The updated meta-analysis first confirms that LCBDE+LC is superior to pre-EST+LC both in perioperative safety and short- and long-term postoperative efficacy, which should be considered as optimal treatment choice for cholecysto-choledocholithiasis.

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BackgroundPancreatic adenocarcinoma is a highly lethal malignancy. Neoadjuvant chemo(radio)therapy [NAC(R)T] is recommended to use for borderline resectable pancreatic cancer (BRPC) and high-risk resectable pancreatic cancer (RPC), but no high-level evidence exists.MethodsWe searched PubMed, EMBASE, Web of Science, and Cochrane library to identify trials comparing survival data of NAC(R)T with SF for RPC or BRPC. Overall survival (OS) was synthesized in analysis of all the patients (intention-to-treat [ITT] analysis) and resected patients respectively.ResultsThe meta-analysis included 17 trials with 2286 participants. For BRPC, NAC(R)T improved OS both in ITT analysis (HR, 0.49; 95% CI, 0.37–0.65; P < 0.001) and in analysis of resected patients (HR, 0.66; 95% CI, 0.51–0.85; P = 0.001) in comparison to SF, accompanied with comparable overall resection rate [odds ratio (OR), 0.69; 95% Cl, 0.41–1.16; P = 0.159]. Disease-free survival, R0 rate, and recurrence were also in favor of NAC(R)T. For RPC, OS in analysis of resected patients was higher with NAC(R)T (HR, 0.75; 95% CI, 0.63–0.89; P = 0.001), but OS in ITT analysis was similar (HR, 1.02; 95% CI, 0.85–1.22; P = 0.818). The overall resection rate (OR, 0.50; 95% Cl, 0.25–0.99; P = 0.048) was lower, but R0 rate was higher with NAC(R)T. No differences in disease-free survival and recurrence between NAC(R)T and SF. Survival benefits of NAC(R)T basically persisted across sensitivity and subgroup analyses.ConclusionsThis meta-analysis demonstrates that NAC(R)T can provide survival benefits in BRPC patients and a subgroup of RPC patients compared with SF. Future research should focus on investigating the potential biomarkers to screen the subgroup of RPC patients who can benefit from neoadjuvant therapy.Trial registrationCRD42018103086.

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Prostate cancer (PCa) is a common cancer worldwide, which mostly occurs in males over the age of 50. Accumulating evidence have determined that long non-coding RNA/microRNA (lncRNA/miRNA) axis plays a critical role in cell progression of cancers, including PCa. However, the pathogenesis of PCa has not been fully indicated. In this study, quantitative real-time polymerase chain reaction was used to detect the expression of HCG11 and miR-543. Western blot was applied to measure the protein expression of proliferating cell nuclear antigen, cleavage-caspase 3 (cle-caspase 3), N-cadherin, E-cadherin, GAPDH, P-AKT, AKT, p-mTOR, and mTOR. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), transwell invasion, and transwell migration assay were used to detect cell proliferation, invasion, and migration, respectively. The function and mechanism of lncRNA HCG11 were confirmed in PCa cell and xenograft mice models. Luciferase assay indicated that miR-543 was a target miRNA of HCG11. Further investigation revealed that overexpression of HCG11 inhibited cell proliferation, invasion, and migration, whereas induced cell apoptosis by regulating miR-543 expression in vitro and in vivo. More than that, lncRNA HCG11 inhibited phosphoinositide-3 kinase/protein kinaseB (PI3K/AKT) signaling pathway to suppress PCa progression. Our data showed the overexpression of HGC11inhibited PI3K/AKT signaling pathway by downregulating miR-543 expression, resulting in the suppression of cell growth in PCa. This finding proved a new regulatory network in PCa and provided a novel therapeutic target of PCa.

Objective To discern the effects of continuous passive motion on inflamed temporomandibular joints (TMJ). Methods The effects of continuous passive motion on TMJ were simulated by exposing primary cultures of rabbit TMJ fibrochondrocyte monolayers to cyclic tensile strain (CTS) in the presence of recombinant human interleukin‐1β (rHuIL‐1β) in vitro. The messenger RNA (mRNA) induction of rHuIL‐1β response elements was examined by semiquantitative reverse transcriptase–polymerase chain reaction. The synthesis of nitric oxide was examined by Griess reaction, and the synthesis of prostaglandin E2 (PGE2) was examined by radioimmunoassay. The synthesis of proteins was examined by Western blot analysis of the cell extracts, and synthesis of proteoglycans via incorporation of 35S‐sodium sulfate in the culture medium. Results Exposure of TMJ fibrochondrocytes to rHuIL‐1β resulted in the induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX‐2), which were paralleled by NO and PGE2 production. Additionally, IL‐1β induced significant levels of collagenase (matrix metalloproteinase 1 [MMP‐1]) within 4 hours, and this was sustained over a period of 48 hours. Concomitant application of CTS abrogated the catabolic effects of IL‐1β on TMJ chondrocytes by inhibiting iNOS, COX‐2, and MMP‐1 mRNA production and NO, PGE2, and MMP‐1 synthesis. CTS also counteracted cartilage degradation by augmenting expression of mRNA for tissue inhibitor of metalloproteinases 2 that is inhibited by rHuIL‐1β. In parallel, CTS also counteracted rHuIL‐1β–induced suppression of proteoglycan synthesis. Nevertheless, the presence of an inflammatory signal was a prerequisite for the observed CTS actions, because fibrochondrocytes, when exposed to CTS alone, did not exhibit any of the effects described above. Conclusion CTS acts as an effective antagonist of rHuIL‐1β by potentially diminishing its catabolic actions on TMJ fibrochondrocytes. Furthermore, CTS actions appear to involve disruption/regulation of signal transduction cascade of rHuIL‐1β upstream of mRNA transcription.

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A bimetallic nanocatalyst Ru–Fe/SBA-15 shows remarkable ability to catalyze selective hydrogenolysis of carboxylic acids to alcoholic chemicals and the optimized catalyst is stable for the hydrogenolysis of acetic acid to ethanol with high catalytic performance for 300 h.