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G H Ding

Publications and source records attributed to G H Ding.

7 recordsLinked to original sources
PubMed1994

Experimental study of chuanxiong on cerebrovascular hemodynamic parameters.

In the experimental rabbit arteriosclerosis, the change of the cerebrovascular hemodynamic parameters (CVHP) and the effect of Chuanxiong (CX) on CVHP were observed. In arteriosclerosis group (AS group), the mean flow (Qmean), mean velocity (Vmean), maximal velocity (Vmax) and minimal velocity (Vmin) of the carotid blood flow and cerebrovascular compliance for zero pressure (CO) were significantly decreased (P < 0.05, 0.01), but the values of cerebrovascular peripheral resistance (R) and characteristic impedance (Zc) were significantly increased (P < 0.05 and 0.01), and the value of R showed significant positive correlation with the extent of carotid lesions (P < 0.01). All indexes of CVHP of the Chuanxiong group (CX group) were close to and had no significant difference from those of the normal group (N group) but Qmean, Vmean, Vmin, CO and R were significantly better than those of the AS group (P < 0.05, 0.01). These results showed that CX can effectively improve cerebrovascular hemodynamics.

Animals↗
PubMed1991

Vasopressin depolymerizes F-actin in toad bladder epithelial cells.

Vasopressin (AVP) induces the rapid fusion of water channel-containing vesicles with the luminal membrane of its target cell. We have carried out a quantitative study of the F-actin content of toad bladder epithelial cells, using the rhodamine phalloidin binding assay. As early as 1 min after AVP stimulation, there is a significant 15% reduction of cellular F-actin, which remains reduced by 20-30% for the duration of action of AVP. Comparable reductions were seen following 8-bromoadenosine 3',5'-cyclic monophosphate, 1-desamino-8-D-arginine vasopressin, and forskolin. F-actin content rose to and then exceeded that of control bladders after AVP washout. Inhibition of prostaglandin synthesis enhanced both water flow and the decrease of F-actin. In the living cell, stabilization of F-actin with NBD-phallacidin selectively inhibited water flow. In view of the rapidity of the response, we conclude that AVP shifts the equilibrium between F-actin and G-actin monomers, and this depolymerization may be required for vesicle fusion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Pharmacokinetics of [6]-gingerol after intravenous administration in rats.

A high-performance liquid chromatographic method to determine [6]-gingerol, a pungent constituent of ginger, in rat plasma was developed and a pharmacokinetic study was performed in rats. Quantitative analysis with high reproducibility was achieved for [6]-gingerol over the concentration range of 0.2-40 micrograms/ml. After bolus intravenous administration at a dose of 3 mg/kg, the plasma concentration-time curve was described by a two-compartment open model. [6]-Gingerol was rapidly cleared from plasma with a terminal half-life of 7.23 min and a total body clearance of 16.8 ml/min/kg. Serum protein binding of [6]-gingerol was 92.4%.

Animals↗
PubMed1987

Endocytosis by cultured mesangial cells and associated changes in prostaglandin E2 synthesis.

The mechanism of macromolecule uptake by cultured mesangial cells was studied by use of transmission electron microscopy. In parallel, we investigated the effect of macromolecular uptake on prostaglandin E2 (PGE2) formation. Cultured rat mesangial cells were studied in their third passage. As model molecules, we used colloidal gold particles (10 nm diameter) coated either with polyethylene glycol (PEG) or fresh serum (SCG). Mesangial cells were incubated from 1 to 60 min and up to 12 h with either PEG or SCG particles. Endocytosis of SCG significantly exceeded that of PEG particles. The mechanism involved binding to coated pits, followed by formation of coated vesicles (endosomes), and eventually delivery of particles to lysosomes. Pretreatment with cytochalasin B virtually prevented endocytosis of SCG particles, indicating active participation of the cytoskeleton. Determination of PGE2 production in parallel showed that SCG significantly stimulated PGE2 synthesis within minutes, whereas PEG-coated gold had no effect. When gold particles were coated with decomplemented serum instead of fresh serum, the stimulation of PGE2 was partially, but not completely, prevented, indicating that complement may be one, but not the only ligand responsible for enhanced PGE2 production. Stimulation of PGE2 synthesis by SCG was not dependent on actual endocytosis, as it was not altered by cytochalasin B pretreatment. Thus, surface ligand-receptor interaction may be sufficient to trigger PGE2 synthesis. The interaction between mesangial endocytosis and PGE2 production may be important for glomerular pathophysiology.

Animals↗
PubMed1987

Morphological aspects of the action of ADH.

Early studies employing biophysical techniques provided a model for ADH-induced water flow in which the number of small water-conducting channels in the outer facing membrane is increased by the hormone. With the development of new concepts and techniques in cell biology, the problem of ADH action now centers on organelle movement, fusion, endocytosis and vesicular traffic with the cell. In this review, endocytosis and vesicular traffic are discussed, and their application to the action of ADH is considered.

Animals↗
PubMed1986

Evidence that the heads of ADH-sensitive aggrephores are clathrin-coated vesicles: implications for aggrephore structure and function.

Antidiuretic hormone (ADH) induces the fusion of long tubular organelles (aggrephores) with the luminal membrane of the receptor cell, and the delivery of particle aggregates to the membrane. Water flow is believed to take place through the particles. Nothing is known about the origin of the particle aggregates, their incorporation into the aggrephores, or the possible relationship of the aggrephores to the vesicular traffic that takes place in the epithelial cell. In the present studies of the ADH-sensitive epithelial cells of the toad urinary bladder, we have found that the spherical heads of the aggrephores appear to be clathrin-coated vesicles. We propose that vesicles originating from sites such as the Golgi or the luminal membrane may be engaged in aggrephore assembly, the resupply of particle aggregates to the aggrephores, and/or the removal of aggregates, and that the aggrephores may be central points in the pattern of vesicular traffic in the cell.

Animals↗