Sentences with phrase «aging phenotypes»

To examine cardiac aging phenotypes, we performed echocardiography in rapamycin - and vehicle - treated aged mice and young controls.

However, rapamycin had limited effects on a large number of murine aging phenotypes.

We observed a large number of aging phenotypes that were not improved by rapamycin in any apparent and measurable way (Table 2), which indicated that rapamycin did not prevent the signs and symptoms of aging in a universal fashion.

Our data identify a distinct senescence response and provide a mechanism by which mitochondrial dysfunction can drive aging phenotypes.

As the investigators note, the rapid age - related arterial stiffening and cardiac arrhythmias that appear to be at cause for the majority of deaths in BubR1H / H mice were not attenuated by ablating p16Ink4a - expressing senescent cells — but these tissues had little burden of such cells, so this finding reinforces the conclusion that the multiple aging phenotypes arrested in these mice when senescent cells were ablated is attributable specifically to the removal of their baleful influence on local tissues.

To impute aging phenotypes directly to p16Ink4a - expressing senescent cells, van Deursen and colleagues with expertise in the aging and senescence of the relevant tissues developed and tested the effects of a pharmacologically - inducible system for the ablation of p16Ink4a - expressing cells.

(6 - 8) and van Deursen and colleagues had already demonstrated that breeding BubR1H / H mice onto a p16Ink4a homozygous - null genetic background attenuated their development of p16Ink4a - senescent cell - associated aging phenotypes and modestly increased their very low survivorship.

We have generated mice that lack Polycomb repressive activity in skin epithelium and presented premature aging phenotypes.

Therefore one of the main challenge of our era is to understand pathways underlay these reversible aging phenotypes with the final goal to identify strategies to prevent age - related diseases and then increase lifespan.

Recent aging researches reveal that some aging phenotypes are reversible, in fact age related dysfunctions may be classified in an early stage then reversible, and as a later stage with permanent damage.

Aging research reveals that some aging phenotypes are reversible, in fact age related dysfunctions may be classified in an early reversible stage, and in a later stage with permanent damage (DNA mutations or deletions or cell death) 1.

In SIRT6 knockout mice, which exhibit accelerated aging phenotype, haploinsufficiency of p65 subunit of NF - kB resulted in improved lifespan 33.

IGF prevents frailty by increasing skeletal muscle mass (sarcopenia), sex drive (infertility), brain thymus (immunosenescence, centenarians maintain a strong immune system), skeletal bone mineralization and marrow stem cell formation (osteoporosis and immune system by bone marrow immune cells working in tandem with thymus and lymphs nodes), I understand that diabetes, an accelerated aging phenotype, is insulin IGF and blood glucose driven.

Her lab explores both cell intrinsic and cell extrinsic (niche) contributions to the aging phenotype.

(9) Indeed, the degenerative aging process is by definition one in which the organism progressively accumulates damage to its cellular and molecular components over time, so any genetic or environmental factor that leads to a greater burden of such damage will bear some resemblance to the aging phenotype, irrespective of the causal origin of the defect or its relationship to «normal» aging.

Second, we note that in the experiments reported here, the DJ - 1 deficient Polg mutator animals all developed the accelerated aging phenotype and that in the quantitative measure of body weight the DJ - 1 - / -; PolgMT / MT group was similar to the DJ - 1 + / +; PolGMT / MT group.

Thus, it may be that a sustained systemic inflammatory state represents a particular aging phenotype, which results from exposure to chronic stressors, perdurable inflammatory responses, and / or some combination of both.

Not exact matches

Using advances in genomic sequencing, the human microbiome, proteomics, informatics, computing, and cell therapy technologies, HLI is building the world's most comprehensive database of human genotypes and phenotypes as a basis for a variety of commercialization opportunities to help solve aging related disease and human biological decline.

Dr. Nguyen then worked at the Buck Institute for Research on Aging and at Stanford University, where she investigated the signaling pathways underlying neurodegeneration and how the modulation of these pathways can influence the AD phenotype.

Cardiovascular phenotyping between the ages of 60 and 64 years with carotid intima media thickness (cIMT; a surrogate marker for cardiovascular events) was used to assess the effect of lifetime exposure to adiposity on cardiovascular risk factors.

Functional changes of the retina were found in three mouse models of human CNS diseases whose phenotype, age of onset and pathological mechanism clearly differ from each other.

Investigating mouse models for biological for research The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotypiPhenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotypiphenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotypingphenotyping imaging.

«It is well established that there is a «hyper - inflammatory phenotype» based largely on genetic factors that is of value in protecting the young from bacterial infection before they have made IgG antibodies to the bacteria they encounter; but which, in later life predisposes to the inflammatory diseases of old age.

Accelerated production of GH is bad, it activates excessive insulin IGF - 1 axis which increases T2D, reduces SIRT / DAF / FOXO genes who activate important oxidative stress genes (SOD, NRF2...)- But LOSS of GH is just as bad Hutchison - Guilford»S progeria children who die at 11 to 15 years old have an extreme accelerated aging (they look like children with ghastly «dying look» of very old people phenotype).

Using advances in genomic sequencing, the human microbiome, proteomics, informatics, computing, and cell therapy technologies, HLI is building the world's most comprehensive database of human genotypes and phenotypes as a basis for a variety of commercialization opportunities to help solve aging related disease and human biological decline.

A late stage treatment may help with some inflammation associated with the senescence - associated secretory phenotype (increased inflammation, MMPs, etc.) but it likely won't be as effective as preventing the aging - related damage in the first place.»

Critical issues include: (i) heterogeneity in stem cell populations (ii) regulation of cell fate choices; (iii) declining tissue performance with age and exposure to environmental injuries; (iv) the use of iPS and Embryonic Stem (ES) cells, and reprogramming methods for phenotyping disease states and potential use of these stem cells in the clinic.

Summary: A two day meeting to review current IMPC progress and discuss future developments such as CRISPR - Cas9 implementation and a mouse ageing pipeline, including several Infrafrontier IPAD - MD sponsored expert group meetings on specific areas of mouse phenotyping Attended by: IMPC members, funders, corporate sponsors, IMPC Panel of Scientific Consultants & invited external researchers Hosted / funded by: Korea Mouse Phenotyping Consortium / Inphenotyping Attended by: IMPC members, funders, corporate sponsors, IMPC Panel of Scientific Consultants & invited external researchers Hosted / funded by: Korea Mouse Phenotyping Consortium / InPhenotyping Consortium / Infrafrontier

Health improvement (allowing to post - pone / escape the diseases and thus live, healthier / disease - free longer, but not above human MLSP of around 122 years; thus these therapies do not affect epigenetic aging whatsoever, they are degenerative aging problems not regular healthy aging problem (except OncoSENS - only when you Already Have Cancer - which cancer increases epigenetic aging, but cancer removal thus does not change anything / makes no difference about what happens in the other cells / about what happens in the normal epigenetic «aging» course in Normal non-cancerous healthy cells) Although there is not such thing as «healthy aging» all aging in «unhealthy» (as seen from elders who are «healthy enough» who show much damage), it's just «tolerable / liveable» enough (in terms of damage accumulating) that it does not affect their quality of life (enough yet), that is «healthy aging»: ApoptoSENS - Clearing Senescent Cells (this will have great impact to reduce diseases, the largest one, since it's all inflammation fueled by the inflammation secretory phenotype (SASP) of these senescent cells) AmyloSENS - Dissolving the Plaques (this will allow humans to evade Alzheimer's, Parkinsons and general brain degenerescence, allowing quite a boost; making people much more easily reach the big 100 - since the brain is causal to how long we live; keeping brain amyloid - free and keeping our memories / neuron sharp / means longer LongTerm Potentiation - means longer brain function means longer heavy brain mass (gray matter / white matter retention seen in «sharp - witted» Centenarians who show are younger brain for their age), and both are correlated to MLSP).

Figure 1: Amelioration of «Premature Aging» Phenotypes in Treated and Untreated BubR1H / H; INK - ATTAC Mice.

(21) Moreover, while the link between excessive visceral adipose tissue and age - independent diabetes and metabolic syndrome widely known, recent studies suggest instead that it is the accumulation of senescent subcutaneous adipocyte progenitors — and their abnormal metabolic function — that drives similar diabetes - like phenotypes during the «normal» aging process.

We tested R6 / 2 transgenic mice, a widely used genetic model of Huntington's disease (Mangiarini et al., 1996), in two studies designed to evaluate progression of the disease phenotype with age.

To date, a screen of the collection of FDA - approved drugs in the Prestwick Library has identified a handful of potential candidates which have demonstrated effectiveness at lowering secretion of IL - 6, a component of SASP whose concentration tends to rise systemically with aging and here used as a preliminary marker of SASP as a phenotype.

To bypass the disruptive effects of the age - related accumulation of senescent cells, some investigators are working on possible ways to manipulate the signaling pathways involved in enforcing the senescent phenotype.

GM1 gangliosidosis can be classified into three major clinical phenotypes according to the age of onset and severity of symptoms: Type I (infantile), Type II (late infantile / juvenile) and Type III (adult).

(6) Some, but not all, of these phenotypes were associated with a high age - related incidence in senescent (p16Ink4a - positive) cells.

(6) Following this initial test of abrogating the early, age - related rise in p16Ink4a - expressing cell burden, the investigators probed the effects of leaving BubR1H / H; INK - ATTAC to undergo 5 months of rapid «premature aging» (and thus, to the attendant accumulation of high levels of p16Ink4a - positive cells and onset of «early - aging» phenotypes), and only then inducing ablation of senescent cells with the INK - ATTAC drug - activated system (see Figure 2 (g) below).

BubR1 insufficiency causes early onset of aging - associated phenotypes and infertility in mice.

Pathobiology of the 129: Stat1 - / - mouse model of human age - related ER - positive breast cancer with an immune infiltrate - excluded phenotype.

Isolated right and left atria and small mesenteric arteries from wild type and tau deficient (KO)... mice of two age groups (13 and 23 months old) were used to assess cardiovascular phenotypes.

The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotypiPhenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotypiphenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotypingphenotyping imaging.

Ageing research and more generally the study of the functional basis of human diseases profit enormously from the large - scale approaches and resources in mouse functional genomics: systematic targeted mutation of the mouse genome, systemic phenotyping in mouse clinics, and the archiving and distribution of the mouse resources in public repositories.

mice of two age groups (13 and 23 months old) were used to assess cardiovascular phenotypes.

His lab's preliminary results suggest an increased prevalence of a variety phenotypes outside of the CNS in Type III patients compared to an age - matched non-SMA population.

These activities are tightly integrated with the current efforts of the International Mouse Phenotyping Consortium (IMPC, www.mousephenotype.org) to set up a standardised late - onset (ageing) pipeline.

We aged a cohort of 27 mice (Table 2) for ∼ 1 year in order to maximize the aging effect of the Polg phenotype.

These data indicate that cellular senescence is causally implicated in generating age - related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.

In tissues — such as adipose tissue, skeletal muscle and eye — in which p16 (Ink4a) contributes to the acquisition of age - related pathologies, life - long removal of p16 (Ink4a)- expressing cells delayed onset of these phenotypes.

Objective: We carried out de novo recruitment of a population - based cohort (MANOLIS study) and describe the specific population, which displays interesting characteristics in terms of diet and health in old age, through deep phenotyping.

This lack of understanding is contributed by the fact that cellular aging is a complex phenotype to measure and comprehensive studies on aging require the application of novel experimental approaches and technological platforms.