Sentences with phrase «systems in our aging mouse»

At the University of Arizona, SENS Research Foundation is funding proof - of - concept research to restore the health of the immune system in aging mice, by simultaneously increasing the ability to produce new killer T - cells while making room for them by purging defective cells from the system.

Not exact matches

In 2014, highly publicized work in the laboratories of Villeda and Tony Wyss - Coray, PhD, professor of neurology at Stanford, showed that connecting the circulatory system of a young mouse to that of an old mouse could reverse the declines in learning ability that typically emerge as mice agIn 2014, highly publicized work in the laboratories of Villeda and Tony Wyss - Coray, PhD, professor of neurology at Stanford, showed that connecting the circulatory system of a young mouse to that of an old mouse could reverse the declines in learning ability that typically emerge as mice agin the laboratories of Villeda and Tony Wyss - Coray, PhD, professor of neurology at Stanford, showed that connecting the circulatory system of a young mouse to that of an old mouse could reverse the declines in learning ability that typically emerge as mice agin learning ability that typically emerge as mice age.

The cardiovascular system, which often fails and causes early death in these prematurely aging mice, also showed improvements in structure and function.

A single gene appears to play a crucial role in coordinating the immune system and metabolism, and deleting the gene in mice reduces body fat and extends lifespan, according to new research by scientists at the Jean Mayer USDA Human Nutrition Research Center (USDA HNRCA) on Aging at Tufts University and Yale University School of Medicine.

Walford's new research is based on the fact that in mice and humans, the immune system malfunctions during aging, losing the ability to distinguish between healthy cells and invasive pathogens such as bacteria and viruses.

In a new study in mice published in the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systeIn a new study in mice published in the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systein mice published in the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systein the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systein the immune system.

«Earlier studies have shown that vitamin E can help regulate the aging body's immune system, but our present research is the first study to demonstrate that dietary vitamin E regulates neutrophil entry into the lungs in mice, and so dramatically reduces inflammation, and helps fight off infection by this common type of bacteria,» said first author Elsa N. Bou Ghanem, Ph.D., postdoctoral scholar in the department of molecular biology and microbiology at Tufts University School of Medicine (TUSM).

Mark Albers uses the olfactory system of mice and humans to help understand the early events of neurodegeneration in order to find ways to intervene early in the disease process before symptoms appear and distinguish early pathologic events from changes produced by aging.

Hypothesis driven approaches to vaccinology can utilise the knowledge gained from mechanistic mouse models and our molecular understanding of intrinsic defects to human cells.5 However, caution is required when extrapolating data from murine models, as there are substantial differences between immune ageing in mice and humans.6 Nevertheless, model systems and ex vivo analyses of molecular alterations in aged human cells have identified multiple changes in the vaccination response with age and the aged immune system in general.

Adenylyl Cyclase Type 5 (AC5): Knockout of AC5 extends life in mice, with the most plausible mechanism being increased resilience of the cardiovascular system to the various slings and arrows of aging.

PER2: Deletion of the PER2 gene in mice, associated with the mechanisms of circadian rhythm, appears to improve DNA repair in stem cell populations relevant to the immune system, resulting in a healhier immune cell population, better immune function in old age, and a modestly extended life span.

Using a technique called parabiosis, in which the vascular systems of two mice are surgically connected, Villeda's lab had previously discovered that infusing old mice with the blood of younger mice leads to brain rejuvenation, including improvements in learning and memory, while infusions of old blood cause premature brain aging in young mice.

(6) In early - aging (2 - mo old) BubR1H / H; INK - ATTAC mice, but not young (3 - wk - old) mice, transcripts of the system and of reporter green fluorescent protein «were significantly elevated in [subcutaneous] adipose tissue, skeletal muscle and eye, but not in tissues in which endogenous p16Ink4a is not induced, including liver and heart.&raquIn early - aging (2 - mo old) BubR1H / H; INK - ATTAC mice, but not young (3 - wk - old) mice, transcripts of the system and of reporter green fluorescent protein «were significantly elevated in [subcutaneous] adipose tissue, skeletal muscle and eye, but not in tissues in which endogenous p16Ink4a is not induced, including liver and heart.&raquin [subcutaneous] adipose tissue, skeletal muscle and eye, but not in tissues in which endogenous p16Ink4a is not induced, including liver and heart.&raquin tissues in which endogenous p16Ink4a is not induced, including liver and heart.&raquin which endogenous p16Ink4a is not induced, including liver and heart.»

«Our findings reveal a critical role for telomere length in a mouse model of age - dependent human disease,» said first author Christina Theodoris, an MD / PhD student in the laboratory of Deepak Srivastava, MD. «This model provides a unique opportunity to dissect the mechanisms by which telomeres affect age - dependent disease and also a system to test novel therapeutics for aortic valve disease.»

Specifically, by using the NeuroCube ® system to measure gait deficits, we found that SOD - 1 mice showed a reduction in step and stride length and an increase in stride, stand and swing duration compared to WT mice, which was evident as early as 8 weeks and progressed with age.

In addition to these routine tests of neurological and motor function, sophisticated algorithm - based systems were employed and determined a strong phenotype effect in the SOD - 1 mice at a much earlier agIn addition to these routine tests of neurological and motor function, sophisticated algorithm - based systems were employed and determined a strong phenotype effect in the SOD - 1 mice at a much earlier agin the SOD - 1 mice at a much earlier age.

The system has no time for people his age who are inept when it comes to modern technology — he holds a mouse up to a computer screen and writes his CV in longhand — and quickly brands Blake as a hopeless case.