Sentences with phrase «aged mouse blood»

We demonstrated that this device could reduce the KLRG1 - positive CD8 cell count in aged mouse blood by a factor of 7.3 relative to the total CD8 cell compartment, reaching a level typically seen only in very young animals.

Not exact matches

http://edition.cnn.com/2014/05/05/health/young-blood-mice-aging/index.html Scientists have recently found that giving old mice transfusions of young mice blood can reverse the aging process, human trials coming soon.

Dr. Issa's team made their discovery after first examining methylation patterns on DNA in blood collected from individuals of different ages for each of three species — mouse, monkey, and human.

Mice ranged in age from a few months to almost three years, monkeys from less than one year to 30 years, and humans from age zero to 86 years (cord blood was used to represent age zero).

The GDF11 protein commonly found in the blood of young mice (the same protein that enhanced neurogenesis in aged mice) and placed in individual older mice was thought to have the same reversal effect on hypertrophy; however, more recent research suggests another molecule besides GDF11 may be at work.

Two years ago, he and his colleagues reported in Aging Cell that cutting the calories ingested by mice by 30 % for up to 4 weeks protected the rodents» kidneys when their blood supply was cut off and then restored.

An MIT - led research team has now found that it can reverse this age - related endurance loss in mice by treating them with a compound that promotes new blood vessel growth.

Similar to humans, the aged mice exhibited enlarged hearts, a general thickening of the heart wall and a reduced efficiency in the hearts ability to pump blood.

Called heterochronic parabiosis the method involves surgically linking the circulatory systems of two mice of different ages by opening a flap of skin on each mouse's side and stitching the two together so that the same blood pumps through both creatures.

Joseph Castellano at Stanford University in California and his colleagues discovered this by collecting blood from people at three different life stages — babies, young people around the age of 22, and older people around the age of 66 — and injecting the plasma component into mice that were the equivalent of around 50 years old in human years.

Studying mouse monocytes in more detail, the researchers found that the increase in TNF levels that occurs with age causes premature release of immature monocytes from the bone marrow into the blood stream.

In a chronic sleep deprivation experiment, young mice were sensitized to insulin and had improved control of their blood sugar, whereas aged animals became hyperglycemic and failed to maintain appropriate plasma insulin concentrations.

«The combined effect of aging and sleep deprivation resulted in a loss of control of blood sugar reminiscent of pre-diabetes in mice,» says Naidoo.

One mode of aging transmission is to give genetically identical mice transfusions of young or old blood.

One substance in the blood of old mice, a protein called Beta ‑ 2 ‑ microglobulin, or B2M, seemed to prematurely age the young ones, Villeda and colleagues reported last year in Nature Medicine (SN: 8/8/15, p. 10).

Although we did observe positive effects on some aging traits, such as memory impairments and reduced red blood cell counts, our studies showed that similar drug effects are also seen in young mice, indicating that rapamycin did not influence these measures by slowing aging, but rather via other, aging - independent, mechanisms.»

A protein in blood can repair age - related damage in the brains and muscles of old mice, returning them to a more youthful state.

NO BARRIER A protein in some cells that form the blood - brain barrier (light blue, as seen in this image of a mouse brain capillary) may have a hand in brain aging, a new study suggests.

As mice and humans age, levels of that protein circulating in the blood rise, Alzheimer researcher Tony Wyss - Coray at Stanford University and colleagues found.

Old blood can prematurely age the brains of young mice, and scientists may now be closer to understanding how.

With use of advanced mouse models, she and her team found that blood stem cells without adequate SIRT1 resembled aged and defective stem cells, which are thought to be linked to development of malignancies.

But now that we know what kinds of changes occur as these cells age, we can ask which of these changes reverse themselves when an old cell goes back to becoming a young cell» — as appeared to be the case when tissues of older mice were exposed to blood from younger mice.

The effects of blood on ageing were first discovered in experiments that stitched young and old mice together so that they shared circulating blood.

The 19 NIH institutes, centers and offices contributing to the Knockout Mouse Project are: the NIH Office of Strategic Coordination / Common Fund; NCRR; the National Eye Institute; NHGRI; the National Institute of Allergy and Infectious Diseases; the National Heart, Lung and Blood Institute; the National Institute on Aging; the National Institute of Alcohol Abuse and Alcoholism; the National Institute of Arthritis and Musculoskeletal and Skin Diseases; the Eunice Kennedy Shriver National Institute of Child Health and Human Development; NIDCD; the National Institute of Dental and Craniofacial Research; the National Institute of Environmental Health Sciences; the National Institute of General Medical Sciences; the National Institute of Mental Health; the National Institute of Neurological Disorders and Stroke; the National Institute of Diabetes and Digestive and Kidney Diseases; the National Cancer Institute; and the Office of AIDS Research.

In Ames dwarrf, Snell Dwarf mice, Klotho mice, GHKO mice who have little IGF and GH; and live longer than wild - type; we see that indeed insulin and glucose / nutrient / energy pathways (which create oxidative stress through excessive nutrient via elevated glycation blood glucose creating high glycated albumin and hemoglobin), that aging is acted on by IGF through hormones, GFs, GHs, acting on insulin signals, which act on survival genes (DAF / SIRT / FOXO).

In recent years, researchers have developed so - called «senolytic» drugs that wipe out senescent cells in aging mice and mouse models of age - related disease, exploiting the high dependence of these cells on specific biochemical survival pathways.9, 10 In these studies, senolytic drugs have restored exercise capacity9 and formation of new blood and immune precursor cells11 in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 2019.

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.

Aged mutant amyloid precursor protein mice with established disease showed a near complete restoration in levels of synaptic and neuronal proteins after exposure to young blood in parabiosis (synaptophysin P =.02; calbindin P =.02) or following intravenous plasma administration (synaptophysin P <.001; calbindin P =.14).

Aging tau KO mice to 23 months resulted in cardiac hypertrophy with significantly attenuated left atrial contractility, increased blood pressure, and sensitivity of isolated mesenteric arteries to angiotensin II contraction and isoprenaline relaxation compared to their younger counterparts.

Here we consider two surface markers thought to define these cells in mice, CD8 and Killer cell lectin - like receptor G1 (KLRG1), and a means we developed to remove these cells from the blood of aged C57BL / 6 mice.

Three recent experimental studies focused on low consumption / exposure.949596 In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.96

Scientists were able to identify the influence caused by factors unique to the blood of young mice, which could ultimately be used as treatments for age - related neurodegenerative disorders.

Utilizing sophisticated genetically engineered mouse models, we will study how these conserved longevity pathways regulate the homeostasis and aging of adult stem cells, including hematopoietic stem cells, the adult stem cells that sustain all blood lineages throughout life.

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The Effect of Acetyl - L - carnitine and R - alpha - lipoic acid Treatment in ApoE4 Mouse as a Model of Human Alzheimer's Disease J Neurol Sci 2009 (Mar 31)[Epub ahead of print] We measured age - dependent effects of human ApoE4 on cerebral blood flow (CBF) using ApoE4 transgenic mice compared to age - matched wild - type (WT) mice by use of -LSB-(14) C] iodoantipyrene autoradiography.