An epidemiological study on mental retardation among children in Chang-qiao area of Beijing.
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Biomedical subjects
Publications and source records attributed to Q Lin.
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Dimethyl sulfoxide (DMSO) stimulates tyrosine phosphorylation of the hepatic EGF receptor in isolated membrane preparations. To determine whether DMSO affects EGF binding, primary cultures of rat hepatocytes were incubated with 1-10% DMSO for 30 min prior to the addition of 125I-EGF. DMSO (1-2%) reduced specific 125I-EGF binding; the effect was maximal (a 40-60% reduction) at 5-7.5% DMSO and was reversed by removing the DMSO. Scatchard analysis showed that the reduction in binding was due to a change in receptor affinity. The decrease in binding was not seen when other, slightly less polar, solvents (eg, acetone and ethanol) were tested. DMSO also reduced 125I-EGF binding to purified rat liver plasma membranes. This reduction was seen in the absence of added ATP and in membranes that had been pretreated with TLCK, a tyrosine kinase inhibitor. Thus, completion of the receptor autophosphorylation reaction was not necessary to effect the change. The data are consistent with a DMSO-induced alteration of receptor conformation that reversibly reduces receptor affinity.
Hydrocortisone and dexamethasone produced a time-dependent increase [125I]epidermal growth factor [( 125I]EGF) binding in primary cultures of isolated rat hepatocytes. Maximally effective doses of glucocorticoids resulted in a 70-100% increase in binding. The effect was similar when hepatocytes were maintained on collagen-coated plates or directly on culture dishes. The glucocorticoid-mediated increase in [125I]EGF binding could be detected after 4 h exposure to glucocorticoid and was substantial by 8 h. The major effect of glucocorticoid appeared to be to increase the number of EGF receptors. While insulin (100 nM) had no effect on basal [125I]EGF binding, it significantly inhibited the increase produced by the glucocorticoid. Since the inhibitory effect of insulin was only observed when insulin was added with the inducing glucocorticoid, insulin appears to inhibit an early hydrocortisone-mediated event.
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The partial purification of human transthyretin (TTR) by high performance affinity chromatography with the help of other separation techniques is described in the present paper. A new affinity medium was prepared with a monosized (ca. 10 microns particle size) macroporous resin as the support and thyroxine (T4) as the ligand. The purification of TTR was carried out in a few simple steps involving serum precipitation, anion exchange, Thyroxine affinity chromatography and gel filtration. The overall yield was 29% and the refined TTR contained less than 2% impurities as analyzed by RP-HPLC. When TTR was administrated to the culture medium DMEM of liver tumor strain SMMC-7721, a true inhibition of cell growth (ca. 50%) was observed as an actual decrease in cell number over time.
A high performance liquid chromatographic method for the simultaneous determination of cimetidine and its major metabolite, cimetidine sulfoxide, was developed. These compounds and the internal standard, ornidazole, were extracted from 0.5 mL of serum using a solid phase Bond Elut C18 analytical column with detection at 229 nm. Absolute recoveries were 94 to 103%, 93 to 104%, and 95 to 105% for cimetidine, cimetidine sulfoxide, and ornidazole, respectively. The minimum detection limit for cimetidine was 0.1 mg/L and for cimetidine sulfoxide was 0.05 mg/L when the concentrating step was used. Cimetidine and cimetidine sulfoxide demonstrated linearity up to 10 mg/L and 7.5 mg/L respectively, with the between-run precision of less than a 5% coefficient of variation for both compounds. Interferences from other drugs tested or endogenous substances in serum were not detected. The mobile phase was recycled to maintain better long term column stability and to minimize solvent cost. The instability of the drugs in solution was circumvented with a reduced-pressure drying process that produced working standards possessing longterm stability. The problem of drug interconversion observed during sample storage and with concentrating steps was controlled also. In addition, a resolution test mixture was chromatographed daily to control chromatographic quality.
Hypertension was induced in Sprague-Dawley and Wistar rats by irregular foot shocks combined with a buzzing noise for 2 h twice a day for 1-2 weeks. The plasma catecholamine, corticosterone, angiotensin II, glucose and lipids were found to increase in parallel. The acetylcholine (ACh) and choline acetyltransferase in rostral ventrolateral medulla (rVLM) increased markedly). Microinjection of ACh or cholinergic agonists into rVLM induced a pressor effect, and microinjection of M receptor blockers had a depressor effect. Electrophysiological studies showed that the stress-induced hypertension was closely related to the activation of a cholinergic system in rVLM. Microinjection of corticoids into rVLM had led to a pressor response which could be blocked by Ru38486, spironolactone, cholinergic blockers or verapamil. Microinjection of morphine and mu- or delta-receptor agonists into rVLM caused bradycardia and a reduction of arterial pressure that could be blocked by naloxone.
Oridonin, an extract from the Chinese herb Rabdosia rubescens, is currently one of the most important traditional Chinese herbal medicines. We investigated the anti-proliferative effect of oridonin on the lung cancer cell line SPC-A-1 and its mechanism of action. Growth inhibition was measured using a microculture tetrazolium assay and apoptosis was measured by several standard methods. Western blot analysis measured the expression of bcl-2 and bax proteins. Oridonin (> 28 micromol/l) inhibited the growth of SPC-A-1 cells and induced apoptosis. Marked morphological changes indicative of apoptosis were observed, especially in cells treated with oridonin for 48 - 60 h. Western blot analysis revealed downregulation of bcl-2 and upregulation of bax proteins following treatment with oridonin for 48 h. We conclude that oridonin demonstrated anti-proliferative and apoptosis-inducing effects on SPC-A-1 cells in vitro, and that changes in bcl-2 and bax protein levels may play an important role in its mechanism of action.