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Objective To investigate the diagnostic value of serum homocysteine in the diagnosis of colon cancer.Methods The performance rate method was used to detect the level of serum homocysteine(Hcy) in colon cancer group(50 cases) who were treated in Beijing Tiantan Hospital Affiliated to Capital Medical University from March 2011 to June 2016 and control group(50 cases).The expression of independent samples t test was used to analysis of the difference of the Hcy levels between the two groups.The ROC curve was used to evaluate the value of Hcy in diagnosis of colon cancer.Results The serum Hcy level in colon cancer group was (18.6±8.9) μmol/L,in healthy control group was (10.7±4.3) μmol/L,colon cancer group serum Hcy levels were significantly higher than those of healthy control group,there was significant difference(t=5.627,P<0.01).AUC of ROC curve was 0.775,cut-off value of 18.5 μmol/L,sensitivity was 0.50,specificity was 0.94,95%CI was 0.682-0.868(P<0.01).Conclusion Serum Hcy can be used as a reference index of the diagnosis of colon cancer.
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Objective To investigate the clinical significance of serum pepsinogen (PG) in gastric cancer screening. Methods The clinical data of 930 patients underwent colonoscopy were retrospectively analyzed. Among them, non chronic atrophic gastritis was in 550 cases (chronic atrophic gastritis group), chronic atrophic gastritis in 300 cases (chronic atrophic gastritis group), gastric cancer in 80 cases (gastric cancer group). The patients in chronic atrophic gastritis group were divided into mild chronic atrophic gastritis subgroup (100 cases), moderate chronic atrophic gastritis subgroup (120 cases) and severe chronic atrophic gastritis subgroup (80 cases) according to the severity of the atrophy. The levels of serum PGⅠand PGⅡwere detected by enzyme linked immunosorbent assay (ELISA) method, and the ratio of PGⅠand PGⅡ(PGR) was calculated. Results There was no statistical difference in PGⅡ among the 3 groups (F = 1.226, P>0.05). The PG Ⅰand PGR in gastric cancer group were significantly lower than those in chronic atrophic gastritis and non chronic atrophic gastritis:(70.41 ± 39.42)μg/L vs. (83.10 ± 30.08) and (165.5 ± 41.40)μg/L, 3.76 ± 2.03 vs. 5.08 ± 1.82 and 6.84 ± 1.88, those in chronic atrophic gastritis were significantly lower than those in non chronic atrophic gastritis group, there were statistical differences (P0.05), and there was no statistical difference between mild chronic atrophic gastritis subgroup and moderate chronic atrophic gastritis subgroup (P>0.05). The receiver operating characteristic (ROC) curve was used, the optimal critical value of PG Ⅰ was 74.8μg/L, the area under curve (AUC) was 0.842, the sensitivity was 90%, specificity was 75%;the optimal critical value of PGR was 4.46, AUC was 0.837, the sensitivity was 75%, specificity was 82%;the AUC of combined detection of PG Ⅰ and PGR was 0.906, the sensitivity was 88%, specificity was 85%. Conclusions Detection of PG Ⅰ combined with PGR can be used as gastric cancer screening, the recommended level of PGⅠ≤74.80μg/L and PGR≤4.46.
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Objective: To observe the effect of oxidative stress on intestinal mucosal barrier dysfunction following traumatic brain injury (TBI). Methods: Seventy-two male Wistar rats were randomly divided into three groups, group B and group C served as TBI models, group A was designated as the normal controlgroup(shame operation). In group C rats were treated with dimethyl sulfoxide(DMSO) prior to TBI, while rats in group A and B were treated with equivalent normal saline. During the experiment period, the morphological changes of intestinal mucosa were observed, and the intestinal mucosal permeability was detected by measuring the level of endotoxin, diamine oxidase(DAO). Superoxide dismutase(SOD), malondiadehycle (MDA), myeloperoxidase(MPO) and xanthine oxidase(XOD) activities were also detected. Results: During the observed period, the intestinal mucosal barrier function was damaged and the intestinal mucosal permeability increased. The content of endotoxin in serum significantly increased(P < 0.05). As early as 3 h after TBI, the DAO activity in the serum began to increase obviously. At 24 hafter TBI it increased to the highest level(P < 0.05).In group TBI the activity of SOD in intestinal mucosal decreased significantly(P < 0.01); however the levels of MDA and the activity of MPO increased significantly (P < 0.01), the activity of XOD increased significantly as well, and then decreased after 6 h. When pr-treatment with DMSO, intestinal mucosal damage was improved, the content of endotoxin in serum was reduced (P < 0.05), and the increased DAO activity in the serum were inhibited (P < 0.05). When compared with group TBI, there was an inhibition in the decreased activity of SOD and the increased level of MDA in group DMSO (P < 0.05), but they were still higher than that of control group(P < 0.05). There were no significant differences in the activity of XOD and MPO between group DMSO and group TBI. Conclusion: The structure and function of intestinal mucosal barrier were damaged following TBI. Oxidative stress played an important role in the intestinal mucosal barrier dysfunction following TBI. Both XOD and activated polymorphonuclear neutrophils(PMN) were the major source of oxygen free radicals.
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<p><b>OBJECTIVE</b>To observe sulfhydryl compound variation in the injury of pancreatic cells and the effects of external sulfhydryl compounds on cytoprotection.</p><p><b>METHODS</b>Male Wistar mice were divided randomly into three groups: groups A and B served as animal models (retrograde duct infusion with 5% sodium taurocholate), in group A, 45 animals were treated with normal saline therapy, in group B, 45 animals were treated with Tiopronin therapy; and group C, 15 animals, were designated as normal control. Animals were killed at 2, 4, 6, 12 and 24 h, and pancreatic tissue was analyzed for total sulfhydryl (TSH), nonprotein sulfhydryl (NPSH) and malondialdehyde (MDA). Histopathology, serum amylase (Sam) and C reactive protein (CRP) were assessed as well.</p><p><b>RESULTS</b>Levels of Sam and CRP increased in both group A and group B, with corresponding pathological changes of acute nerotic pancreatitis (ANP). Levels of TSH, NPSH and protein sulfhydryl (PSH) in group A decreased markedly during pancreatitis (P < 0.01), but MDA increased significantly (P < 0.01). The depletion of NPSH in group B was markedly ameliorated at 4 h or 6 h, when Tiopronin was prophylactically administered (P < 0.05), after which the level of MDA showed very little increase when compared to group A (P < 0.01). Histopathological damage was attenuated to a certain extent, in regards to serum amylase and CRP.</p><p><b>CONCLUSIONS</b>All sulfhydryl compounds decreased significantly during ANP; external sulfhydryl compound could protect the pancreatic cells most likely as a type of scavengers of oxygen free radicals, which are critically involved in the pathophysiology of ANP. Sulfhydryl plays an important role in the action of pancreatic cytoprotection.</p>
Subject(s)
Animals , Male , Rats , Acute Disease , Amylases , Blood , C-Reactive Protein , Cytoprotection , Lipid Peroxidation , Necrosis , Pancreatitis , Drug Therapy , Pathology , Rats, Wistar , Sulfhydryl Compounds , Physiology , Tiopronin , Therapeutic UsesABSTRACT
Objective To study the role of bile reflux in the pathogenesis of stress ulcer after acute brain trauma in rat. Methods The animal model was reproduced by Allen's method with modification. The bile acid concentration in the stomach and blood, the pH value of the gastsic content, and ulcer index (UI) were assayed 1, 3, 6, 24 hour after the stress, and they were compared with that of sham injury group. Results In stress group, compared with sham injury group, the amount of bile acid in the stomach was notably increased( P