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Faster, better, cheaper tests for blood disease

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Development of the test is described in the journal Blood, published in print on Thursday June 09, 2016.

Around three million people worldwide have a rare bleeding or clotting disorder. These diseases are caused by small changes in people’s genes and may be passed on from parents to children. The most familiar and best understood example is the bleeding disorder haemophilia, caused by changes in two clotting genes; however, dozens of other bleeding and platelet genes are known and many remain to be discovered.

Understanding the genetic causes of these diseases helps NHS doctors and nurses to provide better treatments to patients and to provide patients and their families with information predicting the likely development of the disease. A speedy diagnosis is essential to identify affected relatives and to provide support, advice and treatments that will improve a patient’s quality of life and prevent medical emergencies.

“This is great news for NHS patients that, through the work the National Institute of Health Research has done to bring together leading researchers to create better and cheaper diagnostic tests, patients will now get the information they need about the causes of blood diseases,” said the UK’s Minister for Life Sciences, George Freeman, MP.

“Through our commitment to investing £1bn [$1.45bn] every year in the National Institute of Health Research during this Parliament, we’re funding world class medical breakthroughs which can improve patient outcomes and help avoid unnecessary NHS treatment costs.”

Dr Kate Downes from Cambridge University leads the team responsible for facilitating the transfer of the discoveries into clinical practice in the NHS.

“It’s a real privilege that the efforts of my team are providing faster diagnoses to patients by bringing state-of-the-art DNA sequencing technology to the bedside,” said Dr Downes.

“This is an example of how genome science will pave the way for a revolution in medicine that will allow each patient to receive the best possible care tailored to his or her medical needs.”

In the past, the discovery of new genetic changes causing rare diseases did not immediately result in better tests for NHS patients. The cost and time it took to read our genetic code made it impossible to bring better tests to the frontline. With new genetic technologies, more powerful computer analysis and the use of universal descriptions of disease symptoms, this is no longer the case.

“It was intriguing to observe that the symptoms of hundreds of patients with rare disorders of the blood were very diverse and spanned many parts of the body beyond the blood system,” said Dr Ernest Turro, Chief Analyst for the NIHR BioResource at the University of Cambridge and Medical Research Council Biostatistics Unit.

“We had to develop new computer methods to find commonalities between different patients who also shared particular genetic changes. In one example, bringing information together from three families uncovered a genetic link between very big platelets and deafness.”

In the studies published today, researchers working with the National Institute of Health Research (NIHR) and Illumina Cambridge sequenced the genomes of 5,000 patients. The results and the assessment by the treating clinicians were recorded systematically in a computer database. Researchers then applied mathematical and computational approaches to search for variants present in patients’ genomes, but absent from or rare in the general population, that might explain the patients’ symptoms.

Professor John Bradley, a kidney doctor at Cambridge University Hospitals, worked with colleagues across the NHS and overseas to develop a structure for the safe sharing of all this information obtained from patients’ DNA and from their clinical notes.

“Without the NIHR BioResource-Rare Diseases it would never have been possible to make these important discoveries,” explained Professor Bradley.

“I am proud of what the hundreds of doctors and nurses have achieved by working together with patients across the NHS and similar teams in other European countries and the United States. Their work on the tiny cells named platelets is relevant also to patients with fragile bones and possibly even those with heart rhythm problems.”

The developments are a prime example of collaborative genome science. The researchers at Cambridge University Hospitals and NHS Blood and Transplant work hand-in-glove with their colleagues at UCL (University College London) and the Katherine Dormandy Haemophilia and Thrombosis Centre (KD:HT) at the Royal Free London NHS Trust in North London. Teams of computer experts are working with nurses, doctors, patients and their close relatives, as well as with researchers in laboratories, to deliver affordable new blood tests and to use the new knowledge learned about the role of genes in rare diseases.

“In the past four weeks, we have marked ten years of collaborative work in the UK through the National Institute for Health Research,” says Professor Amit Nathwani, Professor of Haematology, UCL Cancer Institute. “These immense improvements in the care of NHS patients could not have been achieved without the National Institute for Health Research, which brings patients together with the best teams of researchers.

“Dr Keith Gomez, from my team, is now leading the introduction of the new DNA test across all NHS hospitals, resulting in tangible patient benefit. This programme is an excellent example of how the NIHR platform enables the best universities in the country to work together, thus accelerating improvements in the care we provide to NHS patients.”

The research team believe that their work was rapidly translated into clinical application because the global community grasped this opportunity to improve diagnosis for patients.

Alongside the new better, faster and cheaper diagnosis sits a hope for better treatment. Leading researchers such as Professor Nathwani are inviting patients to join pioneering studies that can bring long-lasting treatments or even cures for certain rare diseases of the blood.

Identifying genes that cause rare bleeding or clotting disorders will help patients not only with these diseases. A better understanding of the genes involved in platelets will help researchers investigating much more common life-threatening events involving such as heart attacks and strokes.

Source: Eurekalert

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New test allows for one-step diagnosis of HCV infection

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Now researchers have developed a novel enzyme immunoassay that accomplishes screening and diagnosis in one simple and affordable step.

In a Hepatology study that included 365 blood specimens, the assay was highly sensitive and specific for HCV infection.

“Chronic HCV infection affects approximately 170 million individuals worldwide and is associated with risk of progression to cirrhosis and hepatocellular carcinoma,” the authors wrote. “Although health professional practice guidelines advocate screening for HCV infection, recent studies indicated a significant deficit in screening and diagnosis of HCV infection.”

 

Source: Wiley

Study reveals how altered gut microbes cause obesity

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In an earlier study, Gerald I. Shulman, M.D., the George R. Cowgill Professor of Medicine, observed that acetate, a short-chain fatty acid, stimulated the secretion of insulin in rodents. To learn more about acetate’s role, Shulman, who is also an investigator of the Howard Hughes Medical Institute, and a team of Yale researchers conducted a series of experiments in rodent models of obesity.

The research team compared acetate to other short-chain fatty acids and found higher levels of acetate in animals that consumed a high-fat diet. They also observed that infusions of acetate stimulated insulin secretion by beta cells in the pancreas, but it was unclear how.

Next, the researchers determined that when acetate was injected directly into the brain, it triggered increased insulin by activating the parasympathetic nervous system. “Acetate stimulates beta cells to secrete more insulin in response to glucose through a centrally mediated mechanism,” said Shulman. “It also stimulates secretion of the hormones gastrin and ghrelin, which lead to increased food intake.”

Finally, the research team sought to establish a causal relationship between the gut microbiota and increased insulin. After transferring fecal matter from one group of rodents to another, they observed similar changes in the gut microbiota, acetate levels, and insulin.

“Taken together these experiments demonstrate a causal link between alterations in the gut microbiota in response to changes in the diet and increased acetate production,” said Shulman. The increased acetate in turn leads to increased food intake, setting off a positive feedback loop that drives obesity and insulin resistance, he explained.

The study authors suggest that this positive feedback loop may have served an important role in evolution, by prompting animals to fatten up when they stumbled across calorically dense food in times of food scarcity.

“Alterations in the gut microbiota are associated with obesity and the metabolic syndrome in both humans and rodents,” Shulman noted. “In this study we provide a novel mechanism to explain this biological phenomenon in rodents, and we are now examining whether this mechanism translates to humans.”

Source: Yale News

 

Blood test to personalize depression treatment for the first time

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Guided by this test, patients with blood inflammation above a certain threshold could be directed towards earlier access to more assertive antidepressant strategies, such as a combination of antidepressants, before their condition worsens.

Approximately half of all depressed patients do not respond to first-line antidepressants and a third of patients are resistant to all available pharmacological treatments. Until now, it has been impossible to establish if individual patients will respond to common antidepressants or if they need a more assertive antidepressant treatment plan, which may include a combination of more than one medication.

As a result, patients are treated with a trial-and-error approach whereby one antidepressant is tried after another, often for 12 or more weeks for every type of antidepressant. This can result in long periods of ineffective antidepressant treatment for individuals who may not show an improvement in symptoms anyway.

The study, published today by The International Journal of Neuropsychopharmacology, focused on two biomarkers that measure blood inflammation, as previous studies have already shown that elevated levels of inflammation are associated with poor response to antidepressants.

They measured the quantity of two biomarkers – of Macrophage Migration Inhibitory Factor (MIF) and interleukin (IL)-1β- in two independent clinical samples of depressed patients, before or after they took a range of commonly prescribed antidepressants.

The researchers found that blood test results above a specified threshold level could precisely and reliably predict the probability of individuals responding to the treatments. Patients with levels of MIF and IL-1β above the thresholds showed a 100 per cent chance of not responding to conventional, commonly prescribed antidepressants. Those with inflammation below the suggested threshold could be expected to respond to first-line antidepressants, according to the study authors.

The two biomarkers examined in the study are both thought to be important in predicting how people with depression respond to antidepressants, as they are involved in several brain mechanisms relevant to depression. These include the birth of new brain cells and connections between them, as well as the death of brain cells through a process called ‘oxidative stress.’Oxidative stress occurs when the body both overproduces and then struggles to remove molecules called ‘free radicals.’These free radicals break down brain connections and disrupt the brain’s chemical signalling, which in turn can lead to the development of depressive symptoms by reducing the brain’s protective mechanisms.

Professor Carmine Pariante from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London and senior author of the study, said: ‘The identification of biomarkers that predict treatment response is crucial in reducing the social and economic burden of depression, and improving quality of life of patients.

‘This study provides a clinically-suitable approach for personalising antidepressant therapy – patients who have blood inflammation above a certain threshold could be directed toward earlier access to more assertive antidepressant strategies, including the addition of other antidepressants or anti-inflammatory drugs.’

Dr Annamaria Cattaneo, first author from the IoPPN at King’s College London, said: ‘This is the first time a blood test has been used to precisely predict, in two independent clinical groups of depressed patients, the response to a range of commonly prescribed antidepressants.

‘These results also confirm and extend the mounting evidence that high levels of inflammation induce a more severe form of depression, which is less likely to respond to common antidepressants.’ Dr Cattaneo added: ‘This study moves us a step closer to providing personalised antidepressant treatment at the earliest signs of depression.

‘It is really crucial now to carry out a clinical study comparing the current clinical practice in antidepressant prescription, based on trial-and-error, with our novel approach of ‘personalised psychiatry’, where the antidepressant treatment plan is guided by the blood test.’

Source: ScienceDaily

 

War and peace in the human gut: Probing the microbiome

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Athena Aktipis is a researcher in the Biodesign Institute, Assistant Professor in the Psychology Department at Arizona State University and co-Director of the Human Generosity Project. She is also a member of the Center for Evolution and Medicine.

According to Athena Aktipis, a researcher at Arizona State University’s Biodesign Institute, microbes within the body–collectively known as the microbiota–also engage in cooperative and combative behavior with human cells in their environment. This is particularly true in the human gut, where many trillions of them exist in the digestive tract in communities of bewildering diversity.

In research appearing in the current issue of Annals of the New York Academy of Sciences, Aktipis and her colleagues Helen Wasielewski (ASU’s Department of Psychology), and Joe Alcock, (at the University of New Mexico Department of Emergency Medicine), examine the role of microbes in the gut. Their study explores how dietary choices promote cooperation or might fuel conflict between gut microbes and the humans they interact with, maintaining health or encouraging the onset of disease.

The new research provides important insights into the subtle interplay of diet and human health as well as paving the way for management of the microbiome, particularly for the treatment and prevention of inflammatory and metabolic disease.

“Our gut microbes are not just passive recipients of the food that we eat – they evolve and change in response to what we feed our bodies. And there are certain foods that lead to resource sharing between us and our microbes, while other foods can lead to conflict and resource competition between our bodies and our microbes,” Aktipis says. “This cooperation and conflict framework can help us understand certain aspects of why we get sick and how we can stay healthy.”

Bacterial nation

Scientists are only beginning to appreciate the significance and complexity of the bacteria comprising the microbiota, which number approximately 30 trillion, about the same number as human cells. Colonization of the body by a vast array of microbes begins at birth, when a newborn is exposed to maternal vaginal, fecal and skin flora.

Most of the human microbiota resides in the gut. At least 500 different species exist, though most fall into several well-recognized groups. Emerging research suggests the composition of these microbes exerts a profound influence on human health throughout life, including the propensity for obesity and the susceptibility to allergies. They may even affect behavior.

In the new manuscript, Aktipis and her colleagues explore the effects of particular nutrients in food on the behavior of gut bacteria. Their innovative approach applies evolutionary theory to the issue and proposes that the microbes inhabiting the human gut engage in competitive or cooperative behavior, depending in part on the particular diet they are exposed to.

Support vs strife

Cooperation and competition are hallmarks of evolutionary processes, guiding the fate of all living organisms. In the human body, conflict and cooperation between cells of differing genetic makeup can have important consequences for health and disease.

One classic example is that of cancer cells, which mutate genetically, form independent clusters and rob resources from the host for their own benefit. Cell competition can also occur between maternal cells and those of a developing fetus, another topic Aktipis has explored in earlier research.

In the current study, Aktipis and her colleagues examine cooperation and competition between the human and non-human, that is, between the cells making up human tissues and organs and the multitude of microbes (e.g. bacteria, fungi, and archaeons) co-existing in the same individual.

Cooperative behavior between humans and gut microflora occurs when bacterial cells produce energy and vitamins and help to screen out pathogens threatening the host. In return, host cells help maintain the microbial habitat, providing them with an environment conducive to their growth and proliferation–a win-win situation.

The authors propose that a cooperative alignment of needs between gut microbes and the human host should lead to positive health outcomes, while conflicts over resource utilization can often generate disease.

Helen Wasielewski, Postdoctoral Scholar in the Aktipis Lab, argues that taking a microbial perspective is useful in understanding these cooperative relationships: “Thinking about transmission, or how these microorganisms move between hosts, is really important here. If bacteria are able to move between hosts easily, they can exploit the current host and move on, whereas if they’re more limited they can become dependent upon the reproductive success of the host for their own success,” she says. “In extreme cases, symbionts become dependent upon their hosts to such an extent that they no longer have the capacity to live outside the host – we see examples of this in some invertebrates.”

Food fight

Internal disputes can break out when the needs of microbes and humans are at cross-purposes. Should conditions of cooperation break down, gut microbiota may contribute to chronic afflictions including inflammatory, metabolic and cardiovascular diseases or use nutrients intended for the host, causing inflammation and other negative health effects.

Sugar and fat in the diet may constitute a recipe for such internal conflict. Unlike dietary fiber, fats and simple sugars can be used not only by host cells but also by potentially harmful microbes, such as pathogenic E. coli. Instead of resource sharing, a microbial tug-of-war ensues.

When low fiber intake in the diet is combined with abundant sugar, populations of harmful microbes can expand, leading to inflammation-related illness. The ingestion of iron also carries certain health risks and can sometimes lead to internal conflict. A variety of pathogens steal iron directly from host cell proteins. When harmful microbes gain access to key nutrients like iron, the body responds by ramping up immune activity against these microbes. This can result in escalating conflict between human and microbial cells, with deleterious impacts on human health, that may include adipose inflammation, obesity and diabetes.

What’s cooking?

In gauging the health effects of modern Western diets, the new study identifies both benefits and risks associated with cooperation and conflict in the human gut.

The wide availability of foods with high nutritional density and low pathogen load acts to promote health through microbe-human cooperation. Among the specific nutrients examined in the study, breast milk is highlighted for its benefits to both mother and infant. It has been credited with reducing infant mortality and limiting the risk of chronic diseases later in life.

Non-digestible carbohydrates in milk feed protective microbiota in the gut. Specialized proteins in breast milk provide an immunological effect, including cytokines, immunoglobulins, and lactoferrin that act to reduce infection risk.

On the other hand, Western diets may contribute to human disease, including obesity and other chronic inflammatory diseases as a consequence of their low fiber content and high proportion of simple sugars, saturated fats and emulsifying agents.

The research findings highlighted in this paper mark a departure from conventional ideas concerning diet, suggesting the negative health consequences of certain foods may be due to their effects on the subtle interconnection of host and microbiome.

 

Source: Arizona State University

 

Blood-born molecules could predict those who will develop liver cancer

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Hepatocellular carcinoma, the most common type of liver cancer, is increasing in incidence in the United States, and infection with the Hepatitis B virus (HBV) causes about 50 percent of cases. However, it can be difficult to identify who is most likely to develop this cancer. Although earlier research had discovered molecular signatures associated with HBV-driven liver cancer, new research from Thomas Jefferson University has proven that this panel of microRNAs can also predict the patients at high risk for developing the disease before the cancer develops, via a blood test.

The researchers, led by Hushan Yang, Ph.D., an Associate Professor of Medical Oncology and researcher at the Sidney Kimmel Cancer Center at Jefferson studied a large cohort of HBV-infected patients, some of whom eventually developed liver cancer, and analyzed their molecular signature from blood samples. Of the 373 HBV patients who were originally cancer free, 40 developed cancer over a median follow up of 4.5 years. The researchers analyzed a panel of 24 microRNAs — small molecules that regulate gene activity — and showed that 15 of these microRNAs had changed their normal gene expression pattern before patients developed cancer, suggesting these molecules could be used to predict patients with a high likelihood of developing cancer. The study was published in the journal Oncotarget.

Earlier studies had identified the 24 microRNAs that Dr. Yang and colleagues studied. However, it was unclear whether those microRNAs caused the cancer, or were a result of already occurring cancerous processes. By following this cohort of patients prospectively, and using blood samples taken at least one year before liver cancer diagnosis, the researchers were able to answer that question for the first time. In addition, prior studies analyzed samples taken from patient biopsies, which require invasive procedures, whereas the current study showed that microRNAs circulating in the blood could predict disease.

“This research confirms previous work on microRNAs and liver cancer and goes further to show that these microRNAs may be able to predict the development of liver cancer through a non-invasive blood test,” says first author Chun Wang, a visiting scholar in the Department of Medical Oncology.

The current non-invasive test for determining cancer risk among HBV patients is a diagnostic for the molecule alpha-fetoprotein (AFP). It is also associated with Hepatitis C infections, but it isn’t always a good predictor of disease. In fact, the Jefferson researchers identified 15 out of 16 patients, or 94 percent of patients who were misclassified as cancer-free by AFP. Likewise, in the 57 patients who were deemed at high risk of developing liver cancer by AFP, the microRNA testing correctly reclassified 33, or 58 percent, as low risk.

Although the panel of 15 microRNAs was useful, it wasn’t perfect. “We need to find more microRNAs that may predict liver cancer in order to sharpen this tool for identifying high risk patients,” says Dr. Yang. “Through collaboration with Dr. Hann in the Department of Medicine at Jefferson, we continue to work on improving this diagnostic method.”

The work was supported by a Tobacco Grant from the Pennsylvania Department of Health, National Cancer Institute Grant CA159047, American Cancer Society Research Scholar Grant 123741-RSG-13-003-01-CCE, and a V Scholar Grant from the V Foundation for Cancer Research. The authors report no conflicts of interest.

Source: Jefferson.edu

 

Antibiotics disrupt infants’ gut microbiome, studies suggest

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Children repeatedly treated with antibiotics during the first few years of life not only showed lower microbial diversity, but also harbored antibiotic resistance genes, temporarily, after treatment. Further studies are needed to probe the long-term consequences of these gut microbiome disturbances, which have previously been linked to obesity, diabetes, asthma, and to allergies later in life. The community of bugs that resides in our intestines plays a critical role in regulating the body’s metabolism and immune defenses. However, how the gut microbiome develops during early childhood is not fully understood. Less still is known about how the infant microbiome responds to and recovers from environmental perturbations, including those from antibiotic treatment, cesarean section (versus vaginal delivery), and formula feeding (compared to breast-feeding).

Antibiotic treatment among children is routine in most parts of the world, with the average American child receiving three courses of antibiotics by age two. To gain more insights into the possible consequences, Nicholas Bokulich and colleagues tracked the microbial development of 43 U.S. infants for two years after birth, collecting their stool samples as well as additional samples from their mothers before and after birth. They found that antibiotics, cesarean delivery, and formula feeding can delay infants’ microbiome development and reduce bacterial diversity. The mother’s own microbiota, which is known to populate the infant gut during passage through the birth canal, may also influence the healthy development of the infant’s microbiota, as may breast-feeding and skin contact.

In a second study analyzing stool samples collected from 39 children over three years, Moran Yassour and colleagues also found that repeated antibiotic treatment reduced gut microbial diversity and even led to a transient rise in antibiotic resistance genes. In the first few months of life, all infants born by cesarean section and, unexpectedly, about 20% of those born by vaginal delivery lacked Bacteroides, bacteria known to help regulate intestinal immunity, suggesting that birth mode and other factors can strongly influence bacterial diversity. Antibiotic-treated children also had less diverse and less stable microbiota at the level of both species and strain. Furthermore, the researchers detected antibiotic resistance genes that rapidly peaked in abundance following antibiotic treatment, before sharply declining. Interestingly, for reasons not fully understood, some infants as young as two months old harbored antibiotic resistance genes, even without any exposure to antibiotics. In related audio files, authors Yassour and Ramnik Xavier highlight the findings’ public health implications for infants and children who are routinely treated with antibiotics.

Source: Eurekalert

 

Testing blood metabolites could help tailor cancer treatment

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Scientists have found that measuring how cancer treatment affects the levels of metabolites – the building blocks of fats and proteins – can be used to assess whether the drug is hitting its intended target.

This new way of monitoring cancer therapy could speed up the development of new targeted drugs – which exploit specific genetic weaknesses in cancer cells – and help in tailoring treatment for patients.

Scientists at The Institute of Cancer Research, London, measured the levels of 180 blood markers in 41 patients with advanced cancers in a phase I clinical trial conducted with The Royal Marsden NHS Foundation Trust.

They found that investigating the mix of metabolic markers could accurately assess how cancers were responding to the targeted drug pictilisib.

Their study was funded by the Wellcome Trust, Cancer Research UK and the pharmaceutical company Roche, and is published in the journal Molecular Cancer Therapeutics.

Pictilisib is designed to specifically target a molecular pathway in cancer cells, called PI3 kinase, which has key a role in cell metabolism and is defective in a range of cancer types.

As cancers with PI3K defects grow, they can cause a decrease in the levels of metabolites in the bloodstream.

The new study is the first to show that blood metabolites are testable indicators of whether or not a new cancer treatment is hitting the correct target, both in preclinical mouse models and also in a trial of patients.

Using a sensitive technique called mass spectrometry, scientists at The Institute of Cancer Research (ICR) initially analysed the metabolite levels in the blood of mice with cancers that had defects in the PI3K pathway.

They found that the blood levels of 26 different metabolites, which were low prior to therapy, had risen considerably following treatment with pictilisib. Their findings indicated that the drug was hitting its target, and reversing the effects of the cancer on mouse metabolites.

Similarly, in humans the ICR researchers found that almost all of the metabolites – 22 out of the initial 26 – once again rose in response to pictilisib treatment, as seen in the mice.

Blood levels of the metabolites began to increase after a single dose of pictilisib, and were seen to drop again when treatment was stopped, suggesting that the effect was directly related to the drug treatment.

Metabolites vary naturally depending on the time of day or how much food a patient has eaten. But the researchers were able to provide the first strong evidence that despite this variation metabolites can be used to test if a drug is working, and could help guide decisions about treatment.

Dr Florence Raynaud, Senior Researcher in the Clinical Pharmacology and Trials Team at The Institute of Cancer Research, London, said: “We have shown that assessing a patient’s metabolites can be a quick and simple way of assessing whether a cancer drug is specifically hitting its intended target in the body. Our study is an important step in the development of new precision cancer therapies, and is the first to show that blood metabolites have real potential to monitor the effects of novel agents.

“Our method was developed specifically for pictilisib but could now be adapted to discover metabolite markers for other cancer treatments.”

Co-author Professor Paul Workman, Chief Executive of The Institute of Cancer Research, London, said: “In the modern world of precision cancer medicine it is really vital to understand a drug’s mechanism of action, and to know how it is working not just overall but in individual cancer patients.

“By monitoring metabolic signals in the blood, we could make informed decisions about drug development without having to wait years to see the final results of large clinical trials. And our method could eventually be used to monitor patients routinely during the course of treatment, as a quick and easy way of assessing whether a drug is still working, or whether treatment needs to be adapted.”

Source: Sciencedaily

A urine sample could be used to diagnose a complex and serious pregnancy disorder

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In simpler terms, the scientists have found potential biomarkers in the urine of pregnant women. In the future, this urine-based diagnostic method will enable specialists to detect the disease in its early stages. A paper detailing the results has been published in the Journal of Proteomics.

Preeclampsia and why it is dangerous

Preeclampsia is a multisystem disorder that occurs in the second half of pregnancy and is characterized by high blood pressure and proteinuria (a significant increase in the normal level of protein in the urine). Women with the condition suffer headaches, swelling, fainting, and other unpleasant and often dangerous symptoms. Ultimately, preeclampsia puts the health and life of an expectant mother and her baby at serious risk. The symptoms of the condition are ambiguous, so doctors rarely diagnose “pure” preeclampsia. However, even if this diagnosis is made, a new problem arises – it is still not known what causes the disorder, therefore it is not possible to control it effectively.

This means that doctors are only able to prescribe supportive care and treat the symptoms, while trying to delay the birth of the child – a balance has to be made between allowing enough time for full fetal growth (although the baby is also affected by improper development of the placenta as a result of the condition) and preserving the mother’s health.

Clues from the body and a discovery for the medicine of the future

If something is wrong with all the systems in the body, it is logical to assume that the “fault” is at molecular level. Protein is found even in the urine of an absolutely healthy person, although only in very small concentrations. From a doctor’s point of view, one of the main symptoms of preeclampsia is a marked increase in this concentration (from the normal 0.03 g/l to the critical 0.3 g/l and above). The scientists wondered whether peptides (pieces of proteins) that are produced by women with preeclampsia could carry information about the disease. This approach is very much in line with the current focus on non-invasive testing, i.e. analysing available biomaterials such as urine, saliva, or exhaled air.

To identify potential peptide biomarkers, the researchers compared samples of three groups of ten women from the Research Center for Obstetrics, Gynecology and Perinatology: women with a normal pregnancy, and with mild and severe preeclampsia. The researchers were not only interested in comparing healthy women and patients with preeclampsia; they also wanted to examine how certain biomarkers are associated with the severity of the condition. Following the experiments, 35 potential peptide biomarkers of preeclampsia were identified.

They included fragments of alpha-1-antitrypsin (14 peptides), collagen alpha-1(I) and alpha-1(III) chains (6 peptides), and uromodulin (7 peptides).

“In the Research Center for Obstetrics, Gynecology and Perinatology we were able to confirm a number of markers previously proposed by our colleagues abroad, and also identify some new ones. We will obviously need to verify and confirm their significance. What is important is that this non-invasive method has proven effective – it can be used as a basis to develop a clinical method,” said Evgeniy Nikolaev, one of the authors of the study, professor and head of MIPT’s Laboratory of Ionic and Molecular Physics.

Source: MIPT

 

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