Intravenous injection of SPD 10 mg/kg could increase the tolerant dose of ouabain, and prevent the arrhythmias induced by acute myo-cardial ischemia in rats and that elicited by adrenaline-chloroform model in rabbits. SPD 60 mg/kg intraperitoneally could abolish the ventricular fibrillation produced by chloroform inhalation in mice. It inhibited the contractility, prolonged the functional refractory period and decreased the automaticity significantly of the isolated guinea pig papillary muscles, but no significant effect on excitability.

Objective:To examine the expression of VEGF gene in the endometrial carcinoma tissues,para-tumor tissues,normal endometria and peripheral blood,and analyze the role of VEGF in tumor growth and tumor metastasis.Methods:Real-time fluorescence quantitative PCR was used to detect the expression of VEGF gene in 51 endometrial carcinoma samples and the corresponding para-tumor tissues,40 normal endometria samples and their corresponding peripheral blood samples.The relation between the VEGF expression and clinical pathological parameters was analyzed.Results:The expression of VEGF gene was higher in the endometrial carcinoma tissues than in the corresponding para-tumour tissues and normal endometrial tissues(P0.05).The expression of VEGF in peripheral blood was higher in patients with endometrial carcinoma than that in the normal controls;and the expression was significantly correlated with the clinical stage,histological grades,pathological types and the presence of lymph node metastasis(P0.05).Conclusion:Real-time fluorescent quantitative PCR can sensitively,specifically detect the expression of VEGF in the endometrial carcinoma tissues and peripheral blood samples.VEGF might play an important role in the development,invasion,and metastasis of endometrial carcinoma.

This paper reported that lidocaine given intravenously 5mg/kg 9 min before occlusion of left ventricular coronary artery (CO) may shorten the latent period for ventricular arrhythmias from 6.2?1.9 min to 3.7?0.9 min (P

Acute myocardial ischemia and reperfusion led to arrhythmias and increase of glutamic oxalacetic transaminase (GOT),lactate dehydrogenase (LDH),non-csterified fatty acid (FFA) and malondialdehyde (MDA) content, and decrease of superoxide dismutase (SOD) activity in rats. 3, 6-di-methylamino-dibenzopyri-odonium edetate (IHC-72) 5 mg?kg-1 iv significantly reduced the incidence of ventricular tachy-cardia (VT) and ventricular fibrillation(VF) ,shortened the duration of arrhythmias induced by reperfusion, decreased the release of GOT, LDH and FFA, obviously reduced the MDA content,and effectively protected SOD activity in ischemia-reperfused rat hearts. Our experimental results suggested that IHC-72 had protective effects on ischemia-reperfusion injury rat hearts in vivo. The mechanism of the protection might be associated with the inhibition of cellular lipid peroxidation.

Inner ear malformations are anomalies linking to development insults at different periods of embryogenesis,which are common causes of congenital sensorineural hearing loss. The evaluation of pediatric sensorineural hearing loss mostly depends on high-resolution computed tomography and magnetic resonance imaging, which can excellently depict the temporal bones and inner ear malformations.
Ear, Inner ; abnormalities ; diagnostic imaging ; embryology ; Hearing Loss, Sensorineural ; congenital ; Humans ; Magnetic Resonance Imaging ; Temporal Bone ; abnormalities ; diagnostic imaging ; Tomography, X-Ray Computed

0.05). Conclude:The bone type may affect the stability of ITI osseointegrated implants.

This paper summarised related investigations, literature and theoretical and experimental achievements in the field, describing key technology of the methodology of F P of TCMs. The scientific, progressive, practical and feasible significance is discussed.

AIM To get an insight into intracellular signaling steps, a very early step in the signaling cascade, the biphasic Ca 2+ elicited by 5 HT in rat stomach fundus smooth muscle cells was investigated. METHODS Cells were cultured and loaded with Fluo 3 AM. [Ca 2+ ] i was measured by fluorescent intensity (FI) in each cell with confocal microscopy. RESULTS The resting FI level of SFSMC was 264?15. Stimulation of SFSMCs by 5 HT produced an elevation of [Ca 2+ ] i; Depletion of external Ca 2+ by addition of EGTA led to a significant attenuation of [Ca 2+ ] i change induced by 5 HT; Pre treatment of SFSMCs with ryanodine (10 ?mol?L -1 , 5 min) in D Hanks, the effect of 5 HT was completely inhibited; The stimulation of SFSMCs by 5 HT was partly attenuated by miaserin(10 ?mol?L -1 ), however, L type Ca 2+ channel antagonist lacidipine and G protein inhibitor NEM completely abolished the increase of [Ca 2+ ] i mediated by 5 HT; 5 HT mediated Ca 2+ release was reduced by phospholipase C specific inhibitor compound 48/80(1 2 ?g?ml -1 ); When protein kinase C was activated by phorbol 12 myristate 13 acetate (PMA 0 1 ?mol?L -1 , 5 min) the effect of 5 HT was inhibited, and the inhibitory effect of PMA was reversed by D sphingosine, a PKC inhibitor. CONCLUSION Our data suggest that G protein coupled 5 HT 2B receptor in the rat stomach fundus modulates 5 HT stimulated Ca 2+ increase, and it is coupled to calcium influx through L type calcium channels, and also intracellular calcium release by the opening of ryanodine receptor. The 5 HT 2B receptor mediated signal of 5 HT is transduced by PLC and PKC.

BACKGROUND:Basic fibroblast growth factor(bFGF)can promote production of collagen,fibronectin and matrix enzyme in healing wounds.However,dysregulation of this process,such as the abnormal coordination of cell proliferation,extracellular.matrix and neovasculadzation formation,or remodeling of the wound matrix will lead to excess accumulation of scar tissues.OBJECTIVE:To investigate effects of bFGF on normal skin wound healing and hypertrophic scar formation.METHODS:Normal and hypertrophic scar fibroblasts from tissue biopsies from 5 patients who underwent plastic surgery for repairing hypertrophic scars were isolated and cultured.The expressions of collagen,fibronectin and protein synthesis were detected by RT-PCR and ELISA.The mitochonddal membrane potential changes were measured using JC-1 staining and flow cytometry.Simultaneously,adenosine tdphosphate(ATP)levels were determined by chemiluminescence method.The effects of bFGF on these indexes of normal and hypertrophic scar fibroblasts were observed.RESULTS AND CONCLUSION:Hypertrophic scar fibroblasts become slower after being exposed to bFGF,which selectively inhibited type Ⅰ collagen production in hypertrophic scar fibroblasts(P<0.05).Although bFGF inhibited type]collagen production,it had no effect on type Ⅲ collagen expression in both normal and hypertrophic scar fibroblasts.However,fibronectin expression in the normal fibroblasts was up-reguleted after bFGF treatment(P<0.05).In addition,the mitochonddal membrane potential tended to depolarization,although no statistical difference,in hypertrophic scar fibroblasts treated with bFGF(10 or 100 μg/L).bFGF treatment increased the cellular ATP levels in the normal fibroblasts,while there were no significant alterations in the hypertrophic scar fibroblasts over a treatment of bFGF(10 or 100 μg/L,P<0.05).The results suggest that there are differential effects and mechanisms on the skin fibroblasts with bFGF treatment in normal wound healing and hypertrophic scar formation.

Reverse transcription-PCR and methylation-specific PCR (MSP) were used to determine the expression levels of Syk gene and the methylation status of its promoter in tissue samples from 60 patients with cervical cancer, 50 patients with cervical intraepithelial neoplasia (CIN), and 20 normal controls. We also analyzed the association of the methylation status and expression levels of Syk gene with linicopathological features of patients. The expression rates of Syk gene in 20 normal cervical tissue samples and 18 CIN Ⅰ samples were both 100% ; those of CIN Ⅱ- Ⅲ and cervical carcinoma were 56% (18/32)and 35% (21/60) respectively. Among cervical carcinoma patients, the expression of Syk mRNA was detected in one out of 13 cases with lymph node metastasis (1/13) and in 20 out of 47 cases with no lymph node metastasis (43%). The methylation of Syk gene in promoter region was detected in 34 out of 60 cases of cervical carcinoma (57%) ; while there was no methylation in CIN cases. In 13 cases with lymph node metastasis, 11 were found to have the methylation of Syk gene. The methylation rate of Syk promoter in cervical carcinoma was higher than that of CIN tissue( x~2 = 7. 13, P ＜0. 01 ). The methylation status of Syk gene was correlated with the lymph node metastasis ( P＜ 0. 05 ), but not with other clinicopathological parameters ( P ＞ 0. 05). There was a significant correlation between methylation status and expression level of Syk gene ( P ＜ 0. 05 ). The hypermethylation leads to silencing of the Syk gene in human cervicalcarcinoma. Syk hypermethylation may be associated with oncngenesis, metastasis of cervical carcinoma.