Objective:To explore the prognostic value of CysC and NT‐proBNP in patients with non‐ST elevation a‐cute coronary syndrome (NSTE‐ACS) .Methods :A total of 166 NSTE‐ACS patients hospitalized in our hospital from Jan 2012 to Dec 2012 were selected .They were followed up for 12 months ,then general data ,levels of CysC , NT‐proBNP ,hsCRP and cTnI etc .and incidence rate of MACE were recorded and measured .According to MACE occurrence during follow‐up or not ,156 cases were divided into non‐MACE group (n=137) and MACE group (n=19) ,risk factors for MACE in NSTE‐ACS patients were analyzed ,receiver operator characteristic curve (ROC) was performed ,and the optimal cutoffs of related indexes predicting MACE occurrence in these patients were analyzed . Results :Compared with non‐MACE group ,there were significant rise in age [ (60.26 ± 10.45) years vs .(64.16 ± 11.21) years] ,levels of CysC [ (1.02 ± 0.11) mg/L vs .(1.15 ± 0.12) mg/L] ,NT‐proBNP [ (251.97 ± 89.65) pg/ml vs .(347.93 ± 107.29) pg/ml] ,hsCRP [ (14.69 ± 3.53) mg/L vs .(17.13 ± 3.68) mg/L] and cTnI [ (0.36 ± 0.46) ng/ml vs .(0.90 ± 0.88) ng/ml] in MACE group ,P<0.05 or <0.01. Multi‐factor regression analysis indica‐ted that CysC ,NT‐proBNP and cTnI levels were independent predictors for MACE in NSTE‐ACS patients ( P<0.05 or <0.01) .ROC curves of CysC ,NT‐proBNP ,cTnI and hsCRP judging prognosis were drawn , only AUC of CysC and NT‐proBNP curves were >0.7 [CysC:0.784 ,95% CI:0.687~0.881 ;NT‐proBNP:0.753 ,95% CI :0.639~0.867] , and it′s analysis indicated that CysC=1.07 mg/L and NT‐proBNP=279.60 pg/ml were their optimal cutoff predicting MACE .Kaplan‐Meier survival curves with above two cutoffs as risk stratification cutoff indicated that survival time of high risk group was significantly shorter than that of low risk group (P<0.05) .Conclusion:Serum CysC and NT‐proBNP levels are independent predictors assessing prognosis in NSTE‐ACS patients .

Objective: To investigate the characteristic of nasal mucosa absorption in vivo of tetramethylpyrazine hydrochloride (TMP HCl) in rats. Methods: The nasal circulatory perfusion test of TMP HCl was performed in rats.Results: The absorption rate constants was increased with the increasing of the concentration of TMP HCl; The absorption rate constants was increased with the elevating of pH values at the pH value range of 4.70～7.00. Conclusion:When the pH value of nasal circulatory perfusion liquid of TMP HCl is 7.00, the nasal mucosa absorption is optimal.

Objective To investigate the effects of valproic acid ( VPA) on cell proliferation and cell cycle in human pancreatic cancer cell line PaTu8988 in vitro. Methods PaTu8988 cells were treated with VPA in concentration of 0, 0.2, 1.0 or 5.0 mmol/L for 24 h and 48 h respectively. Cell viability was measured by WST-8 assay. Cell cycles were detected by flow cytometery. Dimethyl sulfoxide added to the medium was used as blank control group, while PBS added to the medium was used as PBS group. Results After VPA treatment for 24 h, the inhibition rate of VPA 5.0 mmol/L group was 18.9% , which was significantly higher than those in control group, PBS group and VPA 0.2, 1.0 mmol/L group (0, 4.4% , 6.8%, 6.1% , P <0.05). After 48 h, the inhibition rates of VPA 1.0, 5.0 mmol/L were 12.9%, 25.9% , which was significantly higher than those in control group, PBS group and VPA 0.2 mmol/L group (0, 6.2% , 4.6% , P <0.01). After VPA treatment for 24 h, the proportions of G2 phase cell in VPA 1.0, 5.0 mmol/L group were ( 26.57 ± 1.88) % , ( 34.11 ± 4.74 ) % , which was significantly higher than those in PBS group, control group, VPA 0.2 mmol/L group [(10.72 ± 2.02)% , ( 13.53 ± 2.28)% , (13.81 ±2.40)%, P <0.01 ], the changes 48 h after VPA treatment was consistent with the changes 24 h after VPA treatment. Conclusions VPA may significantly suppress the cell proliferation of human pancreatic cancer cell line PaTu8988, and induce cell cycle arrest in G2 phase in a time and dose-dependent manner.

Objective To investigate the features and clinical value of endoscopic ultrasonography and colonoscopy for appendix mucocele. Methods The patients with mucocele of appendix who were diagnosed by endoscopic ultrasonography and colonoscopy in three hospitals all underwent surgery from January 2008 to March 2015. Appendix mucocele in these patients was confirmed by postoperative pathology and clinical data were retrospectively analyzed. Results A total of 22 patients with appendix mucocele were analyzed retrospectively. The average size of intralumen mucocele was 1. 84±1. 42 cm (0. 6-4. 5 cm) . The colonscopic finding of appendiceal mucocele showed submucosal protuberance at the appendiceal orifice with smooth surface. The appendiceal orifice was found at the edge of appendiceal mucocele. Endoscopic ultrasonogrphy showed low echo with smooth cyst wall in 8 patients, mixed equal echo and low echo in 14 cases. Appendicectomy was performed in 11 patients and resection of ileocecum in 11 others. Conclusion Endoscopic ultrasonography and colonoscopy are valuable for diagnosis and treatment in appendiceal mucocele.

AIM: To explore the mechanism underlying inducible nitric oxide (NO) caused injury of endothelial cells during inflammation. METHODS: The activity of iso-enzymes of NO synthase (NOS), NO level and iNOS expression were examined using NADPH method, Griess reaction and RT-PCR, respectively. Furthermore, the lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) content were also measured. RESULTS:Co-administration of cytokines (TNF-? 5?10 5 U/L, IL-1? 2?10 5 U/L, INF-? 2?10 5 U/L) and LPS (10 mg/L) caused an obvious increase in NOS activity, NO levels (about two-fold) and a significant injury of the cells. At the same time, a significant increase in iNOS mRNA was also detected. Wheareas, treatment of the cells separately with cytokines or LPS for 24 h had no significant effect on NOS activity and NO level in cell lysates, however, it caused a significant increase in LDH release and MDA content. Also, the effect of cytokines and LPS on cell viability was concentration-and time-dependent. L-NMMA, a inhibitor of NOS, can suppress inducible NO production and protect cells against NO induced injury. CONCLUSION:Co-administration of cytokines (TNF-?, IL-1? and INF-?) and LPS significant activated iNOS and NO production which, in turn, induced oxidative reaction in endothelial cells.

nd hypermethylation of HHIP was detected in pancreatic juice,which may be a useful marker in the diagnosis of PCa.

OBJECTIVE: To verify the therapeutic effect and adverse reactions of ?-receptor blocker, domestic urapidil, on severe hypertension. METHODS: Observation was carried out in a multi-center, random sampling and controlled pattern. Drug was iv injected first and then infused. At the same time, the patients' systolic pressure, diastolic pressure, heart rate, EKG, blood & urine routine, serum GPT and urea nitrogen were measured and examined.RESULTS: Of 41 cases in this series. 16 satis- factory(39.0%), 23 improved (56.1%), 2 unsatisfactory(4.9%) .The total effective rate was 95.1%. After drug administra- tion, systolic pressure was lowered by 43 .97mmHg(P

Purpose To assess right ventricular function and synchronous acute response in patients with chronic cardiac failure after cardiac resynchronization therapy (CRT) using equilibrium radionuclide angiography (ERNA).Materials and Methods Twenty-four chronic cardiac failure patients who accepted CRT were included (CRT group) and twenty healthy participants were also selected as the control group.ERNA was performed before and within 48 h after pacemaker implantation to calculate both right ventricular ejection fraction (RVEF) and RV dyssynchrony.RV dyssynchrony was defined as the standard right ventricular phase shift and right ventricular phase standard deviation (RVPS and RVPSD).Results The postoperative RVEF,RVPS and RVPSD in CRT group were significantly improved (P＜0.05).Fifteen patients (62.5％) were classified as acute responders,based on a reduction of at least 15％ in LV end-systolic volume immediately after CRT.The baseline RVEF in responders was higher than that in nonresponders (P＜0.05),while the RVPS and RVPSD were lower (P＜0.05).The postoperative RVPS and RVPSD decreased (P＜0.05),and the RVEF increased (P＜0.05) in both responders and nonresponders after pacemaker implantation,indicating that the right ventricular function and dyssynchrony in CRT group were both improved.Conclusion This study showed a significant improvement in RV ventricular systolic function and synchrony immediately after CRT.ERNA allows assessment of changes in RVEF and RV dyssynchrony before and after CRT implantation.

Objective:To explore the expression of family with sequence similarity 83 member A (FAM83A) in colorectal cancer, and the effect of FAM83A knockdown on the proliferation of colorectal cancer cells and the related mechanism.Methods:The expression of FAM83A in the tissues of 102 patients with colorectal cancer and its adjacent tissues was detected by immunohistochemistry. HCT116 cells were divided into experimental group and control group. The experimental group cells were transfected with FAM83A-siRNA plasmid, and the control group cells were transfected with MOCK-siRNA plasmid. The mRNA content of FAM83A in each group was detected by fluorescence quantitative PCR. The expressions of FAM83A, P13K, p-AKT and p-mTOR in each group were detected by Western blot. CCK8 assay and clonogenesis assay were used to detect cell proliferation.Results:The positive rate of FAM83A in colorectal cancer patients was 88.23% (90 cases /102 cases), and the expression rate of FAM83A in paracancer tissues was 10.78% (11 cases /102 cases). The expression rate of Fam83a in colorectal cancer tissues was significantly higher than that in paracancer tissues, with statistical significance ( P<0.001). After siRNA transfection, the mRNA expression levels of FAM83A in HCT116 cells of the experimental group and control group were 1.23±0.20 and 0.43±0.12, respectively, and the protein expression levels of FAM83A were 1.19±0.11 and 0.23±0.08, respectively. The expression levels of P13K were 1.21±0.17 and 0.28±0.09, the expression levels of p-AKT were 1.35±0.23 and 0.57±0.18, and the expression levels of p-mTOR were 1.48±0.20 and 1.05±0.14. The expression of P13K, p-Akt and p-mTOR was down-regulated (all P<0.05). The absorbance of HCT116 cells in the experimental group and the control group was 1.09±0.22 and 2.21±0.27, respectively. The cloning rate of HCT116 cells in the experimental group and the control group was 21.6%±2.4% and 62.7%±4.1%, respectively. The proliferation ability of HCT116 cells in the experimental group decreased significantly ( P<0.05) . Conclusions:The expression of FAM83A is significantly increased in colorectal cancer tissues, which may be related to the malignant degree of colorectal cancer. FAM83A affects the proliferation of colorectal cancer cells through the P13K/AKT/mTOR signaling pathway.

OBJECTIVES: To study the correlation of intestinal dominant flora with hyperuricemia, and to explore influencing factors of hyperuricemia. METHODS: Data of gut dominant microbiota were collected from subjects who underwent health check-up in Shulan (Hangzhou) Hospital from January 2018 to April 2020. Subjects with high uric acid and normal uric acid were matched by propensity score matching method according to age, gender and body mass index (BMI). This resulted in 178 pairs as hyperuricemia group and control group. The gut dominant microbiota between hyperuricemia and normal control group were compared. Pearson or Spearman correlation coefficient method was used to analyze the correlation between blood uric acid and intestinal dominant flora. Univariate and multivariate logistic regression were used to analyze the influencing factors of hyperuricemia. RESULTS: The abundance of Atopobium, Lactobacillus, Bacteroides, Enterococcus, Clostridium leptum, Fusobacterium prausnitzii, Bifidobacterium, Clostridium butyricum and the ratio of Bifidobacterium to Enterobacter (B/E) in the hyperuricemia group were significantly lower than those in the control group (all P<0.01). The correlation analysis showed that serum uric acid were negatively correlated with the abundance of Atopobium (r=－0.224, P<0.01), Bacteroides (r=－0.116, P<0.05), Clostridium leptum (r=－0.196, P<0.01), Fusobacterium prausnitzii (r=－0.244, P<0.01), Bifidobacterium (r=－0.237, P<0.01), Eubacterium rectale (r=－0.125, P<0.05), Clostridium butyricum (r=－0.176, P<0.01) and B/E value (r=－0.127, P<0.05). Multivariate logistic regression analysis showed that glutamyl transpeptidase was an independent risk factor for hyperuricemia (OR=1.007, 95%CI: 1.002-1.012, P<0.05), and the Atopobium was an independent protective factor for hyperuricemia (OR=0.714, 95%CI: 0.605-0.842, P<0.01). CONCLUSIONS There are alterations in abundance of gut dominant microbiota in patients with hyperuricemia, and Atopobium abundance appears as a protective factor for hyperuricemia.
Humans ; Uric Acid ; Hyperuricemia ; Body Mass Index ; Risk Factors ; Microbiota