Long non-coding RNA MEG3 silencing weakens high glucose-induced mesangial cell injury by decreasing LIN28B expression by sponging and sequestering miR-23c.

Background: Diabetic nephropathy (DN) is a common kidney disease in diabetic patients. Long non-coding RNA maternally expressed gene 3 (MEG3) and microRNA (miR)-23c are reported to be implicated in DN development. Nevertheless, it is unclear that the molecular mechanism between MEG3 and miR-23c in DN remains unclear. Methods: Human mesangial cells (HMCs) were treated with high glucose (HG) to simulate the DN status in vitro. Expression of MEG3 and miR-23c was measured. Effects of MEG3 silencing on HG-stimulated HMC injury were determined. The relationship between MEG3 and miR-23c was verified by the dual-luciferase reporter and RNA immunoprecipitation assays. Results: MEG3 was overexpressed in serums from DN patients and HG-stimulated HMCs. MEG3 knockdown weakened HG-stimulated HMC proliferation, extracellular matrix (ECM) accumulation, and inflammation. MEG3 regulated lin-28 homolog B (LIN28B) expression through adsorbing miR-23c. MiR-23c inhibitor reversed MEG3 knockdown-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation. LIN28B overexpression overturned miR-23c mimic-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation. Conclusion: MEG3 regulated HMC injury via regulation of the miR-23c/LIN28B axis in DN, which can help us better understand the mechanism of DN mediated by MEG3.

RNA sequencing revealed the multi-stage transcriptome transformations during the development of gallbladder cancer associated with chronic inflammation.

Gallbladder cancer (GBC) is a highly malignant tumor with extremely poor prognosis. Previous studies have suggested that the carcinogenesis and progression of GBC is a multi-stage and multi-step process, but most of them focused on the genome changes. And a few studies just compared the transcriptome differences between tumor tissues and adjacent noncancerous tissues. The transcriptome changes, relating to every stage of GBC evolution, have rarely been studied. We selected three cases of normal gallbladder, four cases of gallbladder with chronic inflammation induced by gallstones, five cases of early GBC, and five cases of advanced GBC, using next-generation RNA sequencing to reveal the changes in mRNAs and lncRNAs expression during the evolution of GBC. In-depth analysis of the sequencing data indicated that transcriptome changes from normal gallbladder to gallbladder with chronic inflammation were distinctly related to inflammation, lipid metabolism, and sex hormone metabolism; transcriptome changes from gallbladder with chronic inflammation to early GBC were distinctly related to immune activities and connection between cells; and the transcriptome changes from early GBC to advanced GBC were distinctly related to transmembrane transport of substances and migration of cells. Expression profiles of mRNAs and lncRNAs change significantly during the evolution of GBC, in which lipid-based metabolic abnormalities play an important promotive role, inflammation and immune activities play a key role, and membrane proteins are very highlighted molecular changes.

Feasibility and Tolerability of Lenvatinib, Plus PD-1 Blockades for Patients with Unresectable Hepatocellular Carcinoma: A Retrospective Exploratory Study.

Objective: Lenvatinib was the standard first-line therapy for patients with unresectable HCC. PD-1 blockades demonstrated promising efficacy for patients with previously-treated HCC. Therefore, this study was to investigate the feasibility and tolerability of lenvatinib plus PD-1 blockades for patients with unresectable HCC retrospectively. Methods: A total of 37 patients with unresectable HCC who received lenvatinib plus PD-1 blockades in first-line setting were included in this study retrospectively. Efficacy of the patients was evaluated with the change of target lesion using mRECIST criteria per investigator and all the subjects were followed up regularly. Adverse reactions were collected and documented. Exploratory analysis between prognosis and baseline characteristics was performed using log rank test and multivariate analysis were performed using Cox regression analysis. Results: The best overall response of the 37 patients suggested that complete response was observed in one patient, partial response was noted in 11 patients, stable disease was noted in 16 patients and 9 patients had progressive disease, which yielded an objective response rate (ORR) of 32.4% (95%CI: 18.0-49.8) and a disease control rate (DCR) of 75.7% (95%CI: 58.8-88.2). Furthermore, the median progression-free survival (PFS) of the 37 patients with advanced HCC was 8.3 months (95%CI: 3.34-13.26). And the median overall survival (OS) was 17.8 months (95%CI: 7.19-28.41). In addition, the median duration of response (DoR) in 12 patients with response was 9.6 months (95%CI: 3.03-16.17). Furthermore, adverse reactions that were attributed to the combination administration were detected in 36 patients (97.3%), among whom a total of 22 patients (59.5%) were observed of the grade ≥3 adverse reactions. And the most common adverse reactions were hypertension, fatigue, nausea and vomiting, and hepatotoxicity. Conclusion: Lenvatinib plus PD-1 blockades demonstrated promising anticancer activity and acceptable toxicity for patients with unresectable HCC. And the conclusion should be validated in prospective clinical trials subsequently.

Comprehensive Analysis of the Oncogenic, Genomic Alteration, and Immunological Landscape of Cation-Chloride Cotransporters in Pan-Cancer.

Background: Assessing the phenotypic diversity underlying tumor progression requires the identification of variations in the respective molecular interaction in the tumor microenvironment (TME). Despite emerging studies focusing on the association between cation-chloride cotransporters (CCCs) and carcinogenesis, direct evidence that CCCs (KCC2 and NKCC1) mediate tumor progression in pan-cancer remains unclear. Methods: We conducted a comprehensive assessment of the expression, DNA variation profiles, and prognostic and immunologic implications of CCCs based on a large-scale pan-cancer population, including 10,967 cancer patients from the Cancer Genome Atlas, 9,162 cancer patients from Genomics Expression Omnibus, 48,834 cancer patients from 188 independent studies, and 356 cancer patients from three real-world cohorts. Results: In this study, we first found that CCCs were highly expressed in most tumors, and prominently associated with prognosis. Kaplan-Meier analysis and Cox regression analysis revealed that KCC2 and NKCC1 significantly predicted survival for patients with pan-cancer, suggesting that CCCs have inconsistent tumorigenesis regulatory mechanisms in cancers. Next, we examined the DNA variation landscape of KCC2 and NKCC1 and their prognostic implications in pan-cancer. The results demonstrated that UCEC patients with somatic copy number variation (CNV) of NKCC1 received significantly better outcomes (p < 0.05). Besides emphasizing the clinical implications of CNV of CCCs for cancer patients, we found that NKCC1MUT could prominently prolong progression-free survival (p = 2.59e-04), disease-specific survival (p = 0.019), and overall survival (p = 0.034) compared with NKCC1WT cancer patients possibly via regulation of cell proliferation and oncogenic stress pathways. Additionally, KCC2 positively correlated with the levels of tumor-infiltrating macrophages and CD4+ T cells, but NKCC1 showed a significantly widely negative association with tumor-infiltrated lymphocytes, suggesting an immune-excluded TME in cancers. Similarly, expression of KCC2, rather than NKCC1, was positively correlated with the immune checkpoint molecules, indicating its role as an immune regulator in a wide variety of cancers. Finally, to verify our hypothesis and altered expression of CCCs, we performed IHC analysis and revealed the staining distribution in tumor and adjacent normal tissues of glioma, clear cell renal cell carcinoma, papillary cell renal cell carcinoma, and hepatocellular and breast cancer from three real-world cohorts, and validated prominently prognostic implications of CCCs in patients with clear cell renal cell carcinoma. Conclusion: This study first comprehensively investigated the molecular and clinical role of CCCs, and illustrated the significant association among KCC2/NKCC1 expression, DNA variation profiles prognosis, and TME of pan-cancer. The pan-cancer findings provided an in-depth understanding of potential oncogenic and immunologic of differential expression and DNA alteration of KCC2/NKCC1 cancers.

p53 inhibition attenuates cisplatin-induced acute kidney injury through microRNA-142-5p regulating SIRT7/NF-κB.

Renal tubular epithelial cell apoptosis is the main mechanism of cisplatin-induced acute kidney injury. The role of microRNAs (miRNAs) in the apoptosis of renal tubular epithelial cells has been suggested, but the underlying mechanism has not been fully elucidated. We used microarray analysis to identify miR-142-5p involved in cisplatin-induced acute kidney injury. miR-142-5p was down-regulated in human renal tubular epithelial (HK-2) cells with cisplatin treatment. Notably, the overexpression of miR-142-5p attenuated the cisplatin-induced HK-2 cell apoptosis and inhibition of miR-142-5p aggravated cisplatin-induced HK-2 cell apoptosis. During cisplatin treatment, p53 was activated. The inhibition of p53 by pifithrin-α attenuated the cisplatin-induced kidney injury and up-regulated miR-142-5p expression. We also identified the Sirtuin7 (SIRT7) as a target of miR-142-5p. Furthermore, we demonstrated that the inhibition of SIRT7 prevented cisplatin-induced HK-2 cell apoptosis and decreased the expression of nuclear factor kappa B (NF-κB). Our data revealed that p53 inhibition could attenuate cisplatin-induced acute kidney injury by up-regulating miR-142-5p to repress SIRT7/NF-κB. These findings may provide a novel therapeutic target of cisplatin-induced acute kidney injury.

Long non-coding RNA BZRAP1-AS1 silencing suppresses tumor angiogenesis in hepatocellular carcinoma by mediating THBS1 methylation.

BACKGROUND: Hepatocellular carcinoma (HCC) is the most frequent primary liver cancer associated with a high mortality. Long non-coding RNAs (lncRNAs) have recently emerged as regulators in the development and progression of several cancers, and therefore represent an opportunity to uncover new targets for therapy. In the present study, we aimed to investigate the potential effect of lncRNA BZRAP1-AS1 on the angiogenesis of HCC. METHODS: Microarray-based data analysis was initially employed to screen genes and lncRNAs that are differentially expressed in HCC and the candidate BZRAP1-AS1 was identified as a hit. The expression of BZRAP1-AS1 and thrombospondin-1 (THBS1) in HCC tissues and cells were then determined using RT-qPCR. The gene methylation level was measured by methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) assays. Next, the interactions between BZRAP1-AS1, DNA methyltransferase 3B (DNMT3b), and THBS1 were assessed by RIP, RNA pull-down and ChIP assays. Finally, the roles of BZRAP1-AS1, DNMT3b and THBS1 in angiogenesis in vitro as well as tumorigenesis in vivo were evaluated by a battery of the gain- and loss-of function experiments. RESULTS: BZRAP1-AS1 was identified as a highly expressed lncRNA in HCC tissues and cells. Down-regulation of BZRAP1-AS1 in HCC cells inhibited HUVEC proliferation, migration and angiogenesis. By interacting with DNMT3b, BZRAP1-AS1 induced methylation of the THBS1 promoter and inhibited the transcription of THBS1, resulting in promoted angiogenesis of HUVECs. Moreover, silencing of BZRAP1-AS1 repressed the angiogenesis as well as the tumor growth of HCC in vivo via up-regulating THBS1. CONCLUSION: This study provides evidence that angiogenesis in HCC is hindered by silencing of BZRAP1-AS1. Thus, BZRAP1-AS1 may be a promising marker for the treatment of HCC.

Effect of bone marrow mesenchymal stem cells on RhoA/ROCK signal pathway in severe acute pancreatitis.

The effect of bone marrow mesenchymal stem cells (BMSCs) on RhoA/ROCK signal pathway expression in severe acute pancreatitis (SAP) was investigate in the present study. SAP model was established by retrograde injection of 5% sodium taurocholate into biliopancreatic duct. SD rats were then randomly divided into four groups: normal control, untreated SAP, BMSCs transplant + SAP and ROCK inhibitor + SAP groups (N = 30 each). All rats were sacrificed at 6, 12 and 24 h followed by analysis of serum amylase, TNF-α and IL-6 levels by ELISA, RhoA and ROCK I expression in pancreatic tissues by Western blot, morphological change by HE staining. CM-Dil labelled BMSC can be observed in transplant group. Compared to control group, untreated SAP group had significantly elevated serum amylase, ascites, and levels of TNF-α and IL-6 (P<0.05) in a time-dependent manner, with enhanced pancreatic RhoA and ROCK I protein expression (P<0.05). However, BMSCs transplant group showed decreased serum amylase, ascites, TNF-α and IL-6, plus lower RhoA or ROCK I protein expression (P<0.05). Meanwhile, Y-27632 intervention group also showed lower serum amylase or ascites, plus lower RhoA or ROCK I (P<0.05). HE staining showed improved pathological score in BMSCs transplant or Y-27632 intervention group (only at 6 h time point) compared to untreated SAP group (P<0.05). Pancreatic expression of RhoA and ROCK I is up-regulated in SAP, with severe pancreatic tissue damage. BMSCs can alleviate pancreatic injury possibly through decreasing serum inflammatory factor level and inhibiting RhoA/ROCK signal pathway.

microRNA-135a protects against myocardial ischemia-reperfusion injury in rats by targeting protein tyrosine phosphatase 1B.

microRNAs are an emerging class of molecules that regulate pathogenesis of cardiovascular diseases. Here we aim to elucidate the effects and mechanism of miR-135a, a previously reported regulator of ischemia-reperfusion (I/R) injury, in myocardial I/R injury. Quantitative real-time polymerase chain reaction analysis revealed that the expression level of miR-135a was significantly decreased both in the rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation. Overexpression of miR-135a in vivo markedly decreased the infarct size and inhibited the I/R-induced cardiomyocyte apoptosis. Overexpression of miR-135a in H9c2 also exerted antiapoptosis effects. Furthermore, bioinformatics analysis, luciferase activity, and the Western blot assay indicated that protein tyrosine phosphatase 1B (PTP1B) is a direct target of miR-135a. In addition, the expression of proapoptotic-related genes, such as p53, Bax, and cleaved caspase3, were decreased in association with the downregulation of PTP1B. In summary, this study demonstrates that miR-135a exerts protective effects against myocardial I/R injury by targeting PTP1B.

Pharmacokinetics, bioavailability and metabolism of cligosiban, an antagonist of oxytocin receptor, in rat by liquid chromatography hyphenated with electrospray ionization tandem mass spectrometry.

Cligosiban is a highly-affinity nonpeptide oxytocin receptor antagonist. In this study, a simple an sensitive LC-MS/MS method was developed and validated for the determination of cligosiban in rat plasma. The plasma samples were pretreated with acetonitrile as precipitant and then separated on an ACQUITY BEH C18 column (2.1 × 50 mm, 1.7 µm) with 0.1% formic acid in water and acetonitrile as mobile phase. The analytes were monitored using selected reaction monitoring (SRM) mode with transitions at m/z 420.1→248.1 for cligosiban and m/z 304.1→161.1 for IS. The developed method showed good linearity over the concentration range of 1-1000 ng/mL with coefficient of correlation > 0.996. The lower limit of quantification (LLOQ) is 1 ng/mL. The method was validated for selectivity, precision, accuracy, recovery, and stability in accordance with FDA's guidance. The validated assay has been successfully applied to the pharmacokinetic study of cligosiban in rat plasma after intravenous and oral administration. According to the current results, the oral bioavailability of cligosiban was 63.82%. Furthermore, the metabolites present in rat liver microsomes (RLM), human liver microsomes (HLM) and rat plasma were analyzed by UHPLC-LTQ-Orbitrap-MS method, and four metabolites structurally identified based on their accurate masses, and fragment ions. The proposed metabolic pathways of cligosiban were demethylation and glucuronidation. This study is the first report on the pharmacokinetic and metabolic information of cligosiban, which would provide insights into the effectiveness and toxicity of cligosiban.

Laparoscopic splenectomy: posterolateral approach in patients with liver cirrhosis and portal hypertension with platelet count lower than 1 × 109/l.

INTRODUCTION: Laparoscopic splenectomy for massive splenomegaly secondary to liver cirrhosis and portal hypertension in patients with an extremely low platelet count (< 1 × 109/l) presents several challenges. The posterolateral laparoscopic splenectomy approach may be a feasible and safe technique for these patients. AIM: To evaluate the feasibility and safety of the posterolateral laparoscopic splenectomy approach in patients with platelet counts < 1 × 109/l secondary to liver cirrhosis and portal hypertension. MATERIAL AND METHODS: In the period from January 2013 to December 2016, 11 patients with platelet counts < 1 × 109/l secondary to liver cirrhosis and portal hypertension underwent posterolateral laparoscopic splenectomy in our institution. Pre-, peri-, and postoperative medical managements were reviewed retrospectively. RESULTS: Patients' median platelet count was 0.7 × 109/l at the time of inpatient admission. The median operating time was 75 min, and the median intraoperative blood loss was 30 ml. One patient underwent intraoperative transfusion. The median duration of postoperative hospital stay was 5 days. No intra- or postoperative complications ensued, all patients were followed for 12-32 months (median: 24 months), and none had postoperative complications. CONCLUSIONS: The posterolateral laparoscopic splenectomy approach is a feasible, safe technique in the treatment of patients with platelet counts < 1 × 109/l secondary to liver cirrhosis and portal hypertension.

Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac.

BACKGROUNDS/AIMS: Ras is a control switch of ERK1/2 pathway, and hyperactivation of Ras-ERK1/2 signaling appears frequently in human cancers. However, the molecular regulation following by Ras-ERK1/2 activation is still unclear. This work aimed to reveal whether Ras-ERK1/2 promoted the development of colorectal cancer via regulating H3K9ac. METHODS: A vector for expression of K-Ras mutated at G12 V and T35S was transfected into SW48 cells, and the acetylation of H3K9 was measured by Western blot analysis. MTT assay, colony formation assay, transwell assay, chromatin immunoprecipitation and RT-qPCR were performed to detect whether H3K9ac was contributed to K-Ras-mediated cell growth and migration. Furthermore, whether HDAC2 and PCAF involved in modification of H3K9ac following Ras-ERK1/2 activation were studied. RESULTS: K-Ras mutated at G12 V and T35S induced a significant activation of ERK1/2 signaling and a significant down-regulation of H3K9ac. Recovering H3K9 acetylation by using a mimicked H3K9ac expression vector attenuated the promoting effects of Ras-ERK1/2 on tumor cells growth and migration. Besides, H3K9ac can be deacetylated by HDAC2 and MDM2-depedent degradation of PCAF. CONCLUSION: H3K9ac was a specific target for Ras-ERK1/2 signaling pathway. H3K9 acetylation can be modulated by HDAC2 and MDM2-depedent degradation of PCAF. The revealed regulation provides a better understanding of Ras-ERK1/2 signaling in tumorigenesis.

Appleby operation for carcinoma of the body and tail of the pancreas.

AIMS: The aim of this study is to evaluate the therapeutic efficacy of Appleby operation for carcinoma of the body and tail of pancreas. MATERIALS AND METHODS: From March 2010 to February 2015, Appleby operation was performed in 17 patients with carcinoma of the body and tail of pancreas. The values of fasting plasma blood, body weight (BW), visual analog pain intensity scale (VAS score), and the quality of life indices were evaluated before and 1 day, 1, 2, 6 weeks after surgery. Survival time, tumor recurrence time, hospitalization time, and treatment-related complications were analyzed. RESULTS: There was no hospital mortality. Pancreatic fistula and diarrhea were major and most frequent. The rate of morbidity in general was 47.1%. After operation, all of the patients were completely pain-free. The VAS score decreased more after surgery comparing with before (83.2 ± 8.5 vs. 1.9 ± 3.6, P < 0.05). After operation, patients gained more than their preoperative BW with a mean increment of (4.1 ± 1.3 kg) (68.1 ± 4.3 vs. 64.0 ± 6.7, P < 0.05). A significant rise of the overall quality of life index was observed after surgery (93.8 ± 9.7 vs. 68.6 ± 6.7, P < 0.05). The 1-, 2-, 3-, and 5-year recurrence rates were 22.9%, 58.9%, 72.6%, and 72.6%, respectively. The 1-, 2-, 3-, and 5-year survival rates after operation were 80.4%, 54.2%, 32.5%, and 16.3%, respectively. CONCLUSIONS: Appleby operation is both safe and effective with regard to pain relief and improvement of overall quality of life. Appleby operation can also achieve a high survival rate and a long overall survival time.

Retraction: MicroRNA-371-5p targets SOX2 in gastric cancer.

[This retracts the article DOI: 10.18632/oncotarget.8289.].

Splenic Bed Laparoscopic Splenectomy Approach for Massive Splenomegaly Secondary to Portal Hypertension and Liver Cirrhosis.

This study was performed to evaluate the feasibility of the splenic bed laparoscopic splenectomy approach (SBLS) for massive splenomegaly (≥30 cm) in patients with hypersplenism secondary to portal hypertension and liver cirrhosis. Patients who underwent laparoscopic splenectomy (LS) from January 2012 to December 2016 were retrospectively reviewed. We performed LS in 83 patients with massive splenomegaly (≥30 cm) secondary to portal hypertension and liver cirrhosis. Of these patients, 37 underwent the SBLS and 46 underwent anterior LS (ALS). Five patients in the ALS group and none in the SBLS group underwent conversion to open surgery. The operation time, intraoperative blood loss volume, transfusion volume, frequency of transfusion, hemorrhage of short gastric vessels, conversion rate, postoperative hospital stay, and incidence of pancreatic fistula were all significantly lower in the SBLS than ALS group (all P < 0.05). No death or postoperative bleeding occurred in the two groups, and there were no significant differences in age, gender, spleen size, hemoglobin level, platelet count, prothrombin time, Child-Pugh class, hypoproteinemia, or ascites (all P > 0.05). The SBLS is more feasible and effective than ALS in patients with massive splenomegaly (≥30 cm) secondary to portal hypertension and liver cirrhosis.

Possible Molecular Markers for the Diagnosis of Pancreatic Ductal Adenocarcinoma.

BACKGROUND We aimed to identify pivotal genes and pathways involved in pancreatic ductal adenocarcinoma (PDAC), and explore possible molecular markers for the early diagnosis of the disease. MATERIAL AND METHODS The array data of GSE74629, including 34 PDAC samples and 16 healthy samples, was downloaded from GEO (Gene Expression Omnibus) database. Then, the DEGs (differentially expressed genes) in PDAC samples were compared with healthy samples using limma (linear models for microarray). Gene functional interaction networks were analyzed with Cytoscape and ReactomeFIViz. PPI networks were constructed with Cytoscape software. In addition, PPI (protein-protein interaction) network clustering modules were analyzed with ClusterONE, and the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analyses for modules were performed. RESULTS A total of 630 upregulated and 1,002 downregulated DEGs were identified in PDAC samples compared with healthy samples. Some ribosomal protein genes with higher average correlation in module 0 were enriched in the ribosome pathway. NUP107 (nucleoporin 107 kDa) and NUP160 (nucleoporin 160 kDa) were enriched in module 3. HNRNPU (heterogeneous nuclear ribonucleoprotein U) with higher average correlation in module 8 was enriched in the spliceosome pathway. The ribosome pathway and the spliceosome pathway were significantly enriched in cluster 1 and cluster 2, respectively. CONCLUSIONS Ribosomal protein genes Nup170, Nup160, and HNRNPU, and the ribosome pathway as well as the spliceosome pathway may play important roles in PDAC progression. In addition, ribosomal protein genes Nup170, Nup160, and HNRNPU may be used as possible molecular markers for the early diagnosis of the disease.

Long-term results of hand-assisted laparoscopic gastrectomy for advanced Siewert type II and type III esophagogastric junction adenocarcinoma.

BACKGROUND: Hand-assisted laparoscopic surgery (HALS) combines laparoscopic surgery with the tactile feedback of a hand-assist device for complex laparoscopic operations. This study aimed to comparatively evaluate the long-term outcomes of patients who underwent HALS versus open surgery for the treatment of advanced Siewert type II and type III adenocarcinoma of the esophagogastric junction (AEG). METHODS: A retrospective analysis of 77 patients with advanced Siewert type II and IIIAEG between March 2010 and March 2011. Data concerning the basic characteristics of patients, pathological staging, early postoperative course, and long-term follow-up were collected and analyzed. RESULTS: HALS resulted in significantly lower mean blood loss and mean postoperative hospital stay in comparison to open surgery (P = 0.007 and 0.01, respectively). The mean number of resected lymph nodes was 23.22 ±â€¯9.36 in the HALS group, which was more than in the open surgery group (18.61 ±â€¯6.91, P = 0.015). The cumulative 5-year overall survival (OS) rate was 52.8% (95% CI 43.07-60.09) for all patients in the HALS group (78.6% for stage II patients and 36.4% for stage III patients). The 5-year OS rate was not significantly different between both groups. CONCLUSIONS: While achieving similar oncological outcomes to open surgery, the HALS approach resulted in reduced blood loss, shortened postoperative hospital stay, and the resection of more lymph nodes. This analysis suggests that HALS may serve as a less invasive and as successful alternative to open surgery for the treatment of advanced Siewert type II and type IIIAEG.

Primary Closure Following Laparoscopic Common Bile Duct Exploration Combined with Intraoperative Choledochoscopy and D-J Tube Drainage for Treating Choledocholithiasis.

BACKGROUND This study aimed to assess the clinical short-term results of a primary closure following laparoscopic common bile duct exploration (LCBDE) combined with intraoperative choledochoscopy and D-J tube drainage for choledocholithiasis treatment. MATERIAL AND METHODS Twenty-five patients (14 women and 11 men) who underwent LCBDE with primary duct closure and D-J tube drainage for choledocholithiasis were retrospectively enrolled. The D-J tube (4.7F×14 cm) was removed using a duodenoscope if there was no bile leakage. Before discharge, patients were examined for blood amylase. After discharge or D-J tube removal, all patients were routinely assessed for complications. RESULTS Mean operating time was 135±46 min (range, 78-195 min). Mean intraoperative blood loss was 71±24 mL (range, 25-110 mL). Total hospital stay was 6-9 days (mean, 8.04±1.37 days). Two patients experienced intraoperative bile leakage, which was stopped with re-suturing. None of these patients experienced postoperative bile leaks. Three patients had slight elevation of serum amylase before discharge but without pancreatitis signs. The successful clearance rate of stones was 100%. During 1-year follow-up, no recurrence or severe complications occurred. CONCLUSIONS A primary closure following LCBDE combined with intraoperative choledochoscopy and D-J tube drainage is safe and feasible for choledocholithiasis treatment.

Effective Prevention for Portal Venous System Thrombosis After Splenectomy: A Meta-Analysis.

PURPOSE: Portal venous system thrombosis (PVST) is a common and potentially life-threatening complication of splenectomy for portal hypertension due to cirrhosis. METHODS: A meta-analysis was conducted to study the necessity of pharmacologic prophylaxis of PVST after splenectomy and how to select the feasible treatment method. Articles were searched through the PubMed, EMBASE, Cochrane Library databases, and CNKI. RESULTS: Overall, 404 articles were initially identified, and 11 of them were eligible. Among these selected articles, 7 articles were associated with the necessity of anticoagulation for prevention of PVST, while 5 were about the drug selection. We first demonstrated that the incidence of PVST after splenectomy was significantly lower in patients who received the preventive measures than in those who did not (odds ratio [OR]: 0.22, 95% confidence interval [CI]: 0.13-0.39, P < .00001). Then, we compared the new-style treatment with the conventional treatment and found that patients with new therapy method had lower incidence of PVST than those who received conventional treatment (OR: 0.37, 95% CI: 0.27-0.51, P < .00001). Also, some studies (n = 4) reported that early and combination use of anticoagulation drugs can lead to better outcome for patients with splenectomy and devascularization. CONCLUSION: Preventative use of anticoagulant drugs might decrease the incidence of PVST after splenectomy in patients with portal hypertension, new anticoagulant drugs such as low-molecular-weight heparin should be used, and early or combination use of anticoagulation drugs might lead to lower PVST incidence for patients.

Soluble Triggering Receptor Expressed on Myeloid Cells-1 as a Novel Marker for Abdominal Sepsis.

BACKGROUND: The aim of the study was to investigate the concentration and diagnostic significance of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in acute abdominal conditions. METHODS: Plasma specimens were obtained from 68 patients with abdominal sepsis, 60 patients with systemic inflammatory response syndrome (SIRS), and 60 healthy individuals. The sepsis group was divided into the survival and death groups according to the 28-d outcome. Plasma sTREM-1, procalcitonin (PCT), C-reactive protein (CRP), and white blood cell (WBC) count were measured. A receiver operating characteristic curve (ROC) was used to compare the diagnostic values of sTREM-1, PCT, CRP, and WBC count. In addition, the correlation between plasma sTREM-1 and the Acute Physiology and Chronic Health Evaluation (APACHE) II score in the sepsis group was assessed by Spearman correlation analysis. RESULTS: The plasma concentration of sTREM-1 in the sepsis group was significantly higher than that in the SIRS and healthy groups (both p < 0.001). Also, the plasma concentration of sTREM-1 in the death group was markedly higher than that in the survival group. The ROC for the diagnosis of sepsis vs. SIRS showed that the area under the curve of sTREM-1 (0.82) was greater than that of PCT (0.77), CRP (0.72), and WBC count (0.70). Additionally, in the sepsis group, the plasma sTREM-1 concentration correlated positively with the APACHE II score (r = 0.41; p < 0.05). CONCLUSIONS: The plasma concentration of sTREM-1 may be a significantly sensitive and useful indicator for the rapid diagnosis of abdominal sepsis.