Southern Medical University

The role of ultrasound in small bowel stricturing Crohn's disease (CD) is unclear. We aimed to investigate whether intestinal ultrasound can be used to monitor treatment response, guide treatment strategy, and predict outcomes in small bowel stricturing CD. We performed a multicenter retrospective study of 121 consecutive patients with small bowel stricturing CD who received biological therapy for at least 3 months. Two kinds of ultrasonographic response were evaluated: inflammation response (improvement in bowel wall thickness and vascular intensity) and stricture response (inflammation response with no luminal narrowing). Treatment was optimized when no inflammation response or loss of inflammation response was detected. Cox regression analysis was performed to investigate the predictors of CD-related hospitalization. The rate of inflammation response increased from 57.0% at the end of induction therapy (date 1) to 67.8% 1 year later (date 2) (p = .031). No significant difference was observed for the rate of stricture response between date 1 and date 2 (28.1% versus 27.3%, p = 1.000). Ultrasound led to 91 treatment optimizations, after which 29 patients achieved inflammation response and 9 achieved stricture response. Multivariate analysis showed that stricture response at the end of induction therapy was independently associated with a decreased risk for CD-related hospitalization (hazard ratio 0.29, 95% CI 0.09-0.96; p = .043). Intestinal ultrasound can be used to monitor treatment response and guide treatment strategy in small bowel stricturing CD. Early stricture response on intestinal ultrasound is associated with improved outcomes.

Renal osteodystrophy (ROD), a skeletal complication of chronic kidney disease (CKD)-mineral and bone disorder, may influence perioperative outcomes after total knee arthroplasty (TKA), but its impact remains unclear. This study examined patient characteristics, hospital resource utilization, and postoperative complications in ROD patients undergoing primary TKA. We performed a retrospective cohort analysis of the National Inpatient Sample (2010-2019). Adults undergoing primary TKA were identified and stratified by ROD status. Propensity score matching (PSM; 1:20) was used to balance age, sex, race, comorbidities, and CKD stage. Outcomes included length of stay (LOS), hospital charges, and medical and surgical complications. Among 1,196,522 TKA patients, 283 (0.02%) had ROD. After matching (n = 5,337 controls), ROD patients had a longer median LOS (3 vs. 3 days; p < 0.001) and markedly higher median hospital charges ($58,550 vs. $18,004; p < 0.001). ROD was associated with increased odds of medical complications, including thrombocytopenia (OR: 3.2; 95% CI: 1.9-5.2), convulsion (OR: 6.9; 2.5-19.6), heart failure (OR: 2.3; 1.5-3.4), chest pain (OR: 3.4; 1.2-10.0), acute cerebrovascular disease (OR: 3.0; 1.4-6.4), stroke (OR: 3.3; 1.6-6.8), pneumonia (OR: 3.9; 1.7-9.0), and acute renal failure (OR: 2.3; 1.6-3.5). Surgical risks were also elevated, notably periprosthetic fracture (OR: 7.1; 2.2-22.9), joint dislocation (OR: 4.6; 1.7-12.3), and lower limb peripheral nerve injury (OR: 2.5; 1.4-4.7). ROD patients undergoing primary TKA incur greater hospital resource use and substantially higher rates of diverse medical and surgical complications. These findings highlight ROD as an independent risk factor warranting targeted preoperative risk stratification, multidisciplinary perioperative planning, and bone health optimization to improve outcomes and resource efficiency in this high-risk population. The level of evidence is 3. Trial registration is not applicable.

Joint learning on diverse ultrasonic source scenarios presents a challenge in preserving stable generalization due to the combination of heterogeneity of different sources and the inconsistency of joint learning features. Previous joint learning studies, which are not source-resilient frameworks, may not preserve stable generalization when trained on diverse source scenarios. Furthermore, the limited variations in single-source data and the interference from ultrasound imaging, which are common in ultrasonic source scenarios, further decrease generalization. To address these problems, we proposed a source-resilient joint learning framework consisting of three stages: 1) Source transforming, where our 1-to-N transformation unifies diverse source scenarios for source-resiliency. 2) Our feature enhancement modules model the source-resilient joint learning network, including a manifold-constraint normalization module (MCNM) for addressing heterogeneity by minimizing manifold-based loss, a task-consistent attention module (TCAM) shares the multi-scale features with self-attention to address inconsistency, and an adaptive feature-shifting module (AFSM) for feature-level augmentation to overcome single-source data. 3) Our ultrasound-hybrid linear mapping (USmapping) cascades speckle randomization and mask-guiding Monge-Kantorovitch linear mapping to achieve ultrasonic style randomization for addressing the interference of ultrasonic data. Our framework was evaluated on eight ultrasound datasets from various scanners at multiple centers and surpassed previous comparable studies in both segmentation (DSC$WAvg$ of 75.7%) and classification (AUROC$WAvg$ of 68.8%) tasks. Our framework has the potential to serve as a general framework for enhancing the performance of joint learning under diverse ultrasonic source scenarios.

Heterotopic ossification (HO) within tendons leads to debilitating tissue dysfunction, primarily arising from the abnormal osteogenic differentiation of tendon-derived stem cells (TDSCs). Despite its clinical prevalence, effective pharmacological treatments remain elusive. Farnesol, a natural isoprenoid with potent anti-inflammatory properties, represents a novel but unexplored candidate for musculoskeletal repair. This study aimed to evaluate the therapeutic efficacy of Farnesol in attenuating tendon HO and to elucidate the specific molecular mechanisms driving its effects. The anti-osteogenic effects of Farnesol were assessed using invitro TDSC differentiation assays and an invivo tendon injury model. Integrated RNA sequencing and network pharmacology analysis were employed to identify potential molecular targets. The mechanism was rigorously validated through rescue experiments using a specific GSTP1 inhibitor. Farnesol treatment significantly inhibited osteogenic differentiation invitro and attenuated ectopic bone formation invivo. Mechanistic screening identified the GSTP1/MAPK signaling axis as a critical regulatory pathway. Crucially, the administration of a GSTP1 inhibitor reversed the suppressive effects of Farnesol on osteogenesis, confirming GSTP1 as the primary mediator. Farnesol effectively inhibits the progression of post-traumatic tendon HO by targeting the GSTP1/MAPK pathway. These findings provide the first evidence of Farnesol's therapeutic potential in preventing pathological ossification.