Objective To investigate the correlation of the S100B level with cardiac function and chronic heart failure.Methods A total of 80 elderly chronic heart failure (CHF) patients who accepted treatments in our hospital from March 2012 to December 2013 were recruited,and 80 subjects undergoing health examinations served as the control group.The New York Heart Association (NYHA) functional classification in the experimental group was determined.Serum levels of S100B and NT-proBNP,left ventricular end diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) were compared between the groups,and the correlation of the S100B level with NT proBNP,LVEF and the NYHA functional classification were analyzed.Results The serum S100B level was increased in the experimental group as compared with the control group [(91.4 ±31.9) pg/L vs.(74.9±26.0) pg/L,t=1.980,P=0.000].The serum NT-proBNP level was higher,LVEDD was longer,and LVEF was lower in the experimental group than in the control group (all P＜0.01).The serum S100B level was positively correlated with NT-proBNP (r=0.309,P=0.003) and the NYHA functional classification (r=0.508,P=0.001),and negatively correlated with the LVEF (r=-0.192,P=0.004).Conclusions The serum S100B level is increased in patients with CHF and negatively correlated with cardiac function,suggesting that the S100B protein may serve as a valuable tool for the diagnosis and assessment of CHF.However,more studies are needed to provide more evidence.

Objective To explore the association between serum uric acid (SUA) and all-cause mortality in men. Methods In this prospective cohort study,data being used was derived from the Kailuan study cohort. A total of 81 110 male workers who had taken part in the Kailuan physical examination were enrolled. Subjects with previous myocardial infarction,stroke,cancer, eGFR<30 ml/(min·1.73 m2)accidental deaths and those ever used drugs that seemed to have showed an effect on blood uric acid,were excluded. All the information was gathered from a unified questionnaire,measured by blood biochemistry and with the mean period of follow up as(47.5±4.3) months. Based on the 2006-2007 SUA value,observed objects were divided into five groups,with multivariate Cox proportional hazard regression analysis used to estimate the relationship between SUA and all-cause mortality in men. Results 1)At the end of the follow-up period in 2010-2011, the number of deaths were 315,278,243,292 and 341 among the different SUA quinte,with incidence rates of all-cause mortality as 2.43%,2.36%,1.96%,2.42%and 2.92%,respectively. 2)Data from the Single factor Cox proportional hazard regression analysis showed that,when comparing with the third quinte,HR values of the all-cause mortality were 1.32(1.11-1.56),1.19(1.00-1.41),1.20(1.01-1.43)and 1.41(1.19-1.66)in other four groups,respectively. 3)When factors were adjusted for age, systolic blood pressure,diastolic blood pressure,body mass index,triglyceride,total cholesterol, high-density lipoprotein cholesterol, low density lipoprotein cholesterol, fasting glucose, high-sensitivity C-reactive protein,smoking history and history of drinking,education,profession, economy,etc.,results from the Multiple Cox proportional hazard regression analysis showed the HR values of the all-cause mortality were 1.26(1.06-1.51),1.20(1.01-1.44),1.25(1.05-1.49),1.42 (1.19-1.68) in other four groups,respectively,comparing to the third quinte. Conclusion Using SUA as the independent risk factor of all-cause mortality,the exceptional levels of SUA were associated with an increasing risk for all-cause mortality while the association of SUA with all-cause mortality appeared an“U”shaped curve.

OBJECTIVETo explore the association between serum uric acid (SUA) and all-cause mortality in men.

METHODSIn this prospective cohort study, data being used was derived from the Kailuan study cohort. A total of 81 110 male workers who had taken part in the Kailuan physical examination were enrolled. Subjects with previous myocardial infarction, stroke, cancer, eGFR < 30 ml/(min × 1.73 m(2)) accidental deaths and those ever used drugs that seemed to have showed an effect on blood uric acid, were excluded. All the information was gathered from a unified questionnaire, measured by blood biochemistry and with the mean period of follow up as (47.5 ± 4.3) months. Based on the 2006-2007 SUA value, observed objects were divided into five groups, with multivariate Cox proportional hazard regression analysis used to estimate the relationship between SUA and all-cause mortality in men.

RESULTS1) At the end of the follow-up period in 2010-2011, the number of deaths were 315, 278, 243, 292 and 341 among the different SUA quinte, with incidence rates of all-cause mortality as 2.43%, 2.36%, 1.96%, 2.42% and 2.92%, respectively. 2) Data from the Single factor Cox proportional hazard regression analysis showed that, when comparing with the third quinte, HR values of the all-cause mortality were 1.32 (1.11-1.56), 1.19 (1.00-1.41), 1.20 (1.01-1.43) and 1.41 (1.19-1.66) in other four groups, respectively. 3) When factors were adjusted for age, systolic blood pressure, diastolic blood pressure, body mass index, triglyceride, total cholesterol, high-density lipoprotein cholesterol, low density lipoprotein cholesterol, fasting glucose, high-sensitivity C-reactive protein, smoking history and history of drinking, education, profession, economy, etc., results from the Multiple Cox proportional hazard regression analysis showed the HR values of the all-cause mortality were 1.26 (1.06-1.51), 1.20 (1.01-1.44), 1.25(1.05-1.49), 1.42 (1.19-1.68) in other four groups, respectively, comparing to the third quinte.

CONCLUSIONUsing SUA as the independent risk factor of all-cause mortality, the exceptional levels of SUA were associated with an increasing risk for all-cause mortality while the association of SUA with all-cause mortality appeared an "U" shaped curve.

Adult ; Aged ; Cause of Death ; Humans ; Male ; Middle Aged ; Prospective Studies ; Risk Factors ; Surveys and Questionnaires ; Uric Acid ; blood

Objective: To observe the effect of atorvastatin combined with insulin glargine on renal function in patients with early diabetic nephropathy. Methods: From January 2016 to March 2019, 100 patients with early diabetic nephropathy admitted to Hanzhong 3201 Hospital Affiliated with Xi′an Jiaotong University Medical School were selected as subjects. According to the random number table, patients were divided into control group and observation group, with 50 cases in each group. All patients underwent diet control, blood pressure control and symptomatic treatment. Patients in the control group were treated with insulin glargine to control blood glucose. Patients in observation group were given atorvastatin on this basis. After 16 weeks of treatment, the therapeutic effects of the two groups were observed, as well as the change in urinary albumin excretion rate (UAER), serum creatinine (Scr), C-reactive protein (CRP), total cholesterol (TC), and triglyceride (TG). Adverse reactions were observed during treatment in both groups. Results: After treatment, the levels of UAER, Scr, CRP, TC and TG of the two groups were lower than those before treatment, and the above indexes of the observation group were lower than those of the control group. The difference were statistically significant (P<0.05). During the treatment period, the incidence of adverse reactions in control group and observation group was 4.00%(2/50) and 12.00%(6/50), and there was no significant difference (P>0.05). Conclusions Atorvastatin combined with insulin glargine in the treatment of early diabetic nephropathy can effectively reduce the levels of UAER, Scr, CRP, TC and TG, and has good safety.

OBJECTIVE: To explore the effect of telmisartan on the expression of metadherin in the kidney of mice with unilateral ureter obstruction. METHODS: Eighteen male C57 mice were randomized into sham-operated group, model group and telmisartan treatment group. In the latter two groups, renal interstitial fibrosis as the result of unilateral ureter obstruction (UUO) was induced by unilateral ureteral ligation with or without telmisartan intervention. Renal pathological changes of the mice were assessed using Masson staining, and immunohistochemistry and Western blotting were used to detect the expression of extracellular matrix proteins and metadherin in the kidney of the mice. In the experiment, cultured mouse renal tubular epithelial cells (mTECs) were stimulated with transforming growth factor-β1 (TGF-β1) and transfected with a siRNA targeting metadherin, and the changes in the expressions of extracellular matrix proteins and metadherin were detected using Western blotting. RESULTS: The expressions of extracellular matrix proteins and metadherin increased significantly in the kidney of mice with UUO ( < 0.05). Intervention with telmisartan significantly lowered the expressions of extracellular matrix proteins and metadherin and alleviated the pathology of renal fibrosis in mice with UUO ( < 0.05). In cultured mTECs, siRNA-mediated knockdown of metadherin obviously reversed TGF-β1-induced increase in the expressions of extracellular matrix proteins and metadherin. CONCLUSIONS Telmisartan can suppress the production of extracellular matrix proteins and the expression of metadhein to attenuate UUO-induced renal fibrosis in mice.
Angiotensin II Type 1 Receptor Blockers ; Animals ; Antihypertensive Agents ; Extracellular Matrix Proteins ; metabolism ; Fibrosis ; Kidney ; drug effects ; metabolism ; pathology ; Male ; Membrane Proteins ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; RNA, Small Interfering ; Random Allocation ; Telmisartan ; pharmacology ; Transforming Growth Factor beta1 ; pharmacology ; Ureteral Obstruction ; complications ; metabolism

Objective: To predict the tumor neoantigen peptides in hepatocellular carcinoma (HCC), and examine their specific immune effects against the tumor cells without injury to normal cells. Methods: The data of whole-genome sequencing and exome sequencing of HCC tumor and matched non-tumor liver tissues were analyzed to confirm the HCC-associated somatic mutations. Based on the HLA phenotype of the patients, we used NetMHC software to predict the neoantigen epitopes with high binding affinity to their MHC-I molecules. The predicted peptides with mutation sites included were synthesized. GPL10687 platform was applied to examine the gene expression difference between tumor and normal tissues of the selected genes in GSE25097, one of the GEO databases. The quantitative real-time PCR (qRT-qPCR) and immunohistochemistry were used to confirm the expressions in tumors and normal tissues of the selected genes. By using the predicted peptides, we induced the generation of antigen-specific CD8⁺ cytotoxic T lymphocytes (CTLs) and examined their specific effects against tumor cells. Results: The mutation frequency of TP53 (tumor protein p53) was 40%, and LAMA3 (Laminin Subunit Alpha 3) was 8% in the analyzed HCC tissues. In GSE25097 database, TP53 and LAMA3 mRNA levels in tumors were 1.57±0.02 and 1.37±0.10, which were significantly increased than those in matched no-tumor tissue (0.54±0.01 and 0.36±0.01, P<0.05). The differences of expression levels of TP53 and LAMA3 in tumor and no-tumor tissues were validated by using qRT-qPCR and immunohistochemistry in 10 HCC tissues. The mRNA levels of TP53 and LAMA3 in tumors were 0.24±0.03 and 0.13±0.06, which were significantly elevated than those in matched no-tumor tissue (0.11±0.01 and 0.01±0.01, P<0.05). Among the Chinese population, HLA-A2 and HLA-A11 and HLA-A24 accounted for 70%, representing the major MHC-I molecules. The CTLs induced by predicted peptides showed cytotoxicity to the targets pulsed with mutated peptide, with no effect on the target pulsed with normal peptide and on normal cells. Conclusions TP53 and LAMA3 existed relative higher mutation frequency in HCC, and expressed higher in tumor tissues. The induced CTLs by predicted peptides derived from mutation-associated protein could specific kill the target cells without injury to normal cells.