Well, yes, but the price may send up and coming creatives running for cover. Here is the configuration for the Microsoft Surface Book 2 inch configuration sent to TechRadar for review:. CPU : 1. On the other hand, the Plus, a year later, you should be able to find some deals that up the value proposition of the Surface Book 2. The bigger keyboard base should offer us bigger everything, frankly, not just bigger graphics. In spite of that, the typing experience with the Surface Book 2 is phenomenal, with a brightly backlit keyboard that has punchy feedback and satisfying travel.
All things considered, we like the Surface Book 2 inch design quite a bit — even its p webcam and rear camera should get approving looks at the next meeting or in your Instagram feed. Any latency between drawing on the display with the Surface Pen and its appearance on the screen is definitely indiscernible. Text looks sharp on the screen as do photos and videos, even if the aspect ratio makes for some inelegant thick black bars when viewing the latter. Current page: Introduction, price, design and features. Sometimes the more a person tries to fix a seemingly minor problem, the worse things become.
Cells are no different, it turns out, though attempting to compensate for what begins as a minor deficiency or dysfunction can be dire. In the case of Alzheimer's disease , researchers now show that mitochondrial calcium transport remodeling - what appears to be an attempt by cells to compensate for flagging energy production and metabolic dysfunction - while initially beneficial, ultimately becomes maladaptive, fueling declines in mitochondrial function, memory, and learning.
Altered calcium regulation and metabolic dysfunction have been suspected of contributing to neuronal dysfunction and Alzheimer's development. Calcium transport into mitochondria plays an important part in many cellular functions and requires the involvement of multiple proteins to be carried out effectively. Among the key regulators of this process is a protein known as NCLX , which previously was discovered to mediate calcium efflux from heart cells. NCLX expression is also important in mitochondrial calcium efflux in neurons. In a new study, researchers examined the role of mitochondrial calcium uptake by neurons in Alzheimer's disease.
To do so, the team used a mouse model of familial Alzheimer's disease in which animals harbored three gene mutations that give rise to age-progressive pathology comparable to Alzheimer's progression in human patients.
As mice carrying the three mutations aged, the researchers observed a steady reduction in NCLX expression. This reduction was accompanied by decreases in the expression of proteins that limit mitochondrial calcium uptake, resulting in damaging calcium overload. NCLX loss was further linked to increases in the production of cell-damaging oxidants. When NCLX expression was restored, levels of harmful protein aggregates declined, neuronal mitochondrial calcium homeostasis was reestablished, and mice were rescued from cognitive decline. Moreover, our data suggest that amyloid beta and tau pathology actually lie downstream of mitochondrial dysfunction in the progression of Alzheimer's disease, which opens up a new therapeutic angle.
Exercise achieves benefits to health in large part through upregulation of cellular maintenance processes.
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In this way it is similar to the practice of calorie restriction, but the outcome is of a lesser degree - exercise does not extend life span in laboratory species, while calorie restriction does. Nonetheless, exercise is certainly beneficial. One of the cellular maintenance processes involved is the unfolded protein response , which, as the name might suggest, clears out proteins that are improperly folded, or have otherwise become stuck at the folding stage of protein manufacture, in the endoplasmic reticulum structure of the cell. Like other maintenance processes, the unfolded protein response becomes less effective with age , for reasons that are far from fully explored.
Here, researchers demonstrate this diminished effectiveness in the context of the response to exercise. Aging is associated with the loss of skeletal muscle mass, quality, and function; decrements that have a negative influence on health span. Resistance exercise improves muscle mass and function, but there is emerging evidence that the molecular and cellular responses to anabolic stimuli e. The unfolded protein response UPR has emerged as a key regulatory pathway in skeletal muscle protein quality control and adaptations to exercise. Early evidence points to altered UPR as an explanation for age and disease related changes in protein folding and accumulation and aggregation of proteins within the endoplasmic reticulum ER.
The influence of age on skeletal muscle adaptive UPR in response to exercise, and the relationship to other key exercise-responsive regulatory pathways is not well-understood.
At baseline, there were modest differences in expression of UPR-related genes in young and older adults. Following exercise, transcriptional markers of UPR pathway activation were attenuated in older adults compared to young based on specific salient UPR-related genes and gene set enrichment analysis. In conclusion, older adults exhibited decreased markers of UPR activation and reduced coordination with autophagy and SC-associated gene transcripts following a single bout of unaccustomed resistance exercise.
In contrast, young adults demonstrated strong coordination between UPR genes and key regulatory gene transcripts associated with autophagy and SC differentiation in skeletal muscle post-exercise. Taken together, the present findings suggest a potential age-related impairment in the post-exercise transcriptional response supporting activation of the UPR and coordination with other exercise responsive pathways i.
Senescent cells are created constantly in the body as the result of a number of processes: the Hayflick limit, wound healing, a toxic local environment, DNA damage, and so forth. Near all are destroyed quite quickly, either via programmed cell death or by the immune system. Some few linger, however, and secrete a potent mix of molecules known as the senescence-associated secretory phenotype SASP.
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The SASP produces wide-ranging damage and dysfunction in tissues, causing issues such as chronic inflammation , fibrosis , and harmful behavior or increased senescence in nearby cells. Thus senescent cell burden is one of the important causes of aging , and efforts to produce senolytic therapies capable of selectively destroying these cells are a very important new branch of medicine.
As noted in today's scientific materials, researchers have recently provided data to associate the burden of senescent cells in older individuals with detrimental changes in blood clotting. This adds one more item to a very long list of harmful effects resulting the SASP.
With age, blood clots form more readily, and in inappropriate circumstances, such as inside major blood vessels. This can cause serious issues such as thrombosis , the blocking of blood vessels and consequent ischemia , or worse, such as a stroke or heart attack should a sizable clot fragment and the fragments block a more vital blood vessel elsewhere. The data here associating components of the SASP with increased susceptibility to blood clotting is interesting to compare with a recent review paper on changes in platelet function with age.
The biochemistry of the age-related hyperactivity of platelets, leading to increased clotting, has been examined in a proximate sense, but reaching backwards to root causes is something that the research community has never been all that good at following through on. The work here is a good example of starting with a known cause of aging and working forwards, a much more efficient approach, and one that must become more widespread in the research community if we are to see meaningful progress in treatments for age-related conditions in the years ahead.
Cellular senescence is associated with age-related blood clots. Cells that become senescent irrevocably stop dividing under stress, spewing out a mix of inflammatory proteins that lead to chronic inflammation as more and more of the cells accumulate over time. Researchers have identified 44 specific senescence-associated proteins that are involved in blood clotting, marking the first time that cellular senescence has been associated with age-related blood clots. Over time it becomes a major risk factor for death.
By 80, the condition affects five to six people per thousand individuals. Blood clots are also a serious side effect of chemotherapy , which sets off a cascade of senescence in those undergoing treatment. That's why blood thinners, which carry their own risks, are often included in treatment protocols. In this study, researchers validated the expression of some of the specific factors in cultured cells and in mice, which were treated with doxorubicin , a widely-used chemotherapy drug which induces widespread senescence.
Those mice showed increased blood clotting, similar to what happens in humans who undergo chemotherapy. Cellular senescence irreversibly arrests cell proliferation , accompanied by a multi-component senescence-associated secretory phenotype SASP that participates in several age-related diseases. Using stable isotope labeling with amino acids SILACs and cultured cells, we identify SASP proteins that senescent human fibroblasts secrete at 2-fold or higher levels compared with quiescent cell counterparts.
Bioinformatic analysis reveals that 44 of these proteins participate in hemostasis , a process not previously linked with cellular senescence. We validated the expression of some of these SASP factors in cultured cells and in vivo. Mice treated with the chemotherapeutic agent doxorubicin, which induces widespread cellular senescence in vivo, show increased blood clotting.
Conversely, selective removal of senescent cells using transgenic pMR mice showed that clearing senescent cells attenuates the increased clotting caused by doxorubicin. Our study provides an in-depth, unbiased analysis of the SASP and unveils a function for cellular senescence in hemostasis. Alongside Juvenescence , Life Biosciences is one of the first large investment concerns wholly dedicated to the growing longevity industry. The Life Biosciences principals take the approach of providing the extensive supporting infrastructure needed to wrap a company around a senior scientist in the field of aging research, and then guide their work towards commercialization.
Most scientists have very little interest in founding a company, and in any case lack the skills needed to do so.
This approach of providing an environment that operates in much the same way as academia from the perspective of the researcher, in which the business side of things is handled, is a good way to accelerate progress in a field that presently lacks a sufficiently large population of entrepreneurs for companies to emerge naturally at a good pace.
How far along is longevity in becoming a defined category for investors? Put it on a scale of for us. If fintech has developed to a nine or a ten, where would you score longevity?