Sentences with phrase «activity in human disease»

The answer to this question may open new routes to target age - dependent alterations of stem cell activity in human disease.

Not exact matches

The behavioral tests used here modeled one dimension of the disease — an inability to experience pleasure from normal activities — but not others, such as stress and anxiety, and probably tap into different brain mechanisms in mice than in humans, he says.

From fish in a British lake to lions and corals, many plants and animals have suffered devastating disease outbreaks because of human activity, says Michael Le Page

To understand why the long - spined urchins have not returned to the reef more than 30 years later, Scripps scientists Katie Cramer and Dick Norris analyzed the amount of fossilized urchin spines that accumulated in reef sediment layers over the past 3,000 years to paint a picture of life on the reef before it was altered from the disease outbreak and human activities such as fishing and pollution.

In a novel animal study design that mimicked human clinical trials, researchers at University of California, San Diego School of Medicine report that long - term treatment using a small molecule drug that reduces activity of the brain's stress circuitry significantly reduces Alzheimer's disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative conditioIn a novel animal study design that mimicked human clinical trials, researchers at University of California, San Diego School of Medicine report that long - term treatment using a small molecule drug that reduces activity of the brain's stress circuitry significantly reduces Alzheimer's disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative conditioin a mouse model of the neurodegenerative condition.

For the last decade, neuroscientists have been using the non-invasive brain - mapping technique functional called magnetic resonance imaging or fMRI to examine activity patterns in human and animal brains in the resting state in order to figure out how different parts of the brain are connected and to identify the changes that occur in neurological and psychiatric diseases.

In today's issue of Science Translational Medicine, he and his colleagues present a more efficient way of finding such new uses for old drugs: by bringing together data on how diseases and drugs affect the activity of the roughly 30,000 genes in a human celIn today's issue of Science Translational Medicine, he and his colleagues present a more efficient way of finding such new uses for old drugs: by bringing together data on how diseases and drugs affect the activity of the roughly 30,000 genes in a human celin a human cell.

On the negative side, the researchers found that many of the genes whose activity is unique to modern humans are linked to diseases like Alzheimer's disease, autism and schizophrenia, suggesting that these recent changes in our brain may underlie some of the psychiatric disorders that are so common in humans today.

«Our work allows us to probe the activity of heparanase in human samples — allowing early disease identification and a direct measure of the success of drugs in humans.

Raichle's observation of patterns of ongoing brain activity when the subject is in a resting state, or when the brain is not actively engaged in performing tasks such as recalling events or learning new words, has transformed the way the human brain is now being studied in health and disease.

Often called the «chemistry of life,» metabolism provides the fuel for all cellular activities and goes awry in most human diseases.

Telomere length predicts both cellular health and disease in rodent models and humans.8 Shorter telomeres predict onset of cardiometabolic diseases of aging.9 Chronic stress is associated with higher inflammation, shorter telomeres, and lower activity levels of telomerase, the cellular enzyme that elongates telomeric DNA.10, 11 Levels of amyloid beta (Aβ) proteins circulating in the blood appear to be stress - related in rodent models12 and may be affected by stress reduction, and greater Aβ42 / Aβ40 ratios are associated with lower risk of dementia.13

Research suggests that random fluctuations in gene activity could explain some instances of the phenomenon, known as partial penetrance, which likely plays a role in some human diseases.

Our in vitro study provides a baseline for defining healthy and disease - like states and highlights the power of moving beyond single and dual species applications to capture key players and their orchestrated metabolic activities within a complex human oral microbiome model.

«To then determine how disrupting the gene might play out in the context of disease, we chemically knocked out the activity of SLC16A11 in human liver cells,» explains co-first author Victor Rusu, a former Harvard graduate student at Broad now at Jnana Therapeutics.

In light of the widespread role of oxidative stress in the pathology of diverse human diseases and the ability of the Nrf2 - dependent antioxidant response gene network to protect against oxidative stress, considerable effort has been directed towards discovering compounds that can increase the activity of NrfIn light of the widespread role of oxidative stress in the pathology of diverse human diseases and the ability of the Nrf2 - dependent antioxidant response gene network to protect against oxidative stress, considerable effort has been directed towards discovering compounds that can increase the activity of Nrfin the pathology of diverse human diseases and the ability of the Nrf2 - dependent antioxidant response gene network to protect against oxidative stress, considerable effort has been directed towards discovering compounds that can increase the activity of Nrf2.

In the case of Influenza A, the loss of RNA exosome activity severely compromises viral infectivity, but also manifests in human neurodegeneration suggesting that viruses target essential proteins implicated in rare disease in order to ensure continual adaptatioIn the case of Influenza A, the loss of RNA exosome activity severely compromises viral infectivity, but also manifests in human neurodegeneration suggesting that viruses target essential proteins implicated in rare disease in order to ensure continual adaptatioin human neurodegeneration suggesting that viruses target essential proteins implicated in rare disease in order to ensure continual adaptatioin rare disease in order to ensure continual adaptatioin order to ensure continual adaptation.

Studying heparanase - a key enzyme in the development and metastasis of human cancers — scientists unveiled new fluorescent imaging agents that detect enzyme activity in healthy and diseased tissues.

The misacylation or poor activity of mitochondrial SRS in humans is responsible for a variety of metabolic diseases.

«We already knew that the buildup of fibrin appears early in the development of MS — both in animal models and in human patients, so we wondered whether thrombin activity could in turn serve as an early marker of disease.»

Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem cells, stromal cells, haematopoietic stem cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters

In her essay, she described how the interactions between genes and the environment affect human health and disease, concluding that these environmental influences on gene activity allow people to protect their own well - being by cultivating healthy habits.

Arc is an activity - regulated neuronal protein, but little is known about its interactions, assembly into multiprotein complexes, and role in human disease and cognition.

1) Phytonutrients: * Occur naturally in fruits and vegetables * Promote the function of the immune system * Help fight off viruses as well as reduce inflammation * Associated with the treatment and / or prevention of cancer and cardiovascular disease 2) Enzymes: * Responsible for metabolic processes that occur within a cell and are necessary for sustaining life * Assist and play a large role in digestion, energy production, blood coagulation and contraction of muscles 3) Amino Acids: * The basic building blocks of protein * Absorption of amino acids is essential for your metabolism 4) Essential Fatty Acids: * Reduce the risk of heart disease and some forms of cancer * Improve mood * Decrease inflammation 5) Vitamins: * Essential for the normal growth and development of all human beings * Healthy maintenance of cell tissues and organs * Help process proteins, carbohydrates and fats required for utilization 6 & 7) Macro and Trace Minerals: * Involved in electrolyte balance of body fluids * Essential for normal cellular activity * Provide hardness to bones and teeth

From the producers of the Paranormal Activity franchise, the film is the next installment in their series following Insidious, and «chronicles an unprecedented biological disaster unleashed from the waters of the Chesapeake Bay - an isopod parasite, carrying a horrific untreatable disease, that jumps from fish to human hosts.

During the final cycle of activities, experts worked on the elaboration of recommendations that may contribute in understanding and mitigating the risks of infectious diseases potentially transmitted by companion animals to humans and food animals.

(1) to provide new and additional assistance from the United States to the most vulnerable developing countries, including the most vulnerable communities and populations therein, in order to support the development and implementation of climate change adaptation programs and activities that reduce the vulnerability and increase the resilience of communities to climate change impacts, including impacts on water availability, agricultural productivity, flood risk, coastal resources, timing of seasons, biodiversity, economic livelihoods, health and diseases, and human migration; and