Objective To determine the changes in the prevalence of type 2 diabetes mellitus and prediabetes in residents aged over 20 years in Shandong coastal areas during years 2004-2014. Methods A random stratified cluster sampling was conducted, and 3 944 inhabitants were investigated in Qingdao, Yantai, Weihai, and Rizhao regions. Results (1)The standardized rate of diabetes mellitus prevalence was 10.36% in 2014, increased by 2.38% as compared with 2004 and 0.85% as compared with 2009 (P<0.05). There were 341 newly diagnosed diabetes mellitus patients, accounting for 57.4% of the diabetes mellitus patients, increased by 6.09% as compared with 2004 and decreased by 4.11% as compared with 2009 (P<0.05). The standardized rate of prediabetes was 12.47% in 2014, increased by 2.63% as compared with 2004 and 0.61% as compared with 2009 (P<0.05). (2) The prevalence of diabetes mellitus and impaired glucose regulation in individuals aged under 50 years in 2014 was significantly higher than that in 2004, but lower than that in 2009 (P<0.05). (3) Compared with 2004 and 2009, the levels of diastolic blood pressure, total cholesterol, low density lipoprotein-cholesterol (LDL-C), and high density lipoprotein-cholesterol in subjects with prediabetes and diabetes mellitus increased significantly in 2014 (all P<0.05). The levels of serum uric acid in subjects with prediabetes and diabetes mellitus decreased significantly in 2014 (P<0.05). (4) The logistic regression analysis showed that the age, body mass index, waist-hip ratio, triglyceride, LDL-C, systolic blood pressure, and diabetic family history were the risk factors for abnormal glucose regulation, while total cholesterol was the protective factor. Conclusions The prevalence of diabetes mellitus and prediabetes increased during 10 years (2004-2014), but the growth rate dropped precipitously during last five years as compared with the first five years. The age of diabetes mellitus onset is getting older in residents of Shandong coastal area, especially in females. Aging, overweight, hypertension, lipid disorders, and diabetic family history were the risk factors of diabetes mellitus.

BACKGROUND: Hyperuricemia (HUA), serving as a component of metabolic syndromes (MS), has a major regulatory role in inflammatory responses. However, the correlation between G-308A tumor necrosis factor-α (TNF-α) and MS is still controversial.OBJECTIVE: To study the correlation among G-308A TNF-α genotype distribution, TNF-α mRNA expression and C-reactive protein (CRP) in patients with HUA.DESrGN: Patients with HUA were selected as the subjects, while normal peoplewere taken as the controls.SETTING: Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology.PARTICIPANTS: Subjects were selected from 5 003 people, including 188 patients with HUA and 51 healthy people.Patients with HUA included 40 patients with simple HUA, 42 patients with HUA and dyslipidemia, 80 patients with HUA and dyslipidemia and hypertension, and 26 patients with gout (administration of allopurinol was stopped at one week before the experiment).METHODS: TNF-α gene promoter G-308A genotype was determined by using PCR application followed by Nco/digestion.TNF-α mRNA expression was studied by RT-PCR with semi-quantitative analysis. Antibody sandwich method and enzyme linked immunosorbent assay (ELISA) were adopted to determine the CRP concentration. And the serum uric acid was measured by uricase method, while the insulin resistance index (IRI) was evaluated with homeostasis model.MArN OUTCOME MEASURES: ① Hardy-Weinberg equilibrium test of genotypic frequency. ② Changes in distribution of G-308A TNF-α genotypes and TNF-α mRNA expression in patients with HUA. ③ Changes in TNF-α mRNA expression and other parameters in G-308A TNF-α AA+GA and GG groups. ④ Multiple stepwise regression analysis.RESULTS: A total of 188 patients and 51 normal people were involved in the analysis of results. ① G-308A TNF-α genotypes distribution in 239 enrolled subjects accorded with Hardy-Weinberg equilibrium. ② AA+GA was compared with GG due to lower frequency of AA in population. The results revealed the HUA with dyslipidemia and hypertension group displayed a greater prevalence in G-308A TNF-α AA+GA genotype (30%) than that in the control group (12%) (P ＜ 0.05),while there were no significant differences among other groups. ③ TNF-α mRNA expression and CRP concentration were the highest in the gout group, and HUA accompanied by dyslipidemia and hypertension group listed the second,and then was the HUA and dyslipidemia group, while simple HUA group listed the last, all of which were higher than those in the normal control group (P ＜ 0.05-0.01). TNF-α mRNA expression in HUA accompanied by dyslipidemia and hypertension group, gout group was higher than that in the normal control group (P ＜ 0.05-0.01). The WHR, SBP, DBP,serum uric acid, triglycerides, TNF-α mRNA expression and CRP concentration in AA+GA group were remarkably higher than those in the GG group (P ＜ 0.05-0.01). ④ After adjustment of age, gender, systolic pressure, diastolic pressure,fasting blood glucose, and multiple variable linear stepwise regression showed that triglycerides, uric acid, TNF-α 308 A carrier were related with quantityof TNF-α mRNA expression. Meanwhile, the uric acid concentration, WHR and the quantity expression of TNF-α were significantly in positive association with CRP concentration.CONCLUSTON:The genotype of TNF-α 308 A carriers is associated with TNF-α expression and plasma CRP levels in HUA patients.

Objective:To study the effect of insulin therapy on glucose concentration in saliva in patients with diabetes mellitus(DM), and to study the relationship between blood glucose level and salivary glucose level.Methods: Glucose concentration in blood and in unstimulated mixed saliva was measured with Beckman SYNCHRON CX7 system in 40 DM patients before and after insulin therapy.Results:The average value(mmol/L) of salivary glucose concentration before and after insulin therapy was 2.081?0.287 and 1.571? 0.193 respectively (P

Objective To explore the effects of atorvastatin and valsartan on high glucose-induced human umbilical vein endothelial cells (HUVECs) injury.Methods Cultured HUVECs were divided and assigned to 9 groups:normal control group,mannitol control group,high glucose group,low dose atorvastatin group (0.1 μ mol/L),medium dose atorvastatin group (1 μmol/L),high dose atorvastatin group (10 μ mol/L),low dose valsartan group (0.1 μmol/L),medium dose valsartan group (1 μmol/L),and high dose valsartan group (10 μmol/L).H UVECs were pretreated with or without 30 mmol/L glucose plus various concentrations of atorvastatin and valsartan (0.1,1,10 μmol/L) for 16 hours and then incubated with 5.5 mmol/L glucose for 6 days.The levels of vascular cell adhesion molecule 1 (VCAM-1),monocyte chemotactic protein 1 (MCP-1),and plasminogen activator inhibitor 1 (PAI-1) in the culture supernatant were measured by enzyme-linked immunosorbent assay.Results Compared with normal glucose group,hyperglycemia memory increased the levels of VCAM-1,MCP-1,and PAI-1 (all P＜0.05),which were still maintained at high levels even after withdrawal of high glucose.Atorvastatin and valsartan treatment decreased the levels of VCAM-1,MCP-1,and PAI-1 (all P＜0.05).Conclusion Atorvastatin and valsartan may lower the secretion of VCAM-1,MCP-1,and PAI-1,and prevent high glucose memory-induced injury to endothelial cell.

OBJECTIVE:To observe the efficacy of urapidil hydrochloride in control of blood pressure at the perioperative stage of hemorrhagic apoplexy.METHODS:All80patients with hypertensive cerebral hemorrhage were managed with seda?tive,dehydration,hemostasis,and cerebral nerve nourishment,then when the blood pressure still remained high,or the blood pressure was hard to control after the intubation,urapidi hydrochloride was administered by intravenous infusion at the dose of250mg added with250ml of5%glucose infusion,the infusion drip was set at constant speed,with2mg/min as its starting speed,while at the same time the blood pressure and heart rate were monitored and infusion speed was adjusted every10to15min,after the target blood pressure21.2/13.2kPa was obtained,the infusion speed was kept at0.1～0.4mg/min.The blood pressure and heart rate were observed separately before the administration of urapidil hydrochloride and2,5,10,15,20and30min after the administration as well as after the operation.RESULTS:5min after the administration,blood pres?sure decreased remarkably but not to the extent to cause low blood pressure,and the heart rate increased slightly at the same time,generally not over10beats each minute.CONCLUSION:Urapidil hydrochloride decreases blood pressure steadily and safely at a manageable dosage.It can be used to control blood pressure during hemostasis and clearance of hematoma,which reduces the possibility of rehemorrhagia caused by high blood pressure during and after the operation.

Objective The purpose of this study is to investigate the molecular mechanisms of p.C310R(c.T928C) and p.E396V(c.A1187T) lipoprotein lipase(LPL) gene mutations in vitro, which may help to construct the spectrum of LPL gene mutations and phenotype. It also can provide accurate early diagnosis for high-risk population of familial hypertriglyceridemia and provide the basis for the development of gene targeted therapy. Methods Genomic DNA was extracted from proband′s family members′ peripheral blood cells and screened by whole-exome sequencing to verify candidate gene variations. PCR products were afterwards directly sequenced again to confirm corresponding LPL variants. At the cellular level, lentiviruses containing LPL mutations were constructed and then transfected into COS-1 cells. Functional significance of the mutants was corroborated by analyzing LPL activity and mass in the cell medium and lysates via ELISA and enzyme-fluorescent method. mRNA was assayed by RT-PCR to confirm the effect on gene transcription. Results DNA sequence analysis revealed that the proband was a heterozygote for a novel c.T928C mutation in exon 6 of LPL gene, while his nephew was a compound heterozygote for the c.T928C mutation in exon 6 and a novel c.A1187T mutation in exon 8. In vitro studies, these two mutations can cause decreased activity and mass of extracellular LPL(P<0.05). Moreover, further investigation indicated that LPL C310R mutation tremendously affected post-transcriptional modification of LPL gene, whereas LPL E396V mutation dampened intracellular LPL trafficking. Conclusion Both the mutations are pathogenic by reducing the activity and mass of LPL in the plasma, which affected normal metabolism of triglycerides.

BACKGROUND: What are the influencing factors of serum uric acid of inhabitants from coastal area? What is the critical concentration of serum uric acid to prevent and treat metabolic syndrome?OBJECTIVE: To probe into the relationship between serum uric acid and metabolic syndrome in female inhabitants aged more than 20 years from coastal area of Shandong province.DESIGN: A clusting stratified random sampling survey.SETTING: Department of Endocrinology, Affiliated Hospital of Medical College of Qingdao University.PARTICIPANTS: The survey was carried out in the female inhabitants of five cities from coastal area of Shandong province (Qingdao, Rizhao, Yantai, Weihai and Dongying) between May and October 2004. The inhabitants, aged 20 to 80 years, lived there for 5 or more than 5 years, and they were natural crowd taking family as unit.METHODS: Investigations in the manner of entering every family and being on the spot were combined. Questionnaires were filled in on the first day, and fasting blood was taken to perform serum uric acid examination on the morning of the second day. For those with serum uric acid higher than normal, they were given rechecking on the third day, and education about prevention and treatment of gout and hyperuricemia was conducted at the same time.MAIN OUTCOME MEASURES: ① Investigation on general condition:Including health status, diet, physical activity, labour intensity and economics. ② Investigation on nutrition: Consists of food intake frequency and dietary. ③ Body height, body mass, waistline, hip circum, blood pressure and body mass index. ④ Levels of fasting blood glucose(FBG), serum uric acid, total cholesterol (TC), triacylglycerol (TG), high-density lipoprotein cholesterol(HDL-C), urea nitrogen (UN) and creatinine(Cr).RESULTS: ① With the increase of concentration of serum uric acid, levels of systolic pressure (SP), diastolic pressure (DP), pulse pressure (PP),body mass index(BMI) , waistline, waist-to-hip ratio(WHR), UN, Cr, TG,TC were all gradually increased. Each index was significantly higher in the serum uric acid 280-319 μmol/L group, serum uric acid 320-349 μmol/L group and serum uric acid ＞ 350 μmol/L group (hyperuricemia group)than that in serum uric acid ＜ 280 μmol/L (P ＜ 0.05-0.01 ), While the concentration of HDL-C was decreased with the increase of concentration of serum uric acid (all P ＜ 0.01). ② The incidence of hypertension, lipid metabolic disorder, overweight and obesity, glycometabolism disorder as well as metabolic syndrome was increased with the increase of uric acid;Compared with serum uric acid ＜ 280 μmol/L group, OR value of metabolic syndrome was 2.29(95%CI: 1.81-2.89),4.15(95%CI:3.10-5.55),4.96 (95%CI:3.85-6.39) in the serum uric acid 280-319 μmol/L group,320-349 μmol/L group and hyperuricemia group , respectively. ③Noncondition Logistic multiple stepwise regression analysis showed that age,hypertension, shellfish intake volume, UN, Cr, TG and WHR and light physical activity were the independent risk factors for female patients with hyperuricemia and HDL-C was protective factor.CONCLUSION: The incidence of metabolic syndrome is increased with the increase of concentration of serum uric acid in female inhabitants from coastal area of Shandong province. 280 μmol/L should be as the critical concentration of serum uric acid to prevent and treat metabolic syndrome.Controlling metabolic syndrome and reducing intake of shellfish and other marine products which contain high level of purine is one of means to prevent hyperuricemia. Clinical physicians should paid more attention to the pathopoiesis of hyperuricemia.

Hemichorea associated with ketotic hyperglycemia is a lateral chorea caused by hyperglycemic ketosis, which is very rare clinically, and has not been reported at home and abroad in elderly patients with type 2 diabetes. Two cases with hemichorea associated with ketotic hyperglycemia were reported. One case was an 86-year-old female with primarily diagnosed diabetes and unilateral limb involvement. The other case was an 85-year-old man with chronic poor glycemic control and bilateral limb involvement. In order to improve the understanding of this disease, the clinical and imaging manifestations of this disease were analyzed in combination with relevant literature.

Objective To investigate the correlation between the-308 site,-238 site gene polymorphism of TNF-αa promoter region in hypemricemh and its metabolic phenotype.Methods HUA patients 188,normal people(NHU)51,the-308G/A site single nu-cleofide polymorphism of TNF-a gene promoter region was decided by Polymerase chain reaction-restriction fragment length polymor-phism(PCR-RFLP)method.The level of serum uric acid is detected by uricase.blood glucose by glucose oxidase.Selective inhibition assay for total cholesterol,triglyceride and high-density lipoprotein cholesterol.All these tests were complted within three hours afterextraction.Keep blood samples at-20℃ to detect the concentration of insulin using immunoradiometrie assay.HUA patients 35.NHU 39,the -238G/A site single nucleofide polymorphism of TNF-a gene promoter region was decided by the same method.Results By smdying two single nucleotide polymorphism,the GA+AA frequency of-308 site(23.94%)in HUA was significantly higher than NHU(11.76%)(P=0.0001);the genotype frequencies of GA and GG in-238 site had no significant difference between the two groups(P=0.08).Meanwhile,comparing GA+AA genotype and CG group of-308 site,waist-hip ratio,systolic and diastolic blood pressure,uric acid,triglycerides differences were statistically significant(P=0.05-0.01);the difference in-238 site between the two genotypes waft no significance.Conclusion The results of this study show-308A carriers of TNF-α promoter region in HUA individual is correlated with hyperuficemia and its metabolic phenotype.

OBJECTIVETo investigate the effect of the iron chelator deferoxamine (DFA) in suppressing microglia activation and protecting against secondary neural injury in a rat model of intracerebral hemorrhage (ICH).

METHODSSD rats were randomly divided into sham-operated group, ICH group and DFA treatment group. ICH model was established by infusion of type IV collagenase into the right basal ganglia, and starting from 1 h after the operation, the rats received intraperitoneal DFA injections every 12 h for 7 days. The iron content in the perihematoma brain tissue was determined at different time points after DFA administration, and OX42 immunohistochemistry was used to observe the changes in the microglia. The contents of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the brain tissue were detected by ELISA. The neural death and neurological deficiency were measured using Nissl staining and neurological scores, respectively.

RESULTSThe iron content in the brain tissues around the hematoma was significantly increased 3 days after ICH and maintained a high level till 28 days, accompanied by a marked increase of microglial cells as compared to the sham-operated group. DFA injection caused significantly decreased iron content in the brain tissue, reduced number of microglial cells, and lowered levels of IL-1β and TNF-α. Neuronal loss around the hematoma was obviously reversed after DFA injections, which resulted in improved neurological deficiency.

CONCLUSIONDFA can suppress microglia activation by removing iron overload from the perihematoma brain tissue, thus reducing secondary neuronal death and neurological deficiency in rats with ICH.

Animals ; Cerebral Hemorrhage ; metabolism ; pathology ; Deferoxamine ; pharmacology ; Interleukin-1beta ; metabolism ; Iron ; metabolism ; Male ; Microglia ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism