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ced by the "hero" discourses or overshadowed by professional demands.

COVID-19 is not merely a communicable disease but also a social and political phenomenon that intensifies the effects of social inequities. Current understanding of pandemic stressors affecting HCPs is largely partial in nature. Although workplace stressors of HCPs are real and intense, they need to be explored and understood in the context of stressors that exist in other domains of HCPs' lives such as family and community to ensure these experiences are not being silenced by the "hero" discourses or overshadowed by professional demands.

Telemedicine visit use vastly expanded during the COVID-19 pandemic, and this has had an uncertain impact on cardiovascular care quality.

We sought to examine the association between telemedicine visits and the failure to meet the Controlling High Blood Pressure (BP) quality measure from the Centers for Medicare & Medicaid Services.

This was a retrospective cohort study of 32,727 adult patients with hypertension who were seen in primary care and cardiology clinics at an urban, academic medical center from February to December 2020. The primary outcome was a failure to meet the Controlling High Blood Pressure quality measure, which was defined as having no BP recorded or having a last recorded BP of ≥140/90 mm Hg (ie, poor BP control). Multivariable logistic regression was used to assess the association between telemedicine visit use during the study period (none, 1 telemedicine visit, or ≥2 telemedicine visits) and poor BP control; we adjusted for demographic and clinical characteristics.

During tlemedicine visit use may not negatively impact BP control when BP is recorded.

Ecological momentary assessment (EMA) uses mobile technology to enable in situ self-report data collection on behaviors and states. selleck products In a typical EMA study, participants are prompted several times a day to answer sets of multiple-choice questions. Although the repeated nature of EMA reduces recall bias, it may induce participation burden. There is a need to explore complementary approaches to collecting in situ self-report data that are less burdensome yet provide comprehensive information on an individual's behaviors and states. A new approach, microinteraction EMA (μEMA), restricts EMA items to single, cognitively simple questions answered on a smartwatch with single-tap assessments using a quick, glanceable microinteraction. However, the viability of using μEMA to capture behaviors and states in a large-scale longitudinal study has not yet been demonstrated.

This paper describes the μEMA protocol currently used in the Temporal Influences on Movement & Exercise (TIME) Study conducted with young adultmanner. Data suggest that μEMA may be valuable for understanding behaviors and states at the individual level, thus possibly supporting future longitudinal interventions that require within-day, temporally dense self-report data as people go about their lives.

Black men who have sex with men (BMSM) suffer from alarmingly high rates of HIV in the United States. Pre-exposure prophylaxis (PrEP) can reduce the risk of HIV infection by 99% among men who have sex with men, yet profound racial disparities in the uptake of PrEP persist. Low PrEP uptake in BMSM is driven by poor access to PrEP, including inconvenient locations of PrEP-prescribing physicians, distrust of physicians, and stigma, which limit communication about PrEP and its side effects. Previous work indicates that offering HIV prevention services in pharmacies located in low-income, underserved neighborhoods is feasible and can reduce stigma because pharmacies offer a host of less stigmatized health services (eg, vaccinations). We present a protocol for a pharmacy PrEP model that seeks to address challenges and barriers to pharmacy-based PrEP specifically for BMSM.

We aim to develop a sustainable pharmacy PrEP delivery model for BMSM that can be implemented to increase PrEP access in low-income, undersered 81 individuals who would have been eligible for the pilot phase.

Pharmacies have proven to be a feasible source for offering PrEP for White men who have sex with men but have failed to reach the most at-risk, vulnerable population (ie, BMSM). Increasing PrEP access and uptake will reduce HIV incidence and racial inequities in HIV. Translational studies are required to build further evidence and scale pharmacy-based PrEP services specifically for populations that are disconnected from HIV prevention resources.

DERR1-10.2196/35590.

DERR1-10.2196/35590.Targeting endoplasmic reticulum (ER) stress, inflammation, and metabolic dysfunctions may halt the pathogenesis of obesity and thereby reduce the prevalence of diabetes, cardiovascular disesases, and cancers. The present study was designed to elucidate the mechnaisms by which plant-derived celastrol ameliorated inflammation and lipid accumulation in obesity. The mouse model of diet-induced obesity was induced by feeding high-fat diet for 3 months and subsequently intervented with celastrol for 21 days. Hepatic and adipose tissues were analyzed for lipid accumulation, macrophage activation, and biomarker expression. As result, celastrol effectively reduced body weight, suppressed ER stress, inflammation, and lipogenesis while promoted hepatic lipolysis. RNA-sequencing revealed that celastrol-loaded nanomicelles restored the expression of 49 genes that regulate ER stress, inflammation, and lipid metabolism. On the other hand, celastrol-PEG4-alkyne was synthesized for identifying celastrol-bound proteins in RAW264.7 macrophages. link2 ER chaperone GRP78 (78 kDa glucose-regulated protein) was identified by proteomics approach for celastrol binding to the residue Cys41. Upon binding and conjugation, celastrol diminished the chaperone activity of GRP78 by 130-fold and reduced ER stress in palmitate-challenged cells, while celastrol analog lacking quinone methide failed to exhibit antiobesity effects. Thus, covalent GRP78 inhibition may induce the reprograming of ER signaling, inflammation, and metabolism against diet-induced obesity.The distribution of the generation time (the interval between individuals becoming infected and transmitting the virus) characterises changes in the transmission risk during SARS-CoV-2 infections. link3 Inferring the generation time distribution is essential to plan and assess public health measures. We previously developed a mechanistic approach for estimating the generation time, which provided an improved fit to data from the early months of the COVID-19 pandemic (December 2019-March 2020) compared to existing models (Hart et al., 2021). However, few estimates of the generation time exist based on data from later in the pandemic. Here, using data from a household study conducted from March to November 2020 in the UK, we provide updated estimates of the generation time. We considered both a commonly used approach in which the transmission risk is assumed to be independent of when symptoms develop, and our mechanistic model in which transmission and symptoms are linked explicitly. Assuming independent transmission and symptoms, we estimated a mean generation time (4.2 days, 95% credible interval 3.3-5.3 days) similar to previous estimates from other countries, but with a higher standard deviation (4.9 days, 3.0-8.3 days). Using our mechanistic approach, we estimated a longer mean generation time (5.9 days, 5.2-7.0 days) and a similar standard deviation (4.8 days, 4.0-6.3 days). As well as estimating the generation time using data from the entire study period, we also considered whether the generation time varied temporally. Both models suggest a shorter mean generation time in September-November 2020 compared to earlier months. Since the SARS-CoV-2 generation time appears to be changing, further data collection and analysis is necessary to continue to monitor ongoing transmission and inform future public health policy decisions.Dynamic microtubules play a critical role in cell structure and function. In nervous system, microtubules are the major route for cargo protein trafficking and they specially extend into and out of synapses to regulate synaptic development and plasticity. However, the detailed depolymerization mechanism that regulates dynamic microtubules in synapses and dendrites is still unclear. In this study, we find that KIF2C, a dynamic microtubule depolymerization protein without known function in the nervous system, plays a pivotal role in the structural and functional plasticity of synapses and regulates cognitive function in mice. Through its microtubule depolymerization capability, KIF2C regulates microtubule dynamics in dendrites, and regulates microtubule invasion of spines in neurons in a neuronal activity-dependent manner. Using RNAi knockdown and conditional knockout approaches, we showed that KIF2C regulates spine morphology and synaptic membrane expression of AMPA receptors. Moreover, KIF2C deficiency leads to impaired excitatory transmission, long-term potentiation, and altered cognitive behaviors in mice. Collectively, our study explores a novel function of KIF2C in the nervous system and provides an important regulatory mechanism on how activity-dependent microtubule dynamic regulates synaptic plasticity and cognition behaviors.Regional control of fibrosis after myocardial infarction is critical for maintaining structural integrity in the infarct while preventing collagen accumulation in non-infarcted areas. Cardiac fibroblasts modulate matrix turnover in response to biochemical and biomechanical cues, but the complex interactions between signaling pathways confound efforts to develop therapies for regional scar formation. We employed a logic-based ordinary differential equation model of fibroblast mechano-chemo signal transduction to predict matrix protein expression in response to canonical biochemical stimuli and mechanical tension. Functional analysis of mechano-chemo interactions showed extensive pathway crosstalk with tension amplifying, dampening, or reversing responses to biochemical stimuli. Comprehensive drug target screens identified 13 mechano-adaptive therapies that promote matrix accumulation in regions where it is needed and reduce matrix levels in regions where it is not needed. Our predictions suggest that mechano-chemo interactions likely mediate cell behavior across many tissues and demonstrate the utility of multi-pathway signaling networks in discovering therapies for context-specific disease states.The decarboxylation of pyruvate is a central reaction in the carbon metabolism of all organisms. It is catalyzed by the pyruvateferredoxin oxidoreductase (PFOR) and the pyruvate dehydrogenase (PDH) complex. Whereas PFOR reduces ferredoxin, the PDH complex utilizes NAD+. Anaerobes rely on PFOR, which was replaced during evolution by the PDH complex found in aerobes. Cyanobacteria possess both enzyme systems. Our data challenge the view that PFOR is exclusively utilized for fermentation. Instead, we show, that the cyanobacterial PFOR is stable in the presence of oxygen in vitro and is required for optimal photomixotrophic growth under aerobic and highly reducing conditions while the PDH complex is inactivated. We found that cells rely on a general shift from utilizing NAD(H)- to ferredoxin-dependent enzymes under these conditions. The utilization of ferredoxins instead of NAD(H) saves a greater share of the Gibbs-free energy, instead of wasting it as heat. This obviously simultaneously decelerates metabolic reactions as they operate closer to their thermodynamic equilibrium.