0.05). ConclusionThe expression of VOCC mRNA and BKCa mRNA in kidney tissues of IgA nephropathy patients are abnormal.There is positive correlation between the abnormal expression of VOCC mRNA and BKCa mRNA and total glomerular pathological lesions integrals.The expression of VOCC mRNA and BKCa mRNA in kidney tissues of IgA nephropathy may serve as the indictor for the disease progression.

Objective To estimate the present salt iodine content and iodine nutrition need of high risk population of iodine deficiency disorder in Meixian County. Methods Each primary school was selected from urban and rural areas(Xiyang Town, 20 kilometers away from Meixian County), the goiter rate of 8 to 10 year-old students was examined and urinary iodine and household salt iodine was sampled. Twenty to 40 year-old women of childbearing age nearby schools around the urban and villages around Xiyang Town were selected to collect their urine and salt samples. At urban hospitals and rural health centers, 0 to 2 year-old infant urine samples were collected, Thyroid gland was palpated and urinary iodine was determined by iodine in urine by As3+-Ce4+catalytic spectrophotometry, salt iodine was determined by direct titration. Results The goiter rates of 8 to 10 year-old students were 1.5 % (3/200), 1.0% (1/100) for the urban area and 2.0% (2/100) for rural area. Median of urinary iodine in 8 to 10 year-old students, infants, women of childbearing age averaged at 237.1 μg/L and 280.1, 234.7,187.6 μg/L respectively, with each being 287.4,245.0,205.5 μg/L in urban area and 278.9,228.5,176.4 μg/L in rural area. Women of childbearing age had a higher percentage of urinary iodine < 50.0 μg/L than students,students had a higher percentage than infants, each being 7.5%(15/200), 4.5%(9/200), 4.0%(4/100). The ration of urinary iodine > 300.0 μg/L was more in infants than in students, that in students was more than that in women of childbearing age, each being 33.0% (33/100), 30.0% (60/200),22.5% (45/200). The median of salt iodine was 27.2 mg/kg. The coverage of iodized salt was 100.0%(400/400). Ninty-seven percent(194/200) and 96.0% (192/200) of qualified iodized salt were consumed in urban area and in rural area. Conclusions The amount of iodine added to salt meets the requirement in the 3 kinds population risk of iodine deficiency disorder. But a higher iodine status has been found out in students and infants. It is reasonable to decrease the present salt iodine content.

Seven compounds were isolated from Onychium japonicum by macroporous resin, silica gel, ODS, Sephadex LH-20 column chromatography and semi-preparative HPLC. Their structures were identified by NMR, MS and other spectroscopic methods as onychone A (1), quercetin (2), quercetin-3-O-α-L-rhamnoside (3), kaempferol-7-O-β-D-glucopyranoside (4), kaempferol-3-O-α-L-rhamnopyranoside (5), (-)-prunin (6), and norathyriol (7). Compound 1 is a novel macrocyclic flavonoid, and all the others are reported from this plant for the first time. In vitro cytotoxic activities of compounds 1-7 were evaluated by MTS testing with five cancer cell lines. Compound 7 exhibited weak cytotoxicity against tumor cell lines A549, SMMC-7721, and SW480.

OBJECTIVETo explore the effect of Qiangxin Fumai Granule (QFG, a Chinese herbal preparation for treatment of sick sinus syndrome) contained serum (QFG-S) on sinoatrial node cells during Ca2+ overloading induced by simulated ischemia/reperfusion.

METHODSModel Ca2+ overloading cells were established on sinoatrial node cells from newborn rats, with deprivation of oxygen and glucose to simulate ischemia and with restoration of them to simulate reperfusion. Cells were divided into 5 groups, those in the normal and model control groups were modeled directly and those in the treated groups were pre-cultured with UMEM containing respective medicines in aerobic environment for 30 mm before ischemia/reperfusion simulation. Cell Ca2+ concentration and morphology were observed by invert microscope and fluorescence spectrophotometer.

RESULTSMost cells in the model control group revealed cell edema and deformation, even abscission. By HE staining, many minimal vacuole appeared in cytoplasm, with crumpled nuclear membrane, partially damaged. While cells in the QFG-S treated group, either high-dose or low-dose, were attached grew well, with basically smooth and complete membrane and nuclear membrane, normal in size and shape. The intracellular Ca2+ concentration raised significantly after modeling, but it was much lower in the QFG-S treated group than in the model control group (P < 0.01) and it was not changed obviously in the atropine treated group.

CONCLUSIONQFG-S could diminish the injury of cell induced by simulated ischemia/reperfusion, the acting mechanism for treatment of sick sinus syndrome might be related to its effect in relieving Ca2+ overloading and thus protecting cells from injury.

Animals ; Calcium ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Ischemia ; drug therapy ; metabolism ; Male ; Rats ; Rats, Wistar ; Serum ; chemistry ; Sick Sinus Syndrome ; drug therapy ; metabolism ; Sinoatrial Node ; drug effects ; metabolism

OBJECTIVETo observe the development of arrhythmia induced by ischemia/reperfusion (I/R) of the right coronary artery in rabbits and the intervening effect of Chinese medicine Qiangxin Fumai Granule (QFG), a Chinese preparation for activating yang and promoting blood circulation, on it.

METHODSRabbit right coronary artery I/R model was adopted. Forty healthy adult rabbits were randomly divided into 5 groups, the sham-operation group, the model group, the atropine group, the high-dose QFG group, and the low-dose QFG group, eight in each group. The drugs were administered via duodenal perfusion 10 min after ischemia. The changes of AA interval before and after medication were observed and the scores of arrhythmia were calculated.

RESULTSDuring ischemia period, AA interval prolonged for more than 40 ms in the model group, and the scores of arrhythmia showed a rising trend along with the prolonging of ischemia, with the presence of atrial-ventricular block (AVB) and aggravating of sinus and atrial arrhythmia; during reperfusion period, the incidence of AVB decreased, and AA interval somewhat decreased. The AA intervals and scores of arrhythmia in the high and low-dose QFG groups were significantly lower than those in the model group respectively (P < 0.01 or P < 0.05).

CONCLUSIONQFG is beneficial for shortening AA interval and preventing arrhythmia induced by I/R.

Animals ; Anti-Arrhythmia Agents ; administration & dosage ; pharmacology ; therapeutic use ; Arrhythmias, Cardiac ; drug therapy ; physiopathology ; Coronary Artery Disease ; complications ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Female ; Male ; Myocardial Ischemia ; complications ; Myocardial Reperfusion Injury ; etiology ; physiopathology ; Phytotherapy ; Rabbits ; Random Allocation ; Treatment Outcome

OBJECTIVETo explore the molecular mechanism of Qiangxin Fumai granule (QFG, an effective Chinese composite drug) in preventing and treating sick sinus syndrome (SSS).

METHODRabbit model of sinoatrial ischemia/reperfusion was established by occluding and loosening the root of right coronary artery. Effect of QFG on cell apoptosis was observed by TUNEL method, and its effect on apoptotic related gene Bax, Bcl-2 and Fas-L gene protein expression was observed by immunohistochemical method. Average light density values of the expression of Bax, Bcl-2 and Fas-L of SAN cells was determined by Imagepro Plus image analysis system.

RESULTSinoatrial injury induced by ischemia/reperfusion could cause evident sinoatrial cell apoptosis, enhance Fas-L gene protein expression and obviously enhance Bax gene protein expression, reduce Bcl-2/Bax ratio. QFG could significantly down-regulate Fas-L and Bax gene protein expression, up-regulate Bcl-2/Bax ratio, significantly inhibit and block the sinoatrial cell apoptosis.

CONCLUSIONTo inhibit and block the event of cell apoptosis through regulating Bax, Bcl-2 and Fas-L gene protein expression in sinoatrial node after ischemia/reperfusion might be one of the mechanisms of QFG in preventing and treating sinoatrial ischemia/reperfusion injury of SSS.

Animals ; Apoptosis ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Fas Ligand Protein ; metabolism ; Immunohistochemistry ; In Situ Nick-End Labeling ; In Vitro Techniques ; Microscopy, Fluorescence ; Muscle Cells ; cytology ; drug effects ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rabbits ; Random Allocation ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo study the effect of the Chinese medicine Qiangxin Fumai Granule (, QFG) on electrophysiological functions of the sinoatrial node during ischemia-reperfusion (IR) of the right coronary artery in rabbits.

METHODSThe right coronary artery IR model in rabbits was adopted. The modeled rabbits were randomly divided into 4 groups: the model group, the atropine group, the high-dose QFG group, and the low-dose QFG group, with 8 animals in each group. In addition, twelve rabbits were selected for the sham-operative group. The drugs were administered once via duodenal perfusion after modeling had been stabilized for 10 min. The changes in AA interval, the sinoatrial conduction time (SACT), the sinus node recovery time (SNRT), the corrected sinus node recovery time (CSNRT) and the index of sinus node recovery time (ISNRT) at different time points during ischemia and reperfusion were measured.

RESULTSThe AA interval was prolonged for more than 40 ms in the model group during ischemia. Compared with the model group, the four electrophysiological parameters abovementioned in the high-dose QFG group and the low-dose QFG group were decreased to different extents at each time point (P<0.01 or P<0.05), and no statistically significant differences were found between the QFG groups and the atropine group (P>0.05).

CONCLUSIONQFG is beneficial for accelerating the recovery of sinus node autorhythmicity and conduction function, so as to protect electrophysiological functions of the sinoatrial node. Accelerating the recovery of autorhythmicity and conduction function in the sinus node is considered its electrophysiological mechanism in the treatment of sinoatrial node injury induced by ischemia.

Animals ; Coronary Vessels ; drug effects ; physiopathology ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Electrophysiological Phenomena ; drug effects ; Heart Conduction System ; drug effects ; Myocardial Reperfusion Injury ; drug therapy ; physiopathology ; Phytotherapy ; Rabbits ; Sinoatrial Node ; drug effects ; physiopathology ; Time Factors

Adolescent ; Adolescent Development ; Child ; Child Development ; China ; epidemiology ; Female ; Humans ; Male ; Obesity ; epidemiology ; Prevalence

Aim To observe the effect of interventional therapy of 5-fluorouracil(5-Fu), mitomycin C (MMC) and adriamycin (ADM) on solid malignant turmors in association with aterial infusion of NaHCO3.Methods Patients were randomly divided into two groups.With Seldinger technique,through the femoral atery to tumor atery.The patients in the control group were infused by anticarcinoma agents simply ,and patients in the treatment group were initially infused by NaHCO3,and then by NS 30 ml and anticarcinoma agents seperately. Results Partial remission (PR) in the group treated with NaHCO3 and anticarcinoma agents was significantly higher than in the group treated simply with anticarcinoma agents.Conclusion Aterial infusion of NaHCO3 into malignant tumors can increase the efficacy of ADM,MMC and 5-Fu.

The aim of this study is to investigate the effect and mechanism of angiotensin (Ang) II on E-selectin and vascular cell adhesion molecule-1 (VCAM-1) expression in rat brain microvascular endothelial cells (BMEC) and evaluate the effect of compound EXP-2528, a novel Ang II type 1 (AT1) receptor antagonist. The experiment was performed in cultured BMEC of rat. The mRNA and protein expression of E-selectin and VCAM-1 in BMEC was analyzed by RT-PCR and Western blotting, respectively. The results showed that the mRNA and protein expression of E-selectin and VCAM-1 in BMEC were significantly upregulated by 4 h or 18 h exposure to 1 x 10(-7) mol x L(-1) Ang II. These effects were abolished by pretreatment with the selective AT1 receptor antagonists losartan and compound EXP-2528, but not with the AT2 selective antagonist PD123319. Combining losartan with PD123319 also significantly inhibited Ang II-induced E-selectin and VCAM-1 expression in BMEC, but there was no significant difference compared with losartan group. These findings indicated that Ang II upregulated E-selectin and VCAM-1 in BMEC by activating AT1 receptor and then involved in the development of cerebrovascular disease.
Angiotensin II ; pharmacology ; Angiotensin II Type 1 Receptor Blockers ; pharmacology ; Animals ; Brain ; blood supply ; Cells, Cultured ; E-Selectin ; genetics ; metabolism ; Endothelial Cells ; metabolism ; Imidazoles ; pharmacology ; Isoxazoles ; pharmacology ; Losartan ; pharmacology ; Microvessels ; cytology ; RNA, Messenger ; metabolism ; Rats ; Vascular Cell Adhesion Molecule-1 ; genetics ; metabolism