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Background: Of the numerous complications encountered by people with diabetes (PWD), the effect on mental health is concerning. Within mental health, diabetes distress (DD) occurs when a patient has unfavourable emotional stress while managing their condition, which can be managed by coping strategies but are less studied together in Indian settings. So, the present study aimed to determine the proportion of DD and associated factors and coping skills among the PWD.

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Background: Bear bile powder (BBP), a unique animal-derived medicine with anti-inflammatory and antioxidant effects, is used in Shexiang Tongxin dropping pills (STDP), which is applied to treat cardiovascular diseases, including acute myocardial infarction (AMI). The efficacy and compatibility mechanisms of action of BBP in STDP against cardiovascular diseases remain unclear. This study aimed to investigate the compatibility effects of BBP in STDP in rats with AMI.

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Background: Despite prior observational studies suggesting a link between gut microbiota to Kawasaki disease (KD), these findings remain debated. This study aimed to assess the association between gut microbiota and KD on a genetic level using a two-sample Mendelian randomization (MR) analysis.

Methods: This two-sample MR analysis utilized summary statistics from the largest genome-wide association study meta-analysis on gut microbiota conducted by the MiBioGen consortium.

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Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.

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Metabolic rewiring underlies effective macrophages defense to respond disease microenvironment. However, the underlying mechanisms driving metabolic rewiring to enhance macrophage effector functions remain unclear. Here, we demonstrated that the metabolic reprogramming in inflammatory macrophages depended on the acetylation of CLYBL, a citramalyl-CoA lyase, at lysine 154 (K154), and blocking CLYBL-K154 acetylation restricted the release of pro-inflammatory factors.

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