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Ulnar lengthening has gained popularity in treating forearm deformity due to hereditary multiple exostoses (HME). Whether a simultaneous radius angular correction is necessary for bowing deformity remains debatable. We aimed to evaluate effectiveness and safety of ulnar lengthening alone in HME children. HME patients with forearm deformity who underwent ulnar lengthening between 2011 and 2016 were included. Patients were divided into two groups: eight juniors (age ≤ 10 years) and six seniors (>10 years). The mean age of two groups was 8.1 ± 2.5 and 16.7 ± 4.4 years, respectively. The juniors underwent ulnar lengthening alone, and the seniors received an additional radial corrective osteotomy. Pre-operative and post-operative parameters of supination, pronation, ulnar variance (UV), radial articular angles (RAA), and carpal slip (CS) were assessed. The juniors rather the seniors had an improvement in supination ( p < 0.05 and p = 0.109, respectively). The juniors and seniors improved in pronation ( p < 0.05). UV, RAA, and CS were corrected in the seniors ( p < 0.05). In the juniors, parameters improved in UV, RAA, and CS ( p < 0.05). For HME children, ulnar lengthening alone can restore radiologic anatomy and functions, providing comparable surgical outcomes in cosmetic results and clinical parameters., Competing Interests: The authors declare no conflict of interest.

Implant extrusion in subtalar arthroereisis is a common complication for pediatric flexible flatfoot. However, there were a limited number of articles addressing the body weight effects on implant extrusion after the procedure. We conducted a 24-month follow-up assessment after subtalar arthroereisis. Surgical patients who underwent the Vulpius procedure were retrospectively collected from May 2010 to January 2017, including 59 cases of both feet having implants in situ and 43 cases of both feet having implant extrusion. The average age of 102 patients was 9 years old. The mean body mass index (BMI) of the implant in situ group was 19.5, whilst the extrusion group was 21.2 ( p = 0.035). The inter-observer correlation was excellent. There were 11 cases (39.3%) of bilateral extrusion in the overweight group (BMI ≥ 24) and 13 cases (23.2%) in the low body weight group (BMI ≤ 18.5) ( p < 0.0004). Postoperative radiographic angles were corrected in both the implant in situ group and the extrusion group. Nonetheless, the implant in situ group revealed better postoperative outcomes of Meary's angle and the talonavicular angle from an anterior-posterior view, and the talar inclination angle from a lateral view. We conclude that a higher BMI is related to implant extrusion and worse results after subtalar arthroereisis. Further prospective study to investigate whether preoperative weight loss results in improved surgical outcomes is warranted in the future.

Background: Interactions and early warning effects of non-hepatic alkaline phosphatase (NHALP) and high-sensitivity C-reactive protein (hs-CRP) on the progression of vertebral fractures (VFs) in patients with rheumatoid arthritis (RA) remain unclear. We aim to explore whether serum concentrations of NHALP and hs-CRP could serve as a promising dual biomarker for prognostic assessment of VF progression., Methods: Unadjusted and adjusted hazard ratios (aHRs) of VF progression were calculated for different categories of serum NHALP and hs-CRP using the Cox regression model in RA patients. The modification effect between serum NHALP and hs-CRP on VF progression was determined using an interaction product term., Results: During 4489 person-years of follow-up, higher NHALP (>125 U/L) and hs-CRP (>3.0 mg/L) were robustly associated with incremental risks of VF progression in RA patients (aHR: 2.2 (95% confidence intervals (CIs): 1.2⁻3.9) and 2.0 (95% CI: 1.3⁻3.3) compared to the lowest HR category, respectively). The interaction between NHALP and hs-CRP on VF progression was statistically significant ( p < 0.05). In the stratified analysis, patients with combined highest NHALP and hs-CRP had the greatest risk of VF progression (aHR: 4.9 (95% CI: 2.5⁻9.6)) compared to the lowest HR group (NHALP < 90 U/L and hs-CRP < 1 mg/L)., Conclusions: In light of underdiagnoses of VFs and misleading diagnosis by single test, NHALP and hs-CRP could serve as compensatory biomarkers to predict subclinical VF progression in RA patients.

Background: Interactions and joint effects of galectin-3 and vascular cell adhesion molecule 1 (VCAM-1) on risks of all-cause and cardiovascular (CV) mortality remain unclear in patients with maintenance hemodialysis (MHD)., Methods: Unadjusted and adjusted hazard ratios (aHRs) of mortality risks were analyzed between higher and lower concentration groups of serum galectin-3 and VCAM-1. The modification effect between serum galectin-3 and VCAM-1 on mortality risk was investigated using an interaction product term., Results: During follow-up, galectin-3 and VCAM-1 were associated with incremental risks of all-cause mortality (aHR: 1.038 (95% confidence interval (CI): 1.001⁻1.077) and 1.002 (95% CI: 1.001⁻1.003), respectively). Nonetheless, VCAM-1 but not galectin-3 predicted CV mortality (aHR: 1.043 (95% CI: 0.993⁻1.096) and 1.002 (95% CI: 1.001⁻1.003), respectively). In the interaction analysis, patients with combined higher galectin-3 (>29.5 ng/mL) and VCAM-1 (>1546.9 ng/mL) were at the greatest risk of all-cause and CV mortality (aHR: 4.6 (95% CI: 1.6⁻13.4), and 4.2 (95% CI: 1.3⁻14.4), respectively). The interactions between galectin-3 and VCAM-1 with respect to all-cause and CV mortality were statistically significant ( p < 0.01 and < 0.05, respectively)., Conclusion: Galectin-3 and VCAM-1 could serve as a promising dual biomarker for prognostic assessment, considering their joint effects on pathogenesis of leukocyte trafficking and atherothrombosis.

Molecular mechanisms and pathological features of p-Cresyl sulfate (PCS)-induced uremic lung injury (ULI) in chronic kidney disease (CKD) remain unclear. We analyzed pleural effusions (PE) from CKD and non-CKD patients for uremic toxins, reactive oxygen species (ROS), and chemotactic cytokines. Correlations between PE biomarkers and serum creatinine were also studied. Cell viability and inflammatory signaling pathways were investigated in PCS-treated human alveolar cell model. To mimic human diseases, CKD-ULI mouse model was developed with quantitative comparison of immunostaining and morphometric approach. PE from CKD patients enhance expressions of uremic toxins, hydroxyl radicals, and IL-5/IL-6/IL-8/IL-10/IL-13/ENA-78/GRO α/MDC/thrombopoietin/VEGF. PE concentrations of ENA-78/VEGF/IL-8/MDC/PCS/indoxyl sulphate correlate with serum creatinine concentrations. In vitro, PCS promotes alveolar cell death, cPLA2/COX-2/aquaporin-4 expression, and NADPH oxidase/mitochondria activation-related ROS. Intracellular ROS is abrogated by non-specific ROS scavenger N-acetyl cysteine (NAC), inhibitors of NADPH oxidase and mitochondria-targeted superoxide scavenger. However, only NAC protects against PCS-induced cell death. In vivo, expressions of cPLA2/COX2/8-OHdG, resident alveolar macrophages, recruited leukocytes, alveolar space, interstitial edema and capillary leakage increase in lung tissues of CKD-ULI mice, and NAC pretreatment ameliorates alveolar⁻capillary injury. PCS causes alveolar⁻capillary injury through triggering intracellular ROS, downstream prostaglandin pathways, cell death, and activating leukocytes to release multiplex chemoattractants and extracellular ROS. Thus PCS and nonspecific ROS serve as potential therapeutic targets.