Sentences with phrase «cell disease at»

«Secondary benefits of this trial include the significant improvement in clinical care for children with sickle cell disease at each of the 29 sites because each location had a designated hematologist, neurologist, neuroradiologist and psychologist working as a team to identify and decrease further injury to the brain in this vulnerable population.»

Not exact matches

The companies» R&D will focus on on a gene mutation present in a wide swath of patients with ALS, a degenerative nervous system disease that eats away at nerve cells and weakens muscles.

He conducted his postdoctoral research at Brigham and Women's Hospital / Harvard Medical School, where he researched the role of the Wnt signaling pathway in mouse models of kidney disease, and was part of a team that discovered a stem cell subtype responsible for solid organ fibrosis.

bluebird bio (BLUE)- The company's BCMA CAR - T drug candidate bb2121 remains attractive despite overblown fears on durability (peak sales of $ 2 billion or more), LentiGlobin has a good shot at success in TDT (Transfusion - Dependent ß - Thalassemia) and SCD (Severe Sickle Cell Disease), and they have a strong cash position.

What Stephen Hawking Missed: Small Biotechs Developing Promising Cell Therapies for Devastating Disease Source: Streetwise Reports (5/2/18) In the second of a two - part series exploring the disruptive cell therapy space, Maxim Group analyst Jason McCarthy takes a look at small - cap companies targeting big - ticket indications and their potential to drive blockbuster value for both patients and investCell Therapies for Devastating Disease Source: Streetwise Reports (5/2/18) In the second of a two - part series exploring the disruptive cell therapy space, Maxim Group analyst Jason McCarthy takes a look at small - cap companies targeting big - ticket indications and their potential to drive blockbuster value for both patients and investcell therapy space, Maxim Group analyst Jason McCarthy takes a look at small - cap companies targeting big - ticket indications and their potential to drive blockbuster value for both patients and investors.

Government funding for research into sickle - cell disease is pitifully inadequate (the Sickle - Cell Society receives no government funds at acell disease is pitifully inadequate (the Sickle - Cell Society receives no government funds at aCell Society receives no government funds at all).

The strict definition of celiac disease — positive antibodies to gliadin, intestinal endomysium, and tissue transglutaminase, together with the presence of HLA - DQ2 or HLA - DQ8 genes and an intestinal biopsy that shows at least 20 - 25 CD3 cells per 100 epithelial cells — will account for about 75 - 80 % of all those sensitive to gluten.

It offers cardio protection, it helps lower bad cholesterol, it may help prevent the progression of multiple sclerosis, it has the ability to regenerate brain cells after a stroke, it has the ability to cross the blood - brain barrier to potentially ward off Alzheimer's disease, apparently it's good at wiping amyloid plaque from the brain (which studies haves linked to Alzheimer's), it may help to prevent certain types of cancer, and studies have shown that it inhibits cancer cell growth and metastases (meaning it keeps cancer from spreading).

No observed local immunological response at cell level after five years of oats in adult coeliac disease.

We are the parents of a severely food allergic college age son, Morgan, first diagnosed at the age of 9 months old with life threatening allergies to peanuts, (tree nuts, sesame, fish and shellfish came later); and a grown daughter, Michaela, diagnosed with celiac disease and a mast cell mediated disorder.

Breech Twins and higher order multiples Previous CS Pre-Eclampsia Placenta praevia Cervical incompetence Previous late stillbirth Previous premature birth Grand multiparty Age under 18 Age over 35 Smoking Drug use Severe mental health issue Epilepsy Type 1 diabetes Type 2 diabetes Gestational diabetes Asthma GBS positive Abnormal antibodies Transplant recipient Congenital heart disease Known foetal abnormality Immunosuppressive medication MS Physical disability Intellectual disability Hypothyroidism Hyperthyroidism Previous shoulder dystocia Previous 3rd or 4th degree tear Sickle Cell anaemia BMI under 18 or over 35 at conception Previous massive PPH APH in current pregnancy HIV / AIDS Hepatitis B or C Active TB IUGR Oligohydramnios Polyhydramnios Child previously removed from custody because of abuse Uterine abnormalities such as uterine septum or double uterus Previous uterine surgery for fibroids Chronic renal problems Hypertension Auto immune condition Previous stroke or blod clot Cancer Domestic violence or abusive home Prisoners Homeless women

(borrowed from Dr Kitty) Breech Twins and higher order multiples Previous CS Pre-Eclampsia Placenta praevia Cervical incompetence Previous late stillbirth Previous premature birth Grand multiparty Age under 18 Age over 35 Smoking Drug use Severe mental health issue Epilepsy Type 1 diabetes Type 2 diabetes Gestational diabetes Asthma GBS positive Abnormal antibodies Transplant recipient Congenital heart disease Known foetal abnormality Immunosuppressive medication MS Physical disability Intellectual disability Hypothyroidism Hyperthyroidism Previous shoulder dystocia Previous 3rd or 4th degree tear Sickle Cell anaemia BMI under 18 or over 35 at conception Previous massive PPH APH in current pregnancy HIV / AIDS Hepatitis B or C Active TB IUGR Oligohydramnios Polyhydramnios Child previously removed from custody because of abuse Uterine abnormalities such as uterine septum or double uterus Previous uterine surgery for fibroids Chronic renal problems Hypertension Auto immune condition Previous stroke or blod clot Cancer Domestic violence or abusive home Prisoners Homeless women

For instance, specific anti-T-cell therapies don't work at all for rheumatoid arthritis (RA), and Edwards doesn't think T - cells explained how the disease persisted.

«But in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the human genome at lupus risk variants (and at the variants for other diseases) and that's what we suspect is increasing risk for the disease.»

«In theory, we could model progression of the disease by reprogramming skin cells from patients at a range of ages, including before symptoms begin.

«Our study results are the first to argue that we may be able to treat inflammatory bowel disease and protect against transplant rejection not only by blocking TNF alpha as is done currently, but also by stimulating ATG16L1 to prevent early death of cells lining the gut,» says study senior investigator Ken Cadwell, PhD, an associate professor at NYU School of Medicine and NYU Langone Health's Skirball Institute for Biomolecular Medicine.

McCallion's strategy to make sense of all this data looks at the active genes in cells affected by a disease, groups of genes that interact with one another, their vulnerability to mutation and information from past scientific studies to filter more than a thousand gene candidates for disease risk down to just a handful within any one implicated region.

The long - term persistence of CD8αα + T cells where initial infection occurs may explain why patients have asymptomatic recurrences of genital herpes because these cells constantly recognize and eliminate the virus, according to Jia Zhu, Ph.D., corresponding author, research assistant professor in Laboratory Medicine at the University of Washington and an affiliate investigator in the Fred Hutch Vaccine and Infectious Disease Division.

Human embryonic stem cells are at last being tested in common, potentially fatal diseases such as heart failure and diabetes

At best, the scientists say, there is a 50 - 50 chance that the gene closest to a mutation will even be active in the cell types affected by a disease.

The team also needs to figure out which types of cancer Th17 cells respond to, and at which stage of the disease.

They isolated blood cells from HIV - positive patients on antiretroviral therapy and at different stages of disease progression, as well as cells from non-infected individuals.

In a groundbreaking study that provides scientists with a critical new understanding of stem cell development and its role in disease, UCLA researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research led by Dr. Kathrin Plath, professor of biological chemistry, have established a first - of - its - kind methodology that defines the unique stages by which specialized cells are reprogrammed into stem cells that resemble those found in the embcell development and its role in disease, UCLA researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research led by Dr. Kathrin Plath, professor of biological chemistry, have established a first - of - its - kind methodology that defines the unique stages by which specialized cells are reprogrammed into stem cells that resemble those found in the embCell Research led by Dr. Kathrin Plath, professor of biological chemistry, have established a first - of - its - kind methodology that defines the unique stages by which specialized cells are reprogrammed into stem cells that resemble those found in the embryo.

«This research represents an important step toward the goal of being able to better treat thyroid diseases and being able to permanently rescue thyroid function through the transplantation of a patient's own engineered pluripotent stem cells,» explained co-corresponding author Anthony N. Hollenberg, MD, Chief of the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Professor of Medicine at Harvard Medical School.

A team of researchers at the Stanford University School of Medicine has used a gene - editing tool known as CRISPR to repair the gene that causes sickle cell disease in human stem cells, which they say is a key step toward developing a gene therapy for the disorder.

Since pseudouridine modifications may affect various RNA molecules in different types of normal and malignant cells, «our discoveries pave the way for future avenues of research aimed at exploring the role of pseudouridine in human development disease,» concludes Cristian Bellodi.

Last year Cuervo collaborated with Sheng Zhang, a professor at The University of Texas Health Science Center at Houston on experiments showing that huntingtin — the Huntington's disease protein — helps the cell's autophagy system identify what it should eliminate.

In preclinical studies using cell models that mimicked liver cells of patients with the rare disease Friedreich's ataxia (FA), a widely used cholesterol - lowering drug increased a precursor of HDL (high - density lipoprotein), the «good cholesterol,» according to new research published in PLOS ONE from the Perelman School of Medicine at the University of Pennsylvania.

The idea to specifically study this group of patients was based on groundbreaking research Garon published in the New England Journal of Medicine last year, which found that among patients who received pembrolizumab, those with PD - L1 expression on at least 50 percent of their cancer cells showed the longest survival and disease control.

«We found that a particular vaginal bacterium, Gardnerella vaginalis, did not cause infection during exposure to the urinary tract, but it damaged the cells on the surface of the bladder and caused E. coli from a previous UTI to start multiplying, leading to another bout of disease,» said the study's senior author, Amanda Lewis, PhD, an assistant professor of molecular microbiology and of obstetrics and gynecology at Washington University.

At the same time, researchers have found that much smaller protein clusters called oligomers — made of only a few copies of these proteins — can be highly toxic to motor neuron - like cells grown in the lab and thus are more likely to be the chief causes of brain - cell death in these diseases.

Researchers at Nagoya University have been studying the therapeutic effect of T cells, vital disease - fighting components in our body's immune system, for fighting cancer.

We believe that they will also lead to the development of a whole new range of therapies for neurodegenerative diseases of the central nervous system,» explains corresponding author of the study Jihwan Song, professor and director of Neural Regeneration and Therapy Group at the CHA Stem Cell Institute of CHA University.

Vamsi Mootha, a mitochondrial biologist at Massachusetts General Hospital, his graduate student Isha Jain, and their colleagues used a popular DNA - editing tool called CRISPR to knock out about 18,000 different genes in human cells that were altered to have the same problems as people with mitochondrial diseases.

But their prominence at sites where nerve cells are damaged by the disease means they deserve careful scrutiny in the desperate search for ways to arrest the most salient cause of dementia.

Researchers at the University of Louisville have discovered a mechanism involved in skeletal muscle repair that may enable clinicians to boost the effectiveness of adult stem cell therapies for diseases such as muscular dystrophy.

But a handful of researchers are getting better at deciphering these gaseous clues, bringing us closer to the day when a kind of disease breathalyzer could be part of a routine checkup or maybe even a cell phone app.

«This is the first demonstration that cells carrying a genetic disease are capable of spreading into the normal mammalian brain and lead to the manifestation of behavioral abnormalities associated with the disease,» says Francesca Cicchetti, professor at the Université Laval Faculty of Medecine and researcher at Centre de recherche du CHU de Québec - Université Laval.

Comparing his study to Surmeier's, Redmond noted: «One is an approach to try to minimize disease progression or maybe even get some recovery, the other is more aimed at the other end, after (dopamine - producing] cells are already dead.»

Mice transplanted with cells grown from a patient suffering from Huntington's disease (HD) develop the clinical features and brain pathology of that patient, suggests a study published in the latest issue of Acta Neuropathologica by CHA University in Korea, in collaboration with researchers at Université Laval in Québec City, Canada.

Previous research conducted at Mount Sinai found that the trafficking of protein molecules between the nucleus (the cellular compartment containing the genetic information of the cell) and the cytoplasm is altered in neurodegenerative disease.

In research that has implications for diabetes and other metabolic diseases, an international study based at UT Southwestern Medical Center found that the protein connexin 43 (Cx43) forms cell - to - cell communication channels on the surface of emerging beige fat cells that amplify the signals from those few nerve fibers.

«The compounds identified in this study, when administered orally, both reduced the inflammation that is a hallmark of multiple sclerosis and protected against the nerve cell damage seen in mouse models of the disease,» said Jeffery Haines, PhD, a post-doctoral fellow at Mount Sinai and the study's lead author.

Researchers from Howard University will present their findings today at the American Physiological Society's Physiological and Pathophysiological Consequences of Sickle Cell Disease conference in Washington, D.C.

«Our study reveals a new mechanism that could be harnessed for biological therapies for lupus and other autoimmune diseases, where the immune system mistakenly targets the body's own cells,» says senior study author Boris Reizis, PhD, professor of Pathology and Medicine at NYU Langone.

At first it was thought that only functioned as cellular debris warehouses but in recent years has been that could have an important role as a messenger between cells of the body and now many groups focus their research on the role that could be played exosomes in various diseases, including cancer.

«By learning how tau spreads, we may be able to stop it from jumping from neuron to neuron,» said Karen Duff, PhD, professor in the department of pathology and cell biology (in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) and professor of psychiatry (at New York State Psychiatric Institute.)

A comparison of these two cancers, published April 9 in the journal Cancer Cell, suggests that they are similar in origin, leading researchers at the University of Cambridge to believe that devils simply may be at greater risk for these kinds of diseases.

Gene Yeo, a professor of cellular and molecular medicine at UCSD, led the research and showed he could target RNA in living cells, a first step toward treating diseases like muscular dystrophy and neurodegeneration.

After an earlier stint as a senior writer at Science, where she was widely known for her coverage of the Human Genome Project, Leslie returned as a deputy news editor in 2000, specializing in public health, infectious diseases, stem cells, and ecology.