Sentences with phrase «as senescent»

These women are mostly rendered either nude in a youthful, cartoonish manner with the curvaceous bodies and voluptuous breasts of soft porn, or as senescent — overly clothed in long dresses and turbans, suggesting babushkas or Mormons.

This series addresses the contribution of cellular senescence to cardiovascular, neurodegenerative, and arthritic disorders as well as the senescent phenotypes in various tissues and cell types.

A cell that's no longer dividing is known as senescent; it continues to live but no longer functions as it once did.

Not exact matches

I remember a pathologist describing a post-term stillbirth as the fault of a senescent placenta.

As a postdoctoral researcher at Harvard Medical School, he investigated the use of small - molecule drugs to manipulate signaling pathways to enable otherwise senescent progenitor cells of the cochlea to divide and form new sensory cells.

In addition to their cell - intrinsic effects, senescent cells develop the ability to negatively influence healthy neighboring cells and immune cells by secreting senescence - associated set of cytokines and mediators known as the SASP.

A recent study, led by an international team of researchers confirms that targeted removal of senescent cells (SnCs), accumulated in many vertebrate tissues as we age, contribute significantly in delaying the onset of age - related pathologies.

Masters et al. discuss the often overlooked contribution of the stromal microenvironment as an extrinsic factor to immunosenescence and inflammation.12 Accumulation of senescent stromal cells which demonstrate the senescent associated secretory phenotype (SAPS), may alter tissue structure and function, and increase local inflammation.13 The impact of altered lymphoid stromal microenvironment may be widespread and include altered haematopoiesis, reduced lymphatic flow and disrupted secondary lymphoid organisation, which consequently will alter antigen transportation and presentation to T cells.12

Then I wonder whether we'd get a better idea by clearing senescent cells in mice that receive the same medical care (anti-cancer etc) as humans.

Clearance of senescent cells has been advocated as a part of the SENS vision for the medical control of aging for more than a decade now, and it is very encouraging to see the research and development community at last coming round to this view and making tangible progress.

P16: P16 is perhaps best known as an indicator of cellular senescence, a part of the mechanisms that cause damaged cells or those at the Hayflick limit to become senescent or self - destruct.

Soon the cell becomes senescent as she loses nuclear chromosome telomeric DNA.

The mouse lifespan study is the important news here, as it demonstrates meaningful extension of median life span through removal of senescent cells, the first such study carried out in normal mice for this SENS - style rejuvenation technology.

Moreover, there are yet other cell types — such as visceral adipose tissue macrophages and cytotoxic CD8 + T - cells — in which the age - related supernumerary accumulation of dysfunctional and apoptosis - resistant cells appears to play a highly deleterious role on tissue function, but where the cells are not «senescent» cells in the classical sense of p16Ink4a expression and the senescence - associated secretory profile observed in senescent fibroblasts.

Oisín has shown as much as an 80 % reduction in senescent cells in cell culture and significant reductions of senescent cell burden in naturally aged mice.

The most well - known of these are so - called «senescent» cells, originally characterized by Leonard Hayflick as mitotic cells that reached growth arrest after a limited replicative lifespan (later associated with telomere attrition) under unphysiological conditions in culture.

Persistent DNA damage and DDR signaling triggers senescent cells to secrete immunomodulatory proteins, a phenomenon known as the senescence - associated secretory phenotype (SASP).

As a recent study has shown, clearing senescent cells both reduces negative effects of aging pathologies and also extends median lifespan and survival.

And, to be clear, in the long run, you have to remove senescent cells, restore cells as quickly as they're lost, repair (to stable condition) or replace the ECM when it's contaminated, remove amyloids as they accumulate, and scrub out arterial plaques.

Interestingly, many of those on the side of nuclear DNA damage as being important in aging beyond cancer risk tend to pull senescent cells into the picture they paint.

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 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 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).

This sets the company apart from its main competitors who only pursue senolytics (agents eliminating senescent cells) as potential anti-aging drugs.

Improved rejuvenation biotechnologies would target senescent cells more selectively, and SENS Research Foundation is helping to advance those next - generation «senoablatives» even as UNITY prepares for human testing.

Sure enough, when the researchers examined the brains of PD patients, they found more cells exhibiting signs of senescence than in people without the disease — and especially astrocytes, as they had expected.7 This was true even after matching patients for age, meaning that PD subjects had even more senescent astrocytes in their SNcs than is typical for people their age (ranging in this case from 50 — 92 years at autopsy)-- and remember, aging already drives an increase in the burden of these cells as compared with young people, even in those who have yet to develop Parkinson's disease.7

(8) Imputation of these results specifically to the animals» age - related, low - BubR1 - driven rise in p16Ink4a - expressing senescent cells was, however, limited: limited by the very nature of so - called «accelerated aging» models such as BubR1H / H, (9) and limited by the lifelong, global absence of p16Ink4a expression in the backcrossed mice.

To test this notion, the researchers put paraquat - exposed mice on a regimen of the drug serving as a trigger for the suicide device now armed in all their senescent cells, rapidly eliminating the excess senescent astrocytes from their brains (Figure 1, (a-c)-RRB-.

And sure enough, this increased burden of senescent cells caused the same problems in living mice as in the researchers» cell culture experiments, as well as in previous work in paraquat - exposed mice.

Senescent cells began their existence skin cells, or as related cells that normally play supporting roles in other organs, but were forced into an abnormal state where they lost the ability to divide and reproduce themselves as a protective response to some danger.

And just as in the case of the paraquat model, all of these effects were greatly reduced or prevented entirely when senescent astrocytes were ablated by the suicide - gene activating drug.8

Oisín's platform has shown as much as an 80 % reduction in senescent cells in cell culture and significant reductions of senescent cell burden in naturally aged mice.

Later research has revealed that few cells reach a «senescent» state through sheer replicative exhaustion: instead, senescence has emerged as a programmed response to DNA damage or oncogenic stress, and as part of the resolution of wound healing.

But for reasons that are not fully known, as we age, persistently senescent cells accumulate, leading to a vast number of age - related diseases.

It should be noted, however, that while a study on senescent cell ablation in genetically normal mice would provide at least some evidence on the effect of senescent cells (and their ablation) on promoting cancer, even such a study would likely show less effect than could be anticipated in a large mammal model, since even normally - aging mice rarely suffer metastatic disease to the extent of aging humans, as sheer primary tumor volume is generally sufficient to be fatal to mice.

But while substantial data (including AFFiRiS» [15] and Prothena's [20,22] preclinical work) give good reason to think that early clearance of AS neuropathology will decelerate the rate of SN DA neuronal loss, astrocytosis, and possibly accumulation of senescent glial cells in PD, there is no reason to think that doing so will prevent these phenomena entirely, if for no other reason than because many other factors also contribute to their occurrence.

Studying the mechanism (s) of formation, as well as recognition and elimination of senescent cells, has been hindered by the lack of senescence - specific markers.

Senescent cells lose their normal function in the tissue, cease dividing, and begin secreting a deadly mix of inflammatory and tissue - degrading factors collectively known as the senescence - associated secretory phenotype (SASP) that damages and deranges local tissues.

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.

D. Frescas et al (2017) Senescent cells expose and secrete an oxidized form of membrane - bound vimentin as revealed by a natural polyreactive antibody (http://www.pnas.org/content/early/2017/02/09/1614661114.short)

One well - known characteristic of senescent cells is the production of pro-inflammatory and matrix - degrading molecules, known as the senescence - associated secretory phenotype (SASP).

They found that a significant portion of these immune cells converted from a senescent form, which isn't as effective at combating disease, to a naïve form, ready to fight cancer and infections.

But Campisi also made clear the new findings about senescent cells may signal a regime shift in aging research because if proven true, huge gains could be made in living healthfully as our clocks run out.

With help from postdoctoral fellow Peter de Keizer, former graduate students Lilli Zhou and Adam Freund, former fellow Francis Rodier, consultant Pierre Desprez and fellows in the Hughes and Kapahi laboratories Melissa Sarantos and Su Liu, Remi identified cortisol and corticosterone as potent suppressors of the deleterious secretions of senescent cells.

Sophisticated cell targeting systems such as the gene therapy approach developed for senescent cell clearance by Oisin Biotechnologies could also be turned to stem cell or immune cell destruction, given suitable markers of cell chemistry.

If we're lucky, a substantial proportion of these cells will become senescent as a result of their mutant mitochondria, and will thus be destroyed by senescent cell clearance therapies.

What follows is an introduction to the senescent cell - clearing therapies known as senolytics, these therapies are poised to enter human trials and if successful could revolutionize how we treat age - related diseases.

Apparently, most (epi) mutations in the cell are recognized as critical and trigger the apoptosis program, or make the cell senescent - and the rest, unfortunately, do contribute to cancer.