#VanguardSTEM is an online community and platform that centers women, girls, and non-binary people of color in science, technology, engineering, and mathematics (STEM) fields. We publish original and curated content, using cultural production to include a multiplicity of identities as worthy of recognition and thus redefine STEM identity and belonging. #VanguardSTEM is rooted firmly in Queer, Black feminisms which delineate the experiences and critiques of Black women matter and that these insights can foster a restorative and regenerative construction of the cultures in which we exist. In describing how #VanguardSTEM descended from counterspaces, we draw on speculative fiction to define a #VanguardSTEM hyperspace as a fluid “place-time” that is born digital and enabled by social media, but materializes in the physical world for specific purposes. As Black women in STEM, we consider how our situated knowledges and scientific expertise inform our process. We propose an intersectional scientific methodology to address the influence of embodied observation, embedded context and collective impact on scientific inquiry. Through #VanguardSTEM, we assert, without apology, the right of Black, Indigenous, women of color to self-advocate by fully representing ourselves, our STEM identities and interests, without assimilation.
The decline in the mass and function of bone and muscle is an inevitable consequence of healthy aging with early onset and accelerated decline in those with chronic disease. Termed osteo-sarcopenia, this condition predisposes the decreased activity, falls, low-energy fractures, and increased risk of co-morbid disease that leads to musculoskeletal frailty. The biology of osteo-sarcopenia is most understood in the context of systemic neuro-endocrine and immune/inflammatory alterations that drive inflammation, oxidative stress, reduced autophagy, and cellular senescence in the bone and muscle. Here we integrate these concepts to our growing understanding of how bone and muscle senses, responds and adapts to mechanical load. We propose that age-related alterations in cytoskeletal mechanics alter load-sensing and mechano-transduction in bone osteocytes and muscle fibers which underscores osteo-sarcopenia. Lastly, we examine the evidence for exercise as an effective countermeasure to osteo-sarcopenia.
I Na,late could not be converted to an ''increasing'' morphology by application of isoproterenol, calmodulin, AP-like ramp voltage command or command APs recorded from guinea pig cells. Conventional voltage clamp experiments revealed that the ''increasing'' I Na,late profile in guinea pig is determined by the slow decay of I Na,late in this species. I Na,late was increased by isoproterenol but not by calmodulin in canine myocytes. When APs were recorded from multicellular ventricular preparations with sharp microelectrode, tetrodotoxin decreased AP duration in a reverse rate-dependent manner, which effect was the largest in human, while smaller in canine and the smallest in guinea pig preparations. The shape of I Na,late under the AP is likely determined by the different inactivation kinetics of the sodium channels that generate I Na,late . Variances between different species in the actual sodium channel subtypes that contribute to I Na,late might underlie the differences observed in the macroscopic current. Canine myocytes seems to be the best model of human ventricular cells regarding I Na,late .
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