Effectiveness and safety of acupuncture for postoperative ileus following gastrointestinal surgery: A systematic review and meta-analysis.

BACKGROUND: Postoperative ileus (POI) is an important complication of gastrointestinal (GI) surgery. Acupuncture has been increasingly used in treating POI. This study aimed to assess the effectiveness and safety of acupuncture for POI following GI surgery. METHODS: Seven databases (PubMed, Embase, the Cochrane Library, China National Knowledge Infrastructure, Wan fang Data, VIP Database for Chinese Technical Periodicals, and Chinese Biomedical Literature Database) and related resources were searched from inception to May 30, 2021. Randomized controlled trials (RCTs) reporting the acupuncture for POI in GI were included. The quality of RCTs was assessed by the Cochrane Collaboration Risk of Bias tool, and the certainty of the evidence was evaluated by the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. A meta-analysis was performed by using RevMan 5.4 software. RESULTS: Eighteen RCTs involving 1413 participants were included. The meta-analysis showed that acupuncture could reduce the time to first flatus (TFF) (standardized mean difference [SMD] = -1.14, 95% confidence interval [CI]: -1.54 to -0.73, P < 0.00001), time to first defecation (TFD) (SMD = -1.31, 95% CI: -1.88 to -0.74, P < 0.00001), time to bowel sounds recovery (TBSR) (SMD = -1.57, 95% CI: -2.14 to -1.01, P < 0.00001), and length of hospital stay (LOS) (mean difference [MD] = -1.68, 95% CI: -2.55 to -0.80, P = 0.0002) compared with usual care. A subgroup analysis found that acupuncture at distal acupoints once daily after surgery had superior effects on reducing TFF and TFD. A sensitivity analysis supported the validity of the finding. Acupuncture also manifested an effect of reducing TFF, TFD and TBSR compared with sham acupuncture but the result was not stable. Relatively few trials have reported whether adverse events have occurred. CONCLUSIONS: Acupuncture showed a certain effect in reducing POI following GI surgery with very low-to-moderate quality of evidence. The overall safety of acupuncture should be further validated. More high-quality, large-scale, and multicenter original trials are needed in the future.

Downregulation of a long noncoding RNA-ncRuPAR contributes to tumor inhibition in colorectal cancer.

In recent years, the role of long noncoding RNAs (lncRNAs) in cancer is increasingly focused. ncRuPAR is a newly detected lncRNA; in previous study, we found out that ncRuPAR could inhibit tumor progression by downregulating protease-activated receptor-1 (PAR-1), but its role in colorectal cancer (CRC) is never elucidated. Here, we conducted a self-control study which includes 105 CRC samples. By quantitative real time PCR (qRT-PCR) and immunohistochemical staining, we detected the expression of ncRuPAR and PAR-1 as well as their correlation; we further associated these data with the clinicopathologic parameters. A receiver operating characteristic (ROC) curve was constructed to evaluate the diagnostic value of ncRuPAR and PAR-1, respectively. Our results indicated that the expression of ncRuPAR was significantly downregulated in CRC compared with paired adjacent nontumor tissues, but the level of PAR-1 mRNA in cancerous tissues was significantly higher than in adjacent normal areas. The expression of ncRuPAR was significantly correlated with lymph node metastasis, distant metastasis, Duck's stage, differentiation, and TNM stage and was potentially negatively associated with the mRNA levels and EI scores of PAR-1. The area under the ROC curve of ncRuPAR was 0.81 (95% confidence interval (CI): 0.75-0.87); at a cutoff value of 8.34, the ncRuPAR measurement had a sensitivity of 97.14%, a specificity of 65.87%, and an accuracy of 82.86% to predict CRC.

Decreased expression of IGFBP7 was a poor prognosis predictor for gastric cancer patients.

Increasing evidence indicated that insulin-like growth factor binding protein 7 (IGFBP7) was regarded as a potential tumor suppressor in various human cancers, but its role in gastric cancer is still largely unknown. In the present study, we performed a retrospective study which includes 247 gastric cancer patients. Among them, the IGFBP7 expression was detected by qRT-PCR in 138 cases of gastric cancer and adjacent non-tumor tissues and was further correlated with the expression of p53, Ki-67, and the clinicopathologic features. The results indicated that both IGFBP7 mRNA and protein in gastric cancer tissues were significantly lower than those in the adjacent non-tumor tissues. Additionally, the expression of IGFBP7 was correlated with the depth of invasion, lymph node metastasis, and TNM stage. Interestingly, the expression of IGFBP7 was negatively associated with Ki-67 (r = -0.227, P < 0.001) but positively associated with p53 (r = 0.140, P = 0.028). Univariate analysis showed that low expression of IGFBP7 was associated with poor prognosis (P < 0.001), and multivariate analysis showed that IGFBP7 (HR = 1.87; 95 % CI 1.65-2.17), distant metastasis (HR = 2.68; 95 % CI 1.58-4.56), and tumor size (HR = 1.45; 95 % CI 0.90-2.32) were independent prognostic factors for gastric cancer patients. These results demonstrated that IGFBP7 was downregulated in gastric cancer, and its low expression was potentially correlated with increased cancer cell proliferation and could be used to predicate poor prognosis in these patients.

ncRuPAR inhibits gastric cancer progression by down-regulating protease-activated receptor-1.

ncRuPAR is a newly discovered long noncoding RNA molecule that can upregulate protease-activated receptor-1 (PAR-1) during embryonic growth; however, its role in cancer has not been elucidated. Here, we conducted a study to investigate the role of ncRuPAR in gastric cancer. Significant downregulation of ncRuPAR was detected in gastric cancer tissues compared with paired adjacent nontumor tissues; however, both PAR-1 and vascular endothelial growth factor (VEGF) messenger RNA (mRNA) levels were significantly higher in cancerous tissues compared with adjacent normal tissues. Additionally, the expression level of ncRuPAR was found to be significantly correlated with tumor invasion depth, lymph node metastasis, distant metastasis, tumor size, and tumor-nodes-metastasis (TNM) stage and inversely associated with the mRNA levels and extent (E) × intensity (I) scores of PAR-1 and VEGF. The protein level of PAR-1 was significantly correlated with tumor size only, while the VEGF protein level was significantly correlated with invasion depth and tumor size. The area under the receiver operating characteristic (ROC) curve of ncRuPAR was 0.84 (95 % CI 0.79-0.88) at a cutoff value of 4.97; ncRuPAR had a sensitivity of 88.41 %, a specificity of 73.91 %, and an accuracy of 81.16 % for the prediction of gastric cancer. These results suggest that ncRuPAR inhibits gastric cancer development, and its underlying mechanism involves the inhibition of PAR-1. In addition, ncRuPAR could be regarded as a marker for gastric cancer in the future.

Elevated plasma D-dimer levels correlate with long term survival of gastric cancer patients.

BACKGROUND: Increasing evidence indicated plasma D-dimer could be regarded as a marker in cancers, however, its role in gastric cancer is still largely unknown. METHODS: Plasma D-dimer levels were measured by enzyme linked fluorescent immunoassays and evaluated by receiver operating characteristic (ROC) curves for peritoneal dissemination in gastric cancer and healthy subjects. The overall survival (OS) characteristics were determined using Kaplan-Meier and Cox regression analyses. RESULTS: The average of the plasma D-dimer levels for gastric cancer patients was significantly higher than the healthy subjects. A Spearman correlation analysis showed that plasma D-dimer levels correlated with the depth of invasion, lymph node metastasis, peritoneal dissemination, distant metastasis, tumor size and TNM stage. The mean plasma D-dimer level was 2.20 ± 1.51 µg/mL in peritoneal dissemination patients and 1.01 ± 0.79 µg/mL in non-peritoneal dissemination patients (P<0.001). Additionally, the mean plasma D-dimer concentration in patients alive at the final follow-up evaluation was 0.79 ± 0.72 µg/mL,which was significantly lower than the amounts determined for the deceased patients (1.36 ± 1.13 µg/mL) (P<0.001). The AUC of D-dimer was 0.833 (95%CI: 0.780-0.885). At a cut-off value of 1.465 µg/mL, the D-dimer measurement had a sensitivity of 78.00%, a specificity of 83.76% and an accuracy of 82.59%. The median OS was 48.10 months (95% CI: 43.88-52.31) in patients with plasma D-dimer levels less than 1.465 µg/mL and 22.39 months (95% CI: 16.95-27.82) in patients with plasma D-dimer levels exceeding 1.465 µg/mL (log-rank test, P<0.001). Importantly, plasma D-dimer levels exceeding 1.465 µg/mL were significantly associated with poor OS, as determined using a multivariate Cox regression analysis (hazard ratio [HR], 2.28; 95%CI: 1.36-3.81; P = 0.002). CONCLUSIONS: Plasma D-dimer levels are increased in gastric cancer patients and may be a valuable biomarker for peritoneal dissemination, with high D-dimer levels predicting poor outcomes for gastric cancer patients.

The identification and characterization of novel N-glycan-based biomarkers in gastric cancer.

BACKGROUND AND AIMS: To identify and validate N-glycan biomarkers in gastric cancer (GC) and to elucidate their underlying molecular mechanism of action. METHODS: In total, 347 individuals, including patients with GC (gastric cancer) or atrophic gastritis and healthy controls, were randomly divided into a training group (n=287) and a retrospective validation group (n=60). Serum N-glycan profiling was achieved with DNA sequencer-assisted/fluorophore-assisted carbohydrate electrophoresis (DSA-FACE). Two diagnostic models were constructed based on the N-glycan profiles using logistic stepwise regression. The diagnostic performance of each model was assessed in retrospective, prospective (n=60), and follow-up (n=40) cohorts. Lectin blotting was performed to determine total core-fucosylation, and the expression of genes involved in core-fucosylation in GC was analyzed by reverse transcriptase-polymerase chain reaction. RESULTS: We identified at least 9 N-glycan structures (peaks) and the levels of core fucose residues and fucosyltransferase were significantly decreased in GC. Two diagnostic models, designated GCglycoA and GCglycoB, were constructed to differentiate GC from control and atrophic gastritis. The areas under the receiver operating characteristic (ROC) curves (AUC) for both GCglycoA and GCglycoB were higher than those for CEA, CA19-9, CA125 and CA72-4. Compared with CEA, CA19-9, CA125 and CA72-4, the sensitivity of GCglycoA increased 29.66%, 37.28%, 56.78% and 61.86%, respectively, and the accuracy increased 10.62%, 16.82%, 25.67% and 28.76%, respectively. For GCglycoB, the sensitivity increased 27.97%, 35.59%, 55.09% and 60.17% and the accuracy increased 21.26%, 24.64%, 31.40% and 34.30% compared with CEA, CA19-9, CA125 and CA72-4, respectively. After curative surgery, the core fucosylated peak (peak 3) and the total core fucosylated N-glycans (sumfuc) were reversed. CONCLUSIONS: The results indicated that the diagnostic models based on N-glycan markers are valuable and noninvasive alternatives for identifying GC. We concluded that decreased core-fucosylation in both tissue and serum from GC patients may result from the decreased expression of fucosyltransferase.