Gastric cancer (GC) is the fifth most commonly diagnosed malignant disease and the third leading cause of cancer‑related deaths worldwide. Recently, numerous microRNAs (miRNAs) have been determined to contribute to GC initiation and progression, suggesting that miRNAs may be developed as effective diagnostic and prognostic molecular biomarkers and can be investigated as therapeutic targets for patients with this disease. Therefore, further investigation of the miRNAs involved in GC development represents an opportunity to improve the prognosis of GC patients. miRNA‑454 (miR‑454) is abnormally expressed in multiple types of human cancer. However, the expression pattern, biological roles and underlying mechanism of miR‑454 in GC remain unclear and require further investigation. In the present study, we assessed miR‑454 expression in GC tissues and cell lines. We also explored the effects of miR‑454 on the biological behaviours of tumour cells and the underlying molecular mechanisms of miR‑454. The results revealed that miR‑454 was significantly downregulated in GC tissues and cell lines. Low miR‑454 expression was positively associated with lymph node metastasis, invasive depth and TNM stage. Additionally, upregulation of miR‑454 inhibited cell proliferation and invasion and induced the apoptosis of the GC cells. Subsequently, mitogen‑activated protein kinase 1 (MAPK1) was identified as a direct target of miR‑454. MAPK1 was upregulated in GC tissues and was found to be negatively correlated with the miR‑454 expression level. Downregulation of MAPK1 also suppressed GC cell proliferation and invasion and increased apoptosis, thereby resembling the suppressive effects of miR‑454 overexpression in GC. Moreover, upregulation of MAPK1 reversed the tumour‑suppressive effects of miR‑454 in GC. Collectively, our data demonstrated that miR‑454 may play tumour‑suppressing roles in GC through the regulation of MAPK1, suggesting that miR‑454 may be a novel biomarker and therapeutic target for patients with this disease.

BACKGROUND:Benign anastomotic esophageal stricture after surgical resection frequently occurs and requires endoscopic balloon dilation (EBD) or incision to maintain patency because of the significant recurrence rate. Our study was designed to evaluate the effectiveness and safety of endoscopic incision and selective cutting (EISC) as primary treatment on 5 patients for benign anastomotic esophageal stricture.METHODS:Five patients with benign stricture of the esophageal anastomosis after radical resection for esophageal cancer underwent EISC in our center between April, 2018 and January, 2019. The effectiveness and safety of the procedure were observed during at least 12 months follow-up.RESULTS:The EISC was successfully performed in all 5 patients. The diameters of the anastomoses were increased from 1-3 preoperatively to 14-18 mm (mean: 15.6 mm) intraoperatively (P<0.05). The duration of the operation ranged from 30-55 min (mean: 42.8 min). During at least 12 months follow-up observations, all patients resumed eating solid meals and had no recurrence of dysphagia.CONCLUSIONS:EISC as primary treatment is a safe and effective treatment for benign anastomotic esophageal stricture.

特发性嗜酸性粒细胞增多症(idiopathic hypergranulocytosis,IHES)是一组发病原因不明的疾病,临床工作中不常见,它累及多个器官系统,激素是一线治疗药物.现报道1例我院收治的IHES的诊疗经过,供临床参考.

非甾体类抗炎药(NSAIDs)为抗炎、解热镇痛、抑制血小板聚集的有效药物,被广泛应用于临床.但其不良反应众多,应用不恰当则弊大于利,严重危害患者生命健康.其最主要的不良反应为胃肠道(GI)损伤.近年来,学者们就NSAIDs对胃黏膜损伤的研究较多,而在一定程度上忽略了其对肠道黏膜损伤的影响,本文就NSAIDs对肠道黏膜损伤的发生机制、临床表现、检查异常及防治等进行综述.

Objective:To analyze the clinical characteristics of ischemic colitis(IC) and further improve the diagnosis and treatment of the disease.Methods:The clinical manifestations, risk factors, colonoscopy and abdominal CT examination results of 35 patients with IC confirmed from January 2014 to December 2018 in the Second Hospital of Jilin University were retrospectively analyzed, and their clinical characteristics were summarized.Results:The sudden manifestation of abdominal pain and blood in 31 cases of the 35 patients were the main manifestations.Ten patients who underwent abdominal CT scan showed a thickened bowel wall with a thickness of (7.92±1.41)mm.The CT value of the thickened bowel wall decreased significantly to (21.20±2.27)Hu.In 35 cases of colonoscopy, 42.86%, 31.42%, 20.00%, 2.86% and 2.86% were involved in the descending colon, sigmoid colon, transverse colon, ascending colon and whole colon, respectively.The left colon was the main part, with clusters and bands Mucosa-like erythema, ecchymosis, erosion, and even ulcers.No rectum was involved in 35 patients.Conclusion:The typical manifestation of IC is sudden abdominal pain and bloody stool.Abdominal CT in emergency department has obvious suggestive value for early diagnosis of this disease.Colonoscopy is the main diagnostic method for this disease.

内镜下全层切除术(endoscopic full-thickness resection,EFR)治疗胃肠间质瘤,治疗成功的关键是内镜下成功修补术中发生的迟发性穿孔.本例患者胃间质瘤(gastric stromal tumor,GST)行EFR治疗,术后患者恢复良好,术后3个月并发膈下脓肿,现报道如下.

双氯芬酸钠因具有解热、消炎、镇痛等作用,被广泛用于临床,其不良反应研究多以胃十二指肠损害为主,而下消化道损伤报道较少.现报道本院发现的双氯酚酸钠致消化道溃疡2例,以提高临床医生的认识. 1 病例资料 病例1:患者男,56岁,因反复乏力、头晕4年于2016年11月22日入本院.多次在当地医院检查发现贫血,Hb波动于60 ～ 80 g/L,最低至25 g/L,多次便隐血(+).2016年3月5日当地医院胃镜示:胃体、胃窦陈旧出血点及糜烂,胃窦小弯侧一凹陷性溃疡,表面覆白苔及出血,胃窦前壁大片糜烂.2016年3月11日结肠镜示:乙状结肠、横结肠散在数个大小不一溃疡,部分溃疡见新鲜出血.

AA型(血清淀粉样蛋白A型,继发性)淀粉样变性是以血清淀粉样物质沉积于组织、器官的系统性病变,多与感染、炎性反应相关[1].该病本身为少见疾病,继发于原发性胆汁性胆管炎且多器官累及的病例更为罕见.现报道本院治疗的AA型淀粉样变性多器官累及1例,以提高临床医生对该病的认识.

目的 观察胃镜电凝止血联合瑞巴派特三联疗法治疗胃溃疡出血的临床疗效.方法 将106例胃溃疡出血患者按随机数字表法分为研究组与对照组,每组53例.对照组在基础治疗基础上给予胃镜电凝止血;研究组在基础治疗基础上给予胃镜电凝止血联合施奥美拉唑+铝碳酸镁+瑞巴派特三联疗法治疗;2组均治疗4周.比较2组的临床疗效、治疗前后炎症反应指标[包括白细胞介素-6(IL-6)、白细胞介素-17(IL-17)、白细胞介素-23(IL-23)]与相关血清学指标[包括超氧化物歧化酶(SOD)、血管内皮生长因子(VEGF)、表皮生长因子(EGF)]变化情况及预后质量(包括止血时间、输血量、住院时间).结果 研究组治疗总有效率明显高于对照组(92.45％比75.47％,χ2=5.67,P=0.02).2组治疗后VEGF、EGF、SOD水平均较治疗前显著升高(P<0.05),IL-6、IL-17、IL-23水平较治疗前显著降低(P<0.05);且研究组改善较对照组更为显著(P<0.05).研究组止血时间、输血量、住院时间与对照组比较均明显减少(P<0.05).结论 胃镜电凝止血联合瑞巴派特三联疗法可明显改善胃溃疡出血患者临床症状以及机体高炎症状态,且对其预后质量的改善效果显著.

Background This study was aimed to determination the tumor inhibitory effect and explore the potential mechanisms of Lagopsis supine ethanol extract (Ls) on colorectal cancer. Methods The cell growth inhibition experiment of Ls in colorectal cancer cell lines was determined by MTT method in the time course of 24, 48 and 72 h in four gradient drug concentrations. The protein expression levels of pSTAT3, pJAK2, STAT3, JAK2, Bcl-2 and caspase 3 were measured by Western blot method. The mRNA levels of the downstream genes of STAT3 were detected through semi-quantitative RT PCR. Sixty Balb/c-nude mice were xenograft with HCT116 colorectal cancer cells through subcutaneously. The xenografts were divided into five groups: model group, positive group (capecitabine 300 mg/kg) and three dosages of Ls treated groups (75, 150 and 300 mg/kg). Tumor size and tumor weight were calculated for evaluation the anti-tumor effects. H & E staining and immunohistochemical analysis were used to determine the histopathological changes and the levels of pSTAT3 and pJAK2 in the tumor tissues. Results Ls exhibited a significant anti-proliferation effect in HCT116 and SW480 cells in vitro. The protein levels of pSTAT3, pJAK2 and Bcl-2, and the mRNA levels of Bcl-2 and Bak notably reduced with a dose-dependent manner. While the protein levels of caspase 3, and mRNA levels of Bax and caspase-3 remarkably increased in the gradient dosage of Ls in HCT116 cells. HCT116 in vivo xenografts experiment showed that the growth of the tumors significantly inhibited by Ls administration, which with no any significant body weight changes in each experiment group. The histopathology analysis displayed that Ls significantly reduced the inflammatory cells in tumor tissue. Furthermore, Ls also significantly down-regulate the protein levels of pSTAT3 and pJAK2 in the tumor tissues, compared with the model group. Conclusions This work shows that Ls inhibited the cell proliferation of colorectal cancer in vitro and significantly reduced the tumor growth in HCT116 xenografts in vivo, which is probably related with the JAK/STAT signal pathway.

Colon cancer is one of the most fatal cancers in the United States, and is characterized by the presence of chromosomal instability (CIN), causes of which are largely unclear. Emerging evidence indicates that abnormal spindle geometry and supernumerary centrosomes lead to CIN in cells. However, if and how spindle geometry defects and centrosomes amplification occur in colon cancer remains unknown. Here we show that decrease in the cell cycle regulatory protein, cyclin A2, induces spindle geometry defects in colon cancer cells. In mechanistic studies, we found that cyclin A2 is located at the centrosomes, and its depletion reduces phosphorylation of EG5, which is important for centrosome localization and movement of duplicated centrosomes to opposite poles. We also found that cyclin A2 silencing leads to centrosome amplification in the cells. Collectively, these findings demonstrate previously unrecognized role for cyclin A2 in preventing centrosomal defects in colon cancer cells and provide insights into mechanisms that may potentially cause CIN in these tumors.

Objective To investigate the safety and efficacy of the therapeutic methods in the plant gastrolith.Methods According to the methods of treatment,61 patients with plant gastrolith were divided into drug dissolved stone group and endoscopic lithotripsy group.In the drug dissolved stone group,there were 40 patients taken 50 g/L sodium bicarbonate with several times daily,and reviewed the gastroscope in order to observe the clinical effects after 6 or 7 days.In the endoscopic lithotripsy group,there were 21 patients received lithotripsy under the gastroscope after 50 g/L sodium bicarbonate with several times daily for 2-3 days.Results In the drug dissolved stone group,there were 37 patients successfully dissolved the plant gastrolith,and only 3 patients unsuccessfully.The probability of dissolving stone was 92.5％.In the endoscopic lithotripsy group,there were only 2 patients' plant gastrolith were disappeared after drug dissolving stone for 3 days,and the other 19 patients received lithotripsy under the gastroscope after lithotripsy 2-3 days.After 3 days,the gastroscope was checked,the plant gastrolith successfully dispeared in 17 patients,and the other 2 patients were received lithotripsy under the gastroscope again.The success rate was 89.5％ of the first crushing stone treatment.There was no statistically significant difference in cure rate between the two groups (P ＞ 0.05).The average hospitalization expenses was 6 200 yuan in drug dissolved stone group,and 9 000 yuan in the endoscopic lithotripsy group,which had obvious differences (P ＜ 0.05).The average length of hospital stay had no obvious differences in the two groups.Conclusion Drug therapy for plant gastrolith is cheap,effective,safe and less side effects,superior than endoscopy.

目的 探讨腹部CT在诊断急性出血糜烂性胃炎中的价值.方法 对吉林大学第二医院收治的7例急性出血糜烂性胃炎患者的临床表现、腹部CT及内镜检查进行回顾性分析.结果 7例急性出血糜烂性胃炎患者的急诊腹部CT可见胃壁明显增厚,厚度为(1.2±0.4)cm,可见增厚部分胃壁有分层现象,即中间为低密度影,两边为高密度影,增厚的胃壁中间部分CT值明显下降,CT值为(23±3.5)HU.结论 典型的腹部CT表现对急性出血糜烂性胃炎的诊断有明显的提示作用.

Recent studies have demonstrated that the dysregulation of miRNAs are frequently associated with cancer progression including gastric cancer (GC). MiR-211 was found to act as tumor suppressor in GC, however, the functional role of miR-211 involved in GC cell epithelial-mesenchymal transition (EMT) process still to be investigated. In the study, we demonstrated that miR-211 was lower expression in gastric cancer tissues compared with adjacent normal tissues. Lower miR-211 expression was positively associated with distant metastasis and lymph node metastasis in GC patients. Survival curve by Kaplan-Meier method and log rank test revealed that lower miR-211 expression indicated a poor outcome in GC patients. Function assays showed that miR-211 inhibited cell invasion and cell epithelial-mesenchymal transition (EMT) process in GC by upregulating E-cadherin expression and down-regulating twist1 and N-cadherin expression. Furthermore, we demonstrated that miR-211 suppressed cell EMT by targeting MMP9 expression in GC. These results showed that miR-211 acted as a tumor suppressor in GC and may be a potential target of GC treatment.

Postoperative adhesion (POA) is a common complication that often occurs after a variety of surgeries, such as plastic surgery, repair operations of abdominal, pelvic, and tendon, and so forth. Moreover, POA leads to chronic abdominal pain, secondary infertility in women, intestinal obstruction, and other severe complications, which significantly reduce the life quality of patients. In order to prevent the formation of POA, a number of strategies have been developed, among which an emerging method is physical barriers consisting of polymer materials. This review highlights the most commonly used natural and synthetic polymer materials in anti-adhesion physical barriers. The specific features of polymer materials are analyzed and compared, and the possible prospect is also predicted.Statement of SignificancePostoperative adhesion (POA) is a serious complication accompanied with various surgeries. Polymer material-based physical barriers have attracted a large amount of attention in POA prevention. The polymer barriers can effectively avoid the formation of fibrous tissues among normal organs by reducing the interconnection of injured tissues. In this review, specific features of the natural and synthetic polymer materials for application in POA prevention were presented, and the possible prospects were predicted. All in all, our work can provide inspiration for researchers to choose proper polymer materials for preclinical and even clinical anti-adhesion studies. (C) 2017 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.

Objective To investigate the effect of ethanol on HCO3 - secretion induced by CFTR from guinea - pig pancreatic duct cells and to analyse the mechanisms of alcoholic pancreatitis. Methods Interlobular duct segments( diameter,100 ~ 150 μm)were microdissected under a dissection microscope using sharp needles. The lumen of the interlobular duct segment was microperfused. The bath and luminal solutions were modified separately. Intracellular pH(pHi)in the duct cells was estimated by microfluorometry using the pH - sensitive fluoroprobe BCECF. Transepithelial fluxes of HCO3 - were estimated under the anion gradients favoring rapid exchange of intracellular HCO3 - . Results ①When in vitro pancreatic duct pipe cavity,when filled with high concentration of sodium bicarbonate buffer micro pHi from epithelial cells after alkaline pH unit recovery rate was was 0. 048 ± 0. 009 pH unit·min - 1(n = 9),add 1 mm when ethanol pHi decline accelerated significantly(0. 066 ± 0. 005 pH unit·min - 1 ,n = 7,t = 0. 0009,P < 0. 05). ②Luminal application of CFTRinh - 172(10 μM)significantly( P < 0. 05)inhibited apical HCO3 - secretion(0. 039 ± 0. 010 pH unit·min - 1 ,n = 7,t = 0. 001). ③When the duct was stimulated with ethanol,luminal application of CFTRinh - 172 decrease the rate of pHi(0. 054 ± 0. 008 pH unit·min - 1 ,n = 7,t = 0. 0015,P < 0. 05). Conclusion Ethanol stimulated api-cal HCO3 - secretion of guinea - pig pancreatic ducts. The augmentation by ethanol appears to be mediated by CFTR.

Epidermal growth factor receptor (EGFR) signalling promotes growth of colorectal cancer (CRC) cells and also is known to induce the production of a tumorigenic cytokine parathyroid hormone related peptide (PTHrP) in some malignancies. Sphingosine-1-phosphate (S1P), through its G-protein-coupled receptors S1PR, has been shown to transactivate multiple membrane-bound receptors, notably EGFR. S1P promotes tumorigenic and inflammatory responses that favour cell transformation and malignancy progression. We hypothesize that blocking EGFR signalling and PTHrP production in CRC could mitigate malignant growth. We found that vitamin K2 (menaquinone-4, MK4) reduced the proliferation of KRAS mutant LoVo cells and KRAS wild type Caco 2 cells induced by EGF and S1P. In both cell lines, MK4 attenuated EGF-induced proliferation, survival, phosphorylation of EGFR and production of PTHrP. The EGF-induced PTHrP secretion was responsible for EGF’s proliferation-promoting effect that has been demonstrated by the suppression of EGF-induced cell growth by PTH receptor antagonist, PTH (7-34). S1P, via its receptor S1PR1, increased proliferation and transactivation in CRC cell lines. Transactivation of EGFR by S1PR1 was dependent on the activation of matrix metalloproteases (MMP), particularly MMP-2 and MMP-9 (albeit partially). S1P-induced EGFR transactivation was blocked by S1P receptor 1 (S1PR1) inhibitor which led to inhibition of PTHrP secretion. MK4 suppressed transactivation of EGFR by S1P, leading to inhibition of S1P-induced PTHrP secretion and cell proliferation. Taken together, our data show that MK4 attenuated the pro-malignant effects of EGF and S1P on CRC lines by attenuating their ability to activate EGFR signalling and the downstream production of PTHrP.

Objective In order to improve SpO2 of obese patients during sedative gastroscopy,we investigated the effect of tracheal catheter without sack(catheter without sack)placed around hypopharynx on affording oxygen.Methods 1274 obese patients with sedative gastroscopy were randomly divided into group A(nasal catheter group)and group B(tracheal catheter group).When SpO2 decreased more than 10%,the hypoxemia of group A was improved by increasing the oxygen flow and raising submaxilla,but catheter without sack was placed around hypopharynx in group B.Results There are no differences between group A(617,96.86%)and group B(598,93.86%)whose SpO2 decreased more than 10% during anesthesia(P﹥0.05).303patients(49.11%)of group A accomplished sedative gastroscopy by taking some correcting measures,which is lower than group B(577,96.48%,P0.05).The lowest SpO2 of group A after anesthesia was(83.12±1.65)%,which are no differences with group B(84.92±1.78)%.The SpO2 of patients who suffered from hypoxemia of group A was increased to(90.57±1.74)% by correcting method,which is significantly lower than group B(96.41±1.56)%(P0.05).Conclusion The hypoxemia of obese patients during sedative gastroscopy can be improved by placing tracheal catheter without sack around hypopharynx,which increases the achievement ratio of sedative gastroscopy.

核糖核苷酸还原酶（Ribonucleotide Reductase.RR）在DNA合成、修复及细胞增殖中起关键作用,近来被认为是癌症治疗的重要靶点。RR包含3个亚单位,分别是大亚基RRM1、小亚基RRM2和小亚基p53R2。RRM2亚基不仅和DNA的合成密切相关,对恶性肿瘤生物学行为、转移潜能和肿瘤耐药的产生都具有影响.在绒癌、胰腺癌、膀胱癌、胃癌、直肠癌、乳腺癌等多种人体癌组织中发现RRM2的表达水平有异常升高的情况,抑制RRM2的高表达,可以降低酶的活性,抑制癌细胞的生长,增

目的:观察给予氟(F-)后糖尿病大鼠切牙的病理性改变以及氟对糖尿病大鼠生理指标的影响,阐明氟在糖尿病进程中的作用.方法:雄性Wistar大鼠54只,按体质量平均分成对照组、10 mg·kg1·d-1氟组和20 mg·kg-1·d-1氟组,每组18只;按相应剂量灌胃给氟4周后,每组随机选12只,一次性腹腔注射50 mg·kg-1体质量剂量的STZ,复制大鼠1型糖尿病模型(分别为STZ对照组、10 mg F+STZ组和20 mg F+STZ组),与每组剩余6只大鼠(分别为正常对照组、10 mg F组和20 mg F-组)同时继续给氟饲养4周(STZ对照组和正常对照组不给氟).实验周期内用电子天平每周测量1次大鼠体质量;便携式血糖仪每周测量1次大鼠血糖;利用数码相机对大鼠牙齿的渐进性变化进行拍照;实验结束前采用腹腔注射胰岛素进行糖耐量实验(ITT),观察大鼠胰岛素的敏感性.结果:10 mg F-和20 mg F-组大鼠切牙面逐渐由棕黄色转向淡黄色,着色不匀,部分区域有白色不透光改变,牙面粗糙,呈现氟斑牙病变;与正常对照组比较,单纯氟中毒大鼠体质量无变化.腹腔注射STZ后的3组大鼠体质量均呈下降的趋势,20 mg F-组降幅最大,但与正常对照组比较差异无统计学意义(P＞0.05);腹腔注射STZ后各组大鼠血糖明显上升,与正常对照组比较差异有统计学意义(P＜0.05),20 mg F+STZ组大鼠血糖水平最高,但与STZ对照组比较差异无统计学意义(P＞0.05).ITT结果,20 mg F-组大鼠腹腔注射胰岛素0.5、1和2h时血糖水平显著高于正常对照组(P＜0.05),而10 mg F-组大鼠血糖水平虽高于正常对照组,但差异无统计学意义(P＞0.05).结论:高剂量氟可短期内引起大鼠氟斑牙,并加剧糖尿病引起的大鼠体质量下降和血糖升高,明显降低大鼠胰岛素敏感性.