic. In the current study, McNamara and his colleagues sought to confirm if TrkB was important for status epilepticus-induced epilepsy.

Using an approach combining chemistry and genetic analyses, the researchers studied normal and genetically altered mice. The genetically altered mice were unique in that a drug, 1NMPP1, inhibited TrkB in their brains. If the drug stopped the genetically altered mice from becoming epileptic, this genetic approach would prove that inhibiting TrkB prevents the onset of epilepsy.

When the researchers caused status epilepticus in the animals, both the normal and genetically modified mice developed epilepsy. However, treatment with 1NMPP1 after the prolonged period of seizures prevented epilepsy in the genetically altered but not the normal mice.

"This demonstrated that it is possible to intervene following status epilepticus and prevent the animal from becoming epileptic," McNamara said.

Importantly, the researchers only administered treatment with 1NMPP1 for two weeks, which was sufficient to prevent epilepsy from developing in the mice when tested many weeks later. The results suggest that a preventive therapy may only need to be given for a limited period of time following the initial bout of prolonged seizures, not an individual's entire life, which could prevent unnecessary side effects that come with long-term use of drugs.

In future studies, the researchers hope to determine the exact time window in which TrkB signaling needs to be repressed to prevent the onset of epilepsy. Long term, this research provides a molecular target for developing the first drugs to prevent epilepsy.

The study was recently published in the journal Neuron.

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Scientists identify genetic risk for pulmonary fibrosis factor

Team, including doctors and scientists of the Faculty of the University of Colorado's watched medicine a fairly common variant of the mucin 5b gene, a protein that is a component of the produced by bronchial mucosa. This variant of the gene MUC5B is fairly common, pulmonary fibrosis is a disease rarely reported.

In a review of CT over 2 600 adults don't have a diagnosis of pulmonary fibrosis, the researchers found evidence of imaging of inflammation of the lungs and the scars in about 9% of the people over 50 years. In this age group, these abnormal results on computer tomography were significantly more common in people of 21 percent with the genetic variant of MUC5B.

What is important, final pulmonary fibrosis seen on CT scan has been strongly linked to the genetic variant of MUC5B. Although these anomalies do not necessarily indicate a disease that progresses, the presence of these abnormalities have been associated with more shortness of breath and cough as well as smaller lung sizes and capacity of oxygen transfer.

The results suggest that pulmonary fibrosis, which is a condition where the lung tissue becomes thickened, rigid and scarred, may be part of a syndrome less severe, much more common, but probably and could potentially be predicted on the basis of the genetic variant of MUC5B.

A paper describing the discovery was published recently in the New England Journal of Medicine.

Twenty-one authors share credit for the paper, including researchers from Brigham and Women hospital and Boston University.

Source-ANI

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Scientists Solve White Tiger Mystery

"The white tiger represents part of the natural genetic diversity of the tiger that is worth conserving, but is now seen only in captivity," says Shu-Jin Luo of China's Peking University.

Luo, Xiao Xu, Ruiqiang Li, and their colleagues advocate a proper captive management program to maintain a healthy Bengal tiger population including both white and orange tigers. They say it might even be worth considering the reintroduction of white tigers into their wild habitat.

The researchers mapped the genomes of a family of 16 tigers living in Chimelong Safari Park, including both white and orange individuals. They then sequenced the whole genomes of each of the three parents in the family.

Those genetic analyses led them to a pigment gene, called SLC45A2, which had already been associated with light coloration in modern Europeans and in other animals, including horses, chickens, and fish. The variant found in the white tiger primarily inhibits the synthesis of red and yellow pigments but has little to no effect on black, which explains why white tigers still show characteristic dark stripes.

Historical records of white tigers on the Indian subcontinent date back to the 1500s, Luo notes, but the last known free-ranging white tiger was shot in 1958. That many white tigers were hunted as mature adults suggests that they were fit to live in the wild. It's worth considering that tigers' chief prey species, such as deer, are likely colorblind.

Captive white tigers sometimes do show abnormalities, such as crossed eyes, but Luo says any frailties are likely the responsibility of humans, who have inbred the rare tigers in captivity. With the causal gene identified, the researchers ultimately hope to explore the evolutionary forces that have maintained tigers in both orange and white varieties.

Source-Eurekalert

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Scientists Make New Discovery in Fight Against Deadly Meningococcal Disease

"Until now we have not known how it attaches to the human host. It has been a long-standing mystery how it attaches to the airway to colonise "People can be carriers of the bug and not get any symptoms, while some people progress to invasive disease.

To understand why, we need to know the detail of how the bacterium colonises the airway. Now that the pathway has been identified we can study this process to understand how invasive disease occurs. This is especially important considering the rapidly progressing and serious outcomes of meningococcal disease."If you understand how the bug first attaches and how it first signals its attachment then we may identify new risk factors or treatment procedures," Professor Jennings said.

The findings were published Friday in the highly regard PLOS Pathogens journal as featured research "Dual Pili Post-translational Modifications Synergize to Mediate Meningococcal Adherence to Platelet Activating Factor Receptor on Human Airway Cells." The paper states: There is no fully protective vaccine against this pathogen in current use and the key processes that dictate the transition from harmless carriage of the bacterium in the airway (the case for the vast majority of colonised hosts) to invasive disease are largely undefined.

A key missing link in this organism's interaction with the human host is the identity of the receptor that is the first point of contact for the organism within the airway.Professor Jennings said the receptor is used by a range of airway pathogens and the bacterium mimics a human structure to attach to this receptor."It's not actually protein that attaches to the receptor but decorations on the protein that are known as post-translational modifications. One of these is a sugar structure, which of course is of great interest to our work here at Glycomics," he said.The Institute of Glycomics is a world leader in the study of glycans and carbohydrates (sugars) and how they behave in terms of disease prevention and cure.

Source-Eurekalert

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To Test the Effects of Drugs Scientists Develop Worm EEG

NeuroChip is a microfluidic electrophysiological device, which can trap the microscopic worm Caenorhadbitis elegans and record the activity of discrete neural circuits in its 'brain' - a worm equivalent of the EEG.

C. elegans have been enormously important in providing insight into fundamental signalling processes in the nervous system and this device opens the way for a new analysis. Prior to this development, electrophysiological recordings that resolve the activity of excitatory and inhibitory nerve cells in the nervous system of the worm required a high level of technical expertise - single microscopic (1mm long) worms have to be trapped on the end of a glass tube, a microelectrode, in order to make the recording. The worms are very mobile as well as being small and this can be a challenging procedure.

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Scientists Identify Pathogens Associated With Paediatric Diarrhoeal Disease

by Sheela Philomena on? May 19, 2013 at 10:09 AM Child Health News Pathogens associated with moderate-to-severe diarrhoea in infants have been discovered by scientists. The Global Enteric Multicenter Study (GEMS) was designed to identify the aetiology and population-based burden of paediatric diarrhoeal disease in sub-Saharan Africa and south Asia.
It is a 3-year, prospective, age-stratified, matched case-control study of moderate-to-severe diarrhoea in children aged 0-59 months residing in censused populations at four sites in Africa and three in Asia.

The researchers said that recruited children with moderate-to-severe diarrhoea seeking care at health centres along with one to three randomly selected matched community control children without diarrhoea.

From patients with moderate-to-severe diarrhoea and controls, they said they obtained clinical and epidemiological data, anthropometric measurements, and a faecal sample to identify enteropathogens at enrolment.

One follow-up home visit was made about 60 days later to ascertain vital status, clinical outcome, and interval growth.

They enrolled 9439 children with moderate-to-severe diarrhoea and 13 129 control children without diarrhoea.

By analysing adjusted population attributable fractions, they found that most attributable cases of moderate-to-severe diarrhoea were due to four pathogens: rotavirus, Cryptosporidium, enterotoxigenic Escherichia coli producing heat-stable toxin (ST-ETEC; with or without co-expression of heat-labile enterotoxin), and Shigella.

Other pathogens were important in selected sites (eg, Aeromonas, Vibrio cholerae O1, Campylobacter jejuni).

They also found that odds of dying during follow-up were 8.5-fold higher in patients with moderate-to-severe diarrhoea than in controls.

Pathogens associated with increased risk of case death were ST-ETEC and typical enteropathogenic E coli in infants aged 0-11 months, and Cryptosporidium in toddlers aged 12-23 months.

The researchers noted that interventions targeting five pathogens (rotavirus, Shigella, ST-ETEC, Cryptosporidium, typical enteropathogenic E coli) could substantially reduce the burden of moderate-to-severe diarrhoea.

New methods and accelerated implementation of existing interventions (rotavirus vaccine and zinc) are needed to prevent disease and improve outcomes, they added.

The research was published in Lancet.

Source-ANI

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