Objective To study the effect of different doses of atorvastatin in the treatment of coronary heart disease with chronic heart failure. Methods 100 patients with chronic heart failure who were admitted to Ankang Hospital from April 2013 to April 2016 were selected and randomly divided into the experimental group and the control group with a total of 50 patients in each group. Two groups of patients were treated with conventional treatment, the control group was given 20 mg of calcium a day, the experimental group was given a daily dose of 40 mg of calcium. The therapeutic effects of the two groups were compared. Results After treatment, the left ventricular end diastolic diameter in the control group was significantly higher than that in the experimental group, the left ventricular ejection fraction and E/A were significantly lower than those in the experimental group, and the difference was statistically significant (P<0.05). Patients in the control group were significantly higher than those in the experimental group in the incidence of cardiac death and recurrence of heart failure (P<0.05). Before treatment, there was no significant difference between the experimental group and the control group in serum NT-proBNP, hs-CRP levels and 6MWT. After treatment, the serum levels of NT-proBNP, hs-CRP in the control group were significantly higher than those in the experimental group, 6MWT was significantly shorter than that in the experimental group, and the difference was statistically significant (proBNP) (P<0.05). Conclusion Compared with 20mg/d, 40mg/d dose atorvastatin in the treatment of coronary heart disease with chronic heart failure curative effect, low recurrence rate, high safety, worthy of further promotion in clinical.

The aim of the present study is to investigate the effects of Vam3 which is one of the dihydroxystilbene compounds on expressions of ICAM-1 in the lungs of OVA-induced asthmatic mice and the mechanisms of anti-airway inflammation. Balb/c mice were challenged with OVA inhalation. Lung tissues were stained with Mayer's hematoxylin and eosin for histopathologic examination. The expression of ICAM-1 in the lungs of mice was analyzed by Western blotting and immunohistochemistry method. The NF-kappaB activities were detected by NF-kappaB-luc reporter genetic transient transfection method. The activities of MMP-9 induced by LPS, TNF-alpha and PMA in THP-1 cells were determined by gelatin zymography method. The results showed that Vam3 could inhibit the expression of ICAM-1 in the OVA-induced mouse model. In addition, Vam3 could significantly suppress the activities of NF-kappaB in A549 cells and MMP-9 in THP-1 cells induced by LPS, TNF-alpha and PMA. These results suggested that Vam3 could alleviate the asthmatic inflammation by decreasing ICAM-1 expression in asthmatic mice, down regulating NF-kappaB and MMP-9 activities. Compound Vam3 showed inhibitory effects on inflammatory signal pathways involved in asthma.

Objective: To investigate the levels of vitamin D and the correlation between DPN and vitamin D in elderly patients with diabetic peripheral neuropathy(DPN). Methods: A total of 849 patients aged 60 years and over admitted into endocrinology department from June 2016 to September 2017 were enrolled in this retrospective case-control study.According to DPN diagnostic criteria, patients were divided into the non-DPN group(n=542)and the DPN group(n=307). The 25(OH)-vitamin D[25(OH)D]level and blood biochemical parameters were determined and compared between the two groups.The risk factors for DPN were analyzed using logistic regression analysis and plotting receiver operating characteristic(ROC)curves. Results: The mean of serum 25(OH)D level in the 849 patients was 43.9±19.4 nmol/L.Serum 25(OH)D level was lower in the DPN patients than in the non-DPN patients[(40.9±20.4)nmol/L vs.(45.7±18.6)nmol/L, P<0.05]. The incidence of 25(OH)D deficiency was higher in the DPN group than in the non-DPN group(72.3% or 222/307 vs. 64.6% or 350/542, P<0.05). Binary logistic regression analysis indicated that 25(OH)D was a protective factor for DPN(OR=0.980, 95% CI: 0.964~0.995, P<0.05)and the disease duration was a risk factor for DPN(OR=1.048, 95% CI: 1.027~1.070, P<0.001). ROC analysis indicated that the diagnostic cut-off value of serum 25(OH)D for predicting DPN was 37.5nmol/L, with a Youden index of 0.17, sensitivity of 0.65 and specificity of 0.52. Conclusions The 25(OH)D level is much lower in diabetic patients, especially in DPN patients.Higher 25(OH)VD level might be a protective factor for DPN, and vitamin D might be one of potential biomarkers for DPN in diabetic patients.

OBJECTIVEIn order to understand the prevalence of hepatitis B virus (HBV) precore mutants isolated from asymtomatic carriers in Guangxi.

METHODSNested polymerase chain reaction (nPCR) was used for amplification of HBV DNA precore in 77 carrier sera, followed by HBV DNA nPCR products sequencing using direct sequencing.

RESULTS50.7% of 77 carriers was positive for HBV DNA with a prevalence of mutants 22.1% (17/77). HBV DNA positive rate in the southern part of the autonomous region was 55.6% (20/36). Six of them were mutants, counting for 30%. The common mutation in the southern part was seen T-->C at nt1858 while nt1896 stop mutation was discovered in one sample only, which was accompanied by point mutation at nt1837 (A-->G). HBV DNA positive rate in the northern part was 46.3% (19/41) with 11 of them were mutants, counting for 57.9%. The common mutation in that area stopped at nt1896. Among samples with stopped mutation, 4 samples had mutation at nt1846 (A-->T), 2 samples at nt1862 (G-->T). Both mutation at nt1856 (C-->T) and nt1858 (T-->C) could be seen in sample 734.

CONCLUSIONSThe prevalence of HBV precore mutant in asymptomatic carriers in Guangxi was at the average level in China. Further study is needed to determine the difference between the southern and the northern part of the region in the common type of mutation exists.

Base Sequence ; Carrier State ; virology ; DNA, Viral ; chemistry ; Hepatitis B virus ; genetics ; Humans ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction

OBJECTIVE: To identify potential mutations of F11 gene in a pedigree affected with hereditary coagulation factor XI (FXI) deficiency and explore its molecular pathogenesis. METHODS: Prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB), coagulation factor VIII activity (FVIIIC), coagulation factor IX activity (FIXC), coagulation factor XI activity (FXIC), coagulation factor XII activity (FXIIC) and lupus anticoagulation (LA) of the proband and eight family members were determined. FXI antigen (FXIAg) was determined by enzyme-linked immunosorbent assay (ELISA). For the proband, potential mutations in the exons, flanking introns and 5'-, 3'-untranslated regions of the F11 gene were screened by direct DNA sequencing. The results were confirmed by reverse sequencing. Suspected mutations were detected in other family members. ClustalX-2.1-win and four online bioinformatic tools (PolyPhen-2, PROVEAN, SIFT, and Mutation Taster) were used to study the conservation and possible impact of the mutations. The structure of the mutational sites was processed with Swiss-PdbViewer. RESULTS: The propositus had prolonged APTT (69.6 s), whose FXIC and FXIAg were reduced to 6.0% and 10.7%, respectively. Her mother, elder sister, one younger sister, little brother, daughter and son showed slightly prolonged APTT and moderate FXIC and FXIAg levels. Gene sequencing revealed that the propositus carried a heterozygous nonsense mutation c.738G>A (p.Trp228stop) in exon 7 and a heterozygous mutation c.1556G>C (p.Trp501Ser) in exon 13. Her mother, elder sister and daughter were heterozygous for the p.Trp228stop mutation, while one younger sister and little brother and son were heterozygous for p.Trp501Ser. Her husband and the youngest sister were of the wild type. Phylogenetic analysis suggested that Trp501 was highly conserved among all homologous species. The p.Trp501Ser was predicted to be "probably damaging","deleterious", "affect protein function" and "disease causing" corresponding to PolyPhen-2, PROVEAN, SIFT and Mutation Taster. Model analysis demonstrated that the non-polar Trp501 has two benzene rings, forming a hydrogen bond with Gln512 in the wild type. Once substituted by Ser501, the side chain may form another hydrogen bond with the benzene of His396. This may affect the normal space conformation and stability of FXI protein. CONCLUSION The compound heterozygous mutations of the F11 gene probably accounted for the low FXI concentration in this pedigree.
Factor XI ; genetics ; Factor XI Deficiency ; genetics ; Female ; Heterozygote ; Humans ; Male ; Mutation ; Pedigree ; Phylogeny