Children with autism spectrum disorder (ASD) commonly exhibit deficits in postural control and functional mobility, which limit participation in educational and social activities. Kinect sensor-based exergaming offers interactive, feedback-driven practice that may support motor learning within structured rehabilitation. To evaluate whether Kinect-based gaming incorporating structured balance-training components is associated with greater short-term improvement in balance and functional mobility, compared with conventional balance training, in children with ASD. In this prospectively registered randomised controlled trial (CTRI/2026/02/103223; ethics approval granted (initial review 3 December 2025; formal approval 27 January 2026); trial registration completed 11 February 2026, prior to enrolment of the first participant on 16 February 2026; final follow-up assessment completed 14 March 2026), 34 children with ASD aged 6–12 years were allocated equally to an experimental group (Kinect-based gaming incorporating structured balance-training components) or a control group (conventional balance training). These arms constituted two distinct intervention packages rather than an additive comparison: the experimental group did not receive conventional balance exercises in addition to Kinect gaming. Both groups received 15 supervised sessions over three weeks (30 min per session, five sessions per week). The Paediatric Balance Scale (PBS) and Timed Up and Go (TUG) test were assessed at baseline and immediately after intervention. The prespecified primary analysis was ANCOVA of the post-intervention score adjusted for the baseline score; Welch tests, nonparametric tests, repeated-measures ANOVA, and mixed-effects models were prespecified sensitivity analyses. All 34 participants completed the intervention. Baseline characteristics were descriptively similar between groups, although the standardised mean difference for baseline TUG time (SMD = 0.43) was not trivial (Table 1). ANCOVA adjusting for baseline score showed higher adjusted post-intervention PBS scores in the experimental group than the control group (45.08 vs. 40.03 points; adjusted mean difference 5.05, 95
Patients with prior stroke undergoing orthopedic surgery face elevated risks of recurrent stroke and venous thromboembolism, while thromboprophylaxis must be balanced against hemorrhage. Evidence is fragmented across subspecialties. To map the epidemiology, risk stratification, timing, anesthesia and thromboprophylaxis evidence for this population, labeling each recommendation by evidence type. Following PRISMA-ScR and Joanna Briggs Institute guidance, we searched PubMed, Embase and the Cochrane Library from inception through December 2025, with supplementary identification to the final search date of 23 January 2026. No protocol was registered, 76 sources met inclusion criteria, and formal critical appraisal was not undertaken. Deferring elective arthroplasty at least 3 months after stroke is reasonable, but 3 to 6 months is individualized rather than optimal, derived largely from noncardiac surgery; one arthroplasty cohort suggests longer. Hip fracture surgery should proceed within 24 to 48 h after ischemic or remote hemorrhagic stroke; after recent hemorrhagic stroke timing is unestablished, with no fixed delay supported because delay is itself harmful. Mortality advantages of neuraxial anesthesia are observational, randomized trials including REGAIN are null, and technique is individualized. No randomized trial has compared prophylactic agents here, so preferring low-molecular-weight heparin or a direct oral anticoagulant over aspirin is extrapolation, not established standard. Factor XIa inhibition remains investigational: phase 2 trials with venographic endpoints that largely excluded patients with stroke. Management requires individualized, multidisciplinary assessment, not uniform rules; most positions rest on indirect or inferential evidence. Only 8 of 76 charted sources report stroke subtype or the interval since stroke.
Diabetic foot ulcers (DFUs) are among the most serious complications of diabetes and remain a major cause of hospitalization, infection, and lower-extremity amputation. Although clinical examination remains central to risk assessment, earlier identification of patients at high risk for ulceration is still challenging. Vitamin D deficiency is a plausible, modifiable contributor to peripheral neuropathy, endothelial dysfunction, immune dysregulation, and impaired wound healing. The C-reactive protein to high-density lipoprotein cholesterol ratio (CHR) has emerged as a composite biomarker that reflects the combined burden of inflammation and dyslipidemia. This narrative review summarizes current evidence linking vitamin D status and CHR to the pathogenesis, prediction, and potential treatment of DFUs. Its distinctive contribution is the integration of these complementary biological pathways into a unified “vitamin D–inflammation–lipid axis” framework that supports combined-biomarker risk stratification. Evidence from observational studies and meta-analyses consistently associates lower serum 25-hydroxyvitamin D concentrations with greater DFU risk. Mechanistically, vitamin D may influence neural integrity, endothelial function, antimicrobial defense, and tissue repair, whereas CHR captures inflammatory burden together with impaired HDL-mediated vascular protection. Emerging evidence suggests that combining vitamin D with CHR may improve discrimination of DFU risk beyond either biomarker alone. Evidence for vitamin D supplementation in patients with established DFUs is encouraging but remains limited by small trials and heterogeneity. Vitamin D and CHR appear to capture complementary biological pathways relevant to DFU development and progression. Their combined use may support more refined risk stratification, but prospective validation and interventional studies are required before routine clinical implementation.
Insulin resistance and a slow decrease of β-cell activity cause persistent hyperglycemia in type 2 diabetes mellitus (T2DM), a chronic and progressive metabolic disease. While SGLT2 inhibitors, DPP-4 inhibitors, and GLP-1 receptor agonists are among the more recent oral antidiabetic medications (OADs) that have expanded the options for managing diabetes, insulin has always been a crucial therapy option, especially for patients with severe illness. The comparative functions of insulin and OADs are examined in this narrative review, with a focus on glycaemic control, hypoglycemia, changes in body weight, cardiovascular effects, and treatment compliance. Using PubMed, Scopus, Web of Science, and Google Scholar, pertinent literature from the last ten years was examined with a focus on clinical research, randomised controlled trials, and pertinent reviews. Insulin often offers robust and consistent glycaemic control, particularly in advanced type 2 diabetes; nevertheless, hypoglycemia, weight gain, and challenges with long-term adherence may accompany its usage. In contrast, a number of more recent OADs, especially SGLT2 inhibitors and GLP-1 receptor agonists, provide advantages beyond glucose lowering, such as weight loss and protection for the heart and kidneys. However, oral treatment alone may eventually become less effective due to growing β-cell failure, necessitating the initiation or intensification of insulin for certain patients. In general, glycaemic needs, comorbidities, safety, patient preferences, adherence, and disease progression should all be taken into consideration when making treatment decisions. Therefore, more effective long-term management of T2DM can be achieved while lowering complications and enhancing patient quality of life with a timely and balanced mix of OADs and insulin.
