Army Medical University

This study investigated the association of BMI, weight change patterns, and absolute weight change with mortality in adults (≥ 50 years) with diabetes or prediabetes. A longitudinal cohort analysis of 11,518 NHANES (2005-2018) participants assessed BMI categories, weight change patterns (stable normal weight, persistent overweight, obesity transitions, persistent obesity), and absolute weight change (loss, stable, gain). Cox models and restricted cubic splines evaluated mortality risks, adjusting for covariates. BMI showed a U-shaped mortality relationship, with obesity increasing all-cause (HR: 1.60, 95% CI: 1.20-2.13) and diabetes-related mortality (HR: 2.53, 95% CI: 1.35-4.75). Persistent obesity from young adulthood raised mortality risks (all-cause: +60%; diabetes-related: +153%), while later-life persistent overweight reduced risk. Weight loss (≥ 2.5kg) increased mortality, whereas moderate gain (2.5-20kg) was protective. Results remained robust in sensitivity analyses. For person with diabetes or prediabetes prevention, maintaining normal weight in early adulthood and modest weight gain with aging is beneficial. Older adults may benefit from mild overweight to lower mortality risk. Age-specific weight management strategies should guide clinical and public health recommendations. The online version contains supplementary material available at 10.1007/s40200-026-01896-6.

Sepsis is characterized as a life-threatening organ dysfunction resulting from a dysregulated host response to infection, representing a critical clinical syndrome. Uncontrolled infection and inflammation are two main characteristics of sepsis. Neutrophil extracellular traps (NETs) is a major mechanism by which neutrophils resist pathogens invasion, but the mechanism of the NETs formation remain completely unclear. This study aims to elucidate the role of Histone Deacetylase 2 (HDAC2) in NETs formation and its impact on antimicrobial and anti-inflammatory activities in sepsis. We employed flow cytometry, immunofluorescence and western blotting to assess NETs formation. The effects of HDAC2 on NETs and sepsis outcomes were investigated using an HDAC2 inhibitor and HDAC2 knockout mice in CLP-induced and LPS-induced sepsis models. Histone modifications in neutrophils were also analyzed to explore HDAC2's regulatory mechanism. HDAC2 was found to be highly expressed in patients and mice with sepsis. While HDAC2 knockout or inhibition reduced inflammation and improved organ function in non-infectious sepsis, it decreased survival in infectious sepsis. In addition, knockout or inhibition of HDAC2 significantly reduced the NETs formation, and impaired the antimicrobial activities against E. coli infection in mice. Mechanistically, HDAC2 indirectly promoted H3R17 citrullination to induce the NETs formation through down-regulating H3K18 acetylation and interactively inhibiting CARM1-mediated H3R17 methylation in neutrophils. Furthermore, a dual inhibition strategy targeting HDAC2 and CARM1 not only suppressed inflammation, prevented from multiple organ dysfunction, but also enhanced the antimicrobial activities, which finally improved survival rate of mice with sepsis induced by cecal ligation and puncture (CLP). Our findings reveal a novel role for HDAC2 in modulating anti-infectious immunity through NETs formation during sepsis. This study provides a potential therapeutic strategy for sepsis by enhancing both antimicrobial and anti-inflammatory responses, offering a promising approach to preserve organ function and improve survival.

Current frozen shoulder (FS) therapies present a clinical dilemma: although intra-articular corticosteroids with home exercise provide proven medium-term (3-month) benefits, they lack short-term (<4-week) efficacy for rapid recovery; conversely, manipulative treatments achieve faster outcomes but carry invasiveness risks. These limitations highlight the urgent need for developing and validating novel noninvasive approaches with prompt therapeutic effects. To compare the efficacy and safety of ultrasound-guided tendon surface (UGTS) injection versus manipulation under local anesthesia (MULA) and blind tender point (BTP) injection, all combined with intra-articular injection and home exercise. Randomized controlled trial; Level of evidence, 1. The authors first developed a novel ultrasound-based strategy, which they named "ultrasound-guided tendon surface." Then they conducted a multicenter randomized controlled trial (2019-2022). The primary outcome was 4-week shoulder function assessed by the Beijing Friendship Hospital Scale (BFHS), a modified version of the Constant-Murley Score adapted for Chinese populations with demonstrated validity. Secondary outcomes included (1) short-term (1-month) pain (visual analog scale [VAS]) score, active range of motion (ROM), Evaluation Scale of the Shoulder under Ultrasound (ESSU) score, pain relief, treatment sessions, and cartilage thickness; and (2) long-term (2-year) complete remission rates (tele-follow-up). Among 365 screened patients, 139 were enrolled and randomized to receive UGTS (n = 49), MULA (n = 43), and BTP (n = 47). At the 1-week follow-up visit, the UGTS group showed rapid improvement in BFHS scores compared to both the MULA and BTP groups. These early functional advantages were also indicated by the VAS score, ROM, ESSU score, and pain relief. UGTS achieved faster complete remission (1 month: 59.2% vs 31.0% and 34.9% for BTP and MULA, respectively; 3-month: 79.6% vs 53.2% and 69.8% for BTP and MULA, respectively; P < .05), with remission rates converging by 24 months (P = .216), yet retained early rapid response as its key clinical advantage. UGTS showed no significant impact on articular cartilage thickness. Serial ultrasound monitoring demonstrated no rotator cuff injuries attributable to either the UGTS procedure or prescribed exercises. UGTS combined with intra-articular injection and exercise promotes faster recovery without safety concerns, representing an effective noninvasive first-line option for rapid relief in FS. ChiCTR1900025874 (Chinese Clinical Trial Registry number).