[Clinical study on the treatment of postoperative recurrence of lumbar disc herniation with intervertebral fusion].

OBJECTIVE: To explore clinical effect of different intervertebral fusion devices (cage) in treating postoperative recurrent lumbar disc herniation (LDH). METHODS: One hundred and forty-two LDH patients with recurrence after simple intervertebral disc nucleus pulpoideectomy from January 2019 to January 2021 were retrospectively analyzed. All patients were treated with combined underchannel fixation and interbody fusion and divided into a single anatomical group,two-anatomical group and a single banana group according to types and numbers of implanted cage. There were 51 patients in a single anatomical group,included 29 males and 22 females,aged from 39 to 65 years old with an average of (53.74±5.68) years old;body mass index (BMI) ranged from 18.62 to 28.13 kg·m-2 with an average of (22.08±2.15) kg·m-2;the interval between operation and recurrence ranged from 0.5 to 4.0 years with an average of (2.7±0.8) years;5 patients with L3,4,35 patients with L4,5 and 11 patients with L5S1;a single anatomical cage was implanted. There were 46 patients in two-anatomical group,included 25 males and 21 females,aged from 37 to 66 years old with an average of (54.52±6.02) years old;BMI ranged from 18.25 to 28.44 kg·m-2 with an average of (21.74±1.83) kg·m-2;the interval between operation and recurrence ranged from 0.5 to 5.0 years with an average of (2.7±0.9) years;4 patients with L3,4,32 patients with L4,5 and 10 patients with L5S1;two-anatomical cages were implanted. There were 45 patients in a single banana group,included 22 males and 23 females,aged from 38 to 65 years old with an average of (54.49±6.45) years old;BMI ranged from 18.85 to 28.20 kg·m-2 with an average of (21.63±1.59) kg·m-2;the interval between operation and recurrence ranged from 0.5 to 5.0 years with an average of (2.6±1.0) years;3 patients with L3,4,36 patients with L4,5 and 16 patients with L5S1;a single banana cage was implanted. Operation time,intraoperative blood loss,incision length,postoperative incision drainage volume,hospital stay and complications among 3 groups were observed and compared. The height of intervertebral space before and after operation,curvature of lordosis and the postoperative intervertebral fusion were compared. Visual analogue scale (VAS) and Oswestry disability index (ODI) were used to evaluate degree of lumbar pain and lumbar function before operation,1 and 6 months after operation,respectively. RESULTS: All patients among 3 groups were followed up at least 6 months,and no cases were fell out. There were no significant difference in operation time,intraoperative blood loss,incision length,postoperative incision drainage volume and hospital stay among 3 groups (P>0.05). At 6 months after operation,the height of intervertebral space in two-anatomical group and a single group were [(11.08±1.78) mm,(10.95±1.62) mm],curvature of lordosis were [(12.05±1.86) °,(11.63±1.57) °],which were higher than those in a single dissection group (10.14±1.54) mm,(10.92±1.45) °,and the difference were statistically significant (P<0.05). The interbody fusion rate between two-anatomical and a banana group (95.65%,95.56%) were higher than that in a single anatomical group (78.43%) at 6 months after operation (P<0.05). VAS and ODI of lumbar among 3 groups were decreased at 1 and 6 months after operation (P<0.05). There was no significant difference in complications among 3 groups (P>0.05). CONCLUSION: The three fusion devices could achieve significant results in treating postoperative recurrence of LDH,but the implantation of two-anatomical cage and a single banana cage are more helpful to maintain the height of intervertebral space and lordosis curvature of patients with postoperative recurrence of LDH,and obtain good intervertebral fusion results.

Development and validation of a new stage-specific nomogram model for predicting cancer-specific survival in patients in different stages of colon cancer: A SEER population-based study and external validation.

Background: The effects of laterality of the primary tumor on survival in patients in different stages of colon cancer are contradictory. We still lack a strictly evaluated and validated survival prediction tool, considering the different roles of tumor laterality in different stages. Methods: A total of 101,277 and 809 colon cancer cases were reviewed using the Surveillance, Epidemiology, and End Results database and the First Affiliated Hospital of Xi 'an Jiaotong University database, respectively. We established training sets, internal validation sets and external validation sets. We developed and evaluated stage-specific prediction models and unified prediction models to predict cancer-specific survival and compared the prediction abilities of these models. Results: Compared with right-sided colon cancers, the risk of cancer-specific death of left-sided colon cancer patients was significantly higher in stage I/II but was markedly lower in stage III patients. We established stage-specific prediction models for stage I/II and stage III separately and established a unified prediction model for all stages. By evaluating and validating the validation sets, we reported high prediction ability and generalizability of the models. Furthermore, the stage-specific prediction models had better predictive power and efficiency than the unified model. Conclusions: Right-sided colon cancer patients have better cancer-specific survival than left-sided colon cancer patients in stage I/II and worse cancer-specific survival in stage III. Using stage-specific prediction models can further improve the prediction of cancer-specific survival in colon cancer patients and guide clinical decisions.

Circ_0003159 upregulates LIFR expression through competitively binding to miR-221-3p/miR-222-3p to block gastric cancer development.

Gastric cancer (GC) remains a major cause of cancer-related deaths. Increasing studies suggest that cancer development is accompanied by the deregulation of circular RNAs. We investigated the function of circ_0003159 in GC. The expression levels of circ_0003159, miR-221-3p/miR-222-3p and leukemia inhibitory factor receptor (LIFR) mRNA were measured by real-time quantitative polymerase chain reaction. Cell colony formation ability was assessed by colony formation assay, and cell viability was assessed by cell counting kit-8 assay. Cell apoptosis was assessed by flow cytometry assay and caspase3 activity. Cell migration and invasion were assessed by transwell assay. Glycolysis energy metabolism was assessed by 5'-triphosphate production, glucose uptake and lactate production. The protein levels of related marker proteins and LIFR were detected by western blot. The relationship between circ_0003159 and miR-221-3p/miR-222-3p, or LIFR and miR-221-3p/miR-222-3p was obtained from bioinformatics tools and verified by dual-luciferase reporter assay. A cancer tumorogenicity xenograft experiment in nude mice was conducted to determine the role of circ_0003159 in tumor growth by AGS cells. Our results showed that circ_0003159 expression was decreased in GC tissues and cells. Circ_0003159 overexpression sequestered GC cell viability, migration, invasion and glycolysis and induced cell apoptosis. MiR-221-3p and miR-222-3p were targets of circ_0003159, and the inhibition of miR-221-3p and miR-222-3p also blocked GC cell viability, migration, invasion and glycolysis and promoted cell apoptosis. LIFR was a common target of miR-221-3p and miR-222-3p. Interestingly, LIFR knockdown reversed the effects of circ_0003159 overexpression on GC cell behaviors. Circ_0003159 increased the expression level of LIFR by targeting miR-221-3p and miR-222-3p. The tumorigenicity assay showed that circ_0003159 overexpression inhibited tumor growth in vivo. In conclusion, circ_0003159 inhibited GC development in vitro and in vivo by enriching the level of LIFR via direct binding to miR-221-3p/miR-222-3p.

Will Green Finance Contribute to a Green Recovery? Evidence From Green Financial Pilot Zone in China.

In the post-epidemic era, green finance plays a more significant role in supporting the "green recovery" of the economy, so it is necessary to evaluate the implementation effect of previous green financial policies. In 2017, the green finance reform and innovation pilot zone set up in five provinces and autonomous regions made an exploration in the development of green finance. From the perspective of micro-enterprises, can this policy play a beneficial policy effect in the long run? Based on the quasi-natural experiment of green finance pilot, using the data of A-share listed companies, this paper empirically tests the impact of pilot policies on the long-term value of green enterprises in pilot areas. It is found that, compared with non-pilot zones, the green finance pilot enables a significant increase in the Tobin Q-measured value of green enterprises in the pilot zones. Heterogeneity analysis shows that green finance pilot has a more significant impact on non-state-owned enterprises, enterprises in traditional industries, large enterprises, and enterprises in the eastern region of China. Green finance pilot zone can achieve better policy effects in areas with stronger environmental impact regulation and higher financial development levels. The mechanism test shows that the green finance pilot affects the long-term value of green enterprises through the capital market effect improving the stock trading activity of enterprises and through the real effect improving the operational efficiency and profitability of enterprises. From the perspective of micro-enterprises, this paper enriches the research on the development effect of green finance and provides theoretical support for the effect evaluation of green finance pilot policies.

The role of lncRNA ANRIL in the progression of hepatocellular carcinoma.

OBJECTIVES: The aim of the current study was to identify the long noncoding RNAs (lncRNAs) ANRIL function and molecular pathways underlying hepatocellular carcinoma progression. METHODS: ANRIL knockdown with specific siRNA, and transfected into HepG2 cells according to the protocol of Lipofectamine 2000. Cell proliferation, apoptosis, migration and metastasis were assessed with MTT assay, flow cytometry and wound healing assay, respectively. Moreover, the expression level of ANRIL, apoptosis-related genes, and the Wnt pathway-associated genes were assessed by real time-PCR and Western blot assay. KEY FINDINGS: Knocking down of ANRIL led to alleviated cell growth and increased cell apoptosis of HepG2 cells through markedly increased expression levels of Bax and Bad. In contrast, dramatically diminished the expressions of anti-apoptotic factors including Bid and Bcl-2 in comparison to the scrambled control group (si-NC). Furthermore, ANRIL silencing resulted in an inactivated Wnt/ß-catenin pathway by suppressing key genes associated with this pathway. CONCLUSIONS: Taken together, these findings imply new insights into the regulatory network of the Wnt pathway through lncRNA ANRIL that indicate ANRIL may be a therapeutic factor potential for hepatocellular carcinoma.

Potential of C1QTNF1-AS1 regulation in human hepatocellular carcinoma.

The aim of our study is to explore the regulation of C1QTNF1-AS1 on its target miR-221-3p/SOCS3 in human hepatocellular carcinoma (HCC). To explore the underlying molecular regulation of non-coding RNA for HCC, differentially expressed patterns of lncRNAs and genes were examined by RNA-seq. GO and KEGG pathway analysis were done based on the function of mRNAs that mediated by differentially expressed lncRNAs. RT-qPCR and western blot were conducted to detect the mRNA and protein level expression of C1QTNF1-AS1, miR-221-3p, SOCS3 and key proteins in JAK/STAT signaling pathway in HCC tissues and cells. The target miRNA of differentially expressed C1QTNF1-AS1 and SOCS3 was miR-221-3p predicted by bioinformatics analysis. C1QTNF1-AS1 and SOCS3 was downregulated and miR-221-3p was upregulated in HCC tissues and cells. In HepG2 and Huh-7 cells, the overexpression of C1QTNF1-AS1 or SOCS3, and silencing of miR-221-3p inhibited proliferation, migration, invasion and JAK/STAT signaling pathway, while promoted cell apoptosis. The results of dual-luciferase assay indicated that C1QTNF1-AS1 regulated miR-221-3p and miR-221-3p targeted SOCS3 by directly binding. And the growth of HCC in vivo was impeded when C1QTNF1-AS1 was upregulated. Overexpression of C1QTNF1-AS1 could downregulate miR-221-3p thereby inhibited the proliferation, migration and invasion of HCC cells.

Is concomitant splenectomy necessary in radical gastric cancer surgery? A systematic review and meta-analysis.

PURPOSE: This study is a systematic review and meta-analysis compare the short- and long-term outcomes of splenectomy (SP) versus splenic preservation (NSP) in radical gastric cancer surgery. METHODS: A comprehensive search of PubMed, Embase, Cochrane Library and Web of Knowledge was performed. Evaluation of short- and long-term outcomes was collected and analyzed by a fixed or random effects model, according to the heterogeneity using RevMan 5.2 software. RESULTS: A total of 5431 gastric cancer patients who underwent radical surgery (1706 with SP and 3725 with NSP) were reviewed in 11 studies included in this study. Compared with NSP, SP was significantly associated with higher rate of overall postoperative complication and increased incidence of pulmonary complications, abdominal abscess and pancreas complications. No statistical difference was observed regarding mortality, wound infection, anastomotic leakage and postoperative 5-year overall survival. CONCLUSION: There was no difference in long-term oncological outcome but remarkably poorer short-term outcomes in SP group than NSP group. Therefore, SP seems unnecessary in radical gastric cancer surgery. However, well-designed, multicenter, prospective, randomized controlled trials are warranted for further validation.

Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment.

Development of colorectal cancer has been considered as a result of imbalance of pro- and anti-inflammatory intestinal microenvironment accompanied by macrophage recruitment. Despite macrophages are implicated in remodeling tumor microenvironment, the mechanism of macrophage recruitment is not fully elucidated yet. In this study, we reported clinical association of highly expressed pyruvate kinase M2 in colorectal cancer with macrophage attraction. The conditioned medium from Caco-2 and HT-29 cells with depleted pyruvate kinase M2 dramatically reduced macrophage recruitment, which is reversed by addition of, a critical chemotaxis factor to macrophage migration, rCCL2. Silencing of endogenous pyruvate kinase M2 markedly decreased CCL2 expression and secretion by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Endogenous pyruvate kinase M2 interacted with p65 and mediated nuclear factor-κB signaling pathway and mainly regulated phosphorylation of Ser276 on p65 nuclear factor-κB. In addition, inhibition of macrophage recruitment caused by pyruvate kinase M2 silencing was rescued by ectopic expression of p65. Interestingly, pyruvate kinase M2 highly expressed in colorectal cancer tissue, which is correction with macrophage distribution. Taken together, we revealed a novel mechanism of pyruvate kinase M2 in promoting colorectal cancer progression by recruitment of macrophages through p65 nuclear factor-κB-mediated expression of CCL2.

Laparoscopic spleen-preserving hilar lymph node dissection through pre-pancreatic and retro-pancreatic approach in patients with gastric cancer.

BACKGROUND: The conventional radical resection of proximal gastric cancer is even more risky when performed laparoscopically, though this technique is widely used in gastrointestinal surgery and is accepted as the superior method. This paper explores the feasibility of laparoscopic spleen-preserving hilar lymph node dissection using a retro-pancreatic approach for the treatment of proximal gastric cancer. METHODS: Two cadavers were dissected for examination of and the pre-pancreatic and retro-pancreatic spaces. Following the dissection of the cadavers, ten live patients with proximal gastric cancer from May 2008 to May 2013 at Nanfang Hospital, Guangzhou, China, were given total gastrectomy and adjuvant splenic hilar lymph node clearance through pre-pancreatic and retro-pancreatic approach on the precondition of preserving the pancreas and spleen. The clinicopathologic characteristics, as well as the intraoperative and postoperative variables affecting the procedure, were observed and analyzed. RESULTS: Anatomy of the space anterior and posterior to the pancreas in the two cadavers demonstrated the feasibility of pre-pancreatic and retro-pancreatic approach. The surgeries were all successfully performed laparoscopically; conversion to laparotomy was not necessary for any of the ten patients. The overall mean operative time was 243.6 ± 45 min. The mean estimated blood loss was 232 ± 80 ml. At the time of follow-up (median 12 months post-surgery), there had been neither local recurrence nor mortality in any of the patients. CONCLUSION: Laparoscopic spleen- and pancreas-preserving splenic hilar lymph node dissection during total gastrectomy, using both pre-pancreatic and retro-pancreatic approaches, is indicated as a safe and feasible method for the treatment of proximal gastric cancer.

The prognostic roles of ALDH1 isoenzymes in gastric cancer.

Increased aldehyde dehydrogenase 1 (ALDH1) activity has been determined to be present in the stem cells of several kinds of cancers including gastric cancer (GC). Nevertheless, which ones of ALDH1's isoenzymes are leading to ALDH1 activity remains elusive. In this study, we examined the prognostic value and hazard ratio (HR) of individual ALDH1 isoenzymes in patients with GC using "The Kaplan-Meier plotter" database. mRNA high expression level of ALDH1A1 was not found to be significantly correlated with the overall survival (OS) of all patients with GC followed for 20 years, HR =0.86 (95% confidence interval [CI]: 0.7-1.05), P=0.13. mRNA high expression level of ALDH1A2 was also not significantly correlated with OS for all patients with GC, HR =1.13 (95% CI: 0.91-1.41), P=0.25. mRNA high expression level of ALDH1A3 was found to be significantly correlated with worsened OS in either intestinal-type patients, HR =2.24 (95% CI: 1.44-3.49), P=0.00026, or diffuse-type patients, HR =1.91 (95% CI: 1.02-3.59), P=0.04. Interestingly, mRNA high expression level of ALDH1B1 was found to be significantly correlated with better OS for all patients with GC, HR =0.66 (95% CI: 0.53-0.81), P=7.8e-05, and mRNA high expression level of ALDH1L1 was found to be significantly correlated with worsened OS for all patients with GC, HR =1.23 (95% CI: 1-1.51), P=0.048. Furthermore, our results also indicate that ALDH1A3 and ALDH1L1 are potential major contributors to the ALDH1 activity in GC, since mRNA high expression levels of ALDH1A3 and ALDH1L1 were found to be significantly correlated with worsened OS for all patients with GC. Based on our study, ALDH1A3 and ALDH1L1 are potential prognostic markers and therapeutic targets for patients with GC.

Adenovirus encoding XAF-1 and TNF­α in the same open reading frame efficiently inhibits hepatocellular cancer cells.

X­linked inhibitor of apoptosis (XIAP)­associated factor 1 (XAF­1), a tumor suppressor, is downregulated in most human malignant tumors. However, the tumor suppressive role of XAF­1 in hepatocellular carcinoma (HCC) and its therapeutic value require further elucidation. The present study examined the expression of XAF­1 at the mRNA and protein level in the HCC and paired peritumor tissue specimens, as well as in HCC cell lines and a normal liver cell line. A recombinant adenovirus which co­expressed XAF­1 and TNF­α was then constructed, and its effects on the proliferation and colony formation ability of the MHCC97H HCC cell line were assessed using apoptosis induction, flow cytometry, trypan blue staining assay and a clonogenic assay. The results demonstrated that the expression of XAF­1 was significantly reduced in HCC tissues compared with that in their matched peritumor specimens, and a significant correlation with the tumor size, stage and tumor ­ nodes ­ metastasis stage was identified. The reduced levels of XAF­1 were further confirmed the HCC cell lines MHCC97L, HepG2 and MHCC97H compared with those in the L02 normal liver cell line. The recombinant adenovirus Ad­XAF­1&TNF­α, which co­expressed XAF­1 and TNF­α, was shown to efficiently express the two proteins at the mRNA and protein level. Furthermore, infection with Ad­XAF­1&TNF­α synergistically induced apoptosis, reduced the proliferation and colony formation ability of MHCC97L cells to a significantly greater extent than overexpression of XAF­1 or TNF­α individually. To the best of our knowledge, the present study was the first to construct an adenovirus which co­expressed XAF­1 and TNF­α in the same open reading frame and expressed them proportionally. As Ad­XAF­1&TNF­α inhibited HCC cells with enhanced efficiency, it may be applicable for the treatment of HCC.

Is early oral feeding after gastric cancer surgery feasible? A systematic review and meta-analysis of randomized controlled trials.

AIM: To assess the feasibility and safety of early oral feeding (EOF) after gastrectomy for gastric cancer through a systematic review and meta-analysis based on randomized controlled trials. METHODS: A literature search in PubMed, Embase, Web of Science and Cochrane library databases was performed for eligible studies published between January 1995 and March 2014. Systematic review was carried out to identify randomized controlled trials comparing EOF and traditional postoperative oral feeding after gastric cancer surgery. Meta-analyses were performed by either a fixed effects model or a random effects model according to the heterogeneity using RevMan 5.2 software. RESULTS: Six studies remained for final analysis. Included studies were published between 2005 and 2013 reporting on a total of 454 patients. No significant differences were observed for postoperative complication (RR = 0.95; 95%CI, 0.70 to 1.29; P = 0.75), the tolerability of oral feeding (RR = 0.98; 95%CI, 0.91 to 1.06; P = 0.61), readmission rate (RR = 1; 95%CI, 0.30 to 3.31; P = 1.00) and incidence of anastomotic leakage (RR = 0.31; 95%CI, 0.01 to 7.30; P = 0.47) between two groups. EOF after gastrectomy for gastric cancer was associated with significant shorter duration of the hospital stay (WMD = -2.36; 95%CI, -3.37 to -1.34; P<0.0001) and time to first flatus (WMD = -19.94; 95%CI, -32.03 to -7.84; P = 0.001). There were no significant differences in postoperative complication, tolerability of oral feeding, readmission rates, duration of hospital stay and time to first flatus among subgroups stratified by the time to start EOF or by partial and total gastrectomy or by laparoscopic and open surgery. CONCLUSIONS: The result of this meta-analysis showed that EOF after gastric cancer surgery seems feasible and safe, even started at the day of surgery irrespective of the extent of the gastric resection and the type of surgery. However, more prospective, well-designed multicenter RCTs with more clinical outcomes are needed for further validation.

A comparison of whole-genome shotgun-derived mouse chromosome 16 and the human genome.

The high degree of similarity between the mouse and human genomes is demonstrated through analysis of the sequence of mouse chromosome 16 (Mmu 16), which was obtained as part of a whole-genome shotgun assembly of the mouse genome. The mouse genome is about 10% smaller than the human genome, owing to a lower repetitive DNA content. Comparison of the structure and protein-coding potential of Mmu 16 with that of the homologous segments of the human genome identifies regions of conserved synteny with human chromosomes (Hsa) 3, 8, 12, 16, 21, and 22. Gene content and order are highly conserved between Mmu 16 and the syntenic blocks of the human genome. Of the 731 predicted genes on Mmu 16, 509 align with orthologs on the corresponding portions of the human genome, 44 are likely paralogous to these genes, and 164 genes have homologs elsewhere in the human genome; there are 14 genes for which we could find no human counterpart.