Objective To investigate the role of total bile acid (TBA) in pathogenesis of essential hypertension.Methods The concentration of serum TBA was measured by enzymatic method in 127 cases including 30 healthy controls,21 secondary hypertensive patients and 76 essential hypertensive patients.Results There was a significant increase of TBA in essential hypertensive group compared with that of control group and secondary hypertension (P 0.05) .In essential hypertensive group,the levels of TBA in grade 3 hypertension were higher than that of grade 1 hypertension (P0.05).Conclusion The abnormal increasing of TBA may play a role in pathogenesis of essential hypertension.

BACKGROUND:Proliferation, migration and phenotypic changes of vascular smooth muscle cells is the core of the occurrence of atherosclerosis, and a series of related genes via methylation are involved in the process.
OBJECTIVE:To investigate the effects of oxidized low density lipoprotein (ox-LDL) on DNA methylation in the promoter region of the p21 gene and its potential mechanism in the pathogenesis of atherosclerosis.
METHODCultured human vascular smooth muscle cells were treated with different concentrations of ox-LDL (0, 10, 20, 40 mg/L) for 24 hours. The degree of DNA methylation was assayed by methylation-specific polymerase chain reaction, the expression of p21 mRNA was measured by reverse transcriptional polymerase chain reaction and the proliferative activity of vascular smooth muscle cells was determined by the MTT assay.
RESULTS AND CONCLUSION:The ox-LDL treatment resulted in a promotion in the methylation in the promoter region of the p21 gene and a decrease in mRNA expression with a concentration-dependent manner;it also induced a dose-dependent promoting effect on vascular smooth muscle cellproliferation. The atherogenic mechanism of ox-LDL might promote vascular smooth muscle cellproliferation by the hypermethylation of the p21 gene that may lead to the occurrence and development of atherosclerosis.

Objective To consider the clinical significance of retroperitoneal laparoscopic adrenalectomy for adrenal diseases. Methods We analyzed 33 cases of adrenal diseases treated by retroperitoneal laparoscopic adrenalectomy in this hospital from October 1996 to December 2001. Results Retroperitoneal laparoscopy was successfully applied in 31 cases, whereas conversions to open adrenalectomy were required in the other 2 cases. The mean operation time was 158 min (120 min～200 min). The mean intraoperative blood loss was 150 ml, without blood transfusion needed. The mean length of hospital stay was 6.4 days. Conclusions Compared with open surgery, retroperitoneal laparoscopic adrenalectomy has the advantages of minimal invasion, less blood loss, fewer complications, quicker recovery and shorter hospital stay length. This procedure can be applied to in the absence of contraindications (such as tumor size being more than 10cm, metastatic carcinoma and vital organs or blood vessels being involved).

WTBZ]Breast cancer resistance protein (BCRP) is a recently discovered half-transporter belonging to the ABC transporter superfamily as P-glycoprotein(P-gp) and multiple resistance protein (MRP). The latest research results concerned BCRP on construction features of gene, relationship to differentiation of hemopoietic stem cell and correlated transport substrates were reviewed in the article and it's clinical significance was mentioned at the same time.

Objectives To study the relationship between the severity of coronary lesions and serum uric acid.Methods Coronary heart disease(CHD) was diagnosed or excluded by coronary angiography; concentration of serum uric acid was measured with method of uric acid enzyme.Relationship between the severity of coronary lesions and serum uric acid was analysed by linear correlation and multiple stepwise regression.Results The level of serum uric acid in CHD group was significantly higher than that of control group(P

AIM: To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of G?q/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP 3 was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats ( P 0.05). At 10 days, the level of IP 3 significantly increased in left ventricle of CA rats compared with the control animals ( P

Objective To investigate the clinical features and disease-causing mutations of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis.Methods In February 2016,a 24 year old female patient with left kidney stone and nephrocalcinosis in bilateral kidneys was admitted to our hospital.One month prior to this admission,she had been treated by PCNL to remove the most part of left kidney stone in otherhospital.Mter admission,She was found hypomagnesaemia (serum magnesium 0.65 mmol/ L) and hypercalciuria (24h urine calcium 364.0 mg) but with normal renal function (serum creatinine 101.5μmol/L).And the remained part of left kidney stone was removed by flexible ureteroscope.As she was considered probably with an autosomal recessive FHHNC,an analysis of CLDN16 and CLDN19 gene mutations was performed using her and her parents'peripheral white blood cells.Results Mutation analysis revealed this patient had two heterozygous mutations in the CLDN16.One is an one-base deletion mutation in the 123th codon in exon 2:368delA.The other is a missense mutation in the 139th codon in exon 2:416C →T which resulted in an amino acid change Ala139Val.Her parents respectively had one of each heterozygous mutation.In the six months follow-up,an oral administration with hvdrochlorothiazide,potassium citrate,and calcium magesium supplements significantly reduced her hypomagnesaemia (serum magnesiun 1.0 mmol/L) and hypercalciuria (24-h urine calcium 156.0 mg),and no stone recurrence and aggravation of nephrocalcinosis and renal dysfunction occurred.Conclusions We diagnosed a patient with FHHNC who had a novel compound heterozygous mutation of CLDN16.This rare disease should be suspected if there are three constant clinical features of hypomagnesaemia,hypercalciuria and nephrocalcinosis,and verified with CLDN16 and CLDN19 gene test.Currently the option for treatment of FHHNC is symptomatic treatment until severe deterioration of renal function.The hydrochlorothiazide,potassium citrate,and calcium magesium supplements may have considerable effects on hypomagnesaemia and hypercalciuria.

0.8.

AIM: To investigate the changes of Gq-phosphoinositide pathway in left ventricular tissue of rats with chronic heart failure in order to assess the role of this signal pathway in the formation of heart failure. METHODS: Male Sprague-Dawle rats were divided into three groups: control, chronic heart failure and benazepril therapy group. Chronic heart failure was induced with adriamycin. Rats in benazepril group received benazepril 10 mg?kg-1?d-1 and adriamycin at the same time. Hemodynamic measurement was carried out after 4 weeks. The expression of G? q/11 protein in left ventricle was detected by Western blotting analysis and activity of phospholipase C was measured by the method of hydrolysis of nuclear substrate. RESULTS: Compared with control group, the ?dp/dtmax in chronic heart failure group significantly decreased, and protein G? q/11 expression, basic and stimulated phospholipase C activity significantly increased (P

Objective Pentamethylquercetin (PMQ) has a role in cardiovascular protection. We investigate the effects of 3,3' ,4' ,5,7-pentamethylquercetin, a derivative of PMQ, on intimal hyperplasia of the vein grafts in rats both in vivo and in vitro. Methods The proliferation of vascular smooth muscle cells ( VSMC ) was induced with Ang Ⅱ (0. 1μmol/L, 24 h)while PMQ was administrated at six different dosages (0. 1, 0.3, 1,3, 10 and 30 μmoL/L). Cell viability was identified with MTT; ROS was measured with DCFH-DA; and the expression of NADPH oxidase subunits Nox1, p47phox, and p22phox mRNA were measured with real-time PCR. For the experiment in vivo, 24 SD rats were randomly assigned to control group and PMQ groups, the latter was further divided into three different dosage groups. In the control group, solvent was administrated daily via gavage. In PMQ groups, PMQ ( 12.5 mg/kg, 25 mg/kg, 50 mg/kg) was administrated daily respectively in the same way.All SD rats received operation performed by one person. Reversed external jugular vein was implanted into the external carotid of the same side with interrupted suture. 4 weeks after operation, all vein grafts were harvested. Status of the vein grafts was observed and tissue sections were analyzed with HE staining. The intimal hyperplasia ( intima/media area index and intima/media thickness index) of the vein grafts was assessed. Results Cell viability and ROS of VSMC induced by Ang Ⅱ were suppressed by PMQ. Cell viability and ROS of VSMC were increased substantially when treated with Ang Ⅱ. The therapeutic effects of PMQ could be initially identified at dose of0. 3 μmol/L, with a peak at 3 μmol/L. The effects decreased from 30μmol/L to 10 μmol/L. PMQ at dose of 0.1 μmol/L had no effect on cell viability and ROS of VSMC induced by Ang Ⅱ. PMQ also downregulated the mRNA expression of NADPH oxidase subunits Nox1, p47phox and p22phox induced by Ang Ⅱ. A peak effect was observed at 3μmoL/L and decreased at 30 μmol/L. PMQ at o. 1 μmol/L had no effect on mRNA expression of NADPH oxidase subunits induced by Ang Ⅱ. As compared with control group, PMQ decreased intima/media area index ( 1. 64 ±0.20 in control, 0. 74 ±0.18 at 12.5 mg/kg, 1.09 ±0.17 at 25 mg/kg, 1.21 ± 0. 21 at 50 mg/kg) and intima/media thickness index ( 1.34 ± 0. 24 in control, 0.67 ± 0. 17 at 12.5 mg/kg, 0. 74 ± 0.14 at 25 mg/kg, 0.93 ± 0. 18 at 50mg/kg) at three dosages after implantation. Conclusion PMQ may suppress the proliferation of VSMC and inhibit neointima hyperplasia of vein grafts in rats. The effects may be attributed to the anti-oxidative activity and the downregulation of mRNA expression of NADPH oxidase subunits Noxl, p47phox and p22phox.