To explore the influence of angiotensinⅡ(AngⅡ) and aldosterone (Ald) on synthesis of collagen and activity of precollagenase secreted by cardiac fibroblasts.Sirus Red method was employed to evaluate collagen synthesis of cultured cardiac fibroblasts; typeⅠ collagen was measured by competitive ELISA; collagenase activity was tested by fluorescence spectrophotometry.At the doses of 10-9～10-7mol/L, AngⅡ could enhance gross and typeⅠ collagen production in a dose-dependent manner. Collagenase activity decreased with increasing concentration of AngⅡ. These effects of AngⅡcould be completely abolished by its receptor antagonist, saralasin. Ald might enhance gross and typeⅠ collagen production only at a higher concentration (10-7～10-8mol/L), whereas lower concentration (10-9mol/L) had no effect on it. These effects of Ald could be abolished by spironolactone,a specific Ald receptor antagonist. In addition, Ald could significantly decrease the activity of collagenase secreted from cultured cardiac fiboblasts at concentrations of 10-9～10-7mol/L within 24h，which could not be antagonized by 10-6mol/L spironolactone. The results suggested that AngⅡand Ald enhance cardiac fibroblasts collagen synthesis and inhibit collagenase activity ,resulting in net collagen accumulation resulted and acceleration of cardiac fibrosis.

Anopheles dims Peyton et Harrison, 1979 is an important malaria vector in Southeast Asia and China particularly in forested hilly zones. To establisha a laboratory mating colony for this mosquito is one of the subjects to be solved urgently in malaria research.This paper is to report our experience on breeding this mosquito. Ecological environment is created to simulate the natural conditions. The room-temperature of the insectary is 25?-28℃ and its relative humidity is around 80%.Mosquitoes are kept in cages with the si2e of 50 ? 50 ? 100cm. The larvae are fed with a mixture of de-fatted pig liver powder and yeast with a ratio of 1:3. The adults are fed with a mixture syrup containing 4% of orange juice, 10% of sucrose and other materials. The insectary is illuminated with a 3o w fluorescent light in the day time and a 15 w blue light in the night continuously to induce mating.The mating rate of the fourteenth generation reached 68% and the descendants bred can be used in research work now.

Objective To investigate the effect of hypert riglyceridemia on vascular endothelial function. Methods With high-resolution ultrasound, flow and nitroglycerin-induced dilatation of the brachial artery were determined in thirty hypertriglyceridemic patients and thirty healthy subjects as controls. Serum lipid and plasma endothelin (ET) were determined. Results In patients with hypertriglyceridemia,flow-induced vasodilatation was much reduced compared with that in the control subjects[(2.7±2.0)% vs (15.0±8.0)%, P<0.001］.However, vasodilatation in response to nitroglycerin were similar in both groups［(15.0±5.0)% vs (16.8±9.0)%, P>0.05].Plasma ET level in the hypertriglyceridemic group was significantly higher than that in the control group［(106.22±19.16) μg/L vs (72.37±14.06) μg/L, P<0.001].ConclusionEndothelium-dependent vasodilatation was impaired in patients with hypertriglyceridemia.

Very low density lipoprotein receptor (VLDLR) is thought to participate in the patho-genesis of atherosclerosis induced by VLDL and β-VLDL. The present study was undertaken to elu-cidate the effects of VLDL and β-VLDL on VLDLR expression and its signaling pathway. RAW264.7 cells were incubated with VLDL and β-VLDL. The expression of VLDLR mRNA was detected by RT-PCR. The transcriptional activity of VLDLR gene was detected in recombinant plasmid pGL4.2VR-luciferase transfected RAW264.7. Western blot assay was used to detect the changes of phosphorylated ERK1/2 protein. Inhibitors or activators were used to observe the signal pathway in-volving VLDLR expression regulation. The results showed that VLDL and β-VLDL stimulated ERKI/2 activity in a PKC-dependent manner. VLDL or β-VLDL-induced VLDLR expression on macrophages was extremely abolished by inhibitors ERKI/2 or PKC. Our findings revealed that VLDL or β-VLDL-induced VLDLR expression via PKC/ERK cascades and the effect was linked to the transcriptional activation of VLDLR gene promoter.

OBJECTIVETo investigate the effect of micronized fenofibrate on vascular endothelial function in patients with hypertriglyceridemia.

METHODSUsing high-resolution ultrasound, we measured flow- and nitroglycerin-induced dilatation of the brachial artery in 30 patients with hypertriglyceridemia before and after treatment with micronized fenofibrate at a dose of 200 mg once daily for 4 weeks. Simultaneously, both serum lipid and plasma endothelin (ET) levels were determined.

RESULTSAfter micronized fenofibrate therapy, serum triglyceride (TG) levels decreased significantly (P < 0.05). Plasma ET levels also decreased markedly [(82.66 +/- 15.46) microg/L vs. (106.22 +/- 19.16) microg/L, P < 0.001]. Flow-induced vasodilatation was much improved (11.0% +/- 9.0% vs 2.7% +/- 2.0%, P < 0.01). However, no significant changes in vasodilatation occurred in response to nitroglycerin (16.2% +/- 6.0% vs 15.0% +/- 5.0%, P > 0.05) in patients with hypertriglyceridemia.

CONCLUSIONSMicronized fenofibrate can improve impaired endothelium-dependent vasodilatation in patients with hypertriglyceridemia. Improving endothelial function may also be the mechanism responsible for the beneficial effects of micronized fenofibrate.

Adult ; Endothelium, Vascular ; drug effects ; physiology ; Female ; Fenofibrate ; pharmacology ; therapeutic use ; Humans ; Hypertriglyceridemia ; drug therapy ; Male ; Middle Aged ; Vasodilation ; drug effects