Search PubMed⌕ Search

Biomedical subjects

H Ding

Publications and source records attributed to H Ding.

197 records · Page 11Linked to original sources
PubMed1990

Production and characterization of monoclonal antibodies against tissue-type plasminogen activator.

Four hybridoma clones, TA1, TA2, TA3 and TA4, producing monoclonal antibodies against t-PA were obtained by fusion of mouse myeloma cells (SP2/0 or NS-1) with mouse spleen cells previously immunized with purified t-PA. The antibody titers of the four hybridoma ascites were higher than 1 x 10(5) determined by ELISA. The double immune diffusion test showed that all hybridoma supernatants contained mouse IgG1. These monoclonal antibodies reacted only with t-PA, and rt-PA prepared by genetic engineering, but not with UK. t-PA, activity was inhibited by these monoclonal antibodies completely.

Animals↗
PubMed1990

[Preliminary studies on the relationship between the blood pressure and renin-angiotensin system in brain and blood vessels in SHRSP].

This work analyzed the relationship between A I concentration in aorta tissue and systolic blood pressure (SBP) in stroke-prone spontaneously hypertensive rats (SHRSP) at different ages. The SBP of SHRSP increased progressively with the age until the age of 20 weeks, when the SBP of SHRSP no longer elevated but sustained at a relatively high and stable level. The A I concentration in aorta of SHRSP was much higher than that of Wistar Kyoto rats at all of the three different ages. Perfusion of captopril into the lateral cerebroventricle of SHRSP for four weeks evoked a considerable decrease of A I concentration in brain as well as a significant reduction of SBP accompanied by a decrement of A I concentration in aorta and concentration of norepinephrine and epinephrine in aorta tissue and plasma. The results further confirm the close relationship between the changed activity of renin-angiotensin system localized in blood vessels during hypertension and the pathogenesis of hypertension, and indicate the possible regulative control of A I generated from central nervous system over the production of A I from blood vessels by means of facilitating the activity of peripheral sympathetic nerve system.

Angiotensin II↗
PubMed1990

[Effect of the overactivated central renin-angiotensin system on the concentration of brain norepinephrine and epinephrine in stroke-prone spontaneously hypertensive rats and its significances].

The content of norepinephrine (NE) and epinephrine (E) in the brain of spontaneously hypertensive rats has proved abnormal, but the cause remained unknown. It was shown in the recent work that NE content in pons, posterior hypothalamus, nucleus caudatus and E concentration in medulla oblongata, anterior and posterior hypothalamus of 12-week old stroke-prone spontaneously hypertensive rats (SHRSP) were much higher than those of age-matched Wister-Kyoto rats (WKY). SHRSP also showed higher levels of systolic blood pressure (SBP) and brain angiotensin II (A II) than WKY. Intracerebroventricular (icv) perfusion of angiotensin-converting enzyme inhibitor captopril (20 micrograms for each time and three times for each day for four weeks) inhibited the synthesis of brain A II and reduced SBP and NE, E contents in all examined brain areas in SHRSP and WKY. However, the effects of chronically perfused captopril on SBP and brain NE, E levels in SHRSP were much more significant than in WKY. The results indicate that the modulatory effects of central renin-angiotensin system (RAS) on central adrenergic and noradrenergic system might be overactivated in SHRSP, which might partially responsible for the abnormally high levels of NE, E in some of the brain areas of SHRSP.

Angiotensin II↗
PubMed1988

Analysis of the causes of maternal death in China.

Data were analysed on maternal mortality for 1984 in 287 cities, districts, and counties in 21 provinces, municipalities, and autonomous regions of China. The total population covered was 177.55 million, and during the study period there were 2 483 269 live births and 1211 maternal deaths, corresponding to a maternal mortality rate of 48.8 per 100 000. The main cause of maternal death was obstetric haemorrhage, followed, in order, by cardiac diseases, toxaemia of pregnancy, hepatic disease, puerperal infection, and amniotic fluid embolism. The health care measures received by the mothers who died are analysed, and methods of reducing the maternal mortality rate are proposed.

Cause of Death↗
PubMedDate not supplied

Novel endothelium-derived relaxing factors. Identification of factors and cellular targets.

Nitric oxide (NO), together with prostacyclin (PGI2), mediates shear stress and endothelium-dependent vasodilator-mediated vasorelaxation. In the presence of inhibition of NO synthase (NOS) with nitroarginine analogues, such as of N(w)-nitro-L-arginine methyl ester (L-NAME) and N(w)-nitro-L-arginine (L-NNA), and indomethacin, to inhibit cyclooxygenase (COX) and the synthesis of PGI2, many blood vessels still respond with an endothelium-dependent relaxation to either chemical [i.e. acetylcholine (ACh)] or mechanical (shear stress) activation. This non-NO and non-PGI2 vasorelaxation appears to be mediated by hyperpolarization of the vascular smooth muscle cell (VSMC). Although NO can hyperpolarize VSMC, a novel mediator, the endothelium-derived hyperpolarizing factor (EDHF), which opens a VSMC K(+) channel(s) notably in resistance vessels, has been proposed. Little agreement exists as to the nature of this putative factor, but several candidate molecules have been proposed and evidence, notably from the microcirculation, suggests that endothelium-dependent hyperpolarization (EDH) may be mediated via low electrical resistance coupling via myoendothelial gap junctions. We describe a number of techniques that are being used to identify EDHF and present data that address the contribution of a small increase in extracellular K(+) as an EDHF.

Animals↗
PubMedDate not supplied

Acute effects of total suspended particles and sulfur dioxides on preterm delivery: a community-based cohort study.

The acute effects of air pollution on preterm delivery were examined in a prospective cohort in Beijing, China. From early pregnancy until delivery in 1988, we followed all registered pregnant women who lived in four residential areas of Beijing. Information for both mothers and infants was collected. Daily air pollution and meteorological data were obtained independently. The sample for analysis included 25,370 resident women who gave first live births in 1988. Multiple linear regression and logistic regression were used to estimate the effects of air pollution on gestational age and preterm delivery (i.e., < 37 wk), with adjustment for outdoor temperature and humidity, day of the week, season, maternal age, gender of child, and residential area. Very high concentrations of ambient sulfur dioxide (mean = 102 micrograms/m3, maximum = 630 micrograms/m3) and total suspended particulates (mean = 375 micrograms/m3, maximum = 1 0003 micrograms/m3) were observed in these areas. There was a significant dose-dependent association between gestational age and sulfur dioxide and total suspended particulate concentrations. The estimated reduced duration of gestation was .075 wk (12.6h) and .042 wk (7.1 h) for each 100-micrograms/m3 increase in sulfur dioxide and total suspended particulates 7-d lagged moving average, respectively. The adjusted odds ratio for preterm delivery was 1.21 (95% CI = 1.01-1.46) for each in micrograms/m3 increase in sulfur dioxide, and was 1.10 (95% CI = 1.01-1.20) for each 100-micrograms/m3 increase in total suspended particulates. In addition, the gestational age distribution of high-pollution days was more skewed toward the left tail (i.e., very preterm and preterm), compared with low-pollution days. We concluded that high levels of total suspended particulates and sulfur dioxide, or of a more complex pollution mixture associated with these pollutants, appear to contribute to excess risk of preterm delivery in this population. Further work need to be carried out, with more detailed information on personal exposure and effect modifiers.

Adult↗