Galectin-1 promotes gastric cancer peritoneal metastasis through peritoneal fibrosis.

BACKGROUND: Peritoneal metastasis is one of the main causes of death in patients with gastric cancer (GC). Galectin-1 regulates various undesirable biological behaviors in GC and may be key in GC peritoneal metastasis. METHODS: In this study, we elucidated the regulatory role of galectin-1 in GC cell peritoneal metastasis. GC and peritoneal tissues underwent hematoxylin-eosin (HE), immunohistochemical (IHC), and Masson trichrome staining to analyze the difference in galectin-1 expression and peritoneal collagen deposition in different GC clinical stages. The regulatory role of galectin-1 in GC cell adhesion to mesenchymal cells and in collagen expression was determined using HMrSV5 human peritoneal mesothelial cells (HPMCs). Collagen and corresponding mRNA expression were detected with western blotting and reverse transcription PCR, respectively. The promoting effect of galectin-1 on GC peritoneal metastasis was verified in vivo. Collagen deposition and collagen I, collagen III, and fibronectin 1 (FN1) expression in the peritoneum of the animal models were detected by Masson trichrome and IHC staining. RESULTS: Galectin-1 and collagen deposition in the peritoneal tissues was correlated with GC clinical staging and were positively correlated. Galectin-1 enhanced the ability of GC cells to adhere to the HMrSV5 cells by promoting collagen I, collagen III, and FN1 expression. The in vivo experiments confirmed that galectin-1 promoted GC peritoneal metastasis by promoting peritoneal collagen deposition. CONCLUSION: Galectin-1-induced peritoneal fibrosis may create a favorable environment for GC cell peritoneal metastasis.

Galectin-1-mediated high NCAPG expression correlates with poor prognosis in gastric cancer.

Galectin-1 (Gal1) and non-SMC condensin I complex, subunit G (NCAPG) are associated with metastasis in several malignant tumors. However, their precise roles in gastric cancer (GC) remain uncertain. This study explored the clinical significance and relationship of Gal1 and NCAPG in GC. Gal1 and NCAPG expressions were significantly up-regulated in GC compared to adjacent non-cancerous tissues by immunohistochemistry (IHC) and Western blotting. Besides, methods including stable transfection, quantitative real-time reverse transcription PCR, Western blotting, Matrigel invasion and wound-healing assays in vitro, were also conducted. IHC scores for Gal1 and NCAPG had a positive correlation in GC tissues. High Gal1 or NCAPG expression significantly correlated with poor prognosis in GC, and Gal1 combined with NCAPG had a synergetic effect on the prediction of GC prognosis. Gal1 overexpression in vitro enhanced NCAPG expression, cell migration, and invasion in SGC-7901 and HGC-27 cells. Simultaneous Gal1 overexpression and NCAPG knockdown in GC cells partly rescued the migrative and invasive abilities. Thus, Gal1 promoted GC invasion through increased NCAPG expression. The present study demonstrated the prognostic significance of the combination of Gal1 and NCAPG in GC for the first time.

Identification and validation of oxidative stress and immune-related hub genes in Alzheimer's disease through bioinformatics analysis.

Alzheimer's disease (AD) is the leading cause of dementia in aged population. Oxidative stress and neuroinflammation play important roles in the pathogenesis of AD. Investigation of hub genes for the development of potential therapeutic targets and candidate biomarkers is warranted. The differentially expressed genes (DEGs) in AD were screened in GSE48350 dataset. The differentially expressed oxidative stress genes (DEOSGs) were analyzed by intersection of DEGs and oxidative stress-related genes. The immune-related DEOSGs and hub genes were identified by weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) analysis, respectively. Enrichment analysis was performed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. The diagnostic value of hub genes was assessed by receiver operating characteristic analysis and validated in GSE1297. The mRNA expression of diagnostic genes was determined by qRT-PCR analysis. Finally, we constructed the drug, transcription factors (TFs), and microRNA network of the diagnostic genes. A total of 1160 DEGs (259 up-regulated and 901 down-regulated) were screened in GSE48350. Among them 111 DEOSGs were identified in AD. Thereafter, we identified significant difference of infiltrated immune cells (effector memory CD8 T cell, activated B cell, memory B cell, natural killer cell, CD56 bright natural killer cell, natural killer T cell, plasmacytoid dendritic cell, and neutrophil) between AD and control samples. 27 gene modules were obtained through WGCNA and turquoise module was the most relevant module. We obtained 66 immune-related DEOSGs by intersecting turquoise module with the DEOSGs and identified 15 hub genes through PPI analysis. Among them, 9 hub genes (CCK, CNR1, GAD1, GAP43, NEFL, NPY, PENK, SST, and TAC1) were identified with good diagnostic values and verified in GSE1297. qRT-PCR analysis revealed the downregulation of SST, NPY, GAP43, CCK, and PENK and upregulation of NEFL in AD. Finally, we identified 76 therapeutic agents, 152 miRNAs targets, and 91 TFs regulatory networks. Our study identified 9 key genes associated with oxidative stress and immune reaction in AD pathogenesis. The findings may help to provide promising candidate biomarkers and therapeutic targets for AD.

Efficacy of DC-CIK Immunotherapy Combined with Chemotherapy on Locally Advanced Gastric Cancer.

The aim of the study is to explore the efficacy and safety of dendritic cell-cytokine-induced killer cell (DC-CIK) immunotherapy combined with chemotherapy in the treatment of locally advanced gastric cancer (LAGC). Among 106 patients with LAGC, 53 received the treatment of oxaliplatin-5-fluorouracil chemotherapy (control group), while the remaining 53 received DC-CIK immunotherapy combined with chemotherapy (DC-CIK group). The short-term efficacy and the changes in immune function indexes (cluster of differentiation (CD)3+, CD4+, CD8+, CD4+/CD8+, and natural killer (NK) cells) were analyzed. The overall response rate (ORR) was 47.2% (25/53) and 41.5% (22/53), and the disease control rate (DCR) was 69.8% (37/53) and 50.9% (27/53), respectively, in the DC-CIK group and the control group. It could be seen that the ORR had no statistically significant difference between the two groups, while the DCR in the DC-CIK group was significantly better than that in the control group. After treatment, the proportions of CD3+ T lymphocytes, CD4+ T lymphocytes, CD4+/CD8+ cells, and NK cells obviously rose, while the proportion of CD8+ T lymphocytes obviously declined in the DC-CIK group compared with those in the control group. After treatment, the scores in the function module of the QLQ-C30 scale were greatly higher in the DC-CIK group than those in the control group, while the scores of loss of appetite, constipation, dyspnea, fatigue, pain, and sleep disorders in the symptom module were significantly lower in the DC-CIK group than those in the control group. The median survival time was 23.4 months and 18.6 months, respectively, in the DC-CIK group and the control group. The results of the log-rank test showed that the OS in the DC-CIK group was remarkably superior to that in the control group. DC-CIK immunotherapy combined with chemotherapy can improve the immune cell function, ameliorate the quality of life, and prolong the survival time of LAGC patients, with fewer adverse reactions.

Steroid Receptor Coactivator-1 (SRC-1) Promoted Cell Metastasis of Gastric Cancer via VEGFC Activator by NF-κB.

The regulatory mechanism and function of steroid receptor coactivator-1 (SRC-1) was determined in vitro and the role played in gastric cancer was investigated. The study collected 64 patients with gastric cancer tissue and paracancerous tissue to investigate the clinical patterns of SRC-1 expression in gastric cancer. Quantitative polymerase chain reaction, Western blot, enzyme-linked immunosorbent assay, and immunofluorescence staining were used in this study. In patients with gastric cancer, SRC-1 serum expression levels were up-regulated. Over-expression of SRC-1 promoted cell growth and cell metastasis in vitro model of gastric cancer. However, down-regulation of SRC-1 reduced cell growth and cell metastasis in vitro model of gastric cancer. SRC-1 over-expression induced vascular endothelial growth factor C (VEGFC) protein expressions in vitro model by activation of nuclear factor-kappa B (NF-kB) expression. The inhibition of NF-κB reduced the pro-cancer effects of SRC-1 on cell growth and cell metastasis in vitro model of gastric cancer through inhibition of VEGFC expression. These results suggest that SRC-1 promoted cell metastasis of gastric cancer via VEGFC activator by NF-κB. These novel findings may shed further light on the pathogenesis of gastric cancer and on potential precursor markers.

Passage of exogeneous fine particles from the lung into the brain in humans and animals.

There are still significant knowledge gaps in understanding the intrusion and retention of exogeneous particles into the central nervous system (CNS). Here, we uncovered various exogeneous fine particles in human cerebrospinal fluids (CSFs) and identified the ambient environmental or occupational exposure sources of these particles, including commonly found particles (e.g., Fe- and Ca-containing ones) and other compositions that have not been reported previously (such as malayaite and anatase TiO2), by mapping their chemical and structural fingerprints. Furthermore, using mouse and in vitro models, we unveiled a possible translocation pathway of various inhaled fine particles from the lung to the brain through blood circulation (via dedicated biodistribution and mechanistic studies). Importantly, with the aid of isotope labeling, we obtained the retention kinetics of inhaled fine particles in mice, indicating a much slower clearance rate of localized exogenous particles from the brain than from other main metabolic organs. Collectively, our results provide a piece of evidence on the intrusion of exogeneous particles into the CNS and support the association between the inhalation of exogenous particles and their transport into the brain tissues. This work thus provides additional insights for the continued investigation of the adverse effects of air pollution on the brain.

Duodenal-Distal Ileal Fistula After Laparoscopic Radical Right Hemicolectomy: A Case Report.

Right hemicolectomy for colon cancer may be complicated by leaks, stenoses, or fistulas. These complications usually occur at the ileocolic anastomosis and can be managed endoscopically. However, fistulas that are large cannot be managed by endoscopy and require surgical intervention. After laparoscopic radical right hemicolectomy, duodenal fistulae is relatively rare. Among duodenal fistulae, internal duodenocolic fistulae is relatively common, but duodeno-ileum fistulae is extremely rare. Here, we report a case of duodeno-distal ileum fistula after right hemicolectomy with short bowel syndrome, that was surgically treated. After surgical treatment, the symptoms of short bowel syndrome disappeared, weight gain was obvious, and the clinical effect was satisfactory.

KLF5 activates lncRNA DANCR and inhibits cancer cell autophagy accelerating gastric cancer progression.

Cancer cell autophagy has been associated with the progression of gastric cancer (GC), but involvement of long noncoding RNAs (lncRNAs) remains unclear. Initial bioinformatics analysis has identified abnormally highly expressed KLF5 in GC, as well as the predicted regulatory mechanism associating with lncRNA DANCR, miR-194, and AKT2. The expression of KLF5, DANCR, and AKT2 in GC tissue was upregulated, and the expression of miR-194 was downregulated. We knocked KLF5 down and manipulated the expression of DANCR, miR-194, and AKT2 to characterize their roles in GC cell viability, autophagy, and apoptosis. The mechanistic investigations revealed that KLF5 activated the transcription of DANCR in the promoter region and elevated its expression. DANCR acted as a miR-194 sponge to repress its expression in GC. MiR-194 targeted and inhibited AKT2 expression. Silencing KLF5 augmented GC cell autophagy, apoptosis and impeded its viability through the DANCR/miR-194/AKT2 axis. The tumor-inhibiting properties of KLF5 knockdown were substantiated in vivo. Together, our study uncovered the oncogenic role of KLF5-dependent lncRNA DANCR transcription in GC in vivo and in vitro, which implicates the miR-194/AKT2 axis in tumor growth regulation, and it may be a potential therapeutic target for human GC.

Fibroblastic galectin-1-fostered invasion and metastasis are mediated by TGF-ß1-induced epithelial-mesenchymal transition in gastric cancer.

Background The gastric cancer (GC) microenvironment has important effects on biological behaviors, such as tumor cell invasion and metastasis. However, the mechanism by which the GC microenvironment promotes GC cell invasion and metastasis is unknown. The present study aimed to clarify the effects and mechanism of galectin-1 (GAL-1, encoded by LGALS1) on GC invasion and metastasis in the GC microenvironment. Methods The expression of GAL-1/ LGALS1 was determined using western blotting, immunohistochemistry, and quantitative real-time reverse transcription PCR in GC tissues. Besides, methods including stable transfection, Matrigel invasion and migration assays, and wound-healing assays in vitro; and metastasis assays in vivo, were also conducted. Results GAL-1 from cancer-associated fibroblasts (CAFs) induced the epithelial-mesenchymal transition (EMT) of GC cells though the transforming growth factor beta (TGF-ß1)/ Sma- and mad-related protein (Smad) pathway, and affected the prognosis of patients with GC. The level of GAL-1 was high in CAFs, and treating MGC-803 and SGC -7901 cell line with the conditioned medium from CAFs promoted their invasion and metastasis abilities. Overexpression of LGALS1 promoted the expression of TGF-ß1 and induced EMT of GC cell lines. A TGF-ß1 antagonist inhibited the invasion and migration of GC cells. In vivo, overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-ß1 antagonist dramatically reversed these events. Conclusions These findings suggested that high expression of GAL-1 in the GC microenvironment predicts a poor prognosis in patients with GC by promoting the migration and invasion of GC cells via EMT through the TGF-ß1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.

Upregulation of circRNA_100395 sponges miR-142-3p to inhibit gastric cancer progression by targeting the PI3K/AKT axis.

Gastric cancer (GC) has a high morbidity and mortality, hence it is very important to elucidate the molecular pathogenesis mechanism of GC progression in order to find new treatment strategies. The present study aimed to explore the biological function of circular RNA_100395 (circRNA_100395) in GC. The expression level of circRNA_100395 in GC tissues, as well as normal epithelial cells and various gastric cancer cell lines, was detected using reverse transcription-quantitative PCR. Cell Counting Kit-8, EdU assay, flow cytometry and Transwell assays were performed to investigate cell proliferation, apoptosis, migration and invasion, respectively. A dual-luciferase reporter assay was performed to detect the correlation between circRNA_100395 and micro (mi)RNA-142-3p. Western blotting was performed to elucidate the potential regulatory mechanism. circRNA_100395 expression was found to be increased in GC tissues and cell lines. However, miR-142-3p expression was significantly reduced. Besides, low expression levels of circRNA_100395 were associated with poor tumor differentiation, advanced Tumor-Node-Metastasis stage, lymph node metastasis and shorter overall survival time. Moreover, overexpression of circRNA_100395 suppressed cell proliferation, increased the apoptosis rate and suppressed cell invasion and migration by inhibiting the PI3K/AKT signaling pathway. These findings also showed that miRNA-142-3p rescued the antitumor effects induced by circRNA_100395-overexpression. cirRNA_100395-overexpression had antitumor effects via regulating the miR-142-3p signaling pathway, which might be a promising treatment target for GC.

Galectin-1 promotes vasculogenic mimicry in gastric adenocarcinoma via the Hedgehog/GLI signaling pathway.

BACKGROUND: Galectin-1 (GAL-1), which is encoded by LGALS1, promotes vasculogenic mimicry (VM) in gastric cancer (GC) tissue. However, the underlying mechanism remains unclear. METHODS: Immunohistochemical (IHC) and CD34-periodic acid-Schiff (PAS) double staining were used to investigate Glioma-associated oncogene-1(GLI1) expression and VM in paraffin-embedded sections from 127 patients with GC of all tumor stages. LGALS1 or GLI1 were stably transduced into MGC-803 cells and AGS cells, and western blotting, IHC, CD34-PAS double staining and three-dimensional culture in vitro, and tumorigenicity in vivo were used to explore the mechanisms of GAL-1/ GLI1 promotion of VM formation in GC tissues. RESULTS: A significant association between GAL-1 and GLI1 expression was identified by IHC staining, as well as a significant association between GLI1 expression and VM formation. Furthermore, overexpression of LGALS1 enhanced expression of GLI1 in MGC-803 and AGS cells. GLI1 promoted VM formation both in vitro and in vivo. The effects of GLI1 on VM formation were independent of LGALS1. Importantly, the expression of VM-related molecules, such as MMP2, MMP14 and laminin5γ2, was also affected upon GLI1 overexpression or silencing in GC cell lines. CONCLUSION: GAL-1 promotes VM in GC through the Hh/GLI pathway, which has potential as a novel therapeutic target for treatment of VM in GC.

High versus low ligation of inferior mesenteric artery during laparoscopic radical resection of rectal cancer: A retrospective cohort study.

Laparoscopic radical resection is standard treatment for resectable rectal cancer. However, whether high or low inferior mesenteric artery (IMA) ligation should be performed remains controversial. This retrospective cohort study compared the advantages and disadvantages of low vs high IMA ligation in patients undergoing laparoscopic total mesorectal excision for rectal cancer.Rectal cancer patients (n = 322) undergoing total mesorectal excision at our institution in 2010 to 17 were enrolled; 174 underwent high IMA ligation group and 148 low IMA ligation (LIMAL group). Baseline data on patients, operative indices, economic indices, pathology findings, perioperative complications, and survival in the 2 groups were analyzed retrospectively.The low IMA ligation group had significantly higher anus retention ratio (P = .022), shorter hospital stay (P = .025), lower medical expenses (P = .032), fewer cases of anastomotic leakage (P = .023) and anastomotic stricture (P < .001), and lower incidence of postoperative genitourinary dysfunction (P = .003). Cox regression analysis indicated that local recurrence, distant metastasis, tumor differentiation, and tumor-node-metastasis stage were independently associated with survival.Low ligation of the IMA during laparoscopic radical resection of rectal cancer appears to be associated with a lower risks for anastomotic leakage, anastomotic stricture, and genitourinary dysfunction, a shorter hospital stay, and lower costs. In contrast, the rate of lymph node harvest, tumor recurrence rate, metastasis, or mortality was not found to be related with the level of IMA ligation.

[Application of double-pouch anastomosis in laparoscopic radical resection of rectal cancer assisted by small incision].

OBJECTIVE: To explore the feasibility, safety and the economical efficiency of double-pouch anastomosis in laparoscopic radical rectal cancer assisted by small incisions. METHODS: Clinical data of 224 patients undergoing gastrointestinal surgery at Taizhou People's Hospital of Jiangsu Province from January 2011 to December 2017 were retrospectively analyzed. Indusion criteria: patients were diagnosed as primary rectal adenocarcinoma by preoperative enteroscopy pathology, the distance of the tumor to anal margin was from 4 to 15 cm, and patients were treated with laparoscopic total mesorectal excision(TME) through small incision. Patients were divided into two groups according to different anastomosis method, double-pouch group(108 cases) and single-pouch group (116 cases). The surgical indexes, tumor safety indexes, short-term efficacy and economic indexes were compared between the two groups. RESULTS: There was no significant difference between two groups in baseline data, operative time, blood loss, number of lymph nodes dissection, average length of proximal and distal bowel, or incidence of urination and sexual dysfunction (all P>0.05). Compared with the single-pouch group, the double-pouch group presented lower anastomotic secondary bleeding rate [0.9%(1/108) vs. 6.0% (7/116), χ²=4.238, P=0.040], lower incidence of anastomotic leakage[1.9%(2/108) vs. 7.8%(9/116), χ²=4.179, P=0.041], lower incidence of anastomotic stricture [1.9% (2/108) vs. 8.6% (10/116), χ²=5.054, P=0.025], shorter hospital stay [(13.4±3.9) days vs. (15.9±9.8) days, t=2.524, P=0.013] and less average hospitalization costs [(34 000±7 000) yuan vs. (46 000±23 000) yuan, t=5.047,P<0.001]. There was no significant difference in local recurrence, distant metastasis or overall survival between the two groups during mean follow-up of 33 months (all P>0.05). CONCLUSION: Laparoscopic TME assisted by small incision with double-pouch anastomosis is a safe, feasible and economical method.

Overexpression of p53 delivered using recombinant NDV induces apoptosis in glioma cells by regulating the apoptotic signaling pathway.

Malignant glioma is the most common primary brain carcinoma in the world and has a poor survival rate. Previous studies have demonstrated that p53 dysfunction contributes to the development and severity of malignant glioma. It has also been demonstrated that Newcastle disease virus (NDV) may be a viable candidate for the treatment of various types of cancer. In the present study, a p53 oncolytic agent delivered using recombinant NDV (rNDV-p53) was constructed and its anti-tumor effects in vitro and in vivo were assessed. Glioma cell lines and a xenograft mouse model were utilized to assess the ability of p53 and rNDV to promote apoptosis and induce immunotherapy, respectively. The mechanism of rNDV-p53 in glioma therapy was investigated using quantitative polymerase chain reaction and immunohistochemistry. Tumor-specific cytotoxic T-lymphocyte (CTL) responses and lymphocyte infiltration were also analyzed in glioma-bearing models. The results of the present study demonstrate that rNDV-p53 may be a potential therapeutic agent that improves the prognosis of mice with glioma. It was revealed that rNDV-p53 inhibits glioma cell growth and aggressiveness in vitro and in vivo compared with rNDV and p53 alone. The results also demonstrated that rNDV-p53 induced glioma cell apoptosis by upregulating apoptosis-related genes. In addition, the present study demonstrated that rNDV-p53 significantly stimulated CTL responses and lymphocyte infiltration whilst increasing the number of apoptotic bodies in vivo. Furthermore, rNDV-p53 therapy inhibited tumor regression and prolonged the survival of glioma-bearing mice. In conclusion, rNDV-p53 invoked an immune response against glioma cells, which may serve as a comprehensive immunotherapeutic schedule for glioma.

[Clinical study of preserving left colic artery during laparoscopic total mesorectal excision for the treatment of rectal cancer].

OBJECTIVE: To evaluate the feasibility, safety, radicality and short-term outcome of preserving left colic artery (LCA) during laparoscopic total mesorectal excision (TME) for the treatment of rectal cancer. METHODS: From January 2013 to December 2016,136 patients with mid-lower rectal cancer received laparoscopic TME in the Gastrointestinal Surgery Department of Taizhou People's Hospital of Jiangsu Province. Patients with rectal tumor within 10 cm to the anal verge were enrolled into the study. All the enrolled patients had complete data of pathology and follow-up. Those receiving neoadjuvant chemoradiotherapy, with severe base diseases, multifocal tumor, tumor invasion of surrounding tissues, fixation of tumor, recurrent tumor, complications such as acute ileus, bleeding, perforation were excluded. In this study, 72 patients did not undergo preservation of LCA (high ligation group) and 64 patients underwent preservation of LCA (low ligation group). Operative parameters, clinicopathological data and short-term outcome were collected and compared between two groups. RESULTS: The baseline data including gender, age, body mass index, tumor stage, and distance of tumor from anal verge of two groups were comparable (P>0.05). The differences between two groups about the mean time of operation and the operative blood loss were not significant [(164.0±12.6) min vs. (167.3±9.4) min, (30.0±3.6) ml vs. (30.1±3.0) ml, all P>0.05]. There was no operative death in both groups. Differences in the lymph node dissection (13.7±2.6 vs. 13.3±2.1) and the specimen length of proximal resection margin [(16.4±1.9) cm vs. (16.7±2.1) cm] or distal resection margins [(3.9±0.6) cm vs. (4.1±0.9) cm] between high and low ligation groups were not significant (all P>0.05). Compared with high ligation group, the low ligation group had higher rate of sphincter preservation [92.2% (59/64) vs. 79.2% (57/72), χ2=4.580, P=0.032], lower rate of anastomotic leakage [1.6% (1/64) vs. 9.7% (7/72), χ2=4.075, P=0.044], anastomotic stenosis [3.1% (2/64) vs. 12.5%(9/72), χ2=4.006, P=0.045], and voiding and sexual dysfunction [6.3%(4/64) vs. 18.1%(13/72), χ2=4.317, P=0.038]. Mean time of follow-up was 19 months. In high ligation group, the local recurrent rate was 5.56%, distant metastasis rate was 13.89%, overall survival rate was 90.28%, disease-free survival rate was 80.56%, while in low ligation group, the local recurrence rate was 4.69%, distant metastasis rate was 12.50%, overall survival rate was 90.63%, disease-free survival rate was 82.81%, whose differences between two groups were not significant (all P>0.05). CONCLUSION: Preservation of LCA during laparoscopic TME for the treatment of rectal cancer is safe and feasible, which can reduce the incidence of anastomotic leakage and stenosis, and voiding and sexual dysfunction.

[Clinical significance of No.12 lymph node dissection for advanced gastric cancer].

OBJECTIVE: To evaluate the clinical significance of No.12 lymph node dissection for advanced gastric cancer with D2 lymphadenectomy. METHODS: Clinicopathologic data and No.12 lymph node dissection of 256 advanced gastric cancer patients undergoing radical operation in our department between January 2005 and December 2010 were retrospectively summarized and the influence factors of metastasis in No.12 lymph nodes were analyzed. RESULTS: Of 256 patients, 179 were male and 77 were female with the average age of 59.2 years. Tumor located in the upper of stomach in 24 cases, middle of stomach in 41 cases, lower of stomach in 174 cases, multi-focus or diffuse distribution of stomach in 17 cases. Tumor diameter was <3 cm in 39 cases, 3 to 5 cm in 100 cases, >5 cm in 117 cases. Serum carcinoembryonic antigen (CEA) level increased in 61 cases, serum carbohydrate antigens (CA)72-4 increased in 56 cases and CA19-9 increased in 61 cases. The number of No.12 lymph nodes resected from all the patients was 1 152, and the average number was 4.5±1.9. The metastasis rate of No.12 lymph nodes was 9.4%(24/256) after hematoxylin eosin staining (positive group). All the patients received effective follow-up to December 2015, and the average follow-up time was 101.2 months. The median survival time of positive No.12 group (24 cases) was 29.8 months and of negative No.12 group (232 cases) was 78.2 months, whose difference was statistically significant (χ2=21.715, P=0.000). Univariate analysis found that No.12 lymph node metastasis was not associated with age, gender, tumor differentiation (all P>0.05), but was associated with tumor location, tumor diameter, invasive depth (all P<0.05), and was closely associated with Borrmann type, outside metastatic lymph nodes of No.12 and high levels of serum CEA, CA72-4 and CA19-9 (all P=0.000). Multivariate regression analysis found that tumor location (RR=2.452, 95%CI:1.537 to 3.267, P=0.000), Borrmann type (RR=1.864, 95%CI:1.121 to 3.099, P=0.016) and number of outside metastatic lymph nodes of No.12 (RR=2.979, 95%CI: 2.463 to 3.603, P=0.000) were the independent risk factors of the No.12 metastasis (P<0.05). CONCLUSIONS: Metastasis in No.12 lymph nodes indicates poorer prognosis. The No.12 lymph nodes of advanced gastric cancer patients with curative resection, especially those with the tumor located in the lower part, Borrmann type IIII(, outside metastatic lymph nodes of No.12, should be regularly cleaned.

[Application study on regional infusion chemotherapy by celiac trunk during operation in advanced gastric cancer patients].

OBJECTIVE: To explore the feasibility, safety and efficacy of intraoperative regional infusion chemotherapy by celiac trunk in advanced gastric cancer patients. METHODS: One hundred and twenty-six patients with advanced gastric cancer(stageII(-III() were screened from database of Gastrointestinal Surgery Department of Taizhou People's Hospital between January 2008 and December 2010 who underwent R0 resection and D2 lymphadenectomy, received postoperative chemotherapy(XELOX or FOLFOX), and had complete follow-up data. They were divided into infusion chemotherapy group (65 cases) and control group (61 cases) according to regional infusion chemotherapy or not (fluorine 1 000 mg and cisplatin 60 mg). The side effects of chemotherapy, parameters related to the operation, long-term survival and relapse rate were compared between the two groups. RESULTS: The baseline data between the two groups were comparable(all P>0.05). Postoperative III( and IIII( adverse reaction of chemotherapy was not significantly different between the two groups (P>0.05). The time of postoperative intestinal function recovery [(67.9±14.8) hours vs. (68.9±15.0) hours, t=-0.380, P=0.705), volume of postoperative 1-week drainage [(66.1±17.1) ml vs.(61.9±18.2) ml, t=1.478, P=0.142], recent morbidity of complications[55.4%(36/65) vs. 49.2%(30/61), χ2=0.256, P=0.613], and the long-term morbidity of complications [16.9% (11/65) vs. 14.8% (9/61), χ2=0.111, P=0.739] were all not significantly different between the two groups. The 3-year survival rate and 3-year relapse-free survival rate in infusion chemotherapy group were significantly higher than those in control group(58.4% vs. 37.7%, χ2=5.382, P=0.020; 58.4% vs. 34.4%, χ2=6.636, P=0.010). CONCLUSION: Regional infusion chemotherapy by celiac trunk during operation for advanced gastric cancer patients is safe and feasible, and can reduce the risk of local recurrence and improve survival rate.

Maresin 1 ameliorates iron-deficient anemia in IL-10(-/-) mice with spontaneous colitis by the inhibition of hepcidin expression though the IL-6/STAT3 pathway.

BACKGROUND: Approximately 50% of patients with inflammatory bowel disease (IBD) suffer from anemia, which is prevalently caused by iron deficiency. Maresin 1 (MaR1) is a novel docosahexaenoic acid-derived pro-resolving agent that promotes the resolution of inflammation. The aim of the present study was to investigate the therapeutic effects of MaR1 on iron-deficient anemia in IL-10 knockout (IL-10(-/-)) mice with spontaneous chronic colitis. METHODS: IL-10(-/-) mice of 16 weeks of age with established colitis were used for the experiments with MaR1 treatment for 2 weeks. Histologic injury, CD4+ lymphocyte values in the lamina propria, blood hemoglobin, hematocrit, serum iron concentrations, transferrin saturation, splenic iron stores, levels of inflammatory cytokines, expression of liver hepcidin mRNA, and western blotting of STAT3 were analyzed in this study. RESULTS: MaR1 treatment (0.3 ng/mouse) effectively attenuated histological colitis typically associated with decreased CD4+ lymphocytes in the lamina propria as well as the concentrations of MPO, TNF-α, IFN-γ, IL-6 and IL-17 (P<0.05). Furthermore, reduced expression of liver hepcidin mRNA and p-STAT3 expression, as well as increased hemoglobin concentration, hematocrit, levels of serum iron, transferrin saturation and splenic iron stores were found in IL-10(-/-) mice after MaR1 treatment (P<0.05). CONCLUSIONS: These results indicate that MaR1 treatment ameliorates iron-deficient anemia by reducing colonic inflammation and inhibiting hepcidin expression though the IL-6/STAT3 pathway.

[Application of protective appendicostomy after sphicter-preserving surgery for patients with low rectal carcinoma who are at high-risk of anastomotic leakage].

OBJECTIVE: To explore the application of protective appendicostomy after sphicter-preserving surgery for patients with low rectal carcinoma who are at high-risk of anastomotic leakage. METHODS: Clinical data of 74 low rectal cancer cases with high-risk anastomotic leakage undergoing laparoscope-assisted total mesorectal excision(TME) sphincter-preserving operation in our department from September 2013 to September 2014 were analyzed retrospectively. Patients were randomly divided into two groups: 36 patients received appendicostomy and catheter was removed 4 to 6 weeks after operation when sinus tract formation in abdominal wall was identified; 38 patients received traditional ileostomy and stoma closure was performed 3 to 6 months after operation. RESULTS: The operation time was (149.2±9.4) min vs. (146.7±12.7) min, postoperative complication morbidity was 8.3%(3/36) vs. 13.2%(5/38), anastomotic leakage rate was 2.8%(1/38) vs. 2.6%(1/36), mean drainage volume of 1-week stoma was (203.2±76.9) ml vs. (195.8±76.5) ml, intestinal function recovery time was (25.5±5.6) h vs. (24.0±5.8) h in intubation colostomy group and ileostomy group respectively, and these differences were not significant (all P>0.05). While total hospital stay was shorter and cost was less in intubation colostomy group as compared to ileostomy group [(8.8±1.7) d vs. (18.0±1.7) d, (32 000±3000) yuan vs. (51 000±4000) yuan], and these differences were significant (all P<0.05). CONCLUSION: For low rectal cancer patients who are at high-risk of developing anastomotic leakage undergoing sphincter-preserving anterior resection, protective appendicostomy can decrease anastomotic leakage rate, avoid second stoma closure, shorten hospital stay and reduce hospital cost.