Objective:To investigate the diagnostic value of the promoter methylation of plasma RNF180 gene and its protein ex-pression for the detection of gastric cancer. Methods:Methylation-specific polymerase-chain reaction (MSP) and enzyme-linked immu-no-sorbent assay (ELISA) were performed to detect DNA methylation and protein expression of the RNF180 gene, respectively. The correlations of DNA methylation and protein expression of the RNF180 gene with the clinico-pathological parameters of gastric carcino-ma were then separately analyzed. Results:MSP showed that the methylation rates of the RNF180 gene were 62.75%and 21.88%in the plasma of patients with gastric carcinoma and healthy volunteers, respectively;this result indicated that the two groups significantly differed (P<0.01). The methylation of the RNF180 gene was associated with tumor size, clinical stage, tumor differentiation, lymph node metastasis, and distant metastasis (P<0.05). ELISA results showed that the protein expression of the RNF180 gene [(23.22 ± 1.36)μg/mL] was significantly lower (P<0.01) in the plasma of patients with gastric carcinoma than in the plasma of healthy volunteers [(34.25 ± 2.44)μg/mL]. However, the protein expression of the RNF180 gene was not associated with clinicopathological parameters (P>0.05). Conclusion:The RNF180 gene is expressed at a hypermethylation rate, and the corresponding protein expression level is de-creased in the plasma of individuals with gastric carcinoma. Therefore, RNF180 gene methylation in plasma could be applied to detect microinvasion for the clinical diagnosis of gastric cancer.

Objective To explore the clinical efficacy of glargine combined with metformin for old patients with type 2 diabetes mellitus (T2DM)and its effect on the glucose,high-sensitivity C-reactive protein (hs-CRP)and malondialdehyde (MDA)levels.Methods Seventy-two old pa-tients with T2DM were randomly divided into treatment group and control group,36 cases in each group.The control group was subcutaneously injected glargine,while the treatment group was added metformin based on this.Both courses of treatment were 6 weeks.The clinical efficacy after treatment,changes of glucose-related indexes,hs-CRP and MDA levels before and after treatment were compared,and the incidence of adverse reactions was observed.Results The overall response rate of treatment group was obviously higher than in control group,with statistical significance(P <0.05).After treatment,the levels of fasting blood glucose (FBG),2 h postprandial glucose (2hPG)and glycosylated hemoglobin (HbA1c)in both groups went down significantly by compari-son to treatment before(P <0.01),in which the decreased range in treatment group was more sig-nificant(P <0.05 or P <0.01).Besides,hs-CRP and MDA levels in two groups after treatment were notably decreased(P <0.05 or P <0.01),and hs-CRP level in treatment group was markedly lower than in control group(P <0.05).Conclusion Glargine combined with metformin can effec-tively decrease the glucose level in old patients with T2DM,and alleviate the degree of oxidative stress,with significant efficacy.

Objective To explore the clinical efficacy of glargine combined with metformin for old patients with type 2 diabetes mellitus (T2DM)and its effect on the glucose,high-sensitivity C-reactive protein (hs-CRP)and malondialdehyde (MDA)levels.Methods Seventy-two old pa-tients with T2DM were randomly divided into treatment group and control group,36 cases in each group.The control group was subcutaneously injected glargine,while the treatment group was added metformin based on this.Both courses of treatment were 6 weeks.The clinical efficacy after treatment,changes of glucose-related indexes,hs-CRP and MDA levels before and after treatment were compared,and the incidence of adverse reactions was observed.Results The overall response rate of treatment group was obviously higher than in control group,with statistical significance(P <0.05).After treatment,the levels of fasting blood glucose (FBG),2 h postprandial glucose (2hPG)and glycosylated hemoglobin (HbA1c)in both groups went down significantly by compari-son to treatment before(P <0.01),in which the decreased range in treatment group was more sig-nificant(P <0.05 or P <0.01).Besides,hs-CRP and MDA levels in two groups after treatment were notably decreased(P <0.05 or P <0.01),and hs-CRP level in treatment group was markedly lower than in control group(P <0.05).Conclusion Glargine combined with metformin can effec-tively decrease the glucose level in old patients with T2DM,and alleviate the degree of oxidative stress,with significant efficacy.

Objective:To explore the neuroprotective effects and mechanisms of memantine on sepsis-associated encephalopathy (SAE) model mice.Methods:Totally 90 male C57BL/6J mice aged 8-12 weeks were randomly divided into 3 groups (with 30 mice in each group) : sham group, model group and memantine group. The SAE mouse model was established by cecum ligation and puncture while mouse in sham group received open and closed abdomen only. The mice in the memantine group were irrigation with memantine (15 mg · kg -1· d -1) 3 hours before surgery and 7 consecutive days after modeling. The mice in the model group and sham group were irrigation with an equal volume of 0.9% sodium chloride solution. The 7-day survival rate was observed, neurobehavioral and cognitive function scores of each group of mice after modeling were assessed.Blood-brain barrier permeability was measured by detecting the content of Evans blue. Immunofluorescence staining was used to detect the expression of astrocytes. Enzyme linked immunosorbent assay was conducted to detect cellular inflammatory factors and the glutamic acid content detection kit was used to detect the expression of glutamic acid. All data were analyzed by Graphpad Prism 8.3.0 software, survival rate was analyzed using Kaplan-Meier survival curve.Multigroup comparisons were conducted by one-way ANOVA or Kruskal-Wallis test. Results:(1) There was a statistically significant difference in the 7-day survival rate among the three groups of mice after modeling ( F=24.11, P<0.01), and the 7-day survival rate of the memantine group was higher than that of the model group (57% (17/30), 27% (8/30), P<0.01). (2)The behavioral results showed that after 7 days of modeling, there were statistically significant differences in the total distance of the open field test, central area stay time, four corner area stay time, neurobehavioral scores, pole climbing test, and preference index for new object recognition test among the three groups of mice ( F/ χ2=17.67, 17.30, 9.39, 14.06, 10.36, 14.81, all P<0.05).The neurobehavioral score, pole climbing test score, preference index for new object recognition test, total distance of open field test, and central area stay time of the model group were all lower than those of the sham group (all P<0.05), while four corner area stay time of the model group was higher than that of the sham group ( P<0.05).The total distance of open field test (1 564.07(1 363.24, 1 988.19) cm, 913.91 (574.32, 1 096.23) cm), central area stay time (5.21 (4.91, 8.76) s, 1.09 (0.25, 1.64) s), neurobehavioral scores (9.75±0.50, 8.25±0.50), pole climbing test scores (5.67±0.52, 4.56±0.53), and preference index for new object recognition test (56.50±10.59, 26.84±2.91) of the memantine group were all higher than those of the model group (all P<0.05). The four corner area stay time was lower than that of the model group ((480.30±50.64) s, (529.80±36.20) s, P<0.05).(3)The comparison of molecular indicators showed that there were statistically significant differences in the content of Evans blue in the brain, the number of astrocytes in the hippocampus and cerebral cortex, pro-inflammatory cytokines (TNF-α、IL-1β、IL-6), anti-inflammatory cytokines (IL-10), and glutamic acid among the three groups of mice ( F/ χ2=8.84, 6.43, 28.46, 23.63, 12.23, 16.04, 69.22, 6.65, all P<0.05).The content of Evans blue, the number of astrocytes in the hippocampus and cerebral cortex, the expression of TNF-α、IL-1β、IL-6, and glutamate in the model group were all lower than those in the sham group(all P<0.05). The levels of IL-10 in the model group was lower than that in the sham group ( P<0.05).The content of Evans blue ((5.67±1.38)μg/g, (11.08±2.79)μg/g), the number of astrocytes in the hippocampus (16.50 (13.75, 22.25)/μm 2), 80.00 (73.50, 83.50)/μm 2) and the cerebral cortex (40.00 (29.00, 48.00)/μm 2, 81.50 (72.25, 89.00)/μm 2) in the memantine group were lower than those in the model group (all P<0.05).The pro-inflammatory factor TNF-α, IL-1β, IL-6 and glutamic acid expression in the memantine group were lower than those in the model group (all P<0.05), and the anti-inflammatory cytokine IL-10 was higher than that in the model group ( P<0.05). Conclusions:Memantine can improve the neurobehaviors and cognitive functions of SAE mice through improving the integrity of the damaged blood-brain barrier, alleviating inflammation in the brain, as well as reducing glutamate levels in the brain.

BACKGROUNDCopious evidence from epidemiological and laboratory studies has revealed that sleep status is associated with glucose intolerance, insulin resistance, thus increasing the risk of developing type 2 diabetes. The aim of this study was to reveal the interaction of sleep quality and sleep quantity on glycemic control in patients with type 2 diabetes mellitus.

METHODSFrom May 2013 to May 2014, a total of 551 type 2 diabetes patients in Tianjin Metabolic Diseases Hospital were enrolled. Blood samples were taken to measure glycosylated hemoglobin (HbA1c), and all the patients completed the Chinese version of the Pittsburgh Sleep Quality Index (PSQI) questionnaire to evaluate their sleep status. "Good sleep quality" was defined as PQSI <5, "average sleep quality" was defined as PQSI 6-8, and "poor sleep quality" was defined as PQSI >8. Poor glycemic control was defined as HbA1c ≥7%. Sleep quantity was categorized as <6, 6-8, and >8 hours/night. Short sleep time was defined as sleep duration <6 hours/night.

RESULTSIn the poor glycemic control group, the rate of patients who had insufficient sleep was much higher than that in the other group (χ(2) = 11.16, P = 0.037). The rate of poor sleep quality in poor glycemic control group was much greater than that in the average control group (χ(2) = 9.79, P = 0.007). After adjusted by gender, age, body mass index, and disease duration, the adjusted PSQI score's OR was 1.048 (95% CI 1.007-1.092, P = 0.023) for HbA1c level. The sleep duration's OR was 0.464 (95% CI 0.236-0.912, P = 0.026) for HbA1c level. One-way analysis of variance showed that the poor sleep quality group had the highest homeostasis model assessment-insulin resistance (P < 0.01).

CONCLUSIONSInadequate sleep, in both quality and quantity, should be regarded as a plausible risk factor for glycemic control in type 2 diabetes. Poor sleep might bring much more serious insulin resistance and could be the reason for bad glycemic control. A good night's sleep should be seen as a critical health component tool in the prevention and treatment of type 2 diabetes. It is important for clinicians to target the root causes of short sleep duration and/or poor sleep quality.

Adult ; Aged ; Aged, 80 and over ; Blood Glucose ; metabolism ; physiology ; Cross-Sectional Studies ; Diabetes Mellitus, Type 2 ; blood ; physiopathology ; Female ; Humans ; Male ; Middle Aged ; Sleep ; physiology ; Young Adult