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1.
BMJ Open ; 12(4): e049789, 2022 04 12.
Article in English | MEDLINE | ID: mdl-35414539

ABSTRACT

OBJECTIVES: The study was designed to clarify the difference between extrahepatic cholangiocarcinoma (ECC) and intrahepatic cholangiocarcinoma (ICC) in postoperative cancer-specific death. DESIGN: Patients diagnosed with ECC and ICC after surgery, who are identified from the Surveillance, Epidemiology and End Results programme, are eligible for this retrospective cohort study. SETTING: Survival between groups was compared using the traditional Kaplan-Meier method and the cumulative incidence function (CIF) method. Propensity score-matched (PSM) analysis was conducted to balance the differences in vital variables between groups. The HR and 95% CI for ECC relative to ICC were used to quantify the risk of death. Subgroup analysis was further used to evaluate the stability of the differences between groups. RESULTS: The study included 876 patients with ECC and 1194 patients with ICC. Before PSM, with the Kaplan-Meier method, postoperative overall survival and cancer-specific death for ECC were worse than those for ICC. However, with the CIF method, no difference in postoperative cancer-specific death was found. After PSM, all differences in the considered traits were balanced, and 173 pairs of patients were retained. Survival analysis found that there was no difference in postoperative all-cause death (Kaplan-Meier method, p=0.186) or cancer-specific death (Kaplan-Meier and CIF methods, p=0.500 and p=0.913, respectively), which was consistent with subgroup analysis. CONCLUSIONS: ECC and ICC showed no difference in postoperative cancer-specific death, both in the natural state and in multiple variable-matched conditions. TRIAL REGISTRATION NUMBER: researchregistry4175.


Subject(s)
Bile Duct Neoplasms , Cholangiocarcinoma , Bile Duct Neoplasms/epidemiology , Bile Duct Neoplasms/surgery , Bile Ducts, Intrahepatic/pathology , Cholangiocarcinoma/diagnosis , Cholangiocarcinoma/surgery , Humans , Prognosis , Retrospective Studies , Risk Factors
2.
Int J Surg ; 56: 83-93, 2018 Aug.
Article in English | MEDLINE | ID: mdl-29906644

ABSTRACT

BACKGROUND: Step-up therapy is the recommended therapy for infected necrotizing pancreatitis (INP). However, the most appropriate secondary therapy for use after initial drainage has not been fully determined. This meta-analysis was designed to evaluate the efficacy and safety of retroperitoneal versus open intraperitoneal necrosectomy as part of a step-up strategy for INP. MATERIALS AND METHODS: Eight online databases were searched for randomized controlled trials (RCTs) and cohorts comparing retroperitoneal and open intraperitoneal step-up approaches for treating INP. The data was pooled with a random-effects model. RESULTS: A total of 21 controlled studies (one RCT and twenty cohorts) and 2177 patients were included in this study. Our meta-analysis showed that the retroperitoneal group had a lower postoperative complication rate [risk ratio (RR) = 0.575, 95% confidence interval (CI) = 0.459 to 0.719, P < 0.001], lower postoperative mortality (RR = 0.525, 95% CI = 0.430 to 0.642, P < 0.001), higher technical success rate (RR = 1.313, 95% CI = 1.017 to 1.694, P = 0.037), similar surgical reintervention rate (RR = 0.930, 95% CI = 0.783 to 1.106, P = 0.411), shorter operative time [standardized mean difference (SMD) = -2.402, 95% CI = -3.642 to -1.161, P < 0.001], and shorter hospital stay (SMD = -2.034, 95% CI = -3.041 to -1.026, P < 0.001) than the open group. These results were supported by a subgroup analysis. CONCLUSION: For treating INP, the retroperitoneal approach is safer and more effective than the open intraperitoneal approach.


Subject(s)
Pancreas/surgery , Pancreatitis, Acute Necrotizing/surgery , Peritoneum/surgery , Retroperitoneal Space/surgery , Adult , Drainage/methods , Female , Humans , Length of Stay , Male , Middle Aged , Operative Time , Postoperative Complications/etiology , Treatment Outcome
3.
Cell Calcium ; 66: 90-97, 2017 09.
Article in English | MEDLINE | ID: mdl-28807153

ABSTRACT

C1q/tumor necrosis factor-related protein-3 (CTRP3) is an adipokine that protects against myocardial infarction-induced cardiac dysfunction through its pro-angiogenic, anti-apoptotic, and anti-fibrotic effects. However, whether CTRP3 can directly affect the systolic and diastolic function of cardiomyocytes remains unknown. Adult rat cardiomyocytes were isolated and loaded with Fura-2AM. The contraction and Ca2+ transient data was collected and analyzed by IonOptix system. 1 and 2µg/ml CTRP3 significantly increased the contraction of cardiomyocytes. However, CTRP3 did not alter the diastolic Ca2+ content, systolic Ca2+ content, Ca2+ transient amplitude, and L-type Ca2+ channel current. To reveal whether CTRP3 affects the Ca2+ sensitivity of cardiomyocytes, the typical phase-plane diagrams of sarcomere length vs. Fura-2 ratio was performed. We observed a left-ward shifting of the late relaxation trajectory after CTRP3 perfusion, as quantified by decreased Ca2+ content at 50% sarcomere relaxation, and increased mean gradient (µm/Fura-2 ratio) during 500-600ms (-0.163 vs. -0.279), 500-700ms (-0.159 vs. -0.248), and 500-800ms (-0.148 vs. -0.243). Consistently, the phosphorylation level of cardiac troponin I at Ser23/24 was reduced by CTRP3, which could be eliminated by preincubation of okadaic acid, a type 2A protein phosphatase inhibitor. In summary, CTRP3 increases the contraction of cardiomyocytes by increasing the myofilament Ca2+ sensitivity. CTRP3 might be a potential endogenous Ca2+ sensitizer that modulates the contractility of cardiomyocytes.


Subject(s)
Adipokines/metabolism , Calcium/metabolism , Adrenergic beta-Antagonists/pharmacology , Animals , Calcium Channels, L-Type/metabolism , Cells, Cultured , Fura-2/chemistry , Fura-2/metabolism , Humans , Male , Membrane Potentials/drug effects , Myocardial Contraction/drug effects , Myocytes, Cardiac/cytology , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Patch-Clamp Techniques , Protein Phosphatase 2/metabolism , Rats , Rats, Sprague-Dawley , Troponin I/metabolism
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