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Biomedical subjects

Z W Li

Publications and source records attributed to Z W Li.

At least 73 records · Page 4Linked to original sources
PubMed1991

Effect of experimental acute hypertension of the biliary tract on hemodynamics and activity of the major splanchnic nerve in rabbits.

An experimental study of the effect of acute biliary hypertension on hemodynamics and activity of the major splanchnic nerve was conducted in Japanese big ear white rabbits. A catheter with an inflatable rubber bag fixed to its anterior end was inserted into the extrahepatic biliary duct via the duodenum, and a biliary high pressure of 20 kFa (150 mmHg) was created and maintained for 2 h by inflating the bag with water. The right major splanchnic nerve was isolated and the impulse frequencies of the nerve were recorded during the study. Arterial blood pressure was also dynamically monitored. A significant fall of the arterial blood pressure (P less than 0.01) and an increase in impulse frequency of the nerve (P less than 0.01) were found in this "simple type" acute biliary high pressure without infection. Biliary decompression immediately eliminated these abnormalities (P less than 0.01). The drop in blood pressure was much less prominent if the right splanchnic nerve was blocked prior to biliary high pressure.

Animals↗
PubMed1991

[Effect of LH-FSH releasing hormone on the sensitivity of cholinergic and adrenergic receptors in toad spinal ganglion neurons].

Intracellular recordings were performed on 81 neurons from 53 isolated toad spinal ganglia (SG). The effects of LH-FSH releasing hormone on the sensitivities of muscarinic receptors and alpha-adrenoceptors located on the soma of SG neurons were observed. Perfusing SG with atropine 10 mumol.L-1 in Ringer's solution depressed the amplitude of depolarization response induced by acetylcholine (ACh, 10-100 mumol.L-1). The depolarization and hyperpolarization induced by norepinephrine (NE, 10-100 mumol.L-1) were blocked by alpha 1-adrenoceptor antagonist prazosin and alpha 2-adrenoceptor antagonist yohimbine respectively. These results indicated that ACh-induced depolarization was mediated by muscarinic receptors while NE-induced depolarization and hyperpolarization were mediated by alpha 1- and alpha 2-adrenoceptors respectively. On the other hand, perfusing SG with LH-FSH releasing hormone 10 mumol.L-1 in Ringer's solution increased the depolarization response caused by ACh or NE, but attenuated NE-caused hyperpolarization response. The above results suggest that LH-FSH releasing hormone may modulate the sensitivities of muscarinic receptors and alpha-adrenoceptors on the soma membrane of toad SG neurons.

Animals↗
PubMed1991

Cloning and expression of penicillin G acylase gene in Bacillus megaterium.

Bacillus megaterium BM1, which produces penicillin G acylase (PGA), has been isolated. Gene encoding for PGA was cloned into E. coli MC1061 using pBR322 as the vector, obtaining a recombinant plasmid pBmPA4 containing 9.9 kb inserted DNA. Restriction map of the plasmid was analyzed. A pBmPA5 containing 4.9 kb was gained by deletion in vitro. Both pBmPA4 and pBmPA5 clones can be expressed in E.coli MC1061, and their expressions were induced by phenylacetic acid.

Bacillus megaterium↗
PubMed1991

[Determination of antitumour drug mitoxantrone in plasma using HPLC column switching technique].

An automated clean up and concentration method by column switching is described for the assay of mitoxantrone, an antitumour drug in plasma. The system uses a YWG-CN short precolumn for on-line clean up and concentration and a Shimpack CLC-ODS analytical column for separation. Water is used as pretreat mobile phase and 48% methanol in ammonium acetate (0.2 mol/L pH 1.9) is used as analytical mobile phase. The plasma sample is treated with methanol and ultrasonated for 10 min. The supernatant of treated sample is directly injected to precolumn. The recovery of clean up is 85%. The wavelength used for detection is 658 nm and the concentration of detection limit is 6 ng/ml in plasma. The procedure is simple and the method is sensitive.

Adult↗
PubMed1991

The crystal structure of silver carp insulin at medium resolution.

It is an important way of surveying the structure-function relationship of insulin to study insulins from different species. Based on the structure model of an orthorhombic crystal obtained by the molecular replacement method, the crystallographic refinement of a hexamer of silver carp insulin in an asymmetric unit has been carried out with 2.8 A resolution data using the restrained least-squares method. The comparisons of insulin structures have shown that the six silver carp insulin molecules have very similar but not identical three-dimensional structures which are similar to the known 2 Zn pig insulin structure but remarkably different in some local conformations.

Animals↗
PubMed1990

[Direct injection of plasma to determine famotidine in plasma using HPLC column switching technique].

An automated high performance liquid chromatographic switching system is described for the analysis of famotidine, an H2-receptor antagonist in plasma. The system used YWG-C18 short precolumn for on-line sample clean-up and a Shimpack CLC-ODS analytical column for separation. A solution of 0.2 mol/L acetic acid was used as pretreatment mobile phase and 14% (v/v) methanol in ammonium acetate (0.2 mol/L) was used as analytical mobile phase. The detection was at 267 nm and the detection limit was 12 ng/ml plasma. Plasma sample was diluted with acetic acid (0.2 mol/L) and injected directly on the HPLC system. The procedure of clean-up is simple and automatic. The recovery of clean-up is 84.1%.

Adult↗
PubMed1990

[Effect of acetylcholine on membrane potential in toad dorsal root ganglion neurons and its ionic basis].

Intracellular recordings were made to investigate the effect of acetylcholine (ACh) on membrane potential of neurons in isolated toad dorsal root ganglion (DRG). In the 73 neurons examined, 67 were of type A, and the remaining 6 of type C cell. The resting membrane potential of these two types of cells was -67.5 +/- 1.3 mV (mean +/- SE). During the application of ACh (4 x 10(-4)-6 x 10(-4) mol/L) four types of the membrane potential changes were observed: (1) hyperpolarization of 9.1 +/- 3.0 mV (mean +/- SE, n = 23); (2) depolarization of 12.9 +/- 2.2 mV (mean +/- SE, n = 20); (3) biphasic response, i.e., hyperpolarization of 8.0 +/- 2.4 mV (mean +/- SE) followed by depolarization of 10.9 +/- 3.1 mV (mean +/- SE, n = 24); (4) no change (n = 6). The hyperpolarization induced by ACh could be blocked by atropine (1.3 x 10(-5) mol/L, n = 23), and ACh-induced depolarization could be abolished by coperfusion of d-tubocurarine (1.4 x 10(-5) mol/L) and hexamethonium (1.4 x 10(-5) mol/L, n = 18). During ACh hyperpolarization the membrane conductance was increased by 13.8% and the reversal potential was about -96 mV (n = 3). TEA (20 mmol/L) enhanced ACh depolarization amplitude by 48.2 +/- 3.2% (mean +/- SE, n = 6), and depressed ACh hyperpolarization by 79.4 +/- 4.3% (mean +/- SE, n = 8), MnCl2 (4 mmol/L) decreased the ACh depolarization and hyperpolarization by 54.2 +/- 7.2% (mean +/- SE, n = 5) and by 69.2 +/- 6.4% (mean +/- SE, n = 14) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Neuropeptide processing in regional brain slices: effect of conformation and sequence.

The central enzymatic stability of des-enkephalin-gamma-endorphin and its synthetic analogs [cycloN alpha 6, C delta 11]beta-endorphin-[6-17] and [Pro7, Lys(Ac)9]-beta-endorphin[6-17] was studied in vitro using a newly developed, regionally dissected rat brain slice, time course incubation procedure. Tissue slice viability was estimated as the ability of the brain slice to take up or release gamma-[3H]aminobutyric acid after high K+ stimulation. Results demonstrated stability of uptake/release up to 5 hr of incubation, suggesting tissue viability over this period. The estimated half-life of peptides based on the results obtained in our incubation protocol suggest that the peptides studied are metabolized at different rates in the individual brain regions tested. A good correlation exists between the high enzyme activity of neutral endopeptidase (EC 3.4.24.11) and the rapid degradation of des-enkephalin-gamma-endorphin and [cycloN alpha 6, C delata 11]beta-endorphin-[6-17] in caudate putamen. Proline substitution combined with lysine acetylation appears to improve resistance to enzymatic metabolism in caudate putamen and hypothalamus. However, cyclization of des-enkephalin-gamma-endorphin forming an amide bond between the alpha-NH2 of the N-terminal threonine and the gamma-COOH of glutamic acid did not improve peptide stability in any brain region tested. The present study has shown that the brain slice technique is a valid and unique approach to study neuropeptide metabolism in small, discrete regions of rat brain where peptides, peptidases and receptors are colocalized and that specific structural modifications can improve peptide stability.

Amino Acid Sequence↗
PubMed1989

Effect of acetylcholine on membrane potential in toad dorsal root ganglion neurons and its underlying ionic basis.

Intracellular recordings were made to investigate the responses of membrane potential to acetylcholine (ACh) on neurons in isolated toad dorsal root ganglion (DRG). In the 73 neurons examined, 67 were of type A, and the remaining 6 of type C cell. The resting membrane potential of these two types of cells was -67.5 +/- 1.3 mV (means +/- SE). During the application of ACh (4 x 10(-4)-6 x 10(-4) mol/L), the changes in membrane potential were as follows: 1) hyperpolarization, with amplitude of 9.1 +/- 3.0 mV (means +/- SE; n = 23); 2) depolarization, with amplitude of 12.9 +/- 2.2 mV (means +/- SE; n = 20); 3) biphasic response, i.e., hyperpolarization with amplitude of 8.0 +/- 2.4 mV (means +/- SE) followed by depolarization with amplitude of 10.9 +/- 2.1 mV (means +/- SE) (n = 24); no effect (n = 6). The hyperpolarization induced by ACh was blocked by superfusion with atropine (1.3 x 10(-5) mol/L; n = 23), while ACh depolarization was blocked by the mixture of d-tubocurarine (1.4 x 10(-5) mol/L) and hexamethonium (1.4 x 10(-5) mol/L) (n = 18). When ACh caused hyperpolarization, the membrane conductance was increased by 13.8% and the reversal potential was about -96 mV (n = 3). TEA (20 mmol/L) superfusion enhanced ACh depolarization amplitude by 48.2 +/- 3.2% (means +/- SE; n = 6), and depressed ACh hyperpolarization amplitude by 79.4 +/- 4.3% (means +/- SE; n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

[Ionic mechanism of noradrenaline-induced membrane potential changes of neurones in toad dorsal root ganglion].

The membrane conductance and reversal potential were determined for neurones in toad dorsal root ganglion (DRG) with intracellular recording technique during depolarization or hyperpolarization induced by noradrenaline (NA). The effects of blocking agents for potassium or calcium channels on NA-induced membrane potential responses were examined. In 15 neurones, the NA-induced depolarization was accompanied by a 32.6% decrease of membrane conductance; in other 4 neurones, the depolarization was accompanied by an initial increase and subsequent decrease in membrane conductance. The NA hyperpolarization was associated with an increase of membrane conductance by 16.2% (n = 8). The mean reversal potential of NA-induced depolarization was -88.5 +/- 0.9 mV (means +/- SE, n = 4). The NA-induced hyperpolarization was nullified at -89 to -92 mV of membrane potentials (n = 3). Tetraethylammonium superfusion enhanced NA depolarization amplitude by 73.7 +/- 11.9% (means +/- SE, n = 7) and depressed NA hyperpolarization amplitude by 40.5% (n = 4). Intracellular injection of CsCl increased phenylephrine-induced depolarization by 34.5% (n = 4). MnCl2 superfusion decreased the amplitudes of NA-induced depolarization by 50.5 +/- 9.9% (means +/- SE, n = 10), and of NA-induced hyperpolarization by 89.5 +/- 4.9% (means +/- SE, n = 7) respectively. The results suggest that the depolarization or hyperpolarization induced by NA might be mediated by the alteration in activation of K+ or Ca2+ channels.

Animals↗