Researchers at the University at Buffalo Research Institute on Addictions have discovered how a gene in the brain’s dopamine system can play an important role in prolonging lifespan: it must be coupled with a healthy environment that includes exercise.
The study was led by Panayotis (Peter) K. Thanos, senior research scientist at RIA.
Thanos and his team studied the genes in dopamine to assess their impact on lifespan and behaviour in mice. Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centres and helps regulate physical mobility and emotional response.
The researchers found that the dopamine D2 receptor gene (D2R) significantly influences lifespan, body weight and locomotor activity, but only when combined with an enriched environment that included social interaction, sensory and cognitive stimulation and, most critically, exercise.
“The incorporation of exercise is an important component of an enriched environment and its benefits have been shown to be a powerful mediator of brain function and behaviour,” Thanos says.
The mice in the enriched environment lived anywhere from 16 to 22 percent longer than those in a deprived environment, depending on the level of D2R expression.
“These results provide the first evidence of D2R gene-environment interaction playing an important role in longevity and aging,” Thanos says. “The dichotomy over genes versus environment has provided a rigorous and long debate in deciphering individual differences in longevity. In truth, there exists a complex interaction between the two which contribute to the differences.”
Research exploring this genetic-environmental interaction should lead to a better understanding and prediction of the potential benefits of specific environments, such as those including exercise, on longevity and health during aging.
University at Buffalo Research Institute on Addictions
www.buffalo.edu/ria/news_events/latest_news.host.html/content/shared/university/news/news-center-releases/2016/04/056.detail.html
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Researchers at UMass Medical School have identified a new molecular pathway critical for maintaining the smooth muscle tone that allows the passage of materials through the digestive system. This finding, based on studying calcium ion-controlled pathways in mice, may lead to new treatments for a host of digestive disorders ranging from common gastroesophageal reflux disease (GERD), to swallowing disorders, incontinence and pancreatitis.
“We are excited about the potential to target identified genes to treat disorders such as reflux and incontinence,” said Ronghua ZhuGe, PhD, associate professor of microbiology and physiological systems and a senior author of the study. “Knowing how these muscles stay contracted for such long periods of time will allow us to develop potential new treatments for these diseases. The next step is to see whether this molecular mechanism in mice also operates in humans.”
The human body, and those of other mammals, contains a number of ring-shaped structures made of smooth muscle encircling openings in hollow organs such as the intestines and bladder called sphincters. Smooth muscle is involuntarily controlled, unlike the muscles we use to walk, for example, so that we don’t need to consciously move digested food from stomach to small intestine. Dysfunction in the sphincters, either structurally or functionally, can have severe consequences leading to diseases that impair the ability of the muscle to contract or relax. This can lead to achalasia, which makes it difficult to swallow; gastroesophageal reflux disease (GERD), which allows stomach acid to enter the oesophagus or incontinence of the bowels.
“A healthy sphincter opens transiently but remains closed most of the time, maintaining a basal tone. This basal tone requires constant generation of force produced by the contraction of smooth muscle cells that make up the sphincters,” said Dr. ZhuGe. “However, the genetics governing how the sphincter smooth muscle stays contracted for such long periods of time remains unknown.”
Smooth muscle operates by generating force as the muscle motor protein myosin and actin filaments move past each other. This happens after a molecule called the myosin regulatory light chain (MLC) is turned on through a common molecular transformation called phosphorylation. How much phosphorylation takes place is controlled by the relative amounts of two enzymes; calcium dependent MLC kinase (MLCK), which promotes phosphorylation, and calcium independent MLC phosphatase (MLCP), which reverses phosphorylation. Through this process, contraction and relaxation of the muscle is achieved.
To understand the molecular mechanism responsible for the involuntary and continuous contraction of the sphincter muscle, Dr. ZhuGe and colleagues examined the internal anal sphincter that controls bowel continence in mice. They showed that genetic deletion of the MLCP enzyme in the smooth muscle had no effect on the basal tone of the mouse sphincter, but deletion of MLCK essentially abolishes the basal tone and mice become incontinent as a result.
“Although previous biochemical studies suggested that lower MLCP activity may be related to the basal tone of this sphincter, our genetic study indicates this doesn’t seem to be the case. It turns out MLCK is essential for the tone formation,” said ZhuGe. “This prompted us to look for specific calcium signals that regulate MLCK.”
Co-author Lawrence Lifshitz, PhD, associate professor of molecular medicine, said, “Calcium signalling is our favourite subject. We originally hypothesized that localized releases of calcium inside the cell, near target ion channels, might do the trick, as we knew that such releases can regulate the contraction of smooth muscle in blood vessels and airways.”
But experiments showed that these local calcium releases have no direct role in muscle tone. Instead, three types of ion channels act in concert to generate a rise in cytosolic calcium which eventually results in MLCK activation and muscle tone.
To test this hypothesis, ZhuGe’s group teamed up with Minsheng Zhu, PhD, at Nanjing University in China, to generate a line of mice in which one of these channels could be turned off in smooth muscle only. “These mice were a powerful tool for establishing our hypothesis,” said ZhuGe. “They helped us identify the Tmem16a (also called Ano1) gene as a critical component for basal tone formation and fecal continence. When we were able to turn off the TMEM16A channels in these mice, they lost the majority of the basal tone and became incontinent. ”
UMass Medical School
www.umassmed.edu/news/news-archives/2016/04/umms-scientists-identify-genes-that-control-smooth-muscle-contraction-in-digestive-system/
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Myopia, also known as short-sightedness or near-sightedness, is the most common disorder affecting the eyesight and it is on the increase. The causes are both genetic and environmental. The Consortium for Refractive Error and Myopia (CREAM) has now made important progress towards understanding the mechanisms behind the development of the condition. This international group of researchers includes scientists involved in the Gutenberg Health Study of the University Medical Center of Johannes Gutenberg University Mainz (JGU). The team has uncovered nine new genetic risk factors which work together with education-related behaviour as the most important environmental factor causing myopia to generate the disorder. The results of the study ‘Genome-wide joint meta-analyses of genetic main effects and interaction with education level identify additional loci for refractive error: The CREAM Consortium’ have recently been published in the scientific journal Nature Communications.
There has been a massive rise in the prevalence of short-sightedness across the globe in recent decades and this upwards trend is continuing. It is known from previous studies of twins and families that the risk of acquiring short-sightedness is determined to a large extent by heredity. However, the myopia-causing genes that had been previously identified do not alone sufficiently explain the extent to which the condition is inherited. In addition to the genetic causes of myopia there are also environmental factors, the most significant of which are education-related behaviour patterns. “We know from the Gutenberg Health Study conducted at Mainz that the number of years of education increases the risk of developing myopia,’ said Professor Norbert Pfeiffer, Director of the Department of Ophthalmology at the Mainz University Medical Center.
With the aim of identifying genetic mutations relating to myopia and acquiring better insight into the development of the condition, the international research group CREAM carried out a meta-analysis of data collected from around the world. The data compiled for this analysis originated from more than 50,000 participants who were analysed in 34 studies. The second largest group of participants was formed by the more than 4,500 subjects of the Gutenberg Health Study of the Mainz University Medical Center. ‘In the field of genetic research, international cooperation is of particular importance. This is also borne out by this study, to which we were able to make a valuable contribution in the form of data from our Gutenberg Health Study,’ continued Professor Norbert Pfeiffer. ‘And in view of the fact that a survey undertaken by the European Eye Epidemiology Consortium with the help of the Gutenberg Health Study shows that about one third of the adult population of Europe is short-sighted, it is essential that we learn more about its causes in order to come up with possible approaches for future treatments.’
Aware that environmental effects and hereditary factors reinforce one another in the development of myopia, the scientists devised a novel research concept for their investigations. They used a statistical analysis technique that takes into account both the effects of the environmental and hereditary factors and does so in equal measure and simultaneously. Their efforts were crowned with success as they were able to classify nine previously unknown genetic risk factors.
Risk-associated gene involved in the development of short-sightedness
These newly discovered genetic variants are associated with proteins which perform important functions when it comes to the transmission of signals in the eye. One of these genes is of particular interest because it plays a major role in the transmission of the neurotransmitter gamma-aminobutyric acid (GABA) in the eye. Previous studies have shown that there is greater activation of the gene in question in eyes that are myopic. The results of current research substantiate this conclusion. The CREAM researchers interpret this as evidence that this newly discovered risk-related gene is actually involved in the development of short-sightedness. This represents significant initial headway towards understanding how genetic causes interact with the level of education as an environmental factor to produce the heterogeneity of myopia. Further research will be needed to clarify the details of how the mechanisms actually work and interact with one another.
The spread of short-sightedness is a worldwide phenomenon. Particularly in South East Asia the incidence of myopia in school children has increased notably over the last decades. This is likely due to an improvement in educational attainment. People who read a great deal also perform a lot of close-up work, usually in poor levels of daylight. The eye adjusts to these visual habits and the eyeball becomes more elongated than normal as a result. But if it becomes too elongated, the cornea and lens focus the image just in front of the retina instead of on it so that distant objects appear blurry. The individual in question is then short-sighted.
Johannes Gutenberg University Mainz www.uni-mainz.de/presse/20232_ENG_HTML.php
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Abbott demonstrated a prototype of the company’s next-generation molecular diagnostics platform at a recent scientific event hosted for its customers from across the globe. At the event, molecular laboratory directors and researchers had hands-on interaction with the prototype and were able to provide additional feedback on the system prior to further stages of development.
Abbott’s new system is currently being designed from the ground up based on extensive input from laboratory customers. For example, health systems around the world are often challenged with higher testing volumes with staffing and budget constraints, including in the molecular laboratories.
“Our molecular lab customers tell us they are facing pressures to do more with less,” said John Carrino, divisional vice president, research and development, Molecular Diagnostics, Abbott. “Abbott’s next-generation molecular system is being designed to have a faster turnaround time, greater flexibility to run any test at any time, an ability to run higher volumes and automation to increase lab efficiency – all without compromising the testing performance and quality for which our organization is highly regarded.”
Additionally, customer insights suggest a need for a broad testing menu in the molecular lab. Abbott currently offers one of the broadest molecular testing menus for infectious diseases such as HIV, hepatitis and tuberculosis, as well as sexually transmitted infections such as human papillomavirus (HPV), chlamydia and gonorrhea, among others tests.
“Abbott’s molecular diagnostics can provide the information needed to help guide some of life’s most important health decisions,” said Andrea Wainer, president, Molecular Diagnostics, Abbott. “Our accurate, reliable and quality tests could allow clinicians to make more informed treatment decisions to help improve patient care.” In addition to the new molecular system, Abbott will be launching next-generation systems in blood screening, immunoassay, clinical chemistry, hematology and point of care testing in the near future. All of the systems will be built on the same software and hardware platforms to enable more automation and to simplify the user experience for Abbott’s customers.
Shimadzu has released the first Application Handbook “Clinical”. It contains most advanced technologies and solutions such as chromatography, mass spectrometry, spectroscopy and life sciences instruments. With nearly 140 pages, the Application Handbook “Clinical” covers 47 real life applications related to hot subjects such as Vitamin D, steroids, immunosuppressants, catecholamines and amino acids analysis. The book is free of charge and can be downloaded (17 MB) at www.shimadzu. eu/clinical.
In clinical applications, analytical instruments unfold a multitude of benefits. They support the quality of human life. The concentration of medications in Therapeutic Drug Monitoring (TDM) is assured, even though this may change according to age and health conditions and is dependent on gender, genetic constitution or interferences with other drugs. They help to save lives, particularly when it comes to time-critical situations, e.g. through acute intoxication, medical or drug abuse. They analyse over- and undersupply of vitamins, minerals and trace elements. They are applied in genomics, proteomics and metabolomics and also uncover fraud in sports, particularly in animal or human doping. At the same time, analytical systems support health protection of animals and humans, even in the long-term. Clinical applications benefit from Shimadzu’s complete portfolio covering chromatography and mass spectrometry (GC, GC-MS, GC-MS/MS, HPLC, UHPLC, LC-MS, LC-MS/MS); spectroscopy (UVVis, FTIR, AAS, EDX, ICP-OES); life sciences (MALDI-(TOF)-MS); microchip- electrophoresis; biopharmaceutical (aggregate sizer); observation of medical microbubbles in targeted drug delivery using the HPV-X2 ultra high-speed camera.
Shimadzu breaks new grounds by rethinking the use of mature technologies to develop new unique systems such as the iMScope TRIO. It combines an optical microscope with a mass spectrometer for insights on the molecular level.
For next-generation brain science, Shimadzu provides LABNIRS, an imaging technology for visualization of brain functions by functional near-infrared spectroscopy (fNIRS).
Some analytical technologies used in the clinical world
Chromatographic separation in gas phase for analysis of volatile and semi volatile components is in use in the clinical field since many years. Gas chromatography is a key technique for quantitative analysis of alcohol in blood.
HPLC and UHPLC systems are able to quantitatively analyse substances in blood, serum, plasma and urine containing multiple compounds by separating and detecting target substances. Shimadzu offers a wide variety of application- specific systems such as automated sample pretreatment systems for amino acid analysis or on-line sample trapping for quantification of drugs or metabolites.
Gas chromatography-mass spectrometry (GC-MS) is a hyphenated technique combining the separating power of GC with the detection power of MS to identify different substances within a sample. Mass spectrometry is a wide-ranging analytical technique which involves the production, subsequent separation and identification of charged species according to their mass to charge (m/z) ratio. It is well known for analysis of drug abuse.
Liquid chromatography-mass spectrometry (LC-MS) is an analytical chemistry technique that combines the physical separation capabilities of LC with the mass analysis capabilities of MS, bringing together very high sensitivity and high selectivity. Its application is oriented towards the separation, general detection and potential identification of compounds of particular masses in the presence of other chemicals (e.g. complex mixtures like blood, serum, plasma or urine). Its use is spreading in the clinical field (research and routine) as a replacement of immunoassays thanks to the capability of multiplexing analysis and reduced risk of cross-reaction in immuno-assays.
Sysmex Corporation and Siemens Healthcare Laboratory Diagnostics announced on April 13, 2016 an extension to their long-standing partnership through at least 2020. The contract extension adds a minimum of two additional years to the global supply, distributorship, and sales and service agreement for hemostasis products. The partnership enables laboratory customers around the world to continue to benefit from the largest portfolio of hemostasis systems and reagents. The companies, which began collaborating more than 20 years ago, also agreed to continue joint hemostasis product development activities that will streamline and optimize testing in laboratories throughout the world.
Siemens Healthcare and Sysmex provide hemostasis products used to test for blood clotting disorders, preoperative bleeding risk management, and the monitoring of patients on anticoagulant therapy medications. In the past few years alone, the companies have introduced several cutting-edge INNOVANCE reagents and multiple new platforms for various laboratory settings, including the recent worldwide launch of the Sysmex CS-2500 System, and the U.S. launch of the Sysmex CS-5100 System with optional track-based automation.
“We are pleased to extend our longstanding partnership with Siemens Healthcare,” said Hisashi Ietsugu, Chairman and CEO, Sysmex Corporation. “With the aging population, hemostasis testing has become even more important. Our partnership provides our customers with the innovative technologies needed to manage the increase in testing volumes, while providing accurate results for improved patient care.”
“The continued collaboration and twenty-year partnership between Siemens and Sysmex is rare in the rapidly changing world of diagnostics,” said Franz Walt, President, Siemens Healthcare Laboratory Diagnostics. “As a leader in hemostasis testing, our combined mission to offer best-in-class solutions has enabled us to meet the needs of diverse laboratories throughout the world.”
www.siemens.com
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Under the banner “GeT Perfect”, Greiner Bio-One has kicked off the European promotion of the Greiner eHealth Technologies Solution – GeT. For this purpose, a modern microsite in German and English has been created. The one page site provides all essential information at a glance. GeT utilizes a flexible modular based software solution whilst applying the advantages of pre-barcoded VACUETTE tubes. The aim is to increase the efficiency of routine procedures in and around the laboratory. This page provides information on events, reference customers as well as study material. Testimonials from reference customers report on their experiences. Advantages of the system and working procedures can be seen in the form of videos and animation. All in all, the user has here a compact version of all initial information required for initiating any further steps.
www.gbo.com/get
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In early May Siemens Healthcare unveiled its new brand name Siemens Healthineers. The new brand underlines Siemens Healthcare’s pioneering spirit and its engineering expertise in the healthcare industry. It is meant to describe the healthcare organization and its people – the people accompanying, serving and inspiring customers – the people behind outstanding products and solutions. As part of its Vision 2020 strategy Siemens AG announced nearly two years ago that its healthcare business would be separately managed as a company within the company with a new organizational setup. Siemens Healthineers will continue to strengthen its leading portfolio across the medical imaging and laboratory diagnostics business while adding new offerings such as managed services, consulting and digital services as well as further technologies in the growing market for therapeutic and molecular diagnostics.
The presence of certain bacteria in the mouth may reveal increased risk for pancreatic cancer and enable earlier, more precise treatment. This is the main finding of a study led by researchers at NYU Langone’s Laura and Isaac Perlmutter Cancer Center.
Pancreatic cancer patients are known to be susceptible to gum disease, cavities, and poor oral health in general, say the study authors. That vulnerability led the research team to search for direct links between the makeup of bacteria driving oral disease and subsequent development of pancreatic cancer, a disease that often escapes early diagnosis and causes 40,000 U.S. deaths annually.
“Our study offers the first direct evidence that specific changes in the microbial mix in the mouth—the oral microbiome—represent a likely risk factor for pancreatic cancer along with older age, male gender, smoking, African-American race, and a family history of the disease,” says senior investigator and epidemiologist Jiyoung Ahn, PhD.
Specifically, researchers found that men and women whose oral microbiomes included Porphyromonas gingivalis had an overall 59 percent greater risk of developing pancreatic cancer than those whose microbiomes did not contain the bacterium. Similarly, oral microbiomes containing Aggregatibacter actinomycetemcomitans were at least 50 percent more likely overall to develop the disease. Doctoral student and lead investigator Xiaozhou Fan, MS, says both types of bacteria have been tied in the past to periodontitis, a disease characterized by inflammation of the gums.
“These bacterial changes in the mouth could potentially show us who is most at risk of developing pancreatic cancer,” adds Ahn, an associate professor at NYU Langone and associate director of population sciences at the Perlmutter Cancer Center.
In another study, Ahn and her colleagues showed that cigarette smoking was linked to dramatic, although reversible, changes in the amount and mix of bacteria in the oral microbiome. But she cautions that further research is needed to determine if there is any cause-and-effect relationship, or how or whether such smoking-related changes alter the immune system or otherwise trigger cancer-causing activities in the pancreas.
Laura and Isaac Perlmutter Cancer Center
nyulangone.org/press-releases/pancreatic-cancer-risk-tied-to-specific-mouth-bacteria
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Cancerous tumours must be fed. Their unregulated growth requires a steady stream of blood flow and nutrients. Thus, one way that researchers have tried to wipe out cancer is to target cells undergoing the metabolic shifts that enable a tumour’s rapid growth.
Yet new findings from University of Pennsylvania researchers suggest that such efforts might have missed a key pathway that enables the changes in metabolism that benefit tumours. Their work finds that mitochondrial stress alone can trigger metabolic shifts through a pathway that involves p53, a protein widely known to play multiple important roles in cancer.
“In all five cancer cell lines we looked at, we saw that p53 was induced when mitochondrial function was affected,” said senior author Narayan Avadhani, the Harriet Ellison Woodward Professor of Biochemistry in Penn’s School of Veterinary Medicine’s Department of Biomedical Sciences. “This led to our discovery that it’s possible to promote tumour growth independent of the HIF-1α pathway, which had up to this point been a prime target of therapeutic interventions.”
The study points to a new factor that could inform our understanding of how cancer progresses. It’s possible that markers of metabolic stress could even serve as a biomarker for a cancer’s aggressiveness or likelihood to spread.
Avadhani teamed with Penn Vet’s Anindya Roy Chowdhury, the lead author and a research associate, and Serge Y. Fuchs, professor of cell biology, as well as Ph.D. student Apple Long and Anil Rustgi, the T. Grier Miller Professor of Gastroenterology, both of Penn’s Perelman School of Medicine. Avadhani and Fuchs are also members of Penn Vet’s Mari Lowe Center for Comparative Oncology Research.
Mitochondrial stress induces expression of nearly 120 genes involved in cell metabolism.
In earlier studies, Avadhani and colleagues had shown that disrupting mitochondria could lead to tumour growth. Mitochondria are often referred to as the “powerhouses” of cells because they produce ATP, the molecular energy currency that cells utilize to perform their diverse functions. In related work, the researchers had also observed that subjecting mitochondria to stress also triggered an increase in p53 but, until now, hadn’t conducted follow-up on that finding.
Because p53 is mutated in nearly 50 percent of human cancers, it is widely believed to have a tumour-suppressor function. The researchers decided to take a more detailed look into the connection between mitochondrial stress and p53.
They experimentally depleted mitochondrial DNA to induce mitochondrial stress in six cell lines, including several cancer cell lines, and found that p53 levels increased in response to the mtDNA depletion in each type of cell. Because HIF-1α activity is known to play both complementary and contradictory roles in cancer to p53, they next looked to see how that protein responded. They found that p53 inhibited HIF-1α activity.
Looking specifically at a human colon cancer cell line in which p53 was experimentally deleted, they again found a relationship with HIF-1α: Its activity was six-times higher in the colon cancer cell line with p53 depleted than in the wild type colon cancer cell line, a further indication that p53 inhibits HIF-1α.
To ensure that this was not strictly associated with depletion of mitochondrial DNA, the researchers induced mitochondrial stress using other means, including with chemicals agents and by disrupting the membrane, and found that all induced p53.
Further investigation revealed that p53 reduced HIF-1α levels in the nucleus and the cytoplasm of cells and that genes responsive to HIF-1α were blunted when mitochondrial DNA was depleted. Notably, they found that the expression of several genes involved with glycolysis, a metabolic process by which cells break down sugar to make energy, jumped dramatically in cells in which mtDNA was depleted. Some of these were the same genes that HIF-1α normally regulates, pointing to mitochondrial stress as a similar but completely separate pathway by which a metabolic shift can occur in cancer cells.
Finally, the team demonstrated that, in cells with depleted mtDNA, p53 physically interferes with HIF-1α by preventing it from binding to gene promoters that it would normally and by promoting ubiquitination of HIF-1α, a process that tags the protein for degradation in the cell.
The findings point to a new direction and possible new targets for preventing the metabolic shift that can foster a supportive environment for cancer growth.
Penn’s School Veterinary Medicine
www.vet.upenn.edu/about/press-room/press-releases/article/penn-team-finds-mitochondrial-stress-induces-cancer-related-metabolic-shifts
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Certain genes, in healthy environments, can lengthen lifespan
, /in E-News /by 3wmediaResearchers at the University at Buffalo Research Institute on Addictions have discovered how a gene in the brain’s dopamine system can play an important role in prolonging lifespan: it must be coupled with a healthy environment that includes exercise.
The study was led by Panayotis (Peter) K. Thanos, senior research scientist at RIA.
Thanos and his team studied the genes in dopamine to assess their impact on lifespan and behaviour in mice. Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centres and helps regulate physical mobility and emotional response.
The researchers found that the dopamine D2 receptor gene (D2R) significantly influences lifespan, body weight and locomotor activity, but only when combined with an enriched environment that included social interaction, sensory and cognitive stimulation and, most critically, exercise.
“The incorporation of exercise is an important component of an enriched environment and its benefits have been shown to be a powerful mediator of brain function and behaviour,” Thanos says.
The mice in the enriched environment lived anywhere from 16 to 22 percent longer than those in a deprived environment, depending on the level of D2R expression.
“These results provide the first evidence of D2R gene-environment interaction playing an important role in longevity and aging,” Thanos says. “The dichotomy over genes versus environment has provided a rigorous and long debate in deciphering individual differences in longevity. In truth, there exists a complex interaction between the two which contribute to the differences.”
Research exploring this genetic-environmental interaction should lead to a better understanding and prediction of the potential benefits of specific environments, such as those including exercise, on longevity and health during aging.
University at Buffalo Research Institute on Addictions www.buffalo.edu/ria/news_events/latest_news.host.html/content/shared/university/news/news-center-releases/2016/04/056.detail.html
Genes that control smooth muscle contraction in digestive system identified
, /in E-News /by 3wmediaResearchers at UMass Medical School have identified a new molecular pathway critical for maintaining the smooth muscle tone that allows the passage of materials through the digestive system. This finding, based on studying calcium ion-controlled pathways in mice, may lead to new treatments for a host of digestive disorders ranging from common gastroesophageal reflux disease (GERD), to swallowing disorders, incontinence and pancreatitis.
“We are excited about the potential to target identified genes to treat disorders such as reflux and incontinence,” said Ronghua ZhuGe, PhD, associate professor of microbiology and physiological systems and a senior author of the study. “Knowing how these muscles stay contracted for such long periods of time will allow us to develop potential new treatments for these diseases. The next step is to see whether this molecular mechanism in mice also operates in humans.”
The human body, and those of other mammals, contains a number of ring-shaped structures made of smooth muscle encircling openings in hollow organs such as the intestines and bladder called sphincters. Smooth muscle is involuntarily controlled, unlike the muscles we use to walk, for example, so that we don’t need to consciously move digested food from stomach to small intestine. Dysfunction in the sphincters, either structurally or functionally, can have severe consequences leading to diseases that impair the ability of the muscle to contract or relax. This can lead to achalasia, which makes it difficult to swallow; gastroesophageal reflux disease (GERD), which allows stomach acid to enter the oesophagus or incontinence of the bowels.
“A healthy sphincter opens transiently but remains closed most of the time, maintaining a basal tone. This basal tone requires constant generation of force produced by the contraction of smooth muscle cells that make up the sphincters,” said Dr. ZhuGe. “However, the genetics governing how the sphincter smooth muscle stays contracted for such long periods of time remains unknown.”
Smooth muscle operates by generating force as the muscle motor protein myosin and actin filaments move past each other. This happens after a molecule called the myosin regulatory light chain (MLC) is turned on through a common molecular transformation called phosphorylation. How much phosphorylation takes place is controlled by the relative amounts of two enzymes; calcium dependent MLC kinase (MLCK), which promotes phosphorylation, and calcium independent MLC phosphatase (MLCP), which reverses phosphorylation. Through this process, contraction and relaxation of the muscle is achieved.
To understand the molecular mechanism responsible for the involuntary and continuous contraction of the sphincter muscle, Dr. ZhuGe and colleagues examined the internal anal sphincter that controls bowel continence in mice. They showed that genetic deletion of the MLCP enzyme in the smooth muscle had no effect on the basal tone of the mouse sphincter, but deletion of MLCK essentially abolishes the basal tone and mice become incontinent as a result.
“Although previous biochemical studies suggested that lower MLCP activity may be related to the basal tone of this sphincter, our genetic study indicates this doesn’t seem to be the case. It turns out MLCK is essential for the tone formation,” said ZhuGe. “This prompted us to look for specific calcium signals that regulate MLCK.”
Co-author Lawrence Lifshitz, PhD, associate professor of molecular medicine, said, “Calcium signalling is our favourite subject. We originally hypothesized that localized releases of calcium inside the cell, near target ion channels, might do the trick, as we knew that such releases can regulate the contraction of smooth muscle in blood vessels and airways.”
But experiments showed that these local calcium releases have no direct role in muscle tone. Instead, three types of ion channels act in concert to generate a rise in cytosolic calcium which eventually results in MLCK activation and muscle tone.
To test this hypothesis, ZhuGe’s group teamed up with Minsheng Zhu, PhD, at Nanjing University in China, to generate a line of mice in which one of these channels could be turned off in smooth muscle only. “These mice were a powerful tool for establishing our hypothesis,” said ZhuGe. “They helped us identify the Tmem16a (also called Ano1) gene as a critical component for basal tone formation and fecal continence. When we were able to turn off the TMEM16A channels in these mice, they lost the majority of the basal tone and became incontinent. ”
UMass Medical School www.umassmed.edu/news/news-archives/2016/04/umms-scientists-identify-genes-that-control-smooth-muscle-contraction-in-digestive-system/
New genetic risk factors for myopia discovered
, /in E-News /by 3wmediaMyopia, also known as short-sightedness or near-sightedness, is the most common disorder affecting the eyesight and it is on the increase. The causes are both genetic and environmental. The Consortium for Refractive Error and Myopia (CREAM) has now made important progress towards understanding the mechanisms behind the development of the condition. This international group of researchers includes scientists involved in the Gutenberg Health Study of the University Medical Center of Johannes Gutenberg University Mainz (JGU). The team has uncovered nine new genetic risk factors which work together with education-related behaviour as the most important environmental factor causing myopia to generate the disorder. The results of the study ‘Genome-wide joint meta-analyses of genetic main effects and interaction with education level identify additional loci for refractive error: The CREAM Consortium’ have recently been published in the scientific journal Nature Communications.
There has been a massive rise in the prevalence of short-sightedness across the globe in recent decades and this upwards trend is continuing. It is known from previous studies of twins and families that the risk of acquiring short-sightedness is determined to a large extent by heredity. However, the myopia-causing genes that had been previously identified do not alone sufficiently explain the extent to which the condition is inherited. In addition to the genetic causes of myopia there are also environmental factors, the most significant of which are education-related behaviour patterns. “We know from the Gutenberg Health Study conducted at Mainz that the number of years of education increases the risk of developing myopia,’ said Professor Norbert Pfeiffer, Director of the Department of Ophthalmology at the Mainz University Medical Center.
With the aim of identifying genetic mutations relating to myopia and acquiring better insight into the development of the condition, the international research group CREAM carried out a meta-analysis of data collected from around the world. The data compiled for this analysis originated from more than 50,000 participants who were analysed in 34 studies. The second largest group of participants was formed by the more than 4,500 subjects of the Gutenberg Health Study of the Mainz University Medical Center. ‘In the field of genetic research, international cooperation is of particular importance. This is also borne out by this study, to which we were able to make a valuable contribution in the form of data from our Gutenberg Health Study,’ continued Professor Norbert Pfeiffer. ‘And in view of the fact that a survey undertaken by the European Eye Epidemiology Consortium with the help of the Gutenberg Health Study shows that about one third of the adult population of Europe is short-sighted, it is essential that we learn more about its causes in order to come up with possible approaches for future treatments.’
Aware that environmental effects and hereditary factors reinforce one another in the development of myopia, the scientists devised a novel research concept for their investigations. They used a statistical analysis technique that takes into account both the effects of the environmental and hereditary factors and does so in equal measure and simultaneously. Their efforts were crowned with success as they were able to classify nine previously unknown genetic risk factors.
Risk-associated gene involved in the development of short-sightedness
These newly discovered genetic variants are associated with proteins which perform important functions when it comes to the transmission of signals in the eye. One of these genes is of particular interest because it plays a major role in the transmission of the neurotransmitter gamma-aminobutyric acid (GABA) in the eye. Previous studies have shown that there is greater activation of the gene in question in eyes that are myopic. The results of current research substantiate this conclusion. The CREAM researchers interpret this as evidence that this newly discovered risk-related gene is actually involved in the development of short-sightedness. This represents significant initial headway towards understanding how genetic causes interact with the level of education as an environmental factor to produce the heterogeneity of myopia. Further research will be needed to clarify the details of how the mechanisms actually work and interact with one another.
The spread of short-sightedness is a worldwide phenomenon. Particularly in South East Asia the incidence of myopia in school children has increased notably over the last decades. This is likely due to an improvement in educational attainment. People who read a great deal also perform a lot of close-up work, usually in poor levels of daylight. The eye adjusts to these visual habits and the eyeball becomes more elongated than normal as a result. But if it becomes too elongated, the cornea and lens focus the image just in front of the retina instead of on it so that distant objects appear blurry. The individual in question is then short-sighted.
Johannes Gutenberg University Mainz
www.uni-mainz.de/presse/20232_ENG_HTML.php
Abbott demonstrates next-generation molecular diagnostics prototype
, /in E-News /by 3wmediaAbbott demonstrated a prototype of the company’s next-generation molecular diagnostics platform at a recent scientific event hosted for its customers from across the globe. At the event, molecular laboratory directors and researchers had hands-on interaction with the prototype and were able to provide additional feedback on the system prior to further stages of development.
Abbott’s new system is currently being designed from the ground up based on extensive input from laboratory customers. For example, health systems around the world are often challenged with higher testing volumes with staffing and budget constraints, including in the molecular laboratories.
“Our molecular lab customers tell us they are facing pressures to do more with less,” said John Carrino, divisional vice president, research and development, Molecular Diagnostics, Abbott. “Abbott’s next-generation molecular system is being designed to have a faster turnaround time, greater flexibility to run any test at any time, an ability to run higher volumes and automation to increase lab efficiency – all without compromising the testing performance and quality for which our organization is highly regarded.”
Additionally, customer insights suggest a need for a broad testing menu in the molecular lab. Abbott currently offers one of the broadest molecular testing menus for infectious diseases such as HIV, hepatitis and tuberculosis, as well as sexually transmitted infections such as human papillomavirus (HPV), chlamydia and gonorrhea, among others tests.
“Abbott’s molecular diagnostics can provide the information needed to help guide some of life’s most important health decisions,” said Andrea Wainer, president, Molecular Diagnostics, Abbott. “Our accurate, reliable and quality tests could allow clinicians to make more informed treatment decisions to help improve patient care.” In addition to the new molecular system, Abbott will be launching next-generation systems in blood screening, immunoassay, clinical chemistry, hematology and point of care testing in the near future. All of the systems will be built on the same software and hardware platforms to enable more automation and to simplify the user experience for Abbott’s customers.
www.abbottmolecular.comClinical application handbook
, /in E-News /by 3wmediaShimadzu has released the first Application Handbook “Clinical”. It contains most advanced technologies and solutions such as chromatography, mass spectrometry, spectroscopy and life sciences instruments. With nearly 140 pages, the Application Handbook “Clinical” covers 47 real life applications related to hot subjects such as Vitamin D, steroids, immunosuppressants, catecholamines and amino acids analysis. The book is free of charge and can be downloaded (17 MB) at www.shimadzu. eu/clinical.
In clinical applications, analytical instruments unfold a multitude of benefits. They support the quality of human life. The concentration of medications in Therapeutic Drug Monitoring (TDM) is assured, even though this may change according to age and health conditions and is dependent on gender, genetic constitution or interferences with other drugs. They help to save lives, particularly when it comes to time-critical situations, e.g. through acute intoxication, medical or drug abuse. They analyse over- and undersupply of vitamins, minerals and trace elements. They are applied in genomics, proteomics and metabolomics and also uncover fraud in sports, particularly in animal or human doping. At the same time, analytical systems support health protection of animals and humans, even in the long-term. Clinical applications benefit from Shimadzu’s complete portfolio covering chromatography and mass spectrometry (GC, GC-MS, GC-MS/MS, HPLC, UHPLC, LC-MS, LC-MS/MS); spectroscopy (UVVis, FTIR, AAS, EDX, ICP-OES); life sciences (MALDI-(TOF)-MS); microchip- electrophoresis; biopharmaceutical (aggregate sizer); observation of medical microbubbles in targeted drug delivery using the HPV-X2 ultra high-speed camera.
Shimadzu breaks new grounds by rethinking the use of mature technologies to develop new unique systems such as the iMScope TRIO. It combines an optical microscope with a mass spectrometer for insights on the molecular level.
For next-generation brain science, Shimadzu provides LABNIRS, an imaging technology for visualization of brain functions by functional near-infrared spectroscopy (fNIRS).
Some analytical technologies used in the clinical world
- Chromatographic separation in gas phase for analysis of volatile and semi volatile components is in use in the clinical field since many years. Gas chromatography is a key technique for quantitative analysis of alcohol in blood.
- HPLC and UHPLC systems are able to quantitatively analyse substances in blood, serum, plasma and urine containing multiple compounds by separating and detecting target substances. Shimadzu offers a wide variety of application- specific systems such as automated sample pretreatment systems for amino acid analysis or on-line sample trapping for quantification of drugs or metabolites.
- Gas chromatography-mass spectrometry (GC-MS) is a hyphenated technique combining the separating power of GC with the detection power of MS to identify different substances within a sample. Mass spectrometry is a wide-ranging analytical technique which involves the production, subsequent separation and identification of charged species according to their mass to charge (m/z) ratio. It is well known for analysis of drug abuse.
- Liquid chromatography-mass spectrometry (LC-MS) is an analytical chemistry technique that combines the physical separation capabilities of LC with the mass analysis capabilities of MS, bringing together very high sensitivity and high selectivity. Its application is oriented towards the separation, general detection and potential identification of compounds of particular masses in the presence of other chemicals (e.g. complex mixtures like blood, serum, plasma or urine). Its use is spreading in the clinical field (research and routine) as a replacement of immunoassays thanks to the capability of multiplexing analysis and reduced risk of cross-reaction in immuno-assays.
www.shimadzu.eu/clinicalSysmex and Siemens extend long-standing global partnership in hemostasis testing
, /in E-News /by 3wmediaSysmex Corporation and Siemens Healthcare Laboratory Diagnostics announced on April 13, 2016 an extension to their long-standing partnership through at least 2020. The contract extension adds a minimum of two additional years to the global supply, distributorship, and sales and service agreement for hemostasis products. The partnership enables laboratory customers around the world to continue to benefit from the largest portfolio of hemostasis systems and reagents. The companies, which began collaborating more than 20 years ago, also agreed to continue joint hemostasis product development activities that will streamline and optimize testing in laboratories throughout the world.
Siemens Healthcare and Sysmex provide hemostasis products used to test for blood clotting disorders, preoperative bleeding risk management, and the monitoring of patients on anticoagulant therapy medications. In the past few years alone, the companies have introduced several cutting-edge INNOVANCE reagents and multiple new platforms for various laboratory settings, including the recent worldwide launch of the Sysmex CS-2500 System, and the U.S. launch of the Sysmex CS-5100 System with optional track-based automation.
“We are pleased to extend our longstanding partnership with Siemens Healthcare,” said Hisashi Ietsugu, Chairman and CEO, Sysmex Corporation. “With the aging population, hemostasis testing has become even more important. Our partnership provides our customers with the innovative technologies needed to manage the increase in testing volumes, while providing accurate results for improved patient care.”
“The continued collaboration and twenty-year partnership between Siemens and Sysmex is rare in the rapidly changing world of diagnostics,” said Franz Walt, President, Siemens Healthcare Laboratory Diagnostics. “As a leader in hemostasis testing, our combined mission to offer best-in-class solutions has enabled us to meet the needs of diverse laboratories throughout the world.”
www.siemens.comGeT online – the new microsite from Greiner Bio-One
, /in E-News /by 3wmediaUnder the banner “GeT Perfect”, Greiner Bio-One has kicked off the European promotion of the Greiner eHealth Technologies Solution – GeT. For this purpose, a modern microsite in German and English has been created. The one page site provides all essential information at a glance. GeT utilizes a flexible modular based software solution whilst applying the advantages of pre-barcoded VACUETTE tubes. The aim is to increase the efficiency of routine procedures in and around the laboratory. This page provides information on events, reference customers as well as study material. Testimonials from reference customers report on their experiences. Advantages of the system and working procedures can be seen in the form of videos and animation. All in all, the user has here a compact version of all initial information required for initiating any further steps.
www.gbo.com/getSiemens Healthcare becomes Siemens Healthineers
, /in E-News /by 3wmediaIn early May Siemens Healthcare unveiled its new brand name Siemens Healthineers. The new brand underlines Siemens Healthcare’s pioneering spirit and its engineering expertise in the healthcare industry. It is meant to describe the healthcare organization and its people – the people accompanying, serving and inspiring customers – the people behind outstanding products and solutions. As part of its Vision 2020 strategy Siemens AG announced nearly two years ago that its healthcare business would be separately managed as a company within the company with a new organizational setup. Siemens Healthineers will continue to strengthen its leading portfolio across the medical imaging and laboratory diagnostics business while adding new offerings such as managed services, consulting and digital services as well as further technologies in the growing market for therapeutic and molecular diagnostics.
www.healthcare.siemens.comPancreatic cancer risk tied to specific mouth bacteria
, /in E-News /by 3wmediaThe presence of certain bacteria in the mouth may reveal increased risk for pancreatic cancer and enable earlier, more precise treatment. This is the main finding of a study led by researchers at NYU Langone’s Laura and Isaac Perlmutter Cancer Center.
Pancreatic cancer patients are known to be susceptible to gum disease, cavities, and poor oral health in general, say the study authors. That vulnerability led the research team to search for direct links between the makeup of bacteria driving oral disease and subsequent development of pancreatic cancer, a disease that often escapes early diagnosis and causes 40,000 U.S. deaths annually.
“Our study offers the first direct evidence that specific changes in the microbial mix in the mouth—the oral microbiome—represent a likely risk factor for pancreatic cancer along with older age, male gender, smoking, African-American race, and a family history of the disease,” says senior investigator and epidemiologist Jiyoung Ahn, PhD.
Specifically, researchers found that men and women whose oral microbiomes included Porphyromonas gingivalis had an overall 59 percent greater risk of developing pancreatic cancer than those whose microbiomes did not contain the bacterium. Similarly, oral microbiomes containing Aggregatibacter actinomycetemcomitans were at least 50 percent more likely overall to develop the disease. Doctoral student and lead investigator Xiaozhou Fan, MS, says both types of bacteria have been tied in the past to periodontitis, a disease characterized by inflammation of the gums.
“These bacterial changes in the mouth could potentially show us who is most at risk of developing pancreatic cancer,” adds Ahn, an associate professor at NYU Langone and associate director of population sciences at the Perlmutter Cancer Center.
In another study, Ahn and her colleagues showed that cigarette smoking was linked to dramatic, although reversible, changes in the amount and mix of bacteria in the oral microbiome. But she cautions that further research is needed to determine if there is any cause-and-effect relationship, or how or whether such smoking-related changes alter the immune system or otherwise trigger cancer-causing activities in the pancreas.
Laura and Isaac Perlmutter Cancer Center nyulangone.org/press-releases/pancreatic-cancer-risk-tied-to-specific-mouth-bacteria
Mitochondrial stress induces cancer-related metabolic shifts
, /in E-News /by 3wmediaCancerous tumours must be fed. Their unregulated growth requires a steady stream of blood flow and nutrients. Thus, one way that researchers have tried to wipe out cancer is to target cells undergoing the metabolic shifts that enable a tumour’s rapid growth.
Yet new findings from University of Pennsylvania researchers suggest that such efforts might have missed a key pathway that enables the changes in metabolism that benefit tumours. Their work finds that mitochondrial stress alone can trigger metabolic shifts through a pathway that involves p53, a protein widely known to play multiple important roles in cancer.
“In all five cancer cell lines we looked at, we saw that p53 was induced when mitochondrial function was affected,” said senior author Narayan Avadhani, the Harriet Ellison Woodward Professor of Biochemistry in Penn’s School of Veterinary Medicine’s Department of Biomedical Sciences. “This led to our discovery that it’s possible to promote tumour growth independent of the HIF-1α pathway, which had up to this point been a prime target of therapeutic interventions.”
The study points to a new factor that could inform our understanding of how cancer progresses. It’s possible that markers of metabolic stress could even serve as a biomarker for a cancer’s aggressiveness or likelihood to spread.
Avadhani teamed with Penn Vet’s Anindya Roy Chowdhury, the lead author and a research associate, and Serge Y. Fuchs, professor of cell biology, as well as Ph.D. student Apple Long and Anil Rustgi, the T. Grier Miller Professor of Gastroenterology, both of Penn’s Perelman School of Medicine. Avadhani and Fuchs are also members of Penn Vet’s Mari Lowe Center for Comparative Oncology Research.
Mitochondrial stress induces expression of nearly 120 genes involved in cell metabolism.
In earlier studies, Avadhani and colleagues had shown that disrupting mitochondria could lead to tumour growth. Mitochondria are often referred to as the “powerhouses” of cells because they produce ATP, the molecular energy currency that cells utilize to perform their diverse functions. In related work, the researchers had also observed that subjecting mitochondria to stress also triggered an increase in p53 but, until now, hadn’t conducted follow-up on that finding.
Because p53 is mutated in nearly 50 percent of human cancers, it is widely believed to have a tumour-suppressor function. The researchers decided to take a more detailed look into the connection between mitochondrial stress and p53.
They experimentally depleted mitochondrial DNA to induce mitochondrial stress in six cell lines, including several cancer cell lines, and found that p53 levels increased in response to the mtDNA depletion in each type of cell. Because HIF-1α activity is known to play both complementary and contradictory roles in cancer to p53, they next looked to see how that protein responded. They found that p53 inhibited HIF-1α activity.
Looking specifically at a human colon cancer cell line in which p53 was experimentally deleted, they again found a relationship with HIF-1α: Its activity was six-times higher in the colon cancer cell line with p53 depleted than in the wild type colon cancer cell line, a further indication that p53 inhibits HIF-1α.
To ensure that this was not strictly associated with depletion of mitochondrial DNA, the researchers induced mitochondrial stress using other means, including with chemicals agents and by disrupting the membrane, and found that all induced p53.
Further investigation revealed that p53 reduced HIF-1α levels in the nucleus and the cytoplasm of cells and that genes responsive to HIF-1α were blunted when mitochondrial DNA was depleted. Notably, they found that the expression of several genes involved with glycolysis, a metabolic process by which cells break down sugar to make energy, jumped dramatically in cells in which mtDNA was depleted. Some of these were the same genes that HIF-1α normally regulates, pointing to mitochondrial stress as a similar but completely separate pathway by which a metabolic shift can occur in cancer cells.
Finally, the team demonstrated that, in cells with depleted mtDNA, p53 physically interferes with HIF-1α by preventing it from binding to gene promoters that it would normally and by promoting ubiquitination of HIF-1α, a process that tags the protein for degradation in the cell.
The findings point to a new direction and possible new targets for preventing the metabolic shift that can foster a supportive environment for cancer growth.
Penn’s School Veterinary Medicine www.vet.upenn.edu/about/press-room/press-releases/article/penn-team-finds-mitochondrial-stress-induces-cancer-related-metabolic-shifts