Post-operative deep vein thrombosis (DVT) significantly compromises outcomes in prostate cancer (PCa) surgery patients. This study aimed to develop and validate a clinically applicable nomogram for individualized DVT risk stratification. In this retrospective matched case-control study, 500 PCa patients (150 DVT, 350 non-DVT) undergoing surgery (2018-2023) were analyzed after rigorous DVT confirmation via duplex ultrasonography (92.2% adherence) and radiologist adjudication (κ = 0.86). To address the inflated DVT incidence due to case-control sampling, inverse probability weighting corrected sampling bias (weighted DVT incidence 12.3% versus true 12.1%), with post-weighting covariate balance confirmed by a standardized mean difference <0.08. Independent predictors were identified through multivariate logistic regression, with nomogram construction and validation (bootstrap optimism correction; temporal validation cohort n = 103). Decision curve analysis (DCA) evaluated clinical utility by quantifying net benefit across threshold probabilities (5%-80%). Age (OR 1.045 [95% CI 1.022-1.072] per year), surgery duration (OR 1.018/10 [95% CI 1.011-1.025 per min), preoperative D-dimer (OR 1.315 [95% CI 1.192-1.451] for every 0.1 mg/L), prostate-specific antigen density (PSAD; OR 4.805 [95% CI 2.761-8.365] per unit), and advanced tumour stage (T3-T4, OR 3.512 [95% CI 2.012-6.115]) were significant predictors. The nomogram demonstrated excellent discrimination (optimism-corrected area under the curve [AUC] = 0.942; temporal validation AUC=0.918) and calibration (slope = 0.94). Clinical thresholds: age ≥68.3 years, surgery ≥159.7 min, D-dimer ≥0.92 mg/L, PSAD ≥2.95 ng/mL/cm³. DCA revealed optimal clinical utility at 10%-60% risk thresholds, with a maximum net benefit (0.111) at 10% threshold probability, consistently outperforming default treatment strategies. This validated nomogram integrates five readily available clinical variables to precisely quantify DVT risk in PCa surgical patients. It enables personalized preoperative risk assessment, facilitating targeted prophylaxis to mitigate thromboembolic complications beyond guideline-compliant prevention.

The long-term immune and metabolic effects of COVID-19 in vaccinated populations remain incompletely characterized. This study aimed to analyze dynamic changes in lymphocyte subpopulations (T, B, and Natural Killer [NK] cells [TBNK]) and key metabolic indicators among college students post-Omicron infection with prior vaccination. A prospective observational cohort of 71 male students infected with the Omicron variant of COVID-19 (Beijing, China; March-April 2022) and 18 uninfected controls was followed for 2 years. TBNK subsets and metabolic parameters (uric acid, lipid profiles, β2-microglobulin) were analyzed at 3, 6, 12, and 24 months post-infection. Immunologically, total lymphocytes were elevated at 3 months when compared with controls (P = 0.0063). Total T cells declined at 6 and 12 months but rebounded by 24 months (P < 0.0001). NK cells increased until 12 months, then declined (P < 0.0001). B cells decreased persistently (P < 0.05). Metabolically, uric acid and lipid parameters (total cholesterol, LDL-C, lipoprotein [a]) showed significant fluctuations, with notable increases at 1 year post-infection (P < 0.05). β2-microglobulin levels decreased significantly over time (P < 0.0001). Omicron infection induces immune and metabolic disturbances lasting at least 1 year, with gradual but incomplete recovery by 2 years. The interplay between immune dysregulation and metabolic alterations may contribute to the long-term health effects of COVID-19. Monitoring both lymphocyte and metabolic dynamics may guide the long-term management of post-COVID-19 sequelae.

This study aimed to evaluate the predictive value of multiparametric transthoracic echocardiography (TTE) in patients with moderate to severe sepsis-associated acute respiratory distress syndrome (SA-ARDS), with a focus on right ventricular function and myocardial strain. This single-centre retrospective cohort study was conducted at a tertiary academic medical centre. Data were collected for adult patients admitted to the ICU between June 2020 and June 2024, who developed sepsis within the first 24 hours of ICU admission. A total of 1,163 patients with moderate to severe SA-ARDS were included, with a mean age of 67.4 (SD 14.0) years. Diabetes and chronic lung disease were the most common comorbidities. Clinical predictors of non-recovery included severe ARDS (p = 0.003), and lower PaO₂/FIO₂ ratios (p < 0.001). In contrast, echocardiographic predictors of recovery included higher tricuspid annular plane systolic excursion (TAPSE) (p < 0.001) and lower right ventricular systolic pressure (RVSP) (p = 0.023), higher right ventricular fractional area change (RV-FAC) (p < 0.001), and more negative global longitudinal strain (GLS) (p < 0.001) compared to the non-recovery group. The combined model integrating RV-FAC, GLS, and right ventricular free wall longitudinal strain (RVFWLS) demonstrated superior predictive performance (area under the receiver operating characteristic curve (AUC) = 0.879 [95% CI 0.854-0.904]), outperforming traditional TTE parameters (TAPSE + RVSP, AUC = 0.783, p < 0.001). Multiparametric echocardiography, particularly RV-FAC, GLS, and RVFWLS, provides a robust tool for predicting SA-ARDS recovery. These findings emphasize the critical role of right ventricular adaptability and myocardial deformation in prognosis.

Thrombocytopenia occurs frequently in patients with acute cholangitis and is considered a risk factor for poor prognosis. The present study aimed to investigate the relationship of thrombocytopenia with 60-day mortality and cholangitis disease severity. This was a single-centre, retrospective, observational cohort study. We analyzed 498 patients with acute cholangitis who were admitted to our hospital between July 2013 and July 2021. The correlation between admission platelet count and disease severity and prognosis were analyzed. In this study, the incidence of thrombocytopenia (platelet count <100×109/L) and severe thrombocytopenia (platelet count <50×109/L) in acute cholangitis was 31.12% and 7.43%, respectively. Median platelet count in the thrombocytopenia group was 64×109/L (IQR 42, 79). Compared with the no-thrombocytopenia group, the thrombocytopenia group had a higher proportion of grade III cases, incidences of complications (including respiratory failure, circulatory failure, bacteremia), and higher Acute Physiologic Assessment and Chronic Health Evaluation (APACHE II) and Sequential Organ Failure Assessment (SOFA) scores (all P < 0.05). The 60-day mortality rate was significantly higher in the thrombocytopenia group than that in the no-thrombocytopenia group (12.90% vs. 2.33%, P < 0.001). Binary logistic regression analysis demonstrated that platelet count on admission was a risk factor for mortality. Receiver operating characteristic (ROC) curve analysis showed 84×109/L as the optimal platelet count cut-off value for predicting 60-day mortality with acute cholangitis (Assessment area under the ROC curve [AUC] 0.79; sensitivity 76.4%, specificity 71.4%). Platelet count is a readily available, prognostic marker that can identify acute cholangitis patients at risk of poorer outcomes.

MD-PhD programs play a critical role in training the next generation of clinician-scientists in Canada. However, since 2015, these programs have faced increasing financial pressures. This review examines the impact of cost-cutting measures on Canadian MD-PhD programs and their implications for equity, diversity, and inclusion initiatives in the Canadian context. Using a mixed-methods approach, we analyzed funding structures across all 11 Canadian MD-PhD programs and compared them with 120 U.S. MD-PhD programs using publicly available data. Eighteen percent of Canadian MD-PhD programs (2 of 11) offer full funding, compared to 43% (52 of 120) of U.S. programs. Canadian MD-PhD applicants from two provinces (British Columbia and Ontario) have access to fully funded in-catchment programs (49% of Canada's population). By contrast, U.S. MD-PhD applicants from 31 states have access to fully funded in-catchment programs through Medical Scientist Training Programs (MSTPs) (85% of the U.S. population). Canadian MD-PhD programs have a more uneven geographical distribution and funding landscape than those in the United States, limiting accessibility for Canadian students from underrepresented and lower socioeconomic backgrounds. Despite recent increases in diversity among MD-PhD trainees, financial constraints threaten to reverse these gains, reducing opportunities for historically marginalized groups. This review highlights the need for renewed provincial and federal investment in MD-PhD training. Without targeted policy and funding supports, the sustainability of Canadian MD-PhD programs-and the future of Canada's clinician-scientist training pipeline-remains uncertain. Addressing these challenges is essential to maintaining Canada's global competitiveness in medical and scientific innovation and ensuring that clinician-scientist leadership reflects the diversity of the patient populations they serve.

[Table: see text].

Kawasaki disease (KD) is an acute vasculitis in children, and the resultant inflammatory process can lead to coronary artery aneurysms. The study aimed to investigate the role of 25-hydroxyvitamin D3 (25-OH-D3), a stable circulating form of vitamin D3, in KD mouse models. The KD mouse model was established through intraperitoneal injection of 500 μg Lactobacillus casei cell wall extract (LCWE). 25-OH-D3 was intraperitoneally injected to mice before and after LCWE injection. The mice were euthanized 7, 14, or 28 days after LCWE injection. Hematoxylin-eosin staining was performed to observe inflammation in mouse coronary artery tissues. ELISA was conducted to assess serum levels of inflammatory cytokines (tumour necrosis factor α and interleukin-1 beta ). Aorta areas and maximal aorta diameters were measured. Western blotting was performed to measure factors involved in JAK1/STAT3 and TLR4 signalling pathways. LCWE caused inflammatory cell infiltration in mouse coronary arteries, leading to high heart vessel inflammation scores, coronary artery lesion scores, and inflammatory cytokine levels within 28 days. In addition, LCWE induced the development of abdominal aorta aneurysms and dilatations. 25-OH-D3 exerted a protective role in the KD mouse model by inhibiting coronary artery lesions and inflammation. Moreover, 25-OH-D3 suppressed LCWE-induced activation of the JAK1/STAT3 and TLR4 pathways in coronary artery tissues. 25-OH-D3 ameliorates LCWE-induced coronary artery lesions and inflammation in mice by inhibiting the JAK1/STAT3 and TLR4 pathways.