Researchers have identified specific genes that may trigger the development of sleep problems, and have also demonstrated a genetic link between insomnia and psychiatric disorders such as depression, or physical conditions such as type 2 diabetes. The study was led by Murray Stein of the University of California San Diego and the VA San Diego Healthcare System. Up to 20 percent of Americans and up to 50 percent of US military veterans are said to have trouble sleeping. The effects insomnia has on a person’s health can be debilitating and place a strain on the healthcare system. Chronic insomnia goes hand in hand with various long-term health issues such as heart disease and type 2 diabetes, as well as mental illness such as post-traumatic stress disorder (PTSD) and suicide. Twin studies have in the past shown that various sleep-related traits, including insomnia, are heritable. Based on these findings, researchers have started to look into the specific gene variants involved. Stein says such studies are important, given the vast range of reasons why people suffer from insomnia, and the different symptoms and varieties of sleeplessness that can be experienced. "A better understanding of the molecular bases for insomnia will be critical for the development of new treatments," he adds. In this study, Stein’s research team conducted genome-wide association studies (GWAS). DNA samples obtained from more than 33,000 soldiers participating in the Army Study To Assess Risk and Resilience in Service members (STARRS) were analysed. Data from soldiers of European, African and Latino descent were grouped separately as part of efforts to identify the influence of specific ancestral lineages. Stein and his colleagues also compared their results with those of two recent studies that used data from the UK Biobank. Overall, the study confirms that insomnia has a partially heritable basis. The researchers also found a strong genetic link between insomnia and type 2 diabetes. Among participants of European descent, there was additionally a genetic tie between sleeplessness and major depression. "The genetic correlation between insomnia disorder and other psychiatric disorders, such as major depression, and physical disorders such as type 2 diabetes suggests a shared genetic diathesis for these commonly co-occurring phenotypes," says Stein, who adds that the findings strengthen similar conclusions from prior twin and genome-wide association studies. Insomnia was linked to the occurrence of specific variants on chromosome 7. In people of European descent, there were also differences on chromosome 9. The variant on chromosome 7, for instance, is close to AUTS2, a gene that has been linked to alcohol consumption, as well as others that relate to brain development and sleep-related electric signalling. "Several of these variants rest comfortably among locations and pathways already known to be related to sleep and circadian rhythms," Stein elaborates. "Such insomnia associated loci may contribute to the genetic risk underlying a range of health conditions including psychiatric disorders and metabolic disease." EurekAlertwww.eurekalert.org/pub_releases/2018-03/s-csc030818.php
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A discovery sheds light on how cancerous cells differ from healthy ones, and could lead to the development of new strategies for therapeutic intervention for difficult-to-treat cancers in the future. An international team of investigators found a “stop sign”—a modified protein researchers named a PIP-stop—inside cells that are overused by cancerous cells that effectively prevents healthy ones from sorting material in the way they were designed to. “We have discovered that breast cancer, leukaemia, lymphoma and neuroblastoma cells have too many PIP-stops. This would upset protein function, and opens up a new avenue for developing drugs that block PIP-stop formation by kinase enzymes,” said Michael Overduin, a University of Alberta cancer researcher and professor of biochemistry, who led the research project. The team named the modification a PIP-stop because it stops proteins from interacting with lipid molecules called PIP. Before making their discovery, the researchers first solved the 3-D structure of a sorting nexin protein, which is key to sorting proteins to their proper locations within the cell. Powerful magnets in the U.K. and in the National High Field Nuclear Magnetic Resonance Centre (NANUC), Canada’s national magnet lab based in Edmonton, were then used to detect signals from within individual atoms within the protein structure. By focusing on the protein structure, the team was able to discover the PIP-stop and see how it blocked the protein’s function. The PIP-stop is a phosphate which is added to the protein surface that binds the PIP lipid, and normally controls how proteins attach to membranes. Samples from cancer patients have too many PIP-stops, which could lead to the unregulated growth seen in tumour cells. Similar PIP-stops were found to be overused in a large number of other proteins involved in other cancer types, where they could also influence tumour growth. “Our goal now is to design inhibitors for the overactive kinases that create PIP-stops, and to use this information to design drug molecules that block the progression of cancers, particularly those which lack effective treatments,” said Overduin. University of Alberta Faculty of Medicine & Dentistrywww.folio.ca/medical-researchers-find-protein-that-marks-difference-between-cancer-and-non-cancer-cells/
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Extremely low birth-weight babies are at risk for a chronic lung disease called bronchopulmonary dysplasia, or BPD. This condition can lead to death or long-term disease, but clinical measurements are unable to predict which of the tiny infants—who get care in hospital intensive-care units and often weigh just one and a half pounds—will develop BPD. University of Alabama at Birmingham researchers now report discovery of a strong predictive biomarker for BPD, and they show a role for the biomarker in the pathogenesis of this neonatal lung disease. These results open the path to possible future therapies to prevent or lessen BPD, which is marked by inflammation and impaired lung development. This biomarker could also help neonatologists plan optimal management and risk stratification of their tiny patients, and it could guide targeted enrolment of high-risk infants into randomized trials of potentially novel treatment strategies. The UAB work is an example of "bedside to bench" research. It began with prospective studies of extremely premature infants to identify potential biomarkers, and then proceeded to lab experiments using animal models and cells grown in culture to learn how the biomarker functions in disease progression. The study was led by Charitharth Vivek Lal, M.D., assistant professor in the UAB Pediatrics Division of Neonatology, and it builds upon Lal’s 2016 report that early microbial imbalance in the airways of extremely premature infants is predictive for development of BPD. The biomarker in the study is microRNA 876-3p. The hunt for the biomarker began with a prospective cohort study at the UAB Regional Neonatal Intensive Care Unit, looking at exosomes obtained from tracheal aspirates of infants with severe BPD, compared with full-term controls. Exosomes are small, membrane-bound blebs or vesicles that are actively secreted by a variety of cells. They are known to contain microRNAs and proteins, and the exosomes act in cell-to-cell signalling. MicroRNAs can regulate gene expression in cells. Lal and colleagues found that airway cells in infants with severe BPD had greater numbers of exosomes, but those exosomes were smaller sized. They also experimentally found that high oxygen exposure for newborn mice or human bronchial epithelial cells grown in culture also caused the release of more exosomes, and the exosomes were smaller in size that those secreted at normal oxygen level. Premature infants often receive extra oxygen to aid their underdeveloped lungs. The UAB researchers then did a prospective discovery cohort study at UAB—they collected tracheal aspirate samples from extremely premature infants within six hours of birth, purified exosomes from the samples and looked for microRNAs in the exosomes. Out of 810 microRNAs that were found, 40 showed differences between infants who later developed BPD and those who were BPD-resistant. Next, in cooperation with researchers at Thomas Jefferson University and Drexel University, a validation cohort was studied in Philadelphia. Thirty-two of the 40 microRNAs were confirmed; six had a higher statistical significance; and one biomarker, a low concentration of microRNA 876-3p, was found to have the highest sensitivity to predict severe BPD in extremely low birth-weight infants. Medical Xpressmedicalxpress.com/news/2018-03-exosomal-microrna-severe-lung-disease.html
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Research from the University of Liverpool identifies a genetic variant that could improve the safety and effectiveness of corticosteroids, drugs that are used to treat a range of common and rare conditions including asthma, and chronic obstructive pulmonary disease (COPD). Corticosteroids are very effective in the treatment of asthma and COPD, with more than 20 million prescriptions issued in the UK annually. Unfortunately, corticosteroids can also cause side effects, one of which is adrenal suppression, seen in up to 1/3 of people tested. People with this condition do not make enough cortisol. Cortisol helps the body respond to stress, recover from infections and regulate blood pressure and metabolism. Adrenal suppression can be very difficult to diagnose, as it can present with a spectrum of symptoms from non-specific symptoms such as tiredness, to serious illness and death. The majority of patients do not develop adrenal suppression, and the reasons why some do, and while other don’t, despite using similar doses of corticosteroids were not previously understood. In researchers from the University’s Institute of Translational Medicine, led by Professor Sir Munir Pirmohamed, conducted a genome-wide association study (GWAS) to pinpoint the genes responsible for increasing the risk of a person developing adrenal suppression. This method searches for single nucleotide polymorphisms (SNPs). Each person carries about three million SNPs, but if a particular SNP occurs more frequently in people with a particular condition than in people without the condition, it can pinpoint the underlying reason for the difference. The researchers identified two groups of children with asthma, and one group of adults with chronic obstructive pulmonary disease (COPD), all of whom used inhaled corticosteroid medications. Each patient’s adrenal function was tested. This is the largest published cohort of children ever tested for adrenal suppression (580 children in total). Individuals who had a particular variation in a specific gene (platelet derived growth factor D; PDGFD) had a markedly increased risk of adrenal suppression, both in the children with asthma and adults with COPD. This risk increased if the patient had two copies of the variation (one from their mother, one from their father). Children with two copies of the high risk variation in PDGFD were nearly six times more likely to develop adrenal suppression than children with no copies. University of Liverpoolnews.liverpool.ac.uk/2018/03/16/genetic-variant-discovery-to-help-asthma-sufferers/
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Atrial fibrillation (AF) is a heart condition that causes an irregular, and often rapid, heart rate. It increases the risk of developing strokes, heart failure, and even dementia. Although it can be associated with aging, high blood pressure, diabetes, heart valve problems, etc, about one-third of patients with AF have no symptoms until they suffer a stroke. Therefore, a means of identifying or predicting AF with the aim of starting preventative therapy is highly desirable. AF is associated with several factors that maintain its progression, including inflammation, electrical disturbances, and structural changes in the heart’s upper chambers (the atria). Moreover, several different short sequences of RNA known as microRNAs (miRNAs) have been linked with AF pathology. miRNAs control gene expression after the transcription stage, and have been suggested as possible markers for some cardiovascular diseases because of their stability in the bloodstream. However, it remains unknown whether the miRNAs shown to be related to AF are suitable as predictive biomarkers of disease. A team of researchers from Tokyo Medical and Dental University (TMDU) addressed this issue by comparing miRNA expression in AF patients and healthy controls, and between control mice and those with a similar abnormal heart rhythm to AF. They showed that four miRNAs not previously associated with AF were significantly upregulated in the serum of AF patients and diseased mice, indicating their potential use as AF biomarkers. The study results were recently published in Circulation Journal. Initially, human serum and mouse atrial tissue were screened for 733 and 672 miRNAs, respectively. These were eventually narrowed down to four by excluding non-detectable and non-specific miRNAs, and focusing on the quantification of their expression. “One of the miRNAs, miR-214-3p, is implicated in inflammation, so we wondered whether this might be the underlying mechanism of miRNA-induced AF pathology,” first author Yu Natsume says. “We compared miRNA expression with levels of a serum inflammatory factor but found no correlation suggestive of an association.” Statistical analysis of diagnostic ability showed that miR-214-3p and miR-342-5p had the highest accuracy as individual biomarkers at predicting AF, but that a combined analysis of all four miRNAs slightly improved this accuracy. “The same two miRNAs showed increased expression in a subset of patients with intermittent AF and another subset with chronic AF,” corresponding author Tetsuo Sasano says. “The increases were in comparison both with healthy controls of the same age and young healthy controls, suggesting these miRNAs may predict AF regardless of the age of the individual.” Tokyo Medical and Dental University (TMDU)www.tmd.ac.jp/english/press-release/20180313/index.html
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Tumour cells circulating throughout the body in blood vessels have long been feared as harbingers of metastasizing cancer — even though most free-floating cancer cells will not go on to establish a new tumour. But if these cast-offs could be accurately counted, they could provide an additional way to track treatment or screen for the disease. New research by University of Wisconsin–Madison School of Pharmacy Professor Seungpyo Hong and his collaborators builds on several years of work in isolating these circulating tumour cells, or CTCs, by demonstrating improved methods for their capture on clinical samples for the first time. By forcing cancer cells to slow down and developing stronger molecular traps specific to CTCs, researchers were able to identify large numbers of the cells in cancer patients undergoing radiation therapy. The number of CTCs dropped during therapy and subsequently rebounded in those patients that ended up requiring additional treatment — suggesting that this technology could supplement other techniques for tracking the progress of treatment. Scientists have recognized CTCs as potentially useful metrics for tracking a patient’s disease for some time. But the cells are the proverbial needle-in-a-haystack, drowned out by billions of ordinary red blood cells and other cells found in the blood. Developing ways to specifically concentrate and trap CTCs has been technically challenging, with existing technologies only identifying a handful of cells from certain patients. Hong’s team was inspired by the behaviour of CTCs in the blood, which attach themselves to blood vessel walls and begin tumbling along looking for suitable places to invade. This behaviour separates them from the oxygen-carrying cells floating by and is mimicked in the CapioCyte technology using an array of sticky proteins that force the CTCs to begin rolling, which slows them down. The cells are then trapped using a series of three cancer-specific antibodies, proteins that tightly bind and hold onto the CTCs. To make the connection even stronger, the researchers developed a nanoscale structure shaped a little like a tree, with each branch tipped with an antibody. As a cancer cell passes nearby, many individual branches can latch on, increasing the strength of the attachment. The cell rolling and multi-tipped branches helped the researchers capture an average of 200 CTCs from each millilitre of a patient’s blood, many times the number of cells captured with previous technology. They identified cancer cells in each of 24 patients undergoing treatment for head-and-neck, prostate, rectal or cervical cancer that enrolled in the study. “The absolute numbers of CTCs don’t represent too much because there’s too much variation individually, but the more important thing we found was the trend — how the CTC numbers change over time upon treatment. So, for example, we’ve shown that the CTCs go down when the patients are responding really well to the radiotherapy,” says Hong. Although the number of cells did not correlate with the stage, and thus severity, of the cancer, the reduction in cells was correlated with successful radiation therapy. In two of the three patients that had recurring or persistent disease, CTC numbers came back up. “Our data suggest that we have a good chance of making CTCs a predictive biomarker or biomarker for surveillance for at least a few cancers, and that’s always exciting,” says Wang. University of Wisconsin – Madisonnews.wisc.edu/improved-capture-of-cancer-cells-in-blood-could-help-track-disease/
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:48Improved capture of cancer cells in blood could help track disease
The role of the placenta in healthy foetal development is being seriously under-appreciated according to a new paper The study was part of the Wellcome-funded “Deciphering the Mechanisms of Developmental Disorders (DMDD)” consortium. Dr Myriam Hemberger at the Babraham Institute, Cambridge led the research, working with colleagues at the Wellcome Sanger Institute, Cambridge, the Francis Crick Institute, London, the University of Oxford and the Medical University of Vienna, Austria. The team studied 103 genetic mutations in mice that cause embryos to die before birth. The results showed that the majority, almost 70 per cent, cause defects in the placenta. Each of the 103 gene mutations causes the loss of a particular factor. Many of these had not been previously linked to placenta development, and hence the study highlights the unexpected number of genes that affect development of the placenta. By studying a select group of three genes in further detail, the team went on to show that the death of the embryo could be directly linked to defects in the placenta in one out of these three cases. This may mean that a significant number of genetic defects that lead to prenatal death may be due to abnormalities of the placenta, not just the embryo. Although this research uses mice, the findings are likely to be highly relevant to complications during human pregnancy and the study highlights the need for more work to be done on investigating development of the placenta during human pregnancies. The placenta is vital for normal pregnancy progression and embryo development in most animals that give birth to live young, including humans. It provides a unique and highly specialised interface between the embryo and the mother, ensuring an adequate provision of nutrients and oxygen to the embryo. The placenta is also involved in waste disposal from the embryo and produces important hormones that help sustain pregnancy and promote foetal growth. Although previous research has highlighted the pivotal role of the placenta for a healthy pregnancy, its potential contribution to pregnancy complications and birth defects continues to be overlooked. Scientists call mutations that cause death in the womb embryonic lethal. Mouse lethal genes are enriched for human disease genes and the affected embryos often show morphological abnormalities, i.e. changes to their shape and structure. Around one-third of all gene mutants studied in mouse are lethal or subviable (i.e. mutant offspring are less likely to survive than non-mutant pups). “Analysis of embryonic lethal mutants has largely focused on the embryo and not the placenta, despite its critical role in development. Of the mutations we’ve studied, far more than expected showed defects in the placenta and this is particularly true for mutations that cause death during the early stages of pregnancy. Intriguingly, our analysis also indicates that issues in the placenta often occur alongside specific defects in the embryo itself.”
“Our data highlight the hugely under-appreciated importance of placental defects in contributing to abnormal embryo development and suggest key molecular nodes governing placentation. The importance of a healthy placenta has often been overlooked in these studies and it is important that we start doing more to understand its contribution to developmental abnormalities.” Wellcome Sanger Institutewww.sanger.ac.uk/news/view/placenta-defects-critical-factor-prenatal-deaths
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After becoming the first to definitively discover genetic markers for major depression, researchers at Virginia Commonwealth University and collaborators have found more genetic clues to the disease. A study details the discovery of three additional genetic risk markers for depression, which builds on the ground breaking discovery of two genetic risk factors in 2015. Lead authors include Roseann Peterson, Ph.D., an assistant professor of psychiatry at the VCU Virginia Institute for Psychiatric and Behavioral Genetics, and Na Cai of the European Bioinformatics Institute and the Wellcome Sanger Institute in the United Kingdom. Initially, the researchers were able to isolate changes in DNA that increase risk for major depression. The most recent findings take this a step further by determining that the additional genetic markers are relevant to the disease in a subset of people who have not experienced extreme adversity. Kendler, M.D., professor of psychiatry and human molecular genetics in the Department of Psychiatry in the School of Medicine, and one of five VCU faculty authors, said the work could shed more light on subtypes of depression and their treatment. “We have struggled for years using twin and family studies to try to understand how genes and environment interrelate in causing depression,” Kendler said. “This is the first study where we have been able to do this using molecular variants. This is an important advance in our understanding of this important, severe and common psychiatric disorder.” The researchers collected information on environmental adversity measures from their subjects. Environmental adversity includes experiences of extreme stressful life events such as childhood sexual and physical abuse. Observing groups who were adversity exposed and non-adversity exposed allowed researchers to account for diverse causes of depression, or the disease’s etiological heterogeneity, in determining genetic causes, Peterson said. “Identifying genetic risk variants for major depressive disorder has been difficult, likely due to associated clinical and etiological heterogeneity,” Peterson said. “Here, we highlight individual differences in clinical presentation and the importance of collecting symptom level data to tackle clinical and etiological heterogeneity in complex psychiatric traits.” Peterson said the ultimate goal is to identify high-risk individuals for early intervention and personalized medicine. Cai said the discovery could lead to additional findings on potential links between metabolism and depression. “Some of the genes implicated by variants we found to be associated with depression are involved in mitochondrial function and metabolism,” Cai said. “So, one potential direction for future research is to try to understand the link between depression and metabolism.” Virginia Commonwealth Universitynews.vcu.edu/article/Three_new_genetic_markers_associated_with_risk_for_depression
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In October 2016, researchers at the Aga Khan University’s microbiology laboratory spotted a number of unusual organisms in blood samples from Hyderabad. Blood culture tests from the city contained a novel strain of typhoid that had developed resistance to an unprecedented range of antibiotics. Over the next few months, several similar cases were detected from the city pointing to an outbreak of a form of the disease that would be especially difficult to treat. The research team, led by Pofessor Rumina Hasan, acted quickly to alert local government, the National Institutes of Health and the World Health Organization to this development. They also contacted the UK-based Wellcome Sanger Institute to explore the genetic cause behind the emergence of this extensively drug-resistant (XDR) typhoid strain. “This was the world’s first outbreak of XDR typhoid,” said Professor Zahra Hasan of the department of pathology and laboratory medicine. “Understanding this new threat required high-level genome sequencing which would enable us to analyse the molecular blueprint of this new form of typhoid.” Over the next six months, the research team collaborated with experts at the Wellcome Sanger Institute to jointly analyse over 100 DNA samples which resulted in a striking finding. The typhoid bacteria had acquired a DNA molecule through a plasmid from a bacterium commonly found in contaminated water and food, making it resistant to the majority of available medications . “We used to think that we had a complete picture of the typhoid ‘puzzle’,” said Dr Sadia Shakoor, assistant professor in pathology and laboratory medicine at AKU. “Together with our partners, we’ve found a missing piece that affects how we diagnose and treat the most complex strains of the disease.” Since patients with XDR typhoid do not respond to commonly prescribed antibiotics, blood culture tests have become an even more important tool for physicians, according to Dr Shakoor. Not only do these tests enable early detection but they also highlight the type of typhoid being tackled that affects the choice of antibiotic. “There are currently three antibiotics available to treat XDR typhoid,” Dr Shakoor stated. “These drugs are expensive and we must only prescribe them when needed. Otherwise, bacteria could develop resistance to the only medications we have left.” Beyond resistance, researchers also warn of the risk of the disease spreading since every patient is a potential ‘disease carrier’. The likelihood of the proliferation of the disease is especially high in developing countries where poor sanitation facilities result in the contamination of drinking water with sewage containing the typhoid bacteria. Aga Khan Universitywww.aku.edu/news/Pages/News_Details.aspx?nid=NEWS-001521
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More than 100 industry experts to highlight the latest medical laboratory and diagnostics trends and innovation The 5th edition of MEDLAB Asia Pacific Exhibition & Congress, leading B2B business and educational platform in the field of laboratory and diagnostics for the Asia Pacific region, will offer visitors the opportunity to attend a series of scientific conferences that will cover advancement in science, technology and application of various laboratory techniques to strengthen cooperation between lab and clinic interface. Supported by The Academy of Medicine, Singapore and accredited by Singapore Medical Council, the 15 CME-certified conferences will empower delegates with the knowledge and skills to guarantee the fastest, safest and most accurate laboratory results in improving patient service and care. During the three-day congress, which takes place from 2 – 4 April 2018 at Suntec Singapore Convention & Exhibition Centre in Singapore, a variety of carefully-designed sessions, panel discussions, demonstrations and interactive activities will enable delegates to network and share best practices with more than 100 regional and international experts who are champions of laboratory medicine in the Asia Pacific. The congress will host 11 dedicated laboratory tracks: Laboratory Management, Clinical Chemistry, Haematology & Blood Transfusion, Infectious Diseases, Point of Care Testing, Cytology, Molecular Diagnostics, Laboratory Informatics, Cardiac Markers, Lab Testing: Obs Gyne & Women’s Health and Lab Testing & Management: Diabetes. During these sessions, delegates will able schooled in a wide variety of key topics including the role of the laboratory director, 4th generation sequencing, updates in assays to improve skills in test accuracy, digital pathology, and the evaluation of current and future biomarkers, to name a few. Due to the expanding role of laboratory medicine, the meeting is combined with other clinical specialties that will underscore the overarching influence of the laboratory in medical decision-making and treatment. New conferences in the MEDLAB Asia Pacific Congress portfolio are: Obs Gyne & Women’s Health, Gynae-Oncology, Diabetes Management and Antimicrobial Resistance. “The advent of groundbreaking diagnostic solutions is gaining pace across the region. By introducing new medical tracks from key specialties that interact with the laboratory, the 2018 MEDLAB Asia Pacific Congress will provide the latest evidence-based research into diagnosis and treatment as well as enhance cooperation between laboratory professionals and clinicians to enable the best possible patient outcomes.” said RejoyPenacerrada, Senior Conference Producer, MEDLAB Asia. MEDLAB Asia Pacific 2018 is supported by a large number of key healthcare federations and associations across the region including The Royal College of Pathologists of Australasia, Singapore Society of Pathology, College of Pathologists, Academy of Medicine of Malaysia, Indonesian Association of Clinical Pathologist and Laboratory Medicine, Singapore Society of Haematology, College of American Pathologists, Philippine Society of Pathologists, Inc., Philippine Society of Biochemistry and Molecular Biology, Philippine Society of Microbiology, Indonesian Association of Clinical Chemistry, Society of Infectious Disease Singapore, and Society of Cytology Singapore and Diabetes Singapore. Held alongside the congress is the MEDLAB Asia Pacific exhibition – a platform for leading companies from across the globe to showcase current technologies and innovations in the field of laboratory and diagnostics to an expected 4,000 visitors. MEDLAB Asia Pacific is also co-located with Asia Health,a trade exhibition for medical equipment, products, services and technologies hosting more than 250 international companies and bringing together the world of medical laboratory and healthcare under one roof.
Registration for the MEDLAB Asia Pacific Congress is now open via www.medlabasia.com.
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Can’t sleep? Could be down to genetics
, /in E-News /by 3wmediaResearchers have identified specific genes that may trigger the development of sleep problems, and have also demonstrated a genetic link between insomnia and psychiatric disorders such as depression, or physical conditions such as type 2 diabetes. The study was led by Murray Stein of the University of California San Diego and the VA San Diego Healthcare System.
Up to 20 percent of Americans and up to 50 percent of US military veterans are said to have trouble sleeping. The effects insomnia has on a person’s health can be debilitating and place a strain on the healthcare system. Chronic insomnia goes hand in hand with various long-term health issues such as heart disease and type 2 diabetes, as well as mental illness such as post-traumatic stress disorder (PTSD) and suicide.
Twin studies have in the past shown that various sleep-related traits, including insomnia, are heritable. Based on these findings, researchers have started to look into the specific gene variants involved. Stein says such studies are important, given the vast range of reasons why people suffer from insomnia, and the different symptoms and varieties of sleeplessness that can be experienced.
"A better understanding of the molecular bases for insomnia will be critical for the development of new treatments," he adds.
In this study, Stein’s research team conducted genome-wide association studies (GWAS). DNA samples obtained from more than 33,000 soldiers participating in the Army Study To Assess Risk and Resilience in Service members (STARRS) were analysed. Data from soldiers of European, African and Latino descent were grouped separately as part of efforts to identify the influence of specific ancestral lineages. Stein and his colleagues also compared their results with those of two recent studies that used data from the UK Biobank.
Overall, the study confirms that insomnia has a partially heritable basis. The researchers also found a strong genetic link between insomnia and type 2 diabetes. Among participants of European descent, there was additionally a genetic tie between sleeplessness and major depression.
"The genetic correlation between insomnia disorder and other psychiatric disorders, such as major depression, and physical disorders such as type 2 diabetes suggests a shared genetic diathesis for these commonly co-occurring phenotypes," says Stein, who adds that the findings strengthen similar conclusions from prior twin and genome-wide association studies.
Insomnia was linked to the occurrence of specific variants on chromosome 7. In people of European descent, there were also differences on chromosome 9. The variant on chromosome 7, for instance, is close to AUTS2, a gene that has been linked to alcohol consumption, as well as others that relate to brain development and sleep-related electric signalling.
"Several of these variants rest comfortably among locations and pathways already known to be related to sleep and circadian rhythms," Stein elaborates. "Such insomnia associated loci may contribute to the genetic risk underlying a range of health conditions including psychiatric disorders and metabolic disease."
EurekAlertwww.eurekalert.org/pub_releases/2018-03/s-csc030818.php
Medical researchers find protein that marks difference between cancer and non-cancer cells
, /in E-News /by 3wmediaA discovery sheds light on how cancerous cells differ from healthy ones, and could lead to the development of new strategies for therapeutic intervention for difficult-to-treat cancers in the future.
An international team of investigators found a “stop sign”—a modified protein researchers named a PIP-stop—inside cells that are overused by cancerous cells that effectively prevents healthy ones from sorting material in the way they were designed to.
“We have discovered that breast cancer, leukaemia, lymphoma and neuroblastoma cells have too many PIP-stops. This would upset protein function, and opens up a new avenue for developing drugs that block PIP-stop formation by kinase enzymes,” said Michael Overduin, a University of Alberta cancer researcher and professor of biochemistry, who led the research project.
The team named the modification a PIP-stop because it stops proteins from interacting with lipid molecules called PIP.
Before making their discovery, the researchers first solved the 3-D structure of a sorting nexin protein, which is key to sorting proteins to their proper locations within the cell. Powerful magnets in the U.K. and in the National High Field Nuclear Magnetic Resonance Centre (NANUC), Canada’s national magnet lab based in Edmonton, were then used to detect signals from within individual atoms within the protein structure.
By focusing on the protein structure, the team was able to discover the PIP-stop and see how it blocked the protein’s function. The PIP-stop is a phosphate which is added to the protein surface that binds the PIP lipid, and normally controls how proteins attach to membranes.
Samples from cancer patients have too many PIP-stops, which could lead to the unregulated growth seen in tumour cells. Similar PIP-stops were found to be overused in a large number of other proteins involved in other cancer types, where they could also influence tumour growth.
“Our goal now is to design inhibitors for the overactive kinases that create PIP-stops, and to use this information to design drug molecules that block the progression of cancers, particularly those which lack effective treatments,” said Overduin.
University of Alberta Faculty of Medicine & Dentistrywww.folio.ca/medical-researchers-find-protein-that-marks-difference-between-cancer-and-non-cancer-cells/
Exosomal microRNA predicts and protects against severe lung disease in extremely premature infants
, /in E-News /by 3wmediaUniversity of Alabama at Birmingham researchers now report discovery of a strong predictive biomarker for BPD, and they show a role for the biomarker in the pathogenesis of this neonatal lung disease. These results open the path to possible future therapies to prevent or lessen BPD, which is marked by inflammation and impaired lung development.
This biomarker could also help neonatologists plan optimal management and risk stratification of their tiny patients, and it could guide targeted enrolment of high-risk infants into randomized trials of potentially novel treatment strategies.
The UAB work is an example of "bedside to bench" research. It began with prospective studies of extremely premature infants to identify potential biomarkers, and then proceeded to lab experiments using animal models and cells grown in culture to learn how the biomarker functions in disease progression.
The study was led by Charitharth Vivek Lal, M.D., assistant professor in the UAB Pediatrics Division of Neonatology, and it builds upon Lal’s 2016 report that early microbial imbalance in the airways of extremely premature infants is predictive for development of BPD.
The biomarker in the study is microRNA 876-3p.
The hunt for the biomarker began with a prospective cohort study at the UAB Regional Neonatal Intensive Care Unit, looking at exosomes obtained from tracheal aspirates of infants with severe BPD, compared with full-term controls. Exosomes are small, membrane-bound blebs or vesicles that are actively secreted by a variety of cells. They are known to contain microRNAs and proteins, and the exosomes act in cell-to-cell signalling. MicroRNAs can regulate gene expression in cells.
Lal and colleagues found that airway cells in infants with severe BPD had greater numbers of exosomes, but those exosomes were smaller sized. They also experimentally found that high oxygen exposure for newborn mice or human bronchial epithelial cells grown in culture also caused the release of more exosomes, and the exosomes were smaller in size that those secreted at normal oxygen level. Premature infants often receive extra oxygen to aid their underdeveloped lungs.
The UAB researchers then did a prospective discovery cohort study at UAB—they collected tracheal aspirate samples from extremely premature infants within six hours of birth, purified exosomes from the samples and looked for microRNAs in the exosomes. Out of 810 microRNAs that were found, 40 showed differences between infants who later developed BPD and those who were BPD-resistant.
Next, in cooperation with researchers at Thomas Jefferson University and Drexel University, a validation cohort was studied in Philadelphia. Thirty-two of the 40 microRNAs were confirmed; six had a higher statistical significance; and one biomarker, a low concentration of microRNA 876-3p, was found to have the highest sensitivity to predict severe BPD in extremely low birth-weight infants.
Medical Xpressmedicalxpress.com/news/2018-03-exosomal-microrna-severe-lung-disease.html
Genetic variant discovery to help asthma sufferers
, /in E-News /by 3wmediaResearch from the University of Liverpool identifies a genetic variant that could improve the safety and effectiveness of corticosteroids, drugs that are used to treat a range of common and rare conditions including asthma, and chronic obstructive pulmonary disease (COPD).
Corticosteroids are very effective in the treatment of asthma and COPD, with more than 20 million prescriptions issued in the UK annually. Unfortunately, corticosteroids can also cause side effects, one of which is adrenal suppression, seen in up to 1/3 of people tested. People with this condition do not make enough cortisol. Cortisol helps the body respond to stress, recover from infections and regulate blood pressure and metabolism.
Adrenal suppression can be very difficult to diagnose, as it can present with a spectrum of symptoms from non-specific symptoms such as tiredness, to serious illness and death. The majority of patients do not develop adrenal suppression, and the reasons why some do, and while other don’t, despite using similar doses of corticosteroids were not previously understood.
In researchers from the University’s Institute of Translational Medicine, led by Professor Sir Munir Pirmohamed, conducted a genome-wide association study (GWAS) to pinpoint the genes responsible for increasing the risk of a person developing adrenal suppression. This method searches for single nucleotide polymorphisms (SNPs). Each person carries about three million SNPs, but if a particular SNP occurs more frequently in people with a particular condition than in people without the condition, it can pinpoint the underlying reason for the difference.
The researchers identified two groups of children with asthma, and one group of adults with chronic obstructive pulmonary disease (COPD), all of whom used inhaled corticosteroid medications. Each patient’s adrenal function was tested. This is the largest published cohort of children ever tested for adrenal suppression (580 children in total).
Individuals who had a particular variation in a specific gene (platelet derived growth factor D; PDGFD) had a markedly increased risk of adrenal suppression, both in the children with asthma and adults with COPD. This risk increased if the patient had two copies of the variation (one from their mother, one from their father). Children with two copies of the high risk variation in PDGFD were nearly six times more likely to develop adrenal suppression than children with no copies.
University of Liverpoolnews.liverpool.ac.uk/2018/03/16/genetic-variant-discovery-to-help-asthma-sufferers/
Potential RNA markers of abnormal heart rhythms identified
, /in E-News /by 3wmediaAtrial fibrillation (AF) is a heart condition that causes an irregular, and often rapid, heart rate. It increases the risk of developing strokes, heart failure, and even dementia. Although it can be associated with aging, high blood pressure, diabetes, heart valve problems, etc, about one-third of patients with AF have no symptoms until they suffer a stroke. Therefore, a means of identifying or predicting AF with the aim of starting preventative therapy is highly desirable.
AF is associated with several factors that maintain its progression, including inflammation, electrical disturbances, and structural changes in the heart’s upper chambers (the atria). Moreover, several different short sequences of RNA known as microRNAs (miRNAs) have been linked with AF pathology. miRNAs control gene expression after the transcription stage, and have been suggested as possible markers for some cardiovascular diseases because of their stability in the bloodstream. However, it remains unknown whether the miRNAs shown to be related to AF are suitable as predictive biomarkers of disease.
A team of researchers from Tokyo Medical and Dental University (TMDU) addressed this issue by comparing miRNA expression in AF patients and healthy controls, and between control mice and those with a similar abnormal heart rhythm to AF. They showed that four miRNAs not previously associated with AF were significantly upregulated in the serum of AF patients and diseased mice, indicating their potential use as AF biomarkers. The study results were recently published in Circulation Journal.
Initially, human serum and mouse atrial tissue were screened for 733 and 672 miRNAs, respectively. These were eventually narrowed down to four by excluding non-detectable and non-specific miRNAs, and focusing on the quantification of their expression.
“One of the miRNAs, miR-214-3p, is implicated in inflammation, so we wondered whether this might be the underlying mechanism of miRNA-induced AF pathology,” first author Yu Natsume says. “We compared miRNA expression with levels of a serum inflammatory factor but found no correlation suggestive of an association.”
Statistical analysis of diagnostic ability showed that miR-214-3p and miR-342-5p had the highest accuracy as individual biomarkers at predicting AF, but that a combined analysis of all four miRNAs slightly improved this accuracy.
“The same two miRNAs showed increased expression in a subset of patients with intermittent AF and another subset with chronic AF,” corresponding author Tetsuo Sasano says. “The increases were in comparison both with healthy controls of the same age and young healthy controls, suggesting these miRNAs may predict AF regardless of the age of the individual.”
Tokyo Medical and Dental University (TMDU)www.tmd.ac.jp/english/press-release/20180313/index.html
Improved capture of cancer cells in blood could help track disease
, /in E-News /by 3wmediaTumour cells circulating throughout the body in blood vessels have long been feared as harbingers of metastasizing cancer — even though most free-floating cancer cells will not go on to establish a new tumour.
But if these cast-offs could be accurately counted, they could provide an additional way to track treatment or screen for the disease.
New research by University of Wisconsin–Madison School of Pharmacy Professor Seungpyo Hong and his collaborators builds on several years of work in isolating these circulating tumour cells, or CTCs, by demonstrating improved methods for their capture on clinical samples for the first time. By forcing cancer cells to slow down and developing stronger molecular traps specific to CTCs, researchers were able to identify large numbers of the cells in cancer patients undergoing radiation therapy.
The number of CTCs dropped during therapy and subsequently rebounded in those patients that ended up requiring additional treatment — suggesting that this technology could supplement other techniques for tracking the progress of treatment.
Scientists have recognized CTCs as potentially useful metrics for tracking a patient’s disease for some time. But the cells are the proverbial needle-in-a-haystack, drowned out by billions of ordinary red blood cells and other cells found in the blood. Developing ways to specifically concentrate and trap CTCs has been technically challenging, with existing technologies only identifying a handful of cells from certain patients.
Hong’s team was inspired by the behaviour of CTCs in the blood, which attach themselves to blood vessel walls and begin tumbling along looking for suitable places to invade. This behaviour separates them from the oxygen-carrying cells floating by and is mimicked in the CapioCyte technology using an array of sticky proteins that force the CTCs to begin rolling, which slows them down.
The cells are then trapped using a series of three cancer-specific antibodies, proteins that tightly bind and hold onto the CTCs. To make the connection even stronger, the researchers developed a nanoscale structure shaped a little like a tree, with each branch tipped with an antibody. As a cancer cell passes nearby, many individual branches can latch on, increasing the strength of the attachment.
The cell rolling and multi-tipped branches helped the researchers capture an average of 200 CTCs from each millilitre of a patient’s blood, many times the number of cells captured with previous technology. They identified cancer cells in each of 24 patients undergoing treatment for head-and-neck, prostate, rectal or cervical cancer that enrolled in the study.
“The absolute numbers of CTCs don’t represent too much because there’s too much variation individually, but the more important thing we found was the trend — how the CTC numbers change over time upon treatment. So, for example, we’ve shown that the CTCs go down when the patients are responding really well to the radiotherapy,” says Hong.
Although the number of cells did not correlate with the stage, and thus severity, of the cancer, the reduction in cells was correlated with successful radiation therapy. In two of the three patients that had recurring or persistent disease, CTC numbers came back up.
“Our data suggest that we have a good chance of making CTCs a predictive biomarker or biomarker for surveillance for at least a few cancers, and that’s always exciting,” says Wang.
University of Wisconsin – Madisonnews.wisc.edu/improved-capture-of-cancer-cells-in-blood-could-help-track-disease/
Placenta defects critical factor in prenatal deaths
, /in E-News /by 3wmediaThe role of the placenta in healthy foetal development is being seriously under-appreciated according to a new paper The study was part of the Wellcome-funded “Deciphering the Mechanisms of Developmental Disorders (DMDD)” consortium. Dr Myriam Hemberger at the Babraham Institute, Cambridge led the research, working with colleagues at the Wellcome Sanger Institute, Cambridge, the Francis Crick Institute, London, the University of Oxford and the Medical University of Vienna, Austria. The team studied 103 genetic mutations in mice that cause embryos to die before birth. The results showed that the majority, almost 70 per cent, cause defects in the placenta.
Each of the 103 gene mutations causes the loss of a particular factor. Many of these had not been previously linked to placenta development, and hence the study highlights the unexpected number of genes that affect development of the placenta. By studying a select group of three genes in further detail, the team went on to show that the death of the embryo could be directly linked to defects in the placenta in one out of these three cases. This may mean that a significant number of genetic defects that lead to prenatal death may be due to abnormalities of the placenta, not just the embryo.
Although this research uses mice, the findings are likely to be highly relevant to complications during human pregnancy and the study highlights the need for more work to be done on investigating development of the placenta during human pregnancies.
The placenta is vital for normal pregnancy progression and embryo development in most animals that give birth to live young, including humans. It provides a unique and highly specialised interface between the embryo and the mother, ensuring an adequate provision of nutrients and oxygen to the embryo. The placenta is also involved in waste disposal from the embryo and produces important hormones that help sustain pregnancy and promote foetal growth. Although previous research has highlighted the pivotal role of the placenta for a healthy pregnancy, its potential contribution to pregnancy complications and birth defects continues to be overlooked.
Scientists call mutations that cause death in the womb embryonic lethal. Mouse lethal genes are enriched for human disease genes and the affected embryos often show morphological abnormalities, i.e. changes to their shape and structure. Around one-third of all gene mutants studied in mouse are lethal or subviable (i.e. mutant offspring are less likely to survive than non-mutant pups).
“Analysis of embryonic lethal mutants has largely focused on the embryo and not the placenta, despite its critical role in development. Of the mutations we’ve studied, far more than expected showed defects in the placenta and this is particularly true for mutations that cause death during the early stages of pregnancy. Intriguingly, our analysis also indicates that issues in the placenta often occur alongside specific defects in the embryo itself.”
“Our data highlight the hugely under-appreciated importance of placental defects in contributing to abnormal embryo development and suggest key molecular nodes governing placentation. The importance of a healthy placenta has often been overlooked in these studies and it is important that we start doing more to understand its contribution to developmental abnormalities.”
Wellcome Sanger Institutewww.sanger.ac.uk/news/view/placenta-defects-critical-factor-prenatal-deaths
Three new genetic markers associated with risk for depression
, /in E-News /by 3wmediaAfter becoming the first to definitively discover genetic markers for major depression, researchers at Virginia Commonwealth University and collaborators have found more genetic clues to the disease.
A study details the discovery of three additional genetic risk markers for depression, which builds on the ground breaking discovery of two genetic risk factors in 2015. Lead authors include Roseann Peterson, Ph.D., an assistant professor of psychiatry at the VCU Virginia Institute for Psychiatric and Behavioral Genetics, and Na Cai of the European Bioinformatics Institute and the Wellcome Sanger Institute in the United Kingdom.
Initially, the researchers were able to isolate changes in DNA that increase risk for major depression. The most recent findings take this a step further by determining that the additional genetic markers are relevant to the disease in a subset of people who have not experienced extreme adversity.
Kendler, M.D., professor of psychiatry and human molecular genetics in the Department of Psychiatry in the School of Medicine, and one of five VCU faculty authors, said the work could shed more light on subtypes of depression and their treatment.
“We have struggled for years using twin and family studies to try to understand how genes and environment interrelate in causing depression,” Kendler said. “This is the first study where we have been able to do this using molecular variants. This is an important advance in our understanding of this important, severe and common psychiatric disorder.”
The researchers collected information on environmental adversity measures from their subjects. Environmental adversity includes experiences of extreme stressful life events such as childhood sexual and physical abuse. Observing groups who were adversity exposed and non-adversity exposed allowed researchers to account for diverse causes of depression, or the disease’s etiological heterogeneity, in determining genetic causes, Peterson said.
“Identifying genetic risk variants for major depressive disorder has been difficult, likely due to associated clinical and etiological heterogeneity,” Peterson said. “Here, we highlight individual differences in clinical presentation and the importance of collecting symptom level data to tackle clinical and etiological heterogeneity in complex psychiatric traits.”
Peterson said the ultimate goal is to identify high-risk individuals for early intervention and personalized medicine. Cai said the discovery could lead to additional findings on potential links between metabolism and depression.
“Some of the genes implicated by variants we found to be associated with depression are involved in mitochondrial function and metabolism,” Cai said. “So, one potential direction for future research is to try to understand the link between depression and metabolism.”
Virginia Commonwealth Universitynews.vcu.edu/article/Three_new_genetic_markers_associated_with_risk_for_depression
A new piece of the typhoid ‘puzzle’
, /in E-News /by 3wmediaIn October 2016, researchers at the Aga Khan University’s microbiology laboratory spotted a number of unusual organisms in blood samples from Hyderabad. Blood culture tests from the city contained a novel strain of typhoid that had developed resistance to an unprecedented range of antibiotics.
Over the next few months, several similar cases were detected from the city pointing to an outbreak of a form of the disease that would be especially difficult to treat.
The research team, led by Pofessor Rumina Hasan, acted quickly to alert local government, the National Institutes of Health and the World Health Organization to this development. They also contacted the UK-based Wellcome Sanger Institute to explore the genetic cause behind the emergence of this extensively drug-resistant (XDR) typhoid strain.
“This was the world’s first outbreak of XDR typhoid,” said Professor Zahra Hasan of the department of pathology and laboratory medicine. “Understanding this new threat required high-level genome sequencing which would enable us to analyse the molecular blueprint of this new form of typhoid.”
Over the next six months, the research team collaborated with experts at the Wellcome Sanger Institute to jointly analyse over 100 DNA samples which resulted in a striking finding. The typhoid bacteria had acquired a DNA molecule through a plasmid from a bacterium commonly found in contaminated water and food, making it resistant to the majority of available medications .
“We used to think that we had a complete picture of the typhoid ‘puzzle’,” said Dr Sadia Shakoor, assistant professor in pathology and laboratory medicine at AKU. “Together with our partners, we’ve found a missing piece that affects how we diagnose and treat the most complex strains of the disease.”
Since patients with XDR typhoid do not respond to commonly prescribed antibiotics, blood culture tests have become an even more important tool for physicians, according to Dr Shakoor. Not only do these tests enable early detection but they also highlight the type of typhoid being tackled that affects the choice of antibiotic.
“There are currently three antibiotics available to treat XDR typhoid,” Dr Shakoor stated. “These drugs are expensive and we must only prescribe them when needed. Otherwise, bacteria could develop resistance to the only medications we have left.”
Beyond resistance, researchers also warn of the risk of the disease spreading since every patient is a potential ‘disease carrier’. The likelihood of the proliferation of the disease is especially high in developing countries where poor sanitation facilities result in the contamination of drinking water with sewage containing the typhoid bacteria.
Aga Khan Universitywww.aku.edu/news/Pages/News_Details.aspx?nid=NEWS-001521
Medical laboratory professionals set to benefit from 15 CME-accredited conferences at MEDLAB Asia Pacific Exhibition & Congress
, /in E-News /by 3wmediaMore than 100 industry experts to highlight the latest medical laboratory and diagnostics trends and innovation
The 5th edition of MEDLAB Asia Pacific Exhibition & Congress, leading B2B business and educational platform in the field of laboratory and diagnostics for the Asia Pacific region, will offer visitors the opportunity to attend a series of scientific conferences that will cover advancement in science, technology and application of various laboratory techniques to strengthen cooperation between lab and clinic interface.
Supported by The Academy of Medicine, Singapore and accredited by Singapore Medical Council, the 15 CME-certified conferences will empower delegates with the knowledge and skills to guarantee the fastest, safest and most accurate laboratory results in improving patient service and care.
During the three-day congress, which takes place from 2 – 4 April 2018 at Suntec Singapore Convention & Exhibition Centre in Singapore, a variety of carefully-designed sessions, panel discussions, demonstrations and interactive activities will enable delegates to network and share best practices with more than 100 regional and international experts who are champions of laboratory medicine in the Asia Pacific.
The congress will host 11 dedicated laboratory tracks: Laboratory Management, Clinical Chemistry, Haematology & Blood Transfusion, Infectious Diseases, Point of Care Testing, Cytology, Molecular Diagnostics, Laboratory Informatics, Cardiac Markers, Lab Testing: Obs Gyne & Women’s Health and Lab Testing & Management: Diabetes.
During these sessions, delegates will able schooled in a wide variety of key topics including the role of the laboratory director, 4th generation sequencing, updates in assays to improve skills in test accuracy, digital pathology, and the evaluation of current and future biomarkers, to name a few.
Due to the expanding role of laboratory medicine, the meeting is combined with other clinical specialties that will underscore the overarching influence of the laboratory in medical decision-making and treatment. New conferences in the MEDLAB Asia Pacific Congress portfolio are: Obs Gyne & Women’s Health, Gynae-Oncology, Diabetes Management and Antimicrobial Resistance.
“The advent of groundbreaking diagnostic solutions is gaining pace across the region. By introducing new medical tracks from key specialties that interact with the laboratory, the 2018 MEDLAB Asia Pacific Congress will provide the latest evidence-based research into diagnosis and treatment as well as enhance cooperation between laboratory professionals and clinicians to enable the best possible patient outcomes.” said Rejoy Penacerrada, Senior Conference Producer, MEDLAB Asia.
MEDLAB Asia Pacific 2018 is supported by a large number of key healthcare federations and associations across the region including The Royal College of Pathologists of Australasia, Singapore Society of Pathology, College of Pathologists, Academy of Medicine of Malaysia, Indonesian Association of Clinical Pathologist and Laboratory Medicine, Singapore Society of Haematology, College of American Pathologists, Philippine Society of Pathologists, Inc., Philippine Society of Biochemistry and Molecular Biology, Philippine Society of Microbiology, Indonesian Association of Clinical Chemistry, Society of Infectious Disease Singapore, and Society of Cytology Singapore and Diabetes Singapore.
Held alongside the congress is the MEDLAB Asia Pacific exhibition – a platform for leading companies from across the globe to showcase current technologies and innovations in the field of laboratory and diagnostics to an expected 4,000 visitors.
MEDLAB Asia Pacific is also co-located with Asia Health, a trade exhibition for medical equipment, products, services and technologies hosting more than 250 international companies and bringing together the world of medical laboratory and healthcare under one roof.
Registration for the MEDLAB Asia Pacific Congress is now open via www.medlabasia.com.