Notes

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33 and 3.09, respectively). ANCOVA indicated that adolescents with a healthy lifestyle index ≥3 at baseline showed higher cardiorespiratory fitness at follow-up than those with a healthy lifestyle index of 2 and ≤1 (74.4 [SE=1.5] vs 68.9 [SE=1.4] and 67.8 [SE=1.5] laps, respectively; p<0.01). Adolescents with a healthy lifestyle index ≥3 at baseline were more likely to have high cardiorespiratory fitness at follow-up (OR=3.10) than their peers with ≤1.

The results showed a cumulative impact of baseline health-related behaviors on cardiorespiratory fitness at 24-month follow-up in adolescents. These findings underline the key role of promoting a healthy lifestyle to improve adolescents' health.
The results showed a cumulative impact of baseline health-related behaviors on cardiorespiratory fitness at 24-month follow-up in adolescents. These findings underline the key role of promoting a healthy lifestyle to improve adolescents' health.
Unmet social needs are linked with greater healthcare utilization, but most studies lack timely and granular data on these needs. The 2-1-1 helpline is a telephone helpline focused on social needs. The objective of the study is to determine whether the number of 2-1-1 requests per 1,000 people is associated with preventable emergency department visits and compare the strength of the association with another commonly used predictor, Area Deprivation Index.

This cross-sectional study linked 2-1-1 requests to emergency department visits from uninsured and Medicaid-insured patients by ZIP code for a large urban hospital system from January 1, 2016 to August 31, 2019. Negative binomial regression analysis was used to estimate the association of 2-1-1 service requests and Area Deprivation Index with preventable emergency department visits.

A total of 233,146 preventable emergency department visits and 520,308 2-1-1 requests were analyzed. For every 1-SD increase in 2-1-1 requests per 1,000 population, preventable emergency department visits increased by a factor of 3.05, even after controlling for local area deprivation and other population characteristics (p<0.001).

Requests to 2-1-1 helplines are strongly associated with preventable emergency department visits. This information may help hospital leaders and policymakers target social needs interventions to the neighborhoods with the greatest need.
Requests to 2-1-1 helplines are strongly associated with preventable emergency department visits. This information may help hospital leaders and policymakers target social needs interventions to the neighborhoods with the greatest need.Oxidized LDL (oxLDL) plays a pivotal role on atherosclerosis development, mainly in the formation of lipid-laden macrophage "foam cells". As a consequence, substances that can modulate LDL oxidation have a pharmacological and therapeutic relevance. Based in previous findings showing the ability of Syzigium cumini leaf extract (ScExt) in preventing LDL oxidation in vitro, this study was aimed to assess the effects of ScExt on oxLDL-mediated toxicity in murine J774 macrophages-like cells. For biochemical analyses, LDL isolated from fresh human plasma and oxidized with CuSO4 was incubated with ScExt pre-treated macrophages. Our results demonstrated that ScExt was efficient in preventing the overproduction of reactive oxygen/nitrogen species (ROS/RNS), the loss of macrophage's viability and the foam cells formation induced by oxLDL. These protective effects of ScExt make it a promising antioxidant for future trials toward atherogenesis.The spindle assembly checkpoint (SAC) is a surveillance mechanism that promotes accurate chromosome segregation in mitosis. The checkpoint senses the attachment state of kinetochores, the proteinaceous structures that assemble onto chromosomes in mitosis in order to mediate their interaction with spindle microtubules. When unattached, kinetochores generate a diffusible inhibitor that blocks the activity of the anaphase-promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase required for sister chromatid separation and exit from mitosis. learn more Work from the past decade has greatly illuminated our understanding of the mechanisms by which the diffusible inhibitor is assembled and how it inhibits the APC/C. However, less is understood about how SAC proteins are recruited to kinetochores in the absence of microtubule attachment, how the kinetochore catalyzes formation of the diffusible inhibitor, and how attachments silence the SAC at the kinetochore. Here, we summarize current understanding of the mechanisms that activate and silence the SAC at kinetochores and highlight open questions for future investigation.Loss of cardiac muscle after cardiac injury is replaced by cardiac fibrosis, due to very limited regenerative capacity of the heart. Although initially beneficial, persistent cardiac fibrosis leads to pump failure and conduction abnormalities, common modes of death following cardiac injury. Thus, directly reprogramming cardiac fibroblasts into induced cardiomyocyte-like cells (iCMs) by forced expression of cardiogenic factors (referred to as cardiac reprogramming) is particularly attractive in that it targets cardiac fibroblasts, a major source of cardiac fibrosis, to induce new cardiac muscle. Over the last decade, remarkable progresses have been made on cardiac reprogramming, particularly focusing on how to enhance conversion of fibroblasts to iCMs in vitro. However, it still remains elusive whether this new regenerative approach can be translated into clinical practice. This review discusses progresses and challenges of cardiac reprogramming in the translational context.Cardiovascular diseases are a common cause of death worldwide. Adult cardiomyocytes have limited regenerative capacity after injury, and there is growing interest in cardiac regeneration as a new therapeutic strategy. There are several limitations of induced pluripotent stem cell-based transplantation therapy with respect to efficiency and risks of tumorigenesis. Direct reprogramming enables the conversion of terminally differentiated cells into target cell types using defined factors. In most cardiac diseases, activated fibroblasts proliferate in the damaged heart and contribute to the progression of heart failure. In vivo cardiac reprogramming, in which resident cardiac fibroblasts are converted into cardiomyocytes in situ, is expected to become a new cardiac regenerative therapy. Indeed, we and other groups have demonstrated that in vivo reprogramming improves cardiac function and reduces fibrosis after myocardial infarction. In this review, we summarize recent discoveries and developments related to in vivo reprogramming.
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