BackgroundPostoperative complications (POCs) remain a major challenge in colorectal cancer (CRC) surgery. Easily accessible composite inflammatory indices derived from routine blood tests hold promise for preoperative risk stratification, but their comparative predictive value for POCs is unclear.MethodsWe conducted a two-center, retrospective study of 1331 patients who underwent radical CRC surgery between January 2021 to October 2025. The associations between preoperative composite inflammatory indices and the complications after surgery were evaluated using logistic regression. Their predictive discriminative performances were further assessed and compared using receiver operating characteristic (ROC) curve analysis, with the areas under the curve (AUC) compared by DeLong’s test.ResultsThe complication rate was 17.2% (229/1331). Patients with complications exhibited a significantly more pronounced pro-inflammatory and immunosuppressive preoperative profile across all indices (all P < 0.05). After adjustment, the systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), C-reactive protein-to-lymphocyte ratio (CLR), and systemic inflammation response index (SIRI) were identified as the strongest independent predictors, with the highest quartile (Q4) conferring substantially increased risks (OR for SII: 7.51; for NLR: 5.86; for CLR: 2.24; for SIRI: 2.99; all P-trend <0.05). ROC analysis confirmed SII as the best single predictor (AUC: 0.738). A combined model integrating SII, NLR, CLR, and SIRI achieved superior discriminative ability (AUC: 0.792), significantly outperforming any single index (all P < 0.05).ConclusionThe SII, NLR, CLR and SIRI, are strongly associated with the risk of POCs after CRC surgery. A model combining these four indices provides superior predictive performance.

BACKGROUND Total laparoscopic distal gastrectomy (TLDG) is increasingly used for advanced gastric cancer, but its comprehensive outcomes vs open distal gastrectomy (ODG) require further validation. AIM To investigate the perioperative safety, postoperative recovery, and mid-term survival between TLDG and ODG for locally advanced gastric cancer. METHODS This retrospective study analyzed patients admitted from January 2020 to January 2022. Patients were divided into TLDG and ODG groups on the basis of surgical approach. Perioperative outcomes, postoperative recovery, tumor pathology, preoperative and postoperative day 1 and 5 blood tests, complications, and 3-year overall survival and recurrence-free survival rates were evaluated. RESULTS A total of 420 patients were included, with 213 in the TLDG group and 207 in the ODG group. The TLDG group had shorter incision lengths (4.51 +/- 0.52 cm vs 17.64 +/- 3.25 cm, P < 0.001) and less blood loss (152.44 +/- 26.55 mL vs 220.07 +/- 21.58 mL, P < 0.001). Postoperative recovery was faster in the TLDG group, with earlier mobilization (1.85 +/- 0.22 days vs 2.51 +/- 0.24 days, P < 0.001), flatus (2.92 +/- 0.24 days vs 3.52 +/- 0.21 days, P < 0.001), and lower visual analog scale scores (postoperative day 5: 26.54 +/- 4.20 vs 45.51 +/- 10.41, P < 0.001). Inflammation was reduced in the TLDG group (postoperative day 1 white blood cell: 11.18 +/- 2.11 & times; 109/L vs 11.81 +/- 2.22 & times; 109/L, P = 0.003). Complication rates were similar, but the ODG group had more grade I-II complications (17.39% vs 10.33%, P = 0.036). Three-year overall survival (90.61% vs 90.34%, P = 0.924) and recurrence-free survival (80.28% vs 81.16%, P = 0.820) showed no significant differences. CONCLUSION Compared with ODG, TLDG for locally advanced cancer offers superior short-term outcomes in terms of reduced trauma, accelerated functional recovery, and pain relief without compromising oncological efficacy or survival rates.

The zinc transporter SLC39A10 serves as a risk factor for malignant progression in gastric cancer (GC), characterized by the formation of an immunosuppressive tumor microenvironment (TME). As key cellular components within this microenvironment, both malignant cells and macrophages are influenced by SLC39A10, yet its regulatory mechanisms at the subpopulation level remain unclear. Using single-cell RNA sequencing and functional experiments, we investigated the cell-type-specific role of SLC39A10 in GC. Results demonstrated that oeSLC39A10 tumor cells exhibit activated MAPK14 signaling pathway, while tumor-associated macrophages (TAMs) display a biased M2 polarization state. These two cell populations establish intercellular communication through secretory factors IL-10 and TGF-β, synergistically promoting tumor proliferation and angiogenesis. This study identifies an SLC39A10-MAPK14-M2 macrophage regulatory axis that critically influences immune microenvironment remodeling and GC progression. Targeting this signaling axis may provide a viable therapeutic approach to alter the TME and suppress disease advancement.

BACKGROUND: To investigate the effect of laparoscopic herniorrhaphy on the treatment of unilateral Gilbert type-III inguinal hernia. METHODS: This study retrospectively reviewed medical records of 325 individuals who underwent minimally invasive laparoscopic surgery for unilateral Gilbert type-III inguinal hernias at the Ninth People's Hospital affiliated with Shanghai Jiaotong University Medical College, with data collection occurring between January 2021 and May 2024. The cohort was stratified into two surgical groups: Partial resection (n = 180) receiving transection procedures versus radical resection (n = 145) undergoing complete sac dissection, determined by intraoperative decision-making. The ages, body mass index values, operation modes, operation times, intraoperative bleeding levels, postoperative pain scores, postoperative hospital stays, postoperative seroma rates, postoperative chronic pain levels, postoperative hematoma rates, incision infection rates, and hernia recurrence rates of the patients in the two groups were analyzed and compared. RESULTS: The transection group demonstrated a marked reduction in postoperative seroma occurrence relative to the complete dissection cohort, with statistical significance confirmed (P < 0.05). There were no significant differences between the two groups in intraoperative bleeding, operation times, postoperative hospital stays, postoperative pain scores, postoperative chronic pain levels, postoperative hematoma rates, or incision infection rates (P > 0.05). Continuous surveillance spanning 12 months revealed equivalent therapeutic durability across both treatment arms, with no hernia reappearance detected. CONCLUSION: For patients requiring laparoscopic repair of unilateral Gilbert type-III inguinal hernias, intraoperative sac transection is an effective strategy, particularly in cases where the hernia sac is long and complete dissection is difficult, as it may be the preferable option and can significantly reduce the risk of postoperative seroma formation.

BACKGROUND:High expression of SETD1A, a histone methyltransferase that specifically methylates H3K4, acted as a key oncogene in several human cancers. However, the function and underlying molecular mechanism of SETD1A in ovarian cancer (OV) remain markedly unknown. METHODS:The expression of SETD1A in OV were detected by Western blot and analyzed online, and the prognosis of STED1A in OV were analyzed online. The protein and mRNA levels were determined by Western blot and RT-qPCR. The cell proliferatin, migration and invasion were measured by CCK-8 and transwell assays. The protein interaction was detected by co-IP assay. The interaction between protein and DNA was performed by ChIP assay. The tumor growth in vivo was performed by xenograft tumor model. RESULTS:SETD1A was overexpressed in OV and a predictor of poor prognosis. Overexpression of SETD1A augmented the abilities of cell proliferation, migration, and invasion in MRG1 and OVCAR5 cells. In comparison, SETD1A knockdown suppressed cell growth, migration, and invasion in SKOV3 and Caov3 cells. Specifically, SETD1A enhanced Notch signaling by promoting the expression of Notch target genes, such as Hes1, Hey1, Hey2, and Heyl. Mechanistically, SETD1A interacted with Notch1 and methylated H3K4me3 at Notch1 targets to enhance Notch signaling. In addition, restoration of Notch1 in SETD1A-knockdown OV cells recovered cell proliferation, migration and invasion, which was inhibited by SETD1A knockdown. Furthermore, reduction of SETD1A suppressed tumorigenesis in vivo. CONCLUSION:In conclusion, our results highlighted the key role of SETD1A in OV development and proved that SETD1A promotes OV development by enhancing Notch1 signaling, indicating that SETD1A may be a novel target for OV treatment.

Introduction This study investigated the effect of complete reduction and transection of the hernia sac during laparoscopic indirect inguinal hernia repair on seroma. Methods Retrospective analysis was performed on 1763 cases undergoing laparoscopic indirect inguinal hernia repair in three centers from January 2017 to September 2019, among them, 311 patients with transection of hernia sac and 1452 patients with reduction of hernia sac, the data of the two groups were tested by t-test. Logistic univariate analysis was performed on 233 cases of postoperative seroma, and variables p < 0.05 in univariate analysis were included for multivariate analysis. Then, the transection group and the reduction group were matched with 1:1 propensity score matching, and the caliper value was set at 0.05. Finally, 274 patients matched in each group were analyzed by univariate analysis again to evaluate whether the transection of hernia sac had an impact on postoperative seroma. Results The results of univariate analysis of 233 patients with postoperative seroma showed that: ASA-3 p = 0.031, classification-L3 p < 0.001, surgery-TEP p < 0.001, transect group p = 0.005. The results of multivariate analysis show that: ASA-3 p < 0.001, classification-L3 p < 0.001, surgery-TEP p < 0.001, transect group p = 0.020. The results of univariate analysis after propensity score matching showed that transection of the hernia sac is significant for postoperative seroma (p < 0.001). Conclusion Transection of the hernia sac during laparoscopic indirect inguinal hernia repair can significantly lead to postoperative seroma.

1病例介绍 患者女,39岁,因腹部胀痛3周伴停止排气、排便10 d余来我院急诊.患者约3周前无明显诱因出现腹胀腹痛,主要位于中下腹,后逐渐变成全腹胀痛,10 d天前出现停止排气、排便,曾予以通便对症治疗,效果欠佳.追问其病史,患者有20余年便秘史,2个月前便秘症状明显加重,急诊腹部CT提示:结肠大量粪气影伴肠腔扩张(见图1).遂急诊以"肠梗阻"收治入院.既往有小细胞低色素性贫血病史,否认其他慢性病史.患者入院后,完善常规检查后,予以通便、灌肠、导泄等对症处理,效果均欠佳,腹部体征未见好转,2次肠镜检查均因肠道内充满粪便无法进行,并且体征呈进行性加重,遂和患者及家属沟通后,决定行手术治疗.

目的 分析比较TEP与改良Kugel术治疗双侧腹股沟疝的临床效果及患者生活质量.方法 选取2012年1月至2017年1月在上海交通大学医学院附属第九人民医院接受手术治疗双侧腹股沟疝患者157例.按照手术方式分为腹腔镜组(TEP组)和开放组(改良Kugel)组.其中,TEP组71例,改良Kugel组86例.分析比较包括2组患者的手术时间、术中出血量、住院时间、术后并发症、术后早期疼痛、慢性疼痛、复发情况和生活质量.采用SPSS 20.0统计学软件进行数据分析.结果 TEP组手术时间(93.5±10.9)min,改良Kugel组(102.6±9.8)min,差异有统计学意义(P<0.05).TEP组住院时间(1.05±0.21)d,改良Kugel组(1.52±0.69)d,差异有统计学意义(P<0.05).TEP组术中出血量(22.1±7.1)ml,改良Kugel组(23.4±6.8)ml,差异无统计学意义(P>0.05).TEP组术后恢复正常活动时间(8.67±2.32)d,改良Kugel组(9.14±2.40)d,差异无统计学意义(P>0.05).TEP组术后并发症5(7％),改良Kugel组10例(11.6％),差异无统计学意义(P>0.05).并发症患者中身体质量指数>27 kg/m2,TEP组1例(20％),改良Kugel组6例(60％),差异无统计学意义(P>0.05).TEP组慢性疼痛3例(4.2％),改良Kugel组14例(16％),差异有统计学意义(P<0.05).截止至随访结束,TEP组术后复发0例,改良Kugel组术后复发1例,占约1％;2组无明显差异(P>0.05).术后1及7 d,2组疼痛视觉模拟评分比较,差异有统计学意义(P<0.05);术前、术后及12个月比较,差异无统计学意义(P>0.05).术前、术后1、2、6及12个月2组生活质量量表评分比较,差异均无统计学意义(P>0.05).结论 通过TEP治疗双侧腹股沟疝能有效地减少患者的手术时间、住院时间、术后疼痛.

目的 探究微小RNA-29a(miR-29a)靶向调控干扰素诱导跨膜蛋白3(IFITM3)表达对肝癌HepG2细胞生长、增殖和凋亡的影响.方法 采用实时荧光定量PCR(qRT-PCR)检测肝癌细胞HepG2和正常肝细胞株LO2中miR-29a的表达水平;采用脂质体法将miR-29a minmic及阴性对照转染至HepG2细胞,并分为过表达组和对照组,转染48 h后用QRCR法检测两组miR-29a水平;采用MTT法和流式细胞术检测各组细胞增殖及凋亡情况;Western blot-ting检测各组Bax、caspase-3凋亡相关基因及IFITM3的表达;采用双荧光素酶报告基因实验验证miR-29a对IFITM3的靶向调控作用.结果 肝癌HepG2细胞miR-29a水平低于正常LO2细胞(P<0.05);过表达组HepG2细胞miR-29a表达低于对照组(P<0.05);过表达组HepG2细胞增殖率低于对照组(P<0.05),凋亡率及Bax、caspase-3、IF-ITM3表达高于对照组(P<0.05);miR-29a可显著抑制野生型FITM3-3'UTR质粒转染细胞的荧光素酶活性(P<0.05),但其对突变型FITM3-3'UTR质粒转染细胞的荧光素酶活性无显著影响(P>0.05).结论 miR-29a在肝癌中表达降低,可靶向调控IFITM3表达,抑制肝癌细胞生长、增殖,并促进其凋亡,可作为肝癌的潜在治疗靶点.

Background In this study, we aimed to identify independent predictive factors for lymph node metastasis (LNM) in T1 colon cancer. Methods Data of 8056 eligible patients were retrospectively collected from the Surveillance, Epidemiology, and End Results (SEER) database during 2004–2012. We performed logistic regression analysis to identify predictive factors for LNM. Both unadjusted and adjusted Cox regression analyses were used to determine the association between LNM and patient survival. Finally, we used competing risks analysis and the cumulative incidence function (CIF) to further confirm the prognostic role of LNM in cancer-specific survival (CSS). Results The overall risk of LNM in patients with T1 colon cancer was 12.0% ( N = 967). Adjusted logistic regression models revealed that mucinous carcinoma [odds ratio (OR) = 2.26, P < 0.001], moderately differentiated (OR 1.74, P < 0.001), poorly differentiated (OR 5.16, P < 0.001), and undifferentiated carcinoma (OR 3.01, P = 0.003); older age (OR 0.66, P < 0.001 for age 65–79 years, OR 0.44, P < 0.001 for age over 80 years); and carcinoma located in the ascending colon (OR 0.77, P = 0.018) and sigmoid colon (OR 1.24, P = 0.014) were independent predictive factors for LNM. Adjusted Cox regression analysis showed that positive lymph node involvement was significantly associated with CSS [hazard ratio (HR) = 3.02, P < 0.001], which was further robustly confirmed using a competing risks model and the CIF. Conclusions This population-based study showed that mucinous carcinoma, tumor grade, age, and primary tumor location were independent predictive factors for LNM in T1 colon cancer. The risk of LNM should be carefully evaluated in patients with T1 colon cancer, before clinical management.

目的 探讨赖氨酸特异性组蛋白去甲基化酶1(KDM1A)对结直肠癌细胞增殖侵袭及AKT信号通路的影响.方法 采用LipofectamineTM 2000转染试剂将si-KDM1A转染至结直肠癌HCT15细胞中,MTT法检测细胞增殖能力,流式细胞仪检测细胞的周期变化,Transwell小室实验检测细胞的侵袭能力,RT-PCR检测细胞中KDM1A mRNA的表达,Western blotting检测KDM1A蛋白和AKT信号通路相关蛋白p21、Cyclin D1、MMP-2和p-AKT的表达.结果 转染si-KDM1A后,HCT15细胞中KDM1A mRNA、KDM1A、Cyclin D1、MMP-2和p-AKT蛋白表达均显著降低,而p21蛋白表达显著升高;细胞的增殖能力和侵袭能力明显减弱;细胞在G1期所占比例明显增加,而在S期和G2期明显减少.结论 下调KDM1A基因可抑制结直肠癌HCT15细胞的增殖、侵袭能力,其分子机制可能与抑制AKT信号通路的活化有关.

Gemcitabine is a first-line drug utilised in the chemotherapy of pancreatic cancer; however, this drug induces chemo-resistance and toxicity to normal tissue during treatment. Here, we firstly report that andrographolide (ANDRO) alone not only has anti-pancreatic cancer activity, but it also potentiates the anti-tumour activity of gemcitabine. Treatment with ANDRO alone inhibits proliferation of the pancreatic cancer cell lines in a dose- and time-dependent manner in vitro. Interestingly, ANDRO induces cell cycle arrest and apoptosis of pancreatic cancer cells by inhibiting STAT3 and Akt activation, upregulating the expression of p21(WAF1) and Bax, and downregulating the expression of cyclinD1, cyclinE, survivin, X-IAP and Bcl-2. Additionally, ANDRO combined with gemcitabine significantly induce stronger cell cycle arrest and more obvious apoptosis than each single treatment. The mechanistic study demonstrates that this synergistic effect is also dependent on the inhibition of STAT3 and Akt activations which subsequently regulates the pathways involved in the apoptosis and cell cycle arrest. Furthermore, both ANDRO alone and the combination treatments exhibit efficacious anti-tumour activity in vivo. Overall, our results provide solid evidence supporting that ANDRO alone or its combination with gemcitabine is a potential chemotherapeutic approach for treating human pancreatic cancer in clinical practice.

Objective To explore the expression of gene DEPDC1 in human pancreatic cancer cell lines,pancreatic cancer tissues and adjacent tissues,and to investigate the effect of silencing DEPDC1 gene of PANC-1 cells on the proliferation,cell cycle and apoptosis by RNA interference.Methods The mRNA expression of DEPDC1 was detected in 4 cell lines of pancreatic cancer,4 cases with pancreatic cancer tissues and adjacent tissues by semi-quantitative reverse transcription PCR.DEPDC1-siRNA was transfected into PANC-1 cells,the expression of DEPDC1 mRNA and protein were determined by real-time PCR and Western blot.Proliferation,cycle and apoptosis of cell were examined by CCK-8 and flow cytometry,respectively.Results DEPDC1 mRNA was expressed in pancreatic cancer cell lines.It was higher expressed in pancreatic cancer tissues than in adjacent tissues.The expression of DEPDC1 mRNA and protein were down-regulated markedly in pancreatic cancer cells by DEPDC1 siRNA.The proliferation of PANC-1 cells was significantly suppressed(P<0.05).The rate of apoptosis of PANC-1 cells differed significantly from that of control groups(P <0.05).The percentage of G0/G1 stage cells was significantly higher,and the percentage of S stage cells lower in experimental group than in control groups(P<0.01 or P<0.05).Conclusions DEPDC1 mRNA is expressed in pancreatic cancer cell lines and it is higher expressed in pancreatic cancer tissues than in adjacent tissues.Down-regulation of DEPDC1 mRNA can inhibit the proliferation of pancreatic cancer PANC-1 cells,induce cell apoptosis and change cell cycle distribution.DEPDC1 may play an important role in the development of pancreatic cancer.

Objective To prevcnt the activation of post-reperfusion syndrome (PRS) in reducedsize liver transplantation in minipigs.Methods Twenty-four minipigs were randomly paired,divided into two groups (group A∶n =6; group B∶n =6) and received reduced-size liver transplantation.Group A allowed the initial 100 ml of portal blood reperfusing hepatic graft to be discarded through the inferior vena cava.Groups A and B were both administered 5％ sodium bicarbonate 5 ml/kg.Blood gas and electrolyte were obtained at preanhepatic phase,anhepatic phase,neohepatic phase and the end of surgery,respectively.PRS and one-week-survival rate were observed in both groups.Results Blood potassium concentration at neohepatic phase was correlated with PRS,while PRS was correlated with poor prognosis after reduced-size liver transplantation.At neohepatic phase,the plasma potassium concentration and PRS rate in group A were significantly lower than in group B (P ＜0.05).As a result,one-week-survival rate (100％) in group A was significantly higher than in group B (only 33.3％) (P ＜ 0.05).Four cases in group B died of cardiac arrest (intraoperation),acute pulmonary edema (3 h postoperation),acute renal failure (2 days postoperation) and intra-abdominal bleeding (3 days postoperation) respectively.Conclusion The abolishment of initial portal vein blood reperfusing graft and venous infusion of 5％ sodium bicarbonate can improve postoperative survival by effectively reducing the potassium concentration after reperfusion and significantly decreasing the incidence of PRS.

Objective To investigate the protective effect of polymyxin B (PMB) to the liver graft after liver transplantation and the underlying mechanism in rats.Methods Male SD rats were selected as the donors and recipients.Non-artery whole liver transplantation model was established in rats according to Kamada's two-cuff method.The rats were divided into two groups by the way of random number table method:control group (normal saline,0.5 ml) and PMB group (PMB,1 mg/ml,0.4 mg/kg+ normal saline 0.5 ml).The levels of portal vein plasma endtotoxin (EU/ml)were determined by endotoxin-analyzing machine of BET-24A. ALT,BUN,and TNF-α,IL-6 in serum were measured by using machine of Automatic Analyzer and ELISA,respectively.The CD14,TLR4,NFκB and AP-1 in the grafts were measured by RT-PCR and Western blotting,and pathological changes were observed. Results PMB decreased the levels of portal vein plasma endotoxin 1 h after reperfusion in PMB group as compared with control group (P＜0.05),and the levels of portal vein plasma endotoxin returned to the normal levels 6 h after reperfusion in both two groups (P＞0.05).After operation,the levels of ALT,TNFα and IL-6 in serum were significantly reduced (P＜0.05),the expression of CD14 and TLR4 mRNA in the grafts was significantly decreased (P＜0.05),the expression of Hsp60 protein and mRNA,and NF-κB and AP1 proteins in the grafts were reduced (P＜0.05),and the pathological damage to the grafts was significantly alleviated in PMB group as compared with control group.Conclusion PMB reduced the levels of portal vein plasma endotoxin after reperfusion in liver transplantation in rats.PMB improved liver function,reduced the injury of inflammatory response,decreased the levels of endotoxin signal pathway markers and alleviated the pathological damage to the grafts.

Objective To study the relationship between hepatic arterial buffer response (HABR),recovery of liver function,early biliary complications and small-for-size syndrome (SFSS).Methods Early hepatic hemodynamic parameters (including hepatic arterial flow (HAF),portal venous flow (PVF) were measured using duplex Doppler sonography in 34 patients who received living donor liver transplantation (preoperatively n＝26,intraoperatively n=26) and on postoperative days 1,2,3,and 7.Alanine aminotransferase (ALT),aspartate aminotransferase (AST) and total bilirubin (TBIL) level were measured preoperatively and on postoperative days 1,2,3,7,14,21,and 28.If TBIL level was elevated,we used B ultrasonography or CT and even ERCP to diagnose early biliary complications.The days taken for AST,AI T and TBIL to recover and the number of patients with early (＜60 days) biliary complications (bile leakage or bile stricture) and with small-for-size syndrome (SFSS) were recorded.Results Passive hepatic artery buffer response (HABR) was present in 11 patients early after living donor liver transplantation (group 1) and it disappeared in 23 patients (group 2).The recovery in days taken for normalization of AST (10.6± 8.8),AIT (11.6±9.0) and TBlL (average of 29) in group 1 were shorter than in group 2.However,the differences did not reach statistics difference (P＞0.05).The overall incidences of early biliary complications and small-for-size syndrome (SFSS) in group 1 were significantly lower than in group 2 (P=0.04).The survival rate in group 1 was 82 ％,compared with 74 ％ in group 2.Conclusions Passive hepatic arterial buffer response (HABR) disappeared in some patients early after living donor liver transplantation.There were high incidences of early biliary complications and small-for-size syndrome (SFSS) in these patients.Measurcment of hepatic buffer response in the early stage after living donor liver tranaplanta tion is valuable for predition of early biliary complications and small-for-size syndrome (SFSS),thus helping to prevent failure in transplantation.