Current indicators lack the precision required to accurately predict the PM(peritoneal metastasis) of gastric cancer (GC). The accurate prediction of GC with PM and the implementation of targeted therapeutic strategies hold substantial clinical significance. This study aimed to evaluate the prognostic value of galectin-1 expression and peritoneal fibrosis in predicting PM in GC patients. Immunohistochemical and Masson’s trichrome staining were conducted on GC tissues and peritoneal tissues from 125 patients who underwent radical gastrectomy. The correlations among galectin-1 expression in GC tissues, peritoneal fibrosis, and PM were analyzed. Univariate and multivariate regression analyses were performed, incorporating clinicopathological parameters, to assess predictors of PM of GC. Both univariate and multivariate analyses revealed significant correlations among pathological Tumor (pT) stage, galectin-1 expression, peritoneal fibrosis, and PM. Patients with pathological pT3-4 stage GC, who had high galectin-1 expression and who were positive for peritoneal fibrosis had a greater risk of PM after pairwise superposition. This study represents the first to systematically elucidate that galectin-1 expression in GC tissues and peritoneal fibrosis are independent predictors of the risk of PM in patients with GC. These two indicators coordinate with pT stage, and the combination of these two indicators increases their predictive accuracy.

Peritoneal metastasis (PM) is the most common cause of death in gastric cancer (GC) patients. Targeting the molecular mechanisms of PM in GC could reduce its incidence and improve clinical outcomes. Using clinical specimen analysis, lentivirus transfection, western blotting, RT-qPCR, immunofluorescence, cell adhesion assays, and a GC peritoneal metastasis (GCPM) animal model, we explored galectin-1's role in promoting peritoneal MMT (mesothelial-mesenchymal transition) and enhancing PM through in vivo and in vitro studies. Galectin-1 in the GC microenvironment reprograms peritoneal mesothelial cells to facilitate PM, with its high expression in GC tissues being a key factor for PM. Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

Objective: This study aimed to explore the utility of transcutaneous electrical acupoint stimulation (TEAS) combined with skin sympathetic response (SSR) in assessing the effectiveness of perigastric autonomic nerve preservation during radical gastrectomy. Methods: A retrospective cohort analysis was conducted involving 221 patients who underwent laparoscopic radical gastrectomy at the Department of Gastric Surgery, Taizhou People's Hospital, affiliated with Nanjing Medical University, between June 2022 and September 2024. The cohort comprised 109 patients who underwent laparoscopic radical total gastrectomy without autonomic nerve preservation (total gastrectomy without nerve preservation group). Additionally, 112 patients underwent laparoscopic radical distal gastrectomy, including 34 patients who received autonomic nerve preservation (nerve preservation group) and 78 patients who did not (without nerve preservation group). TEAS was administered at the Zusanli and Tianshu acupoints one day before and one day after surgery, during which SSR latency and voltage amplitudes in the upper and lower extremities were recorded and compared across groups. Differences in SSR latency and voltage amplitude between the nerve preservation and non-nerve preservation groups of the distal gastrectomy cohort were also analyzed. Further, TEAS was applied at the same acupoints for 15 minutes on the 1st, 2nd, and 3rd postoperative days, and changes in intestinal sounds and intestinal functional recovery time were monitored. Surgical parameters, including operative duration, intraoperative blood loss, and harvested lymph node, were documented. Postoperative inflammatory indicators, including interleukin-6 (IL-6), C-reactive protein (CRP), procalcitonin (PCT), and the incidence of anastomotic leakage, were evaluated. At three months postoperatively, gastroscopy was performed to assess residual gastric food and bile reflux. Additionally, the prognostic nutritional index (PNI) was evaluated across all patient groups. Results: Following total gastrectomy, TEAS of Zusanli combined with arms' SSR revealed a latency of (23 59.71±410.55) ms and a voltage amplitude of (0.43±1.67) mV; for the legs, latency was (2 596.88±369.01) ms and voltage amplitude was (0.25±0.08) mV. TEAS of Tianshu combined with arms' SSR demonstrated a latency of (2 746.47±224.37) ms and a voltage amplitude of (0.31±0.14) mV; for the legs, latency was (2 891.90±193.61) ms and voltage amplitude was (0.19±0.72) mV. Postoperative latency was significantly prolonged, and voltage amplitude was markedly reduced (all P < 0.01). In the distal gastrectomy with nerve preservation group, TEAS of Zusanli combined with arms' SSR showed a latency of (1 668.04±261.91) ms and a voltage amplitude of (0.78±0.26) mV; for the legs, latency was (1 568.86±220.09) ms and voltage amplitude was (0.61±0.24) mV. TEAS of Tianshu combined with arms' SSR demonstrated a latency of (1 519.36±206.99) ms and a voltage amplitude of (0.66±0.34) mV; for the legs, latency was (2 004.80±508.53) ms and voltage amplitude was (0.55±0.28) mV. In the distal gastrectomy without nerve preservation group, TEAS of Zusanli combined with arms' SSR revealed a latency of (2 385.95±710.27) ms and a voltage amplitude of (0.23±0.11) mV; for the legs, latency was (2 506.81±779.37) ms and voltage amplitude was (0.26±1.29) mV. TEAS of Tianshu combined with arms' SSR indicated a latency of (2 697.78±385.55) ms and a voltage amplitude of (0.21±0.14) mV; for the legs, latency was (2 949.14±506.61) ms and voltage amplitude was (0.17±0.11) mV. The group without nerve preservation exhibited significantly prolonged latencies and reduced voltage amplitudes (all P<0.01). No statistically significant differences were observed between the groups in operative time, intraoperative bleeding, the number of dissected lymph nodes, inflammatory indicators (IL-6, CRP, PCT) at 3 days postoperatively, or anastomotic leakage rates (all P>0.05). In the group without nerve preservation, bowel sounds on postoperative days 1, 2, and 3 were (0.36±0.58), (1.04±0.97), and (1.74±1.10) times/min, respectively, with bowel function recovery time of (62.24±9.91) hours. The PNI at 3 months postoperatively was (37.42±3.01). Incidences of food residue in the residual stomach and bile reflux were 21.79% (17/78) and 29.49% (23/78), respectively. In the group with nerve preservation, bowel sounds on postoperative days 1, 2, and 3 were (0.76±0.82), (2.03±1.34), and (3.71±1.27) times/min, respectively, with bowel function recovery time of (44.94±8.05) hours. The PNI at 3 months postoperatively was (41.34±3.40). Incidences of food residue and bile reflux were 5.88% (2/34) and 11.76% (4/34), respectively. Statistically significant differences were observed between the groups (all P < 0.05). Conclusion: TEAS of Zusanli and Tianshu combined with SSR provides an objective measure for assessing the preservation of perigastric autonomic nerves during radical gastrectomy.

BACKGROUND:Peritoneal metastasis (PM) is the predominant mode of gastric cancer (GC) dissemination in patients. The underlying mechanisms remain incompletely understood, and therapeutic interventions are highly challenging. The preemptive interventions of GCPM is particularly important. PURPOSE:This study investigated the role and mechanism of galectin-1 within the GC microenvironment in promoting PM and evaluated the inhibitory effects of dihydroartemisinin(DHA) on galectin-1-induced PM. METHODS:Through immunohistochemical analysis of clinical samples, database mining, and animal model experiments utilizing lentivirus-transfected GC cells, we investigated the promoting effect of galectin-1 on GCPM. Transcriptomic analysis was conducted to identify potential pathways through which galectin-1 facilitates GCPM, with subsequent validation performed using clinical specimen analysis and both in vitro and in vivo experimental approaches. IC50 of DHA on GC cell lines with LGALS1 overexpression was determined via CCK8 assay. The inhibitory effect of DHA on galectin-1-induced GCPM, along with its underlying mechanism, was further confirmed through in vitro experiments and in vivo animal model interventions. Finally, molecular docking assay was employed to investigate the preliminary mechanism underlying the inhibitory effect of DHA on galectin-1. RESULTS:Galectin-1 functions as a key regulatory factor in GCPM and has a significant impact on patient outcomes. It promotes ferroptosis resistance in GC cells by activating the PI3K/Akt/Nrf2/HO-1 signaling pathway, thereby facilitating PM. Moreover, DHA has been shown to target this signaling pathway, effectively inhibiting galectin-1-induced ferroptosis resistance and PM. CONCLUSION:To our knowledge, this study is the first to elucidate the mechanism by which galectin-1 promotes PM through enhancement of ferroptosis resistance and to explore the potential of DHA as an inhibitor of this process, thus providing novel strategies for preventing GCPM.

BackgroundIn the past several decades, cisplatin (DDP), in combination with other drugs, has been used as the mainstay chemotherapy drug for the treatment of gastric cancer (GC). However, the clinical application of DDP is restricted because of its toxic side effects, it is imperative to explore less toxic and more effective treatment strategies. Dihydroartemisinin (DHA) has been shown to exert potent anticancer effects through ferroptosis in multiple malignancies and has shown high efficacy and safety.MethodsCell viability assay, live/dead staining assay, EDU proliferation assay, MitoTracker assay, BODIPY C11 assay and other cell assays in vitro were employed to observe DHA in combination with DDP inducing ferroptosis in GC. Subsequently, proteomic analysis integrated with database analysis and clinical sample detection were utilized to elucidate the mechanism of DHA inducing ferroptosis in GC both in vitro and in vivo.ResultsIn this study, we found that DHA combined with DDP can synergistically inhibit the proliferation, invasion and migration of GC cells and induce ferroptosis. Further studies have shown that DHA acts in combination with DDP to induce ferroptosis in GC cells by inhibiting GPX4 in vivo and in vitro.ConclusionIn summary, this study is the first to report that DHA and DDP synergically promote ferroptosis in GC cells, the combination of DDP and DHA is a promising strategy from the perspective of toxicity of DDP, which may be a promising therapeutic approach.

Vasculogenic mimicry (VM) is a novel model for supplying blood to multiple tumors, including gastric cancer (GC), and is a potential target for its treatment. Dihydroartemisinin (DHA) is a potential natural antitumor substance that inhibits the progression of tumors in many ways. The research aimed to evaluate the impact of DHA on VM formation and its mechanisms. The IC50 of DHA, DHA's effect on proliferation, invasion, and migration in GC cells and VM formation in both cell and animal models were determined through wound healing, MTT, EdU, colony formation, and Transwell assays. Genomics was employed to identify genes related to DHA inhibition of VM formation, and to analyze their relationship to VM formation. qRT‒PCR and western blot (WB) analysis were carried out to analyze the changes in protein and mRNA levels after DHA treatment and the changes in VM-associated protein biomarkers after blocking target gene-related pathways. The mechanism by which DHA inhibits VM in GC was elucidated in vivo. DHA reduced the invasion, proliferation, and migration of GC cells and inhibited VM in cells and in vivo. A total of 220 DEGs were identified in the DHA-treated HGC-27 cells. Among the 146 downregulated genes, fibroblast growth Factor 2 (FGF2) was most closely associated with angiogenesis and VM. The level of FGF2 in GC tissues with VM was markedly greater than in VM lacking tissues. Treatment with DHA or FGFR1 blockade suppressed VM formation and reduced VM-related biomarker proteins. DHA suppressed tumor progression and VM formation by reducing FGF2 in xenograft mouse models. Per our knowledge, this is the first study to demonstrate the inhibitory effect of DHA on VM, providing a novel strategy for the treatment of GC.

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 (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.

Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has induced a worldwide pandemic since early 2020. COVID-19 causes pulmonary inflammation, secondary pulmonary fibrosis (PF); however, there are still no effective treatments for PF. The present study aimed to explore the inhibitory effect of dihydroartemisinin (DHA) on pulmonary inflammation and PF, and its molecular mechanism. Morphological changes and collagen deposition were analyzed using hematoxylin-eosin staining, Masson staining, and the hydroxyproline content. DHA attenuated early alveolar inflammation and later PF in a bleomycin-induced rat PF model, and inhibited the expression of interleukin (IL)-1β, IL-6, tumor necrosis factor α (TNFα), and chemokine (C-C Motif) Ligand 3 (CCL3) in model rat serum. Further molecular analysis revealed that both pulmonary inflammation and PF were associated with increased transforming growth factor-β1 (TGF-β1), Janus activated kinase 2 (JAK2), and signal transducer and activator 3(STAT3) expression in the lung tissues of model rats. DHA reduced the inflammatory response and PF in the lungs by suppressing TGF-β1, JAK2, phosphorylated (p)-JAK2, STAT3, and p-STAT3. Thus, DHA exerts therapeutic effects against bleomycin-induced pulmonary inflammation and PF by inhibiting JAK2-STAT3 activation. DHA inhibits alveolar inflammation, and attenuates lung injury and fibrosis, possibly representing a therapeutic candidate to treat PF associated with COVID-19.

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.

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.

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.

Background This study aims to investigate the expression of galectin-1 and vascular mimicry (VM) in rectal cancer tissues, and to assess their predictive value in the prognostic evaluation of patients with rectal cancer. Methods Immunohistochemistry (IHC) and CD34-periodic acid solution (PAS) double staining were used to detect galectin-1 expression and the formation of VM in rectal cancer tissues from 94 patients with stage I–III rectal cancer and their corresponding paracancerous tissues. We also analyzed the relationship between the expression of galectin-1, VM, various clinicopathological parameters, and the prognosis of rectal cancer patients, as well as their influence on the overall survival (OS) of rectal cancer patients. Results Among the 94 tissue specimens from rectal cancer patients, 43 had positive expression of galectin-1 and 19 had positive expression of VM. There was a positive correlation between VM and galectin-1 expression in rectal cancer tissue. Galectin-1 expression in rectal cancer tissue and the formation of VM were related to tumor differentiation, staging, lymph node metastasis, and intravascular tumor thrombus (P<0.05). Kaplan-Meier analysis showed that the OS time of rectal cancer patients in the galectin-1 positive expression group was shorter than the galectin-1 negative expression patients, and the difference between the 2 groups was statistically significant (P=0.003). The OS time of patients with rectal cancer in the VM positive expression group was shorter than the VM negative expression group, and the difference between the two groups was statistically significant (P<0.001). The OS time of the galectin-1 and VM negative expression group was 57.33±1.13 months, and the OS time of the galectin-1 and VM positive expression group was 43.21±3.97 months, while the OS time of the galectin-1 positive expression and VM negative expression group was 55.42±2.23 months, and the difference between the three groups was statistically significant (P<0.001). Multi-factor analysis results indicated that invasion depth and VM expression were independent risk factors that affected the OS of patients with rectal cancer. Conclusions Galectin-1 and VM expression in rectal cancer tissues may predict poor prognosis in patients after radical surgery. Galectin-1 and VM may therefore become potential new targets for rectal cancer treatment.

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-β1)/ 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-β1 and induced EMT of GC cell lines. A TGF-β1 antagonist inhibited the invasion and migration of GC cells. In vivo , overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-β1 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-β1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.

Dihydroartemisinin (DHA) is a semi-synthetic derivative and the main active metabolite of artemisinin. The purpose of this study was to investigate the effect of DHA on the ulcerative colitis (UC) in both in vivo and in vitro models. Weight, survival rate, colon length, and Disease Activity Index score were used to evaluate the severity of colitis. Reverse transcription quantitative polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expressions of cytokines interleukin (IL)-1, IL-1β, IL-4, IL-6, IL-10, IL-12, and tumor necrosis factor-α (TNF-α). The expressions of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3), and the phosphorylation of JAK2 (p-JAK2) and STAT3 (p-STAT3), were measured by western blot analysis. Western blot analysis and immunohistochemistry were used to detect the expressions of tight junction proteins. We found that the weights and colon lengths of mice in dextran sodium sulfate (DSS)+DHA group were significantly lower and longer than those in the DSS group, respectively. Compared with those in the DSS group, the expressions of IL-1β, IL-6, IL-17, and TNF-α in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. DHA largely increased the expressions of zonula occludens-1 and occludin. Western blot analysis and/or immunohistochemical staining analysis showed that the expressions of JAK2, STAT3, p-JAK2, and p-STAT3 in DSS+DHA and DSS+5-ASA groups were significantly lower than those in DSS group. DHA has a specific therapeutic effect on UC. The anti-inflammatory mechanism of DHA is related to the blockage of the JAK2/STAT3 signaling pathway. These findings provide evidence that DHA may be a useful drug and is expected to become a promising new treatment for human UC.

目的 探讨胃节段切除术治疗早期胃癌的安全性和有效性.方法 将68例早期胃癌患者根据随机数字表法分为对照组和研究组,每组34例.对照组患者行远端胃切除术,研究组患者行胃节段切除术.记录并比较2组患者围术期指标、胃肠激素水平、术后并发症情况、术后生活质量及随访情况.结果 2组患者手术时间、术中出血量及淋巴结清扫数目比较,差异无统计学意义(P>0.05);研究组患者肠鸣音恢复时间、术后排气时间、术后排便时间及术后住院时间均较对照组显著缩短(P<0.05).时间与方法在血浆胃动素(MOT)、血管活性肠肽(VIP)、生长抑素(SS)水平上不存在交互作用(P>0.05),时间与方法在MOT、VIP、SS水平上主效应显著(P<0.05).研究组术后并发症总发生率较对照组显著降低(P<0.05).研究组术后3个月SF-36各项评分均显著高于对照组(P<0.05).随访期间,所有患者均未出现复发及转移情况.结论 胃节段切除术治疗早期胃癌安全、有效,不仅可最大限度地保留患者胃肠功能,促进术后恢复,还可以有效减少术后并发症,改善患者术后生活质量,预后效果满意.

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.

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.

Objective: The operative approach and steps of laparoscopic right hemicolon cancer radical resection have been standardlized and professional consensus has been reached. However, some detailed issues such as the handling of Henle's trunk and whether to preserve the right gastroepiploic vein (RGEV) still remain controversial. This study investigates the safety, feasibility, short- and long-term outcomes of preserving RGEV during laparoscopic right hemicolectomy. Methods: A retrospective cohort study was carried out. Clinical data of 92 patients undergoing laparoscopic right hemicolectomy in Taizhou People's Hospital from March 2016 to May 2018 were retrospectively analyzed. All the patients were treated with complete mesocolon resection (CME) and had complete postoperative pathological data and follow-up data. Based on the tumor location, 49 patients preserved RGEV (preservation group) and 43 did not (non-preservation group). Pathological data, postoperative complications, short- and long-term outcomes were compared between the two groups. Results: There were no significant differences in baseline data between the two groups (all P>0.05). No significant differences were found in operation time, intraoperative blood loss, unplanned reoperation, anastomotic leak, number of harvested lymph nodes, number of metastatic lymph node, and time to food intake after surgery between two groups (all P>0.05). Compared with non-preservation group, the preservation group had faster recovery of anal gas passage after operation [(3.1±1.0) days vs. (4.0±1.7) days, t=-2.787, P=0.007], shorter length of hospitalization [(11.5±1.5) days vs. (15.0±7.9) days, t=-2.823, P=0.007], and reduced the hospitalization expenses [(46 000±5000) yuan to (57 000±33 000) yuan, t=-2.076, P=0.044]. No postoperative gastroparesis (PGS) occurred in the preservation group, while 6 cases in the non-preservation group developed gastroparesis during perioperative period (P<0.05). The median time of follow-up time was 31.8 (5.2-43.7) months. The overall survival time of the preservation group and non-preservation group was (35.4±1.8) months and (37.6±1.7) months, respectively without significant difference (P=0.336); the disease-free survival was (32.0±2.2) months and (35.5±2.0) months, respectively without significant difference as well (P=0.201). Conclusions: Dissection of the Henle's truck and preservation of RGEV is safe and feasible during laparoscopic right hemicolectomy, which can significantly reduce the incidence of postoperative gastroparesis, shorten the recovery time of postoperative intestinal function and hospitalization, and decrease the cost of hospitalization. The efficacy of RGEV preservation is similar to non-preservation of RGEV.