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991.
992.
It is of interest to evaluate the prevalence of systemic disorders in patients undergoing minor oral surgeries at a dental hospital. This will help to take necessary precautions prior to oral surgeries. We used the digital case records of 1288 patients who underwent minor oral surgeries in a hospital. Demographic details and systemic diseases of the patients were recorded from digital case records. Data shows that 103 patients (7.9%) of the total number of patients undergoing minor oral surgeries had systemic diseases with 3.8% of patients diagnosed with diabetes. Statistically significant associations were found between type of minor oral surgery and the type of systemic disease (p<0.001); age of patients and type of minor oral surgery (p<0.001); age and type of systemic diseases (p<0.001) and gender of patient and type of minor oral surgery (p = 0.005). Thus, data shows the prevalence of systemic diseases in patients undergoing minor oral surgeries was 7.9%.  相似文献   
993.
BackgroundDiabetes may be associated with decreased prostate cancer (PCa) risk. However, previous studies have not always accounted for time since diabetes diagnosis or antidiabetic drug use. Futhermore, the role of metabolic syndrome (MetS) in PCa risk is still debated. We investigated the role of diabetes and MetS in PCa risk based on data from the Epidemiological study of PCa (EPICAP).MethodsEPICAP is a population-based case-control study that included 819 incident PCa cases in 2012–2013 and 879 controls frequency matched by age. MetS was characterized according to National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III). Logistic regression models adjusted for age, family history of PCa and ethnicity, were used to assess odds ratios (ORs) and their 95%conficence intervals (CIs) for the associations between diabetes, MetS and PCa risk.ResultsWhereas we did not observed an association between diabetes and PCa, a decreased risk of PCa has been highlighted with an increasing treated diabetes duration (p-trend=0.008). No association has been observed between MetS, the number of MetS criteria and the risk of PCa. However, we suggested that NSAIDs use could modify the association between MetS and PCa risk.ConclusionOur results suggest an inverse association between the duration of diabetes and PCa risk. The role of metabolic factors, such as MetS and its components, in PCa risk remains unclear and requires further investigations.  相似文献   
994.
目的建立检测人体粪便提取液对肠上皮细胞毒性的方法。方法以Caco-2细胞为体外模型,应用建立好的毒性检测方法:用MTT法(四甲基偶氮唑盐微量酶反应比色法)检测细胞毒性,用单细胞凝胶电泳技术检测遗传毒性,对糖尿患者和健康人的粪便提取液进行分析。结果糖尿病患者粪便提取液的细胞毒性显著高于健康人(n=30,P〈0.05);其遗传毒性显著高于阴性对照PBS(P〈0.05),与健康人相比有升高趋势,但差异无统计学意义。结论粪便提取液的毒性检测方法可以简便、有效地检测人体粪便中毒性物质对肠上皮细胞的影响,因此可作为评价肠道菌群状态的方法。  相似文献   
995.
Belamcanda chinensis (Iridaceae) belongs to the family of iridaceae and its rhizoma has been widely used for the treatment of throat ailment. Here we report a new pharmacological activity of B. chinensis leaf extract (BCL), that is, the hypoglycemic effect in normal and STZ-induced diabetic rats. Animals either healthy or STZ-induced diabetic show significantly lowered fasting blood glucose levels after treatment with BCL. The serum insulin concentration in normal rats is also enhanced. Additionally, the increase in blood glucose levels after administration of various carbohydrates in normal rats is significantly decreased and the oral glucose tolerance (OGTT) of STZ-induced diabetic rats is largely improved by BCL treatment. However, co-administration of BCL with Nifedipine, a Ca2+ ion channel blocker, or Nicorandil, an ATP-sensitive K+ ion channel opener thoroughly abolishes the hypoglycemic effect of BCL. HPLC analysis and compound identification showed that several isoflavone glycosides with antidiabetic activities were contained in BCL while pharmacological experiment showed that the polysaccharide fraction of BCL had no significant hypoglycemic effect on normal rats. Therefore, the isoflavone glycosides but not polysaccharides might be the active fraction of BCL in diabetes treatment.  相似文献   
996.
PCK1 and PCK2 as candidate diabetes and obesity genes   总被引:1,自引:0,他引:1  
The PCK1 gene (Pck1 in rodents) encodes the cytosolic isozyme of phosphoenolpyruvate carboxykinase (PEPCK-C), which is well-known for its function as a gluconeogenic enzyme in the liver and kidney. Mouse studies involving whole body and tissue-specific Pck1 knockouts as well as tissue-specific over-expression of PEPCK-C have resulted in type 2 diabetes as well as several surprising phenotypes including obesity, lipodystrophy, fatty liver, and death. These phenotypes arise from perturbations not only in gluconeogenesis but in two additional metabolic functions of PEPCK-C: (1) cataplerosis which maintains metabolic flux through the Krebs cycle by removing excess oxaloacetate, and (2) glyceroneogenesis which produces glycerol-3-phosphate as a precursor for fatty acid esterification into triglycerides. PEPCK-C catalyzes the conversion of oxaloacetate + GTP to phosphoenolpyruvate + GDP + CO2. It is in part the tissue-specificity of this simple reaction that results in the variety of phenotypes listed above. Briefly: (1) A 7-fold over-expression of PEPCK-C in the livers of mice causes excessive glucose production. (2) Mice with a whole-body knockout of Pck1 die within 2–3 days of birth, not from hypoglycemia, but probably because the Krebs cycle slows to approximately 10% of normal in the absence of cataplerosis. (3) Mice with a liver-specific knockout have an inability to remove oxaloacetate from the Krebs cycle, which leads to a fatty liver following a fast. (4) An adipose-specific knockout of Pck1 results in a fraction of the mice developing lipodystrophy due to lost glyceroneogenesis and a consequent decrease in fatty acid re-esterification. (5) Finally, disregulated over-expression of PEPCK-C in adipose tissue increases fatty acid re-esterification leading to obesity. These varied experimental phenotypes in mice have led us to postulate that abnormal production of PEPCK isozymes encoded by two PEPCK genes, PCK1 and PCK2, in humans could have similar consequences (Beale, E. G. et al. (2004). Trends in Endocrinology and Metabolism, 15, 129–135). The purpose of this review is to further explore these possibilities.  相似文献   
997.
目的:研究地黄对于糖尿病模型大鼠血糖以及微炎症状态的作用。方法:采用高糖高脂饲料喂养加腹腔注射链尿佐菌素(STZ)破坏胰岛细胞的方法构建糖尿病大鼠模型。将大鼠分为空白对照组、糖尿病模型组与药物治疗组。空白对照组以及糖尿病模型组给予蒸馏水,用药组分别给予不同剂量丹参、地黄、格列本脲灌胃治疗,每日一次,连续60日。应用血糖仪动态监测血糖,ELISA法检测血清中超敏C反应蛋白(Hs-CRP)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)浓度变化情况,以观察地黄对血糖及糖尿病微炎症状态的改善效果。结果:造模成功后,糖尿病大鼠血糖明显升高(P0.05),血液中炎症因子Hs-CRP、IL-6、TNF-α含量升高,与空白对照组相比,差异显著(P0.05)。地黄治疗后血糖明显降低(P0.05),血液中炎症因子Hs-CRP、IL-6、TNF-α含量均显著减低,差异均有统计学意义(P0.05)。结论:地黄可以明显降低糖尿病大鼠的血糖水平,显著改善糖尿病大鼠的微炎症状态。  相似文献   
998.
目的:比较高通量与低通量血液透析对糖尿病肾病透析患者氧化应激、细胞免疫功能和微炎症状态的影响。方法:选择2011年1月~2017年1月在我院进行诊治的糖尿病肾病透析患者60例,随机分为对照组与观察组,每组各30例。对照组采用低通量血液透析治疗,观察组采用高通量血液透析治疗,两组每次血液透析的时间、透析液流速以及透析液成分均完全相同。比较两组血液透析前后的血清丙二醛、过氧化物歧化酶以及谷胱甘肽过氧化物酶等氧化应激指标,CD~+4、CD~+3、CD~+8以及CD~+4/CD~+8等细胞免疫功能指标,高敏C反应蛋白、白介素-6以及肿瘤坏死因子等微炎症状态指标。结果:治疗后,观察组血清过氧化物歧化酶、谷胱甘肽过氧化物酶、高敏C反应蛋白、白介素-6以及肿瘤坏死因子水平均明显低于对照组(P0.05),血清丙二醛、CD~+4、CD~+3以及CD~+4/CD~+8水平均明显高于对照组(P0.05)。结论:糖尿病肾病血液透析患者体内普遍存在不同程度的微炎症状态以及氧化应激状态,长期采用低通量血液透析会加重体内的炎性反应和氧化应激水平,而高通量血液透析能缓解炎性反应和氧化应激,并且有效改善患者的细胞免疫功能。  相似文献   
999.
Group X secretory phospholipase A2 (GX sPLA2) potently hydrolyzes membrane phospholipids to release arachidonic acid (AA). While AA is an activator of glucose-stimulated insulin secretion (GSIS), its metabolite prostaglandin E2 (PGE2) is a known inhibitor. In this study, we determined that GX sPLA2 is expressed in insulin-producing cells of mouse pancreatic islets and investigated its role in beta cell function. GSIS was measured in vivo in wild-type (WT) and GX sPLA2-deficient (GX KO) mice and ex vivo using pancreatic islets isolated from WT and GX KO mice. GSIS was also assessed in vitro using mouse MIN6 pancreatic beta cells with or without GX sPLA2 overexpression or exogenous addition. GSIS was significantly higher in islets isolated from GX KO mice compared with islets from WT mice. Conversely, GSIS was lower in MIN6 cells overexpressing GX sPLA2 (MIN6-GX) compared with control (MIN6-C) cells. PGE2 production was significantly higher in MIN6-GX cells compared with MIN6-C cells and this was associated with significantly reduced cellular cAMP. The effect of GX sPLA2 on GSIS was abolished when cells were treated with NS398 (a COX-2 inhibitor) or L-798,106 (a PGE2-EP3 receptor antagonist). Consistent with enhanced beta cell function, GX KO mice showed significantly increased plasma insulin levels following glucose challenge and were protected from age-related reductions in GSIS and glucose tolerance compared with WT mice. We conclude that GX sPLA2 plays a previously unrecognized role in negatively regulating pancreatic insulin secretion by augmenting COX-2-dependent PGE2 production.  相似文献   
1000.
IntroductionHearing loss due to noise is considered within the prevention plans of the most common occupational diseases. In addition to evaluation of working conditions, other personal factors increasing the risk of hypoacusis, such as diabetes, should be taken into account.ObjectivesTo explore hearing loss in the workplace and its relationship to impaired fasting baseline blood glucose levels.MethodsAn observational, cross-sectional study enrolling 1636 workers from service companies was conducted. Full audiometric evaluation was performed at different frequencies: high frequency (HF), early loss index (ELI), speech average loss (SAL), and monaural and binaural loss. Results were categorized by baseline blood glucose levels: G1 (< 100 mg/dl), G2 (100-125 mg/dl), and G3 (> 125 mg/dl).ResultsBased on both HF and ELI, 11% of workers had clear indication of deafness. Women with G3 levels showed significant differences in the results of HF and ELI indexes as compared to the G1 group (P = .038 and .046, respectively). A positive association was found between hearing loss and G3 blood glucose levels in HF (OR: .338; p = .002), ELI (OR: .407; p = .007), and the monaural test in the left ear (OR: 4.77 × 10-5; p = .006).ConclusionsDespite the methodological limitations of this study, there is evidence for an increased risk of high frequency hearing loss in workers with high baseline blood glucose levels.  相似文献   
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