表皮生长因子受体在老年大肠癌中的表达及临床意义

目的探讨表皮生长因子受体(EGFR)在老年大肠癌组织中的表达及其临床意义。方法采用免疫组化SABC法对87例大肠癌、14例大肠炎性黏膜和26例大肠腺瘤样息肉进行检测。结果EGFR在大肠炎性黏膜、腺瘤样息肉和大肠癌中阳性率分别为21.43%、46.15%和54.02%,其中EGFR在炎性黏膜中表达率明显低于腺瘤样息肉和大肠癌(P<0.05);EGFR表达与大肠癌浸润深度和淋巴结转移有相关性(P<0.05)。结论EGFR过度表达,在老年大肠癌的发生过程中可能起重要作用;检测EGFR对于指导临床治疗和判断预后有重要意义。

结肠镜活检组织检测MGMT和galectin-3的表达在结肠腺癌中的临床意义

目的检测结肠腺癌活检组织中DNA修复酶O^6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)和半乳糖凝集素-3(galectin-3)的表达在结肠腺癌中的临床意义。方法选取2010年1月～2015年1月广西壮族自治区民族医院结肠镜活检的120例患者标本组织(包括60例结肠腺癌、30例炎性结肠黏膜病变和30例不典型增生结肠黏膜病变),通过免疫组化SP方法检测MGMT蛋白、galectin-3蛋白的表达情况,并通过随访了解预后情况。结果与炎性肠黏膜病变组比较,结肠腺癌组MGMT阳性表达降低,galectin-3阳性表达升高,差异有统计学意义(P <0.05)。与中-高分化结肠腺癌组比较,低分化结肠腺癌组中MGMT阳性表达降低,galectin-3阳性表达升高,差异有统计学意义(P <0.05);与有淋巴结转移的结肠腺癌组比较,无淋巴结转移的结肠腺癌组MGMT阳性表达升高,galectin-3阳性表达降低,差异有统计学意义(P <0.05);MGMT在结肠腺癌组织中的表达随着TNM分期增高而降低,galectin-3的表达随着TNM分期增高而增高,差异有统计学意义(P <0.05);MGMT和galectin-3的表达与结肠腺癌患者的年龄、性别无关(P> 0.05)。MGMT和galectin-3在结肠腺癌中的表达呈负相关(r=-0.399,P=0.002);MGMT和galectin-3在结肠腺癌中的阳性表达率与患者的3年生存率明显相关(P <0.05)。结论 MGMT和galectin-3在结肠腺癌的发生、发展过程中起重要作用,检测结肠腺癌组织中MGMT和galectin-3的表达有助于判断肿瘤的恶性程度、病情进展及预后。

结肠腺癌中MGMT和galectin-3的表达及其与淋巴结转移的关系

研究结肠腺癌活检组织中DNA 修复酶O 6-甲基鸟嘌呤-DNA甲基转移酶(O 6-methylguanine DNA methyltransferase,MGMT)和半乳糖凝集素-3(galectin-3,GAL-3)的表达及其与淋巴结转移的关系。方法:采用免疫组化(SP)法检测51例结肠腺癌、29例转移淋巴结及51例炎性肠病组织中MGMT和galectin-3的表达,并分析MGMT和galectin-3的表达与结肠腺癌侵袭和淋巴结转移的关系以及二者之间的相关性。结果:MGMT在结肠腺癌、转移淋巴结及炎性肠病组织中的阳性率分别为58.82%(30/51)、17.24%(5/29)、78.43%(40/51),差异有统计学意义( P <0.05);galectin-3在结肠腺癌、转移淋巴结及炎性肠病组织中的阳性率分别为56.86%(29/51)、93.10%(27/29)、35.29%(18/51),差异有统计学意义( P <0.05)。在结肠腺癌中,MGMT和galectin-3的表达呈负相关( r =-0.327, P <0.05)。MGMT的低表达和galectin-3的高表达均与淋巴结转移有关( P <0.05)。结论:MGMT和galectin-3的异常表达可能与结肠腺癌的侵袭、转移有关,联合监测MGMT和galectin-3有望成为判断淋巴结转移更为有效的指标。

Protective Action of Acupuncture and Moxibustion on Gastric Mucosa in Model Rats with Chronic Atrophic Gastritis

Objective: To probe the mechanism of acupuncture and moxibustion in atrophic gastritis so as to provide a basis for clinical treatment. Method: Observe the effects of acupuncture and moxibustion at the points of Zusanli, Zhongwan and Tianshu on gastric mucosa in model rats with chronic atrophic gastritis. Results:Acupuncture and moxibustion can increase the contents of PGE2α, PGF2α and cAMP, and decrease the content of cGMP in the tissue of gastric mucosa. Conclusion: Acupuncture and moxibustion shows cytoprotection on gastric mucosa, so it is an effective method for treating chronic atrophic gastritis.

Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus-indica mucilage

AIM： To study the effect of mucilage obtained from cladodes of Opuntia ficus-indica （Cactaceae） on the healing of ethanol-induced gastritis in rats. METHODS： Chronic gastric mucosa injury was treated with mucilage （5 mg/kg per day） after it was induced by ethanol. Lipid composition, activity of 5＇-nucleotidase （a membrane-associated ectoenzyme） and cytosolic activities of lactate and alcohol dehydrogenases in the plasma membrane of gastric mucosa were determined. Histological studies of gastric samples from the experimental groups were included. RESULTS： Ethanol elicited the histological profile of gastritis characterized by loss of the surface epithelium and infiltration of polymorphonuclear leukocytes. Phosphatidylcholine （PC） decreased and cholesterol content increased in plasma membranes of the gastric mucosa. In addition, cytosolic activity increased while the activity of alcohol dehydrogenases decreased. The administration of mucilage promptly corrected these enzymatic changes. In fact, mucilage readily accelerated restoration of the ethanol-induced histological alterations and the disturbances in plasma membranes of gastric mucosa, showing a univocal anti-inflammatory effect. The activity of 5＇-nucleotidase correlated with the changes in lipid composition and the fluidity of gastric mucosal plasma membranes. CONCLUSION： The beneficial action of mucilage seems correlated with stabilization of plasma membranes of damaged gastric mucosa. Molecular interactions between mucilage monosaccharides and membrane phospholipids, mainly PC and phosphatidylethanolamine （PE）, may be the relevant features responsible for changing activities of membrane-attached proteins during the healing process after chronic gastric mucosal damage.

Dynamic changes of IL-2/IL-10, sFas and expression of Fas in intestinal mucosa in rats with acute necrotizing pancreatitis

AIM:To investigate dynamic changes of serum IL-2, IL-10, IL-2/IL-10 and sFas in rats with acute necrotizing pancreatitis. To explore the expression of Fas in intestinal mucosa of rats with acute necrotizing pancreatitis (ANP). METHODS:A total of 64 Sprague-Dawley (SD) rats were randomly divided into two groups:normal control group (C group), ANP group (P group). An ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane. Normal control group received isovolumetric injection of 9 g/L physiological saline solution using the same method. The blood samples of the rats in each group were obtained via superior mesenteric vein to measure levels of IL-2, IL-10, sFas and calculate the value of IL-2/IL-10. The levels of IL-2, IL-10 and sFas were determined by ELISA. The severity of intestinal mucosal injury was evaluated by pathologic score. The expression of Fas in intestinal mucosal tissue was determined by immunohistochemistry staining. RESULTS:Levels of serum IL-2 were significantly higher in P group than those of C group (2.79 ± 0.51 vs 3.53 ± 0.62, 2.93 ± 0.89 vs 4.35 ± 1.11, 4.81 ± 1.23 vs 6.94 ± 1.55 and 3.41 ± 0.72 vs 4.80 ± 1.10, respectively, P < 0.01, for all) and its reached peak at 6 h. Levels of serum IL-10 were significantly higher in P group than those of C group at 6 h and 12 h (54.61 ± 15.81 vs 47.34 ± 14.62, 141.15 ± 40.21 vs 156.12 ± 43.10, 89.18 ± 32.52 vs 494.98 ± 11.23 and 77.15 ± 22.60 vs 93.28 ± 25.81, respectively, P < 0.01, for all). The values of IL-2/IL-10 were higher significantly in P group than those of C group at 0.5 h and 2 h (0.05 ± 0.01 vs 0.07 ± 0.02 and 0.02 ± 0.01 vs 0.03 ± 0.01, respectively, P < 0.01, for all), and it were significantly lower than those of C group at 6 h (0.05 ± 0.02 vs 0.01 ± 0.01, P < 0.01) and returned to the control level at 12 h (0.04 ± 0.01 vs 0.05 ± 0.02, P > 0.05). In sFas assay, there was no significant difference between P group and C group (3.16 ± 0.75 vs 3.31 ± 0.80, 4.05 ± 1.08 vs 4.32 ± 1.11, 5.93 ± 1.52 vs 5.41 ± 1.47 and 4.62 ± 1.23 vs 4.44 ± 1.16, respectively, P > 0.05, for all). Comparison of P group and C group, the pathological changes were aggravated significantly in P group. Immunohistochemistry staining show the expression of Fas was absent in normal intestinal tissues, however, it gradually increased after induction of pancreatitis in intestinal tissue, then reached their peaks at 12 h.CONCLUSION:Fas were involved in the pathogenesis of pancreatitis associated intestinal injury. The mechanisms of Fas may be associated to Fas mediated T helper cell apoptosis.

Persistence of gene expression changes in noninflamed and inflamed colonic mucosa in ulcerative colitis and their presence in colonic carcinoma

AIM： A few studies have applied genomic-wide gene expression analysis in inflamed colon tissue sample in ulcerative colitis （UC）. We reported the first study of non-inflamed mucosal gene expression in UC and explored its clinical implication. METHODS： Non-inflamed mucosa was obtained from 6 UC patients who received total colectomy. The gene expression of UC in noninflamed mucosa was monitored with a microarray. For a selected gene, RT-PCR was performed to verify array results and to further examine expression pattern in inflamed mucosa of UC, colorectal cancer tissue and normal mucosa using additional matched pairs. RESULTS： Two genes showing 2.5-fold decreased expression with significance set at in UC samples were borneo box a4 （HOXa4） and mads box transcription enhancer factor 2, polypeptide B （MEF2b）. RT-PCR showed that MEF2b expression in non-inflamed mucosa was significantly downregulated, whereas the expression of MEF2b increased in accordance with the severity of mucosal inflammation. HOXa4 expression both in inflamed and non-inflamed mucosa in UC was consistently downregulated, and the downregulation of HOXa4 was also found in colorectal carcinoma. CONCLUSION： It is suggested that the MEF2b expression in UC which increase in accordance with inflammation may be induced by the inflammatory mediator. In contrast the downregulation of HOXa4 may be partly involved in the pathogenesis of disease including UC and UC-related carcinogenesis.

B1a lymphocytes in the rectal mucosa of ulcerative colitis patients

AIM:To assess B1a cell expression in the rectal mucosa of ulcerative colitis (UC) patients in comparison with healthy controls.METHODS:Rectal mucosa biopsies were collected from 15 UC patients and 17 healthy controls.CD5 + B cells were analysed by three colour flow cytometry from rectal mucosal samples after mechanical disaggregation by Medimachine.Immunohistochemical analysis of B and T lymphocytes was also performed.Correlations between,on the one hand,rectal B1a cell concentrations and,on the other,erythrocyte sedimentation rate and C-reactive protein levels and clinical,endoscopic and histological disease activity indices were evaluated.RESULTS:Rectal B-lymphocyte (CD19 + /CD45 +) rate and concentration were higher in UC patients compared with those in healthy controls (47.85% ± 3.12% vs 26.10% ± 3.40%,P=0.001 and 501 ± 91 cells/mm 2 vs 117 ± 18 cells/mm 2,P < 0.001);Rectal B1a cell density (CD5 + CD19 +) was higher in UC patients than in healthy controls (85 ± 15 cells/mm 2 vs 31 ± 6.7 cells/mm 2,P=0.009).Rectal B1a cell (CD5/CD19 +) rate correlated inversely with endoscopic classification (Rs=-0.637,P < 0.05).CONCLUSION:B1a lymphocytes seem to be involved in the pathogenesis of UC,however,the role they play in its early phases and in disease activity,have yet to be defined.

H pylori exist in the gallbladder mucosa of patients with chronic cholecystitis

AIM:To study whether H pylori locate in the gallbladder mucosa of patients with chronic cholecystitis.METHODS:Using Warthy-Starry(W-S)silver stain and immunohistochemistry stain with anti-H pylori antibodies,we screened paraffin specimens in 524 cases of cholecystitis.H pylori urease gene A(HPUA)and H pylori urease gene B(HPUB)were analyzed by polymerase chain reaction(PCR)in the fresh tissue specimens from 81 cases of cholecystitis.RESULTS:H pylori-like bacteria were found in 13.55% of the gallbladders of the cholecystitis patients using W-S stain.Meanwhile,bacteria positive for H pylori antibodies were also found in 7.1% of the gallbladders of patients with cholecystitis by immunohistochemistry.Of 81 gallbladders,11 were positive for both HPUA and HPUB,4 were positive for HPUA only and 7 were positive for HPUB only.CONCLUSION:H pylori exist in the gallbladders of patients with chronic cholecystitis.

Extraintestinal heterotopic gastric tissue simulating acute appendicitis

We describe the case of a 68-year-old otherwise healthy male who presented to our emergency room with signs and symptoms of acute appendicitis. Exploratory surgery revealed a normal appendix. Further examination revealed an enlarged lymph node-like mass of tissue near the appendix, in the ileocecal mesentery. This mass was removed and was found to be inflamed heterotopic gastric tissue. Although reports of heterotopic gastric tissue in the literature are common, we believe that this case represents the first report of inflamed heterotopic gastric tissue simulating appendicitis.

Role of scintigraphy in inflammatory bowel disease

The diagnosis of inflammatory bowel disease(IBD) depends on direct endoscopic visualization of the colonic and ileal mucosa and the histological study of the obtained samples.Radiological and scintigraphic methods are mainly used as an adjunct to endoscopy.In this review,we focus on the diagnostic potential of nuclear medicine procedures.The value of all radiotracers is described with special reference to those with greater experience and more satisfactory results.Tc-99m hexamethylpropylene amine oxime white blood cells remain a widely acceptable scintigraphic method for the diagnosis of IBD,as well as for the evaluation of disease extension and severity.Recently,pentavalent Tc-99m dimercaptosuccinic acid has been recommended as an accurate variant and a complementary technique to endoscopy for the follow-up and assessment of disease activity.Positron emission tomography alone or with computed tomography using fluorine-18 fluorodeoxyglucose appears to be a promising method of measuring inflammation in IBD patients.

Lansoprazole-associated collagenous colitis:Diffuse mucosal cloudiness mimicking ulcerative colitis

There have only been a few reports on lansoprazole-associated collagenous colitis. Colonic mucosa of collagenous colitis is known to be endoscopically normal. We present a case of collagenous colitis where the mucosa showed diffuse cloudiness mimicking ulcerative colitis. A 70-year-old woman developed watery diarrhea four to nine times a day. She had interstitial pneumonia at 67 and reflux esophagitis at 70 years. Lansoprazole 30 mg/d had been prescribed for reflux esophagitis for nearly 6 mo. Lansoprazole was withdrawn due to its possible side effect of diarrhea. Colonoscopy disclosed diffuse cloudiness of the mucosa which suggested ulcerative colitis. Consequently sulfasalazine 2 g/d was started. The patient's diarrhea dramatically disappeared on the following day. However, biopsy specimens showed subepithelial collagenous thickening and infi ltration of inflammatory cells in the lamina propria, confirming the diagnosis of collagenous colitis. One month after sulfasalazine therapy was initiated, colonoscopic and histological abnormalities resolved completely. Five months later the diarrhea recurred. The findings on colonoscopy and histology were the same as before, confirming a diagnosis of collagenous colitis relapse. We found that the patient had begun to take lansoprazole again 3 mo ahead of the recent diarrhea. Withdrawal of lansoprazole promptly resolved the diarrhea. Endoscopic and histological abnormalities were also completely resolved, similar to the first episode. Retrospectively, the date of commencement of sulfasalazine and discontinuation of lansoprazole in the first episode was found to be the same. We conclude that this patient had lansoprazole-associated collagenous colitis.

Effect of He-Ne Laser on the Expressions of EGF and EGFR in Gastric Mucosa of Chronic Atrophic Gastritis

To investigate the histological change and the expressions of epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) in atrophic gastric mucosa in rats so as to appraise the effect of these regulators on the formation of atrophic gastritis, to study the expressions of EGF and EGFR in rats with chronic atrophic gastritis (CAG) after the irradiation of He-Ne laser, and to investigate the relations of He-Ne laser and precancerous lesion or apoptosis. The rats were divided into normal group, model group and laser group. The models of CAG rats were established with enema which was the mixed liquor consisted of sodium salicylate and alcohol, combined with irregular fasting and compulsive sporting as pathogenic factors. He-Ne laser(3.36 J/cm2 ) was used to irradiate CAG rats, once a day for 7 min, 20 days as a course of treatment; the expressions of EGF and EGFR were detected with immunohistochemical method. During the process of antral atrophy, the expressions of EGF and EGFR increased, they were higher in model group than those in normal group (P<0.05). After the irradiation of He-Ne laser, the expressions of EGF and EGFR were obviously lower than those in model group (P<0.05). We draw the conclusion as follows: gastric mucosa of model rat is in a hyper-proliferation status, with high protein expressions of apoptosis suppressor EGF and EGFR. CAG has some correlation with the imbalance between cell proliferation and apoptosis. He-Ne laser (3.36 J/cm2 ) can reduce the expressions of EGF and EGFR, which is an effective physiostimulator to stimulate the gastric mucosa of rat. The appropriate secretions of EGF and EGFR are propitious to the repair and regeneration for the gastric mucosa tissues, thus preventing CAG to canceration.