Ssd Lifespan Software

[Hermalindo Lepicier]

Meetingthe American Heart Association's recommendation of 10,000 daily can significantly reduce the risk of heart disease, extending your lifespan. Yet, when you're sitting in an office desk eight hours a day, you might not have time to walk five miles every day. And if you do, you're likely putting chores and hobbies aside. Instead, active workstations offer you the chance to get to 10,000 steps and make your fitness tracker happy while you're at work.

Create a fitness-friendly space that encourages healthier habits and makes you happy. Not interested in a Treadmill Desk? No worries! We offer all types of fitness equipment that suit people of all experience levels. We're confident that our equipment, whether it's a standing desk or bike desk, can be the push a person needs to start their fitness journey.

With its pedal-powered internals, this under-desk bike is capable of delivering 65W of power via USB-C and 15W with wireless charging. In addition, the bike has comforts such as an all-day comfort cushion, wheels that make it easy to move around, a backside seat handle, and a solid aluminum base frame. If you want to do your part to help the environment, the Ampera Bike Desk is a great way to do that.

LifeSpan has been in the home fitness market for 25 years. With well-made, reliable products like theTR5500iMfolding treadmill, theTR7000iMcommercial treadmill, and theSP1000Stretch Partner Pro, LifeSpan established itself as one of the leading fitness equipment manufacturers. But, when we noticed a need for fitness equipment tailored specifically to the work-from-home crowd, we began developing our office wellness series. Now, LifeSpan Fitness is known for both its fitness and office wellness equipment.

A healthier planet means healthier people, which is why we're committed to doing our part to fight climate change. Our new Ampera Bike Desk speaks to our ideals, with the product able to generate electricity and power a user's laptop.

In addition to the Ampera Bike Desk, we've also partnered with Greenspark to increase our impact. With Greenspark, we can reduce our carbon footprint with every purchase by planting one tree for every $300 spent on our site, and we can recuse 10 plastic bottles from the ocean for every review.

Equipment that is built to last for multi-housing communities, recreation and rehabilitation centers, and offices. Office wellness is the future of the workplace. It draws in employees, keeps them happy, and allows them to have more time after work to focus on what matters most. As an employer that invests in the tools for an active workforce, you'll see:

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Ageing studies to date have focused largely on lifespan extension, particularly in yeast, worms and fruit flies, but lifespan extension does not necessarily reflect longer healthspan12,13,14. There is a need for integrated studies to determine the effects of interventions on both healthspan and lifespan. Laboratory mice are particularly suited for such experiments, as ageing pathologies that are important for human wellbeing and function are apparent and lifespan studies are well established in mice1,15.

Studies of germline genetic loss of function on healthspan and/or lifespan should be complemented by interventions in late life only to identify phenotypes that are carried through from younger animals and for translational relevance. This is pertinent to the current study, in which some beneficial effects of Il11 loss of function (such as increased muscle mass and strength) are apparent even in young Il11-deleted mice (Fig. 2 and Extended Data Fig. 6). To achieve this goal, we administered a neutralizing IL-11 antibody (X203) or IgG control to aged mice and studied healthspan indices29,38 (Fig. 3a).

Compared with controls, mice receiving X203 from 75 to 100 weeks of age progressively lost body weight that was defined by a reduction in indexed fat mass (Fig. 3b,c). Impaired glucose metabolism was apparent across experimental groups at study start that was improved in mice receiving X203, whereas IgG had no effect (Fig. 3d). Frailty scores were mildly increased across experimental groups at study initiation (Fig. 3e). Over the study period, mice receiving no treatment or IgG exhibited frailty progression (for example, tremor and gait disorder), whereas those on X203 did not (Fig. 3e and Supplementary Table 3). Muscle strengths of 100-week-old mice receiving anti-IL-11 were higher than aged-matched controls receiving IgG or untreated, and also higher than those of 75-week-old mice at the start of the experiment (Fig. 3f and Extended Data Fig. 7a).

After six weeks of antibody administration, mice were studied in metabolic cages. The RER of mice receiving X203 was higher than that of IgG-treated mice but lower than that of a cohort of young mice (Fig. 3g and Extended Data Fig. 7b), suggesting that X203 slows age-associated metabolic inflexibility. Administration of X203 was associated with higher core temperatures and increased food intake, whereas locomotor activity levels and faecal caloric densities were similar between study groups (Fig. 3h and Extended Data Fig. 7b,c).

Fibrosis is a canonical feature of ageing and a hallmark of senescence, and IL-11 is known to be pro-fibrotic in human cells and in young adult mice22,39. We quantified fibrosis in aged vWAT, skeletal muscle and livers of old mice across experimental groups, which showed reversal of tissue fibrosis across organs of mice receiving X203 (Fig. 3l).

To support our findings, we showed age-related suppression of UCP1 expression in vWAT of female control mice, which was mitigated in female mice lacking Il11 and in mice of both sexes lacking Il11ra1 (Fig. 4f and Extended Data Fig. 9b). A targeted assessment of mitochondrial gene expression in vWAT revealed significant increases in terms associated with mitochondrial biogenesis and function in mice receiving anti-IL-11 (Extended Data Fig. 9c,d).

The metabolic effects seen with inhibition of IL-11 in old mice phenocopy those of young mice with WAT-specific deletion of Raptor41. Although we did not study mice at thermoneutrality, we surmise that inhibition of IL-11 prevents mTORC1 activation in fat, affording age-repressed WAT beiging that can be particularly prominent in mice40,41. We highlight that although we excluded food intake and enteric or locomotor-related energy expenditure and showed WAT beiging across genetic and therapeutic models, we did not pinpoint the specific physiology leading to weight loss with IL-11 inhibition.

Beyond metabolism, inhibition of IL-11 improved deterministic features of ageing that are common among vertebrates (such as frailty and sarcopenia), showing generic anti-ageing benefits at the organismal level. Intriguingly, some of the beneficial effects of germline Il11ra1 or Il11 deletion, notably in muscle and fat, were apparent even in young mice, perhaps suggesting primacy of metabolic benefits. We did not discern cell-type specificity but infer that tissue-localized IL-11 activity is important, given its known autocrine and paracrine activities22.

Inhibition of IL-11 increased lifespan in both male and female mice. The magnitude of lifespan extension remains to be fully determined but current data suggest that anti-IL-11 therapy given in late life increases median lifespan by more than 20% in both sexes. In these experiments, anti-IL-11 was injected in mice from 75 weeks of age (human equivalent to approximately 55 years of age) and it remains to be seen whether administration to older mice has similar effects and/or if short term anti-IL-11 therapy is effective for lifespan extension, as seen for rapamycin. Mouse mortality in old age is often cancer-related44 and our end-of-life autopsy data support the notion that inhibition of IL-11 significantly reduces age-related cancers. Of note, IL-11 is important for tumorigenesis and tumour immune evasion and clinical trials of anti-IL-11 in combination with immunotherapy to treat cancer are planned22.

Inhibition of ERK or mTOR or activation of AMPK by trametinib, rapamycin or metformin, respectively, increase lifespan in model organisms and such drugs are advocated by some for use in humans. However, these agents have on- and off-target toxicities along with variable, and sometimes detrimental, effects on healthspan and inflammation12,13,35,49. Our data suggest that anti-IL-11 therapy, which has a reassuring safety profile and is currently in early-stage clinical trials for fibroinflammatory diseases, is a potentially translatable approach for extending human healthspan and lifespan22.

All experimental protocols involving human subjects (commercial primary human cell lines) were performed in accordance with the ICH Guidelines for Good Clinical Practice. All participants provided written informed consent and ethical approvals have been obtained by the relevant parties as written in the datasheets provided by ScienCell from which primary human cardiac fibroblasts and primary human hepatocytes were commercially sourced.

Animal studies were carried out in compliance with the recommendations in the Guidelines on the Care and Use of Animals for Scientific Purposes of the National Advisory Committee for Laboratory Animal Research (NACLAR). All experimental procedures were approved (SHS/2019/1481 and SHS/2019/1483) and conducted in accordance with the SingHealth Institutional Animal Care and Use Committee (IACUC). Certified veterinarians were responsible for all animal experiment procedures according to the laws governing animal research in Singapore.

Mouse body composition (total body fat and lean mass measurements) was performed 1 day prior to GTT/ITT or euthanasia by Echo MRI analysis using 4in1 Composition Analyzer for live small animals (Echo Medical Systems).

3a8082e126