Cardiac Troponin to Adjudicate Subclinical Heart Failure in Diabetic Patients and a Murine Model of Metabolic Syndrome.

Background: Cardiovascular disease, kidney health, and metabolic disease (CKM) syndrome is associated with significant morbidity and mortality, particularly from congestive heart failure (CHF). Guidelines recommend measurement of cardiac troponin (cTn) to identify subclinical heart failure (HF) in diabetics/CKM. However, appropriate thresholds and the impact from routine screening have not been elucidated.

Dietary lipids inhibit mitochondria transfer to macrophages to divert adipocyte-derived mitochondria into the blood.

Adipocytes transfer mitochondria to macrophages in white and brown adipose tissues to maintain metabolic homeostasis. In obesity, adipocyte-to-macrophage mitochondria transfer is impaired, and instead, adipocytes release mitochondria into the blood to induce a protective antioxidant response in the heart. We found that adipocyte-to-macrophage mitochondria transfer in white adipose tissue is inhibited in murine obesity elicited by a lard-based high-fat diet, but not a hydrogenated-coconut-oil-based high-fat diet, aging, or a corn-starch diet.

A systematic review and meta-analysis of obesity and COVID-19 outcomes.

Some studies report that obesity is associated with more severe symptoms following SARS-CoV-2 infection and worse COVID-19 outcomes, however many other studies have not reproduced these findings. Therefore, it is uncertain whether obesity is in fact associated with worse COVID-19 outcomes compared to non-obese individuals. We conducted a systematic search of PubMed (including MEDLINE) and Google Scholar on May 18, 2020 to identify published studies on COVID-19 outcomes in non-obese and obese patients, covering studies published during the first 6 months of the pandemic.

Intercellular Mitochondria Transfer to Macrophages Regulates White Adipose Tissue Homeostasis and Is Impaired in Obesity.

Recent studies suggest that mitochondria can be transferred between cells to support the survival of metabolically compromised cells. However, whether intercellular mitochondria transfer occurs in white adipose tissue (WAT) or regulates metabolic homeostasis in vivo remains unknown. We found that macrophages acquire mitochondria from neighboring adipocytes in vivo and that this process defines a transcriptionally distinct macrophage subpopulation.

Myeloid-specific Asxl2 deletion limits diet-induced obesity by regulating energy expenditure.

We previously established that global deletion of the enhancer of trithorax and polycomb (ETP) gene, Asxl2, prevents weight gain. Because proinflammatory macrophages recruited to adipose tissue are central to the metabolic complications of obesity, we explored the role of ASXL2 in myeloid lineage cells. Unexpectedly, mice without Asxl2 only in myeloid cells (Asxl2ΔLysM) were completely resistant to diet-induced weight gain and metabolically normal despite increased food intake, comparable activity, and equivalent fecal fat.

Return to Play and Complications After Hook of the Hamate Fracture Surgery.

Purpose: The purpose of this study was to evaluate the efficacy of hook of the hamate excision for fracture in a large cohort of patients to better understand recovery time and complications.

Methods: We retrospectively reviewed the medical records of patients treated with surgical excision for hook of the hamate fractures at 2 different centers. We collected information on demographics, clinical presentation, and postoperative complications.