No abstract

Background: The prognostic nutritional index (PNI) has been proposed as a useful prognostic tool in multiple populations. However, its prognostic value has not been fully evaluated in the hip fracture population. We aimed to assess the relationship between PNI and postoperative complications as well as 2-year all-cause mortality in the hip fracture population. Materials and methods: We included patients aged 45 or older who underwent surgery for hip fracture between 2000 and 2022. The baseline serum albumin and total lymphocyte count were used to calculate PNI with the following formula: 10 × serum albumin level (g/dL) + 0.005 × total lymphocyte count (per mm3). Patients were classified into low, medium, and high categories based on tertiles of PNI (≤ 43.23, 43.23-47.35, and > 47.35, respectively). Logistic regression and Cox proportional hazards models were used to calculate the odds ratio (OR) for postoperative compilations and the hazard ratio (HR) for mortality, adjusting for potential confounders. Results: Of 3,351 hip patients, 236 (7.04%) developed postoperative complications, and 305 (9.10%) died during the 2-year follow-up. Compared to the low-category patients, the medium- and high-category patients showed lower odds of postoperative complications (ORs 0.69, 95% CI, 0.48-0.98; and 0.61, 95% CI, 0.40-0.93, respectively), and lower hazard of 2-year mortality (HRs 0.66, 95% CI 0.49-0.88; and 0.61, 95% CI 0.42-0.88, respectively). These associations were robust across a series of analyses, including subgroup analyses and dose-response sensitivity analyses. Conclusion: PNI is an independent predictor of postoperative complications and 2-year all-cause mortality in hip fracture patients. PNI can be used to identify patients who may be at high risk of a poor prognosis.

Rotator cuff tendinopathy (RCT) is the most common cause of shoulder pain, therefore posing an important clinical problem. Understanding the mechanism and biochemical changes of RCT would be of crucial importance and pave the path to targeting novel and effective therapeutic strategies in translational perspectives and clinical practices. Phosphorylation, as one of the most important and well-studied post-translational modifications, is tightly associated with protein activity and protein functional regulation. Here in this study, we generated a global protein phosphorylation atlas within the pathological site of human RCT patients. By using Tandem Mass Tag (TMT) labeling combined with mass spectrometry, an average of 7,741 phosphorylation sites (p-sites) and 3,026 proteins were identified. Compared with their normal counterparts, 1,668 p-sites in 706 proteins were identified as upregulated, while 73 p-sites in 57 proteins were downregulated. GO enrichment analyses have shown that majority of proteins with upregulated p-sites functioned in neutrophil-mediated immunity whereas downregulated p-sites are mainly involved in muscle development. Furthermore, pathway analysis identified NF-κB–related TNF signaling pathway and protein kinase C alpha type (PKCα)–related Wnt signaling pathway were associated with RCT pathology. At last, a weighted kinase-site phosphorylation network was built to identify potentially core kinase, from which serine/threonine-protein kinase 39 (STLK3) and mammalian STE20-like protein kinase 1 (MST1) were proposed to be positively correlated with the activation of Wnt pathway.

Degenerative musculoskeletal diseases (DMDs), including osteoporosis, osteoarthritis, degenerative disc disease, and sarcopenia, present major challenges in the aging population. Patients with DMDs present with pain, functional decline, and reduced exercise tolerance, which result in long‐term or permanent deficits in their ability to perform daily activities. Current strategies for dealing with this cluster of diseases focus on relieving pain, but they have a limited capacity to repair function or regenerate tissue. Cell‐based therapies have attracted considerable attention in recent years owing to their unique mechanisms of action and remarkable effects on regeneration. In this review, current experimental attempts to use cell‐based therapies for DMDs are highlighted, and the modes of action of different cell types and their derivatives, such as exosomes, are generalized. In addition, the latest findings from state‐of‐the‐art clinical trials are reviewed, approaches to improve the efficiency of cell‐based therapies are summarized, and unresolved questions and potential future research directions for the translation of cell‐based therapies are identified.