Not exact matches
THE ELUSIVE LIQUID BIOPSY Intervention Track Ballroom C1 Every
protein fragment, every strand of microRNA, every sentence and mis - sentence of DNA, every immune system marker, every signature of
disease in the
human being.
In reality, the amount of
protein associated with optimal
human health, as supported by science and epidemiology (the incidence of
disease amongst various populations), is much lower than you think.
Some of the marketing material highlighted
in Lion's cross claim includes: «A2 will improve
human health through the consumption of a2 dairy milk products», «studies suggest that milk containing only the A2 type of
protein may benefit you and your family if you're concerned with certain allergies, immune function or digestive wellbeing» and «there is significant evidence to suggest that beta casein A1 may be a primary risk factor for heart
disease in adult men and also be involved
in the progression of insulin dependent diabetes
in children... Beta casein A1... is the most powerful risk factor ever discovered.»
While the difference
in molecular make - up and easier solubility of
proteins in spelt means it may be easier for
humans to digest than wheat, it does however contain gluten and is not suitable for anyone with a gluten intolerance or Coeliac
disease.
If any of these components is reduced
in food products and
human consumption these will leads to the Deficiency
diseases for example Kwashiorkor and Marasmus caused by the deficiency of dietary
proteins.
Findings of the research, published April 22
in the journal Mucosal Immunology, reveal that a substance found
in animal and
human breast milk called epidermal growth factor, or EGF, blocks the activation of a
protein responsible for unlocking the damaging immune cascade that culminates
in NEC, a
disease marked by the swift and irreversible death of intestinal tissue that remains one of the most - challenging - to - treat conditions.
less than or equal to lamivudine Acquired Immune Deficiency Syndrome Antiretroviral therapy, usually means 1 - 2 drugs, used
in early studies Antiretroviral zidovudine (also known as ZDV) Breastfeeding Baby Friendly Hospital Initiative Breastfeeding and HIV International Transmission Study Combined antiretroviral therapy Centers for
Disease Control and Prevention Deoxyribonucleic Acid Exclusive Breastfeeding Enzyme Linked Immunosorbent Assay Food and Agrigulture Organization Fixed dose combination ART, e.g., lamividine, stavudine, and nevirapine Highly Active Antiretroviral Therapy, 3 or more drugs for more effective treatment used
in later studies
Human Immunodeficiency virus International Atomic Energy Agency Infant feeding Infant and young child feeding Lopinavir cubic millimetre Mother - to - Child Transmission of HIV Non-governmental organization Nevirapine Polymerase Chain Reaction People Living with HIV Prevention of Mother - to - Child Transmission Replacement Feeding Ritonavir Ribonucleic acid, one of the three major macromolecules (along with DNA and
proteins) that are essential for all known forms of life single dose NVP United Nations Agencies Joint United Nations Programme on HIV / AIDS United Nations Population Fund United Nations Commissioner for Refugees United Nations Children's Fund U.S. Agency for International Development World Alliance for Breastfeeding Action United Nations World Food Programme World Health Assembly WHO 2010 Guidelines on HIV and infant feeding World Health Organization Zidovudine (same drug as AZT)
Studies have shown that a
protein in human milk aids
in brain development, and breast - fed babies are less likely to get gastrointestinal infections and diarrhea, respiratory and ear infections or more serious
diseases such as pneumonia, and there is a lower risk of Sudden Infant Death Syndrome.
Besides DNA, entire mitochondria, mitochondrial
proteins and mitochondrial RNA can also be found
in the nucleus; but their roles
in human health and
disease remain relatively unexplored.
«Small loop
in human prion
protein prevents chronic wasting
disease.»
These findings allowed researchers to create a chimera virus: a mouse virus with a
human viral gene that can be used to test molecules that inhibit
human LANA
protein in an animal model of
disease, treating not only
human herpes virus infection but also its associated cancers.
Degenerative brain
diseases like mad cow
disease (officially known as bovine spongiform encephalopathy, or BSE), scrapie
in sheep, and vCJD
in humans are thought to be caused by prions, misfolded versions of a normal cellular
protein called PrPC.
By directly manipulating a portion of the prion
protein - coding gene, Whitehead Institute researchers have created mouse models of two neurodegenerative
diseases that are fatal
in humans.
In humans, Huntington's is an inherited
disease caused by a gene encoding a toxic
protein, called mutant huntingtin, which causes brain cells to die.
Reductions
in biodiversity from illegal wildlife trade can have other substantial negative
human health impacts, including the loss of potential sources of pharmaceuticals, experimental models for studying
disease, crop pollination and micronutrients for
humans lacking alternative sources of
protein.
An inflammatory
protein that triggers a pregnant mouse's immune response to an infection or other
disease appears to cause brain injury
in her fetus, but not the premature birth that was long believed to be linked with such neurologic damage
in both rodents and
humans, new Johns Hopkins - led research suggests.
The newly identified gene affects accumulation of amyloid - beta, a
protein believed to be one of the main causes of the damage that underpins this brain
disease in humans.
Groundbreaking research from the University of Alberta has identified the structure of the infectious prion
protein, the cause of «mad cow
disease» or BSE, chronic wasting
disease in deer and elk and Creutzfeldt - Jakob
disease in humans, which has long remained a mystery.
«This paper represents an exciting advance
in a field that has become increasingly important with the discovery that defects
in RNA - binding
proteins contribute to
human diseases such as metabolic disorders, cancer and neurodegeneration,» Lipshitz said.
Several fatal neurological
diseases — including Creutzfeldt - Jakob
disease (CJD)
in humans and scrapie
in sheep — are marked by the accumulation of
protein deposits
in the brain.
They found that although the
protein stayed soluble for a week or two, it eventually polymerized into long fibers resembling those
in so - called prion
diseases — brain
diseases such as scrapie
in sheep, «mad cow
disease»
in cattle, and Creutzfeldt - Jakob
disease in humans.
Membrane
proteins make up about one third of all
proteins in the
human body, and their malfunction is associated with more than 500
diseases.
Prion
diseases originate when normally harmless prion
protein molecules become abnormal and gather
in clusters and filaments
in the
human body and brain.
In response to the recent revelations, an international group of researchers has launched a project called the
Human Dark Proteome Initiative to study how disordered
proteins cause
disease.
When mice with the
disease were given increased amounts of the
protein PGC -1-alpha, which is naturally present
in both mice and
humans, the neural decay was dramatically reduced.
In humans, normal prion
proteins may generally protect against Alzheimer's
disease.
«Further work
in our lab will be aimed at understanding the detailed mechanism of how these
proteins regulate editing,
in turn providing an inroad to developing therapeutics that modulate editing for the treatment of
human diseases.»
Mathias Uhlen, director of the
Human Protein Atlas project and co-author of the paper, says: «I am extremely pleased that the resource created through the
Human Protein Atlas effort has been used
in the analysis of clinical data obtained from liver
disease patients and that this analysis has led to the identification of liver - specific drug targets that can be used for treatment of this clinically important patient group.»
Mardinoglu says the team's network modeling approach, which relied on data from the Sweden - based
Human Protein Atlas project and The Genotype - Tissue Expression (GTEx) project consortia, can be used
in the identification of drug targets and eventually
in the development of efficient strategies for treating a number of chronic liver
diseases.
In experiments in mice and human cells, researchers found that blocking CXCR4 — a so - called homing receptor protein molecule that helps T cells mature and attracts blood cells to the bone marrow — halted disease progression in bone marrow and spleen tissue within two week
In experiments
in mice and human cells, researchers found that blocking CXCR4 — a so - called homing receptor protein molecule that helps T cells mature and attracts blood cells to the bone marrow — halted disease progression in bone marrow and spleen tissue within two week
in mice and
human cells, researchers found that blocking CXCR4 — a so - called homing receptor
protein molecule that helps T cells mature and attracts blood cells to the bone marrow — halted
disease progression
in bone marrow and spleen tissue within two week
in bone marrow and spleen tissue within two weeks.
Additional experiments using a combination of maraviroc and a drug that blocks the VEGF
protein suggest that the treatment duo could be an effective way to prevent metastatic
disease in human breast cancer patients, according to the researchers.
The program works by connecting computer - generated drug profiles — including mechanisms of action, clinical efficacy, and side effects — with information about how a molecule may interact with
human proteins in specific
diseases, such as ovarian cancer.
UBC Psychiatry Professor Dr. Weihong Song and Neurology Professor Yan - Jiang Wang at Third Military Medical University
in Chongqing attached normal mice, which don't naturally develop Alzheimer's
disease, to mice modified to carry a mutant
human gene that produces high levels of a
protein called amyloid - beta.
Auriel Willette, a researcher
in food science and
human nutrition at Iowa State University, found evidence that an elevated presence of a
protein called neuronal pentraxin - 2 may slow cognitive decline and reduce brain atrophy
in people with Alzheimer's
disease.
The inhibition of this signaling pathway by NT219 protected worms from toxic
protein aggregation that
in humans is associated with the development of Alzheimer's or Huntington's
disease.
«Single enzyme's far - reaching influence
in human biology,
disease: Enzyme Fam20C chemically modifies more than 100 different secreted
proteins, thus directing numerous cellular processes.»
Auriel Willette, a researcher
in food science and
human nutrition, found evidence that an elevated presence of a
protein called neuronal pentraxin - 2 may slow cognitive decline and reduce brain atrophy
in people with Alzheimer's
disease.
«The ultrasensitive detection of interferon -
protein in human material can provide novel insights into
disease - causing pathways,» explains co-senior author Duffy.
The researchers used mouse models that mimic the
disease characteristics of pulmonary hypertension and pulmonary fibrosis
in humans to study the effect of triciribine, which inhibits production of a
protein called Akt1.
Excessive numbers of glutamine - rich repeats
in various
human proteins are known to result
in severe neurodegenerative disorders such as Huntington's
disease.
In principle, we can make any
protein fluorescent, be it from HIV, from another
disease or from a
human cell.»
Taken together, these findings indicate that inadequate levels of the
protein, known as RBFOX1, may be a factor
in the faulty connections that are a hallmark of Alzheimer's
disease, says Hamed S. Najafabadi, senior author of the paper and an assistant professor
in McGill's Department of
Human Genetics.
Of the roughly 50,000
proteins in the
human body, researchers have zeroed
in on four that appear most likely to contribute this chronic
disease.
In research published in Molecular Cell, Rutgers scientists discovered that a protein (p62), which is supposed to act as an antioxidant to prevent cell damage, was not working efficiently in laboratory mice with liver and heart disease that mimicked these conditions in human
In research published
in Molecular Cell, Rutgers scientists discovered that a protein (p62), which is supposed to act as an antioxidant to prevent cell damage, was not working efficiently in laboratory mice with liver and heart disease that mimicked these conditions in human
in Molecular Cell, Rutgers scientists discovered that a
protein (p62), which is supposed to act as an antioxidant to prevent cell damage, was not working efficiently
in laboratory mice with liver and heart disease that mimicked these conditions in human
in laboratory mice with liver and heart
disease that mimicked these conditions
in human
in humans.
Wayne Anderson is one of the leaders of Northwestern's structural genomics programs, which use state - of - the - art expertise and technology to map the three - dimensional atomic structure of
proteins involved
in human disease.
This accomplice, the researchers say, allows the
protein to cause disorders like «mad cow»
disease in cattle, scrapie
in sheep, and Creutzfeldt - Jakob
disease (CJD)
in humans.
Scientists have located two possible receptors for the so - called prion
protein (PrP) believed to be at fault
in fatal neurological conditions such as «mad cow
disease,» Creutzfeldt - Jakob
disease in humans, and scrapie
in sheep.
«
Proteins are the workhorses
in the cell, and are more directly related to
disease and
human function» than genomes, he says.
BEIJING — Hoping to create an encyclopedia of
proteins in the
human body, China's Ministry of Science and Technology today kicked off a $ 40 million effort to map the
human proteome — the full complement of
proteins — of 10 major organs and tissues, including the heart and liver,
in healthy and
diseased states.
Professor Hayday added: «This is very significant because antibodies make up one of the largest sectors of the pharmaceutical market, and one of the great quests
in the pharmaceutical industry is to be able to routinely generate antibodies against
human proteins implicated
in diseases.