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Archive for category: E-News

E-News

Siemens Healthineers to acquire Epocal from Alere to complete its blood gas portfolio

, 26 August 2020/in E-News /by 3wmedia

Siemens Healthineers has entered into a definitive agreement to acquire Epocal Inc., a subsidiary of Alere Inc. Epocal Inc. develops and provides point-of-care blood diagnostic systems for healthcare enterprises, including the epoc Blood Analysis System, a handheld, wireless testing solution. Financial details of the transaction are not being disclosed. The transaction is subject to the completion of Abbott’s acquisition of Alere, as well as antitrust approvals and other customary closing conditions.
“We want to help our customers innovate care delivery. As one of the market leaders in blood gas, the acquisition of the epoc product line will enable us to provide the right solution in the right setting, all from one partner,” said Peter Koerte, President, Point of Care Diagnostics, Siemens Healthineers. “The epoc product line will seamlessly integrate with our digital ecosystem offering customers the broadest solution available in the market. The acquisition complements our existing offerings in the point of care diagnostics space, with a view to provide customers globally with a full range of blood gas solutions.”
Healthcare systems continue to look for ways to elevate patient experience and satisfaction as well as the quality of care. It is a strategic goal of Siemens Healthineers to support healthcare providers worldwide to meet their challenges and excel in their respective environments. Health networks may have varying testing needs near to their patients at the point of care in physician’s offices, clinics, emergency departments and labs. With a complete offering for blood gas diagnostics from a low-volume, single-use handheld device up to a high-volume, multi-use benchtop solution, Siemens Healthineers can help customers improve their workflows and utilize the correct system for the needs of their particular settings.
Arterial blood gases are an important routine investigation to monitor the acid-base balance of patients. They play an important role in the work-up and management of critically ill patients and may help in diagnosing pulmonary and metabolic disorders. They indicate the severity of a condition and help to assess treatment. Blood gas test systems are an important component in critical care settings such as hospitals, clinics, emergency departments and pulmonary laboratories.
The epoc Blood Analysis System is a handheld, wireless testing solution that provides blood gas, electrolyte and metabolite results near the patient in approximately 30 seconds after sample introduction. The epoc Blood Analysis System is comprised of the epoc room-temperature stable BGEM test card, epoc reader and epoc host2 mobile computer. Each single-use epoc BGEM test card features smartcard technology with a full menu of tests on one card.
www.siemens.com/healthineers

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New biomarker assay detects neuroblastoma with greater sensitivity

, 26 August 2020/in E-News /by 3wmedia

Investigators at The Saban Research Institute of Children’s Hospital Los Angeles have developed and tested a new biomarker assay for quantifying disease and detecting the presence of neuroblastoma even when standard evaluations yield negative results for the disease.  In a study, led by Araz Marachelian, MD, of the Children’s Center for Cancer and Blood Diseases, researchers provide the first systematic comparison of standard imaging evaluations versus the new assay that screens for five different neuroblastoma-associated genes and determine that the new assay improves disease assessment and provides prediction of disease progression. 
Neuroblastoma is a cancer of the nervous system that exists outside the brain and typically is diagnosed in children 5 years or age or younger. Forty-five percent of patients have high-risk, metastatic tumours (stage 4) when diagnosed.
While children with neuroblastoma often respond to therapy and many are declared to be in a “remission” based on standard tests, many will still relapse. “Clearly, there is some remaining tumour in the body that we cannot detect with standard tests and physicians have a hard time predicting if a patient is likely to relapse,” said Marachelian, who is medical director of the New Approaches to Neuroblastoma (NANT) consortium, headquartered at CHLA.
The new assay, which was developed in the laboratories of Robert Seeger, MD, and Shahab Asgharzadeh, MD, at CHLA, tests for five different genes that are specific to neuroblastoma. The test evolved to address the need for a better way to quantify the disease and fully understand its impact on the patient. Previously, assays used for detecting disease screened for only one NB-associated gene at a time, which was less effective. Instead of running five different tests, the research team figured out a way to test for multiple neuroblastoma-associated genes, simultaneously, using a different technology platform. This test can quantify infinitesimal amounts of tumour, akin to finding “a needle in a haystack”.
According to Marachelian, in a population of patients with relapsed or refractory neuroblastoma, it is important to understand if the therapeutics given to patients are working. But standard clinical evaluations such as scans (CT, MRI and MIBG) and bone marrow evaluation can be limited in their ability to do this because of variability and an inability to indicate severity of disease or how aggressive the treatment should be.
“With imaging scans, disease that is starting to grow versus disease that is getting better can look very similar when you first look,” explained Marachelian, who is also an assistant professor of Clinical Pediatrics at the Keck School of Medicine of the University of Southern California. “This assay could have the potential to be like an advance warning system – we can see if things are getting worse and be poised to take action. Alternately, if we see things are getting better or the disease is no longer detectable even with this very sensitive test, we can decrease the treatment to protect the patient from unnecessary exposure to toxicity and side effects.”

Children’s Hospital Los Angeles
www.chla.org/press-release/finding-needle-haystack-new-biomarker-assay-detects-neuroblastoma-greater-sensitivity

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Researchers validate a clinical test for fusion genes

, 26 August 2020/in E-News /by 3wmedia

An assay that identifies a peculiar but important abnormality in cancer cells has been developed and validated by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James).
The assay, called OSU-SpARKFuse (Ohio State University-Spanning Actionable RNA Kinase Fusions), detects a genetic change called gene fusions in solid tumours.
Gene fusions happen when parts of two different genes join together. Gene fusions can happen, for example, when a piece of one chromosome becomes attached to another. Such chromosome “translocations” can join two genes that together become a major driver of cancer-cell and tumour growth.
Targeted therapies are becoming increasingly available that block the activity of fusion genes, particular those involving kinase genes. Whereas current assays for detecting gene fusions require previous knowledge of both genes involved in the fusion, OSU-SpARKFuse was designed to accurately detect fusions when only one of the genes is known, which allows for the discovery of novel gene fusions.
“We designed OSU-SpARKFuse to meet these needs and to identify patients who are eligible for novel therapies such as FGFR inhibitors or NTRK inhibitors that target gene fusions,” says principal investigator Sameek Roychowdhury, MD, PhD, assistant professor in the Division of Medical Oncology at Ohio State.
“Along with detecting gene fusions, OSU-SpARKFuse can provide gene-expression analysis, detect single-nucleotide changes and identify alternative splicing events and resistance genes,” says first author Julie Reeser, PhD, technical supervisor of the OSUCCC – James Cancer Genomics Laboratory.
“Additionally, OSU-SpARKFuse does not require information regarding the location of the fusion in each gene. It is an accurate, reproducible, cost-effective assay that detects gene fusions across many genes and from the small samples of tumour tissue obtained by biopsy,” Reeser adds.
The Ohio State University Comprehensive Cancer Centerhttp://tinyurl.com/yczce7e2

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Cause for male infertility discovered

, 26 August 2020/in E-News /by 3wmedia

Researchers at Ben-Gurion University of the Negev and Soroka University Medical Center in Beer-Sheva, Israel have discovered a new genetic mutation that prevents sperm production.
Five percent of men suffer from infertility and approximately one percent suffer from azoospermia, a condition in which sperm cells are completely absent.
For the first time, the researchers identified a mutation in the gene TDRD9 using whole genome genotyping and sequencing.
The findings were possible only because five men from a single Bedouin family suffered from lack of sperm and spermatogenic arrest in their testis with no obvious cause. The men were being treated by Dr. Eitan Lunenfeld and his team at Soroka’s In Vitro Fertilization Unit.
Profs. Ruti Parvari and Mahmoud Huleihel of the Shraga Segal Department of Microbiology, Immunology and Genetics discovered the mutation in the gene, which normally protects the full DNA sequence in sperm. This mutation inactivates the function of the gene and arrests sperm production.
“With the link between this damaged gene and male infertility now identified, specific scans will be available to test for the mutation that will be important for treatment of a couple’s infertility,” the researchers say.

American Associates, Ben-Gurion University of the Negev (AABGU)
aabgu.org/cause-male-infertility-discovered/

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Siemens employees as finalists for the 2017 European Inventor Award

, 26 August 2020/in E-News /by 3wmedia

The European Patent Office has announced Dutch product manager Jan van den Boogaart (57) and Austrian researcher Prof. Dr. Oliver Hayden (45) as finalists for the 2017 Inventor Award in the “Industry” category. The two Siemens Healthineers employees have invented an automated method for detecting the life-threatening disease malaria. On the basis of their own research, they jointly developed a method for the Siemens Healthineers Advia 2120i hematology systembased on a combination of parameters that define whether a patient has  malaria. With this method, the Advia 2120i hematology system can run malaria tests automatically as part of a full blood panel. The great advantage is the high throughput at lower cost than with other methods, such as microscopic examination.
Until now, the most reliable method has been a microscopic examination of the blood for plasmodia, which calls for experienced, trained personnel, as recognizing plasmodia under the microscope is not easy. The process is also very time-consuming. In recent years, malaria has also been diagnosed more and more with fast tests: a test strip that detects parasite-specific antigens. But if used improperly, that test is unreliable, and it’s also expensive. www.siemens.com/press/PR2017040278HCENwww.epo.org/news-issues/press.html

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”Superior vena cava (or SVC) – derived atrial fibrillation attributes to both clinical and genetic factors”

, 26 August 2020/in E-News /by 3wmedia

Normally, the heart contracts and relaxes to a regular beat. In atrial fibrillation, the upper chambers of the heart beat irregularly, which affects blood flow into the two lower large chambers. This can lead to stroke, heart failure and other heart-related complications.
Atrial fibrillation triggers were first identified in the pulmonary veins. Hence, the isolation of these veins has become one of the standard treatments for atrial fibrillation. Subsequently, other sites in the heart have been found to trigger and/or drive atrial fibrillation, including the superior vena cava (SVC). Notably, patients with arrhythmogenic SVC have long myocardial sleeves (circularly and longitudinally oriented bundles of heart cells) around the SVC and high amplitude electrical potentials within them.
Although these anatomical features in arrhythmogenic SVC all point to the possibility of genetic factors being involved in atrial fibrillation, this topic has remained largely unstudied. Furthermore, findings of genetic studies previously conducted in people of European ancestry could not be generalized and transferred to those of Asian ancestry.
This critical knowledge gap drove a team of researchers from Tokyo Medical and Dental University(TMDU) in Japan to study the clinical and genetic factors associated with atrial fibrillation in an Asian population. The team discovered two variants of single-nucleotide polymorphism (SNP), a variation in a single nucleotide that occurs at a specific position in the genome, which were significantly associated with SVC arrhythmogenicity.
“We found that among six variants identified in a previous genome-wide association study in Japanese patients, SNPs rs2634073 and rs6584555 were associated with SVC arrhythmogenicity,” said Yusuke Ebana, first author of the study.
“We also determined that SVC arrhythmogenicity was conditionally dependent on age, body mass index, and left ventricular ejection fraction,” Ebana added.
To arrive at that conclusion, the research team conducted a meta-analysis of clinical and genetic factors of 2,170 atrial fibrillation patients with and without SVC arrhythmogenicity across three major hospitals in Japan. Surface electrocardiogram and bipolar intracardiac electrograms were continuously monitored. Additionally, a mapping catheter was placed in the SVC to map the circumferential SVC region using computed tomography (CT) or transesophageal echocardiography as a reference. All the patients were followed-up at least every three months.
“The genes closest to the two SVC variants we found were PITX2 and NEURL1, with the former reported as a left-right determinant in cardiac development,” said Tetsushi Furukawa, senior author of the study. “We speculate that the suppression of NEURL1 in SVC patients with the risk genotype could be the cause of arrhythmogenic SVC leading to atrial fibrillation,” Furukawa added.

Tokyo Medical and Dental University (TMDU)
www.tmd.ac.jp/english/press-release/20171018/index.html

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Biomarkers associated with chronic fatigue syndrome severity

, 26 August 2020/in E-News /by 3wmedia

Researchers at the Stanford University School of Medicine have linked chronic fatigue syndrome to variations in 17 immune-system signalling proteins, or cytokines, whose concentrations in the blood correlate with the disease’s severity.
The findings provide evidence that inflammation is a powerful driver of this mysterious condition, whose underpinnings have eluded researchers for 35 years.
“Chronic fatigue syndrome can turn a life of productive activity into one of dependency and desolation,” said Jose Montoya, MD, professor of infectious diseases, who is the study’s lead author. Some spontaneous recoveries occur during the first year, he said, but rarely after the condition has persisted more than five years.
The study’s senior author is Mark Davis, PhD, professor of immunology and microbiology and director of Stanford’s Institute for Immunity, Transplantation and Infection.
“There’s been a great deal of controversy and confusion surrounding myalgic encephalomyelitis (ME) CFS — even whether it is an actual disease,” said Davis. “Our findings show clearly that it’s an inflammatory disease and provide a solid basis for a diagnostic blood test.”
Many, but not all, ME/CFS patients experience flulike symptoms common in inflammation-driven diseases, Montoya said. But because its symptoms are so diffuse —sometimes manifesting as heart problems, sometimes as mental impairment nicknamed “brain fog,” other times as indigestion, diarrhea, constipation, muscle pain, tender lymph nodes and so forth — it often goes undiagnosed, even among patients who’ve visited a half-dozen or more different specialists in an effort to determine what’s wrong with them.
The sporadic effectiveness of antiviral and anti-inflammatory drugs has spurred Montoya to undertake a systematic study to see if the inflammation that’s been a will-o’-the-wisp in those previous searches could be definitively pinned down.
To attack this problem, he called on Davis, who helped create the Human Immune Monitoring Center. Since its inception a decade ago, the centre has served as an engine for large-scale, data-intensive immunological analysis of human blood and tissue samples. Directed by study co-author Holden Maecker, PhD, a professor of microbiology and immunology, the centre is equipped to rapidly assess gene variations and activity levels, frequencies of numerous immune cell types, blood concentrations of scores of immune proteins, activation states of intercellular signalling models, and more on a massive scale.
This approach is akin to being able to look for and find larger patterns — analogous to whole words or sentences — in order to locate a desired paragraph in a lengthy manuscript, rather than just try to locate it by counting the number of times in which the letter A appears in every paragraph.
The scientists analysed blood samples from 192 of Montoya’s patients, as well as from 392 healthy control subjects. The average age of patients and controls was about 50. Patients’ average duration of symptoms was somewhat more than 10 years.
Importantly, the study design took into account patients’ disease severity and duration. The scientists found that some cytokine levels were lower in patients with mild forms of ME/CFS than in the control subjects, but elevated in ME/CFS patients with relatively severe manifestations. Averaging the results for patients versus controls with respect to these measures would have obscured this phenomenon, which Montoya said he thinks may reflect different genetic predispositions, among patients, to progress to mild versus severe disease.
When comparing patients versus control subjects, the researchers found that only two of the 51 cytokines they measured were different. Tumour growth factor beta was higher and resistin was lower in ME/CFS patients. However, the investigators found that the concentrations of 17 of the cytokines tracked disease severity. Thirteen of those 17 cytokines are pro-inflammatory.
TGF-beta is often thought of as an anti-inflammatory rather than a pro-inflammatory cytokine. But it’s known to take on a pro-inflammatory character in some cases, including certain cancers. ME/CFS patients have a higher than normal incidence of lymphoma, and Montoya speculated that TGF-beta’s elevation in ME/CFS patients could turn out to be a link.
One of the cytokines whose levels corresponded to disease severity, leptin, is secreted by fat tissue. Best known as a satiety reporter that tells the brain when somebody’s stomach is full, leptin is also an active pro-inflammatory substance. Generally, leptin is more abundant in women’s blood than in men’s, which could throw light on why more women than men have ME/CFS.

Stanford Medicinehttp://tinyurl.com/y7agngxn

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Glioblastoma ‘ecosystem’ redefined for more effective immunotherapy trials

, 26 August 2020/in E-News /by 3wmedia

A research team has revealed the intrinsic gene expression patterns of glioblastoma (GBM) tumours, insights that could drive more effective treatments for GBM, the most common and deadly malignant primary brain tumours in adults.
Jackson Laboratory (JAX) Professor Roel Verhaak, Ph.D., is the senior author of a paper showing tumour gene expression patterns distinct from those of the surrounding immune cells, and characterizing the effects of chemotherapy and radiation treatments.
Verhaak was the first author of a 2010 paper that established four subclasses of GBM — proneural, mesenchymal, neural and classical — based on molecular markers found in patient tumours. That paper was widely influential in the glioblastoma research field, observes Verhaak. “However, these four subtypes have not translated into differential treatment strategies. Every glioblastoma patient receives essentially the same treatment. We hope that our latest work will improve understanding of how to optimally stratify patients, another step towards precision medicine and more targeted, effective treatments.”
The cells that surround a tumour are known as its microenvironment, usually consisting of immune cells, supporting cells and other normal cells. Tumours donated to tissue banks consist of a mixture of microenvironment cells and cancer cells.
In the new paper, the research team isolated the intrinsic gene expression of 364 GBM tumours and observed the impact of the standard cancer treatment regimens of temozolomide and radiation on that expression after subtracting out the effects of therapy on the tumour-associated non-cancer cells.
“By separating out the contributions of the microenvironment, we developed a much clearer picture of the ‘ecosystem’ of hundreds of tumours,” Verhaak says. “We determined what types of cells are in the microenvironment and what their contributions are, and also assessed how treatment affects the microenvironment as well as the tumour cells themselves.”
Through this approach, the researchers found that the molecular markers defining the neural subtype of GBM was actually ascribed by the presence of normal neural tissue in the tumour margin, thus not representing a true tumour subtype.
By studying gene expression patterns in glioblastomas after treatment, their analysis also revealed that the presence of macrophages correlates with poorer outcomes for GBM patients receiving radiation therapy, and that tumours with a relatively high number of point mutations have an increased number of positive T cells, indicating they could respond to a kind of immunotherapy known as checkpoint inhibitors.
The resulting gene expression datasets, which are publicly available to researchers, provide comprehensive profiles of glioblastoma characteristics to more accurately guide immunotherapy trials.


Jackson Laboratory
www.jax.org/news-and-insights/2017/july/glioblastoma-ecosystem-redefined

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Link between bacterial imbalances and breast cancer

, 26 August 2020/in E-News /by 3wmedia

In a newly published study, Cleveland Clinic researchers have uncovered differences in the bacterial composition of breast tissue of healthy women vs. women with breast cancer. The research team has discovered for the first time that healthy breast tissue contains more of the bacterial species Methylobacterium, a finding which could offer a new perspective in the battle against breast cancer.
Bacteria that live in the body, known as the microbiome, influence many diseases.
Most research has been done on the “gut” microbiome, or bacteria in the digestive tract. Researchers have long suspected that a “microbiome” exists within breast tissue and plays a role in breast cancer but it has not yet been characterized. The research team has taken the first step toward understanding the composition of the bacteria in breast cancer by uncovering distinct microbial differences in healthy and cancerous breast tissue.
“To my knowledge, this is the first study to examine both breast tissue and distant sites of the body for bacterial differences in breast cancer,” said co-senior author Charis Eng, M.D., Ph.D., chair of Cleveland Clinic’s Genomic Medicine Institute and director of the Center for Personalized Genetic Healthcare. “Our hope is to find a biomarker that would help us diagnose breast cancer quickly and easily.  In our wildest dreams, we hope we can use microbiomics right before breast cancer forms and then prevent cancer with probiotics or antibiotics.”
The study examined the tissues of 78 patients who underwent mastectomy for invasive carcinoma or elective cosmetic breast surgery. In addition, they examined oral rinse and urine to determine the bacterial composition of these distant sites in the body.
In addition to the Methylobacterium finding, the team discovered that cancer patients’ urine samples had increased levels of gram-positive bacteria, including Staphylococcus and Actinomyces. Further studies are needed to determine the role these organisms may play in breast cancer.
Co-senior author Stephen Grobymer, M.D., said, “If we can target specific pro-cancer bacteria, we may be able to make the environment less hospitable to cancer and enhance existing treatments. Larger studies are needed but this work is a solid first step in better understanding the significant role of bacterial imbalances in breast cancer.” Dr. Grobmyer is section head of Surgical Oncology and director of Breast Services at Cleveland Clinic.

Cleveland Clinic
newsroom.clevelandclinic.org/2017/10/05/cleveland-clinic-researchers-find-link-between-bacterial-imbalances-and-breast-cancer/

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Make way for haemoglobin

, 26 August 2020/in E-News /by 3wmedia

Every cell in the body, whether skin or muscle or brain, starts out as a generic cell that acquires its unique characteristics after undergoing a process of specialization. Nowhere is this process more dramatic than it is in red blood cells.
In order to make as much room as possible for the oxygen-carrying protein haemoglobin, pretty much everything else inside these precursor red blood cells–nucleus, mitochondria, ribosomes and more–gets purged. Jam-packing red blood cells with haemoglobin is essential. Doing so ensures that all the body’s tissues and organs are well nourished with oxygen to carry on their normal functions.
But how does this cell remodelling take place to begin with?
For more than 20 years, Daniel Finley, professor of cell biology at Harvard Medical School, has been on a quest to unravel the process behind this profound cellular transformation.
Now, thanks to advances in technology and a fortuitous meeting with researchers in a lab at Boston Children’s Hospital, Finley and his collaborators have identified the mechanism behind red blood cell specialization and revealed that it is controlled by an enzyme he first studied in 1995.
During cell specialization, unwanted parts of a generic, immature cell are removed by the proteasome, protein-gobbling strings of molecules, or the cells’ "trash compactors," says study first author Anthony Tuan Nguyen, an HMS MD-PhD student.
The researchers set out to find the mechanism that controls which parts get destroyed and which parts are spared before the precursor red blood cell becomes a full-fledged one.
Finley had a hunch that the process was controlled by an enzyme called UBE2O, which he and colleagues identified in the 1990s. The enzyme marks cell parts for destruction by tagging them with a small protein called ubiquitin. This tagging allows the proteasome to recognize cells destined for destruction. The vast machinery, known as the ubiquitin-proteasome system (UPS), is switched on constantly throughout the body to remove unnecessary proteins and keep cells free of clutter.
Previously, UPS had not been linked to the specialization of red blood cells. However, in his early research on UBE2O, Finley had noticed large amounts of the enzyme present in immature red blood cells. That was a powerful clue. The combination of UBE2O’s pronounced presence and its known function as cellular debris-remover made it a promising candidate for the role of a key regulator of cell specialization. Yet, back when he first came to this realization, Finley had neither the technology nor the funding to analyse red blood cell development at the necessary molecular detail.
"It was the fish that got away," he said.
Twenty years later, the pieces Finley needed to reopen his abandoned investigation fell into place when he met Mark Fleming, HMS professor of pathology at Boston Children’s Hospital. While studying blood cells, Fleming had identified a mutant mouse that lacked the UBE2O enzyme. Knowing that Finley was interested in the enzyme and its possible role in cell specialization, Fleming contacted him.
The researchers observed that mice without the enzyme were anaemic, a marker of red blood cell deficiency. The observation supported the notion that UBE2O may play a role in red blood cell development.
Using a series of tests that relied on large-scale protein analyses not available in earlier decades, the researchers confirmed the enzyme’s role. Their results revealed that immature red blood cells lacking UBE2O retained hundreds of proteins and failed to become specialized.
The researchers also demonstrated that when isolated from immature red blood cells and tested in other cell types, UBE2O still marked the right proteins for destruction, suggesting that the enzyme is the primary regulator of red blood cell specialization.
The researchers have yet to determine whether the mechanism they found in red blood cells controls specialization of other cells as well. Finley says it probably does.
"I think our work calls attention to the complicated processes behind the development of specialized cells, which is seen throughout nature," Finley said.
Because the enzyme plays an important role in the development of red blood cells, the researchers say they hope their work could lead to therapies for certain blood disorders and blood cancers. The present study revealed that, in mice, UBE2O deficiency powerfully suppressed the symptoms of a blood disorder known as beta thalassemia. This aspect of the research is particularly tantalizing to Nguyen, who has a gene mutation linked to the condition.

EurekAlert
www.eurekalert.org/pub_releases/2017-08/hms-mwf081817.php

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