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Biomedical subjects

Y Ruan

Publications and source records attributed to Y Ruan.

77 records · Page 5Linked to original sources
PubMed1989

[Polymorphism of the affinity of muscarinic receptors in the gastric smooth muscles of guinea pigs].

In the experiment of contraction of guinea pig gastric smooth muscle, it was found that pD2 of acetylcholine for longitudinal and circular smooth muscles from guinea pig gastric fundus and body were 6.5 and 4.0 respectively. The pA2 values of atropine for these smooth muscles were approximately 10 and 8.5 respectively. This suggests that there were two kinds of muscarinic receptors of different affinities in the stomach and these receptors played a role in contractile function in longitudinal and circular smooth muscles. Specific [3H]-QNB binding to homogenates of gastric smooth muscles were also studied by using the method described by Yamamura et al. It was also found that high and low affinity bindings in the homogenates of gastric smooth muscles. The KD values of various homogenates of high and low affinity bindings were 1.8 and 18 nmol/L respectively. Since protein modulators with various functions showed different effects of the bindings of two components to labeled ligand, it is therefore concluded that the two components were the binding sites with different affinities.

Acetylcholine↗
PubMed1987

Identification of the Serratia marcescens hemolysin determinant by cloning into Escherichia coli.

A cosmid bank of Serratia marcescens was established from which DNA fragments were cloned into the plasmid pBR322, which conferred the chromosomally encoded hemolytic activity to Escherichia coli K-12. By transposon mutagenesis with Tn1000 and Tn5 IS50L::phoA (TnphoA), the coding region was assigned to a DNA fragment, designated hly, comprising approximately 7 kilobases. Two proteins with molecular weights of 61,000 (61K protein) and 160,000 (160K protein) were expressed by the pBR322 derivatives and by a plasmid which contained the hly genes under the control of a phage T7 promoter and the T7 RNA polymerase. When strongly overexpressed the 160K protein was released by E. coli cells into the extracellular medium concomitant with hemolytic activity. The genes encoding the 61K and the 160K proteins were transcribed in the same direction. Mutants expressing a 160K protein truncated at the carboxy-terminal end were partially hemolytic. Hemolysis was progressively inhibited by saccharides with increasing molecular weights from maltotriose (Mr 504) to maltoheptaose (Mr 1,152) and was totally abolished by dextran 4 (Mr 4,000). This result and the observed influx of [14C]sucrose into erythrocytes in the presence of hemolytic E. coli transformants under osmotically protective conditions suggest the formation of defined transmembrane channels by the hemolysin.

Bacterial Proteins↗
PubMedDate not supplied

Studies on the characterization of the subtype(s) of muscarinic receptor involved in prostacyclin synthesis in rabbit cardiomyocytes.

The present study was conducted to localize and characterize the subtype(s) of muscarinic receptor involved in prostacyclin (PGI2) production elicited by the cholinergic transmitter acetylcholine (ACh) in various cell types in the rabbit heart. ACh increased PGI2 synthesis measured as 6-keto-PGF1 alpha, in cultured coronary endothelial cells and freshly dissociated ventricular myocytes in a dose dependent manner but not in cultured coronary smooth muscle cells of rabbit heart. McN-A-343, a partially selective M1 muscarinic ACh receptor (mAChR) agonist, did not alter 6-keto-PGF1 alpha synthesis in these cell types. ACh induced 6-keto-PGF1 alpha synthesis in coronary endothelial cells and ventricular myocytes was not altered by a low concentration (10(-8) M) of pirenzipine, an M1 mAChR antagonist but was reduced by a higher concentration (10(-6) M). In coronary endothelial cells ACh induced 6-keto-PGF1 alpha production was reduced by hexahydro-sila-difendial (HHSiD), an M3 mAChR antagonist, and in ventricular myocytes by both 11-¿2-[(di-ethylamino) methyl]-1-piperidinyl]acetyl-5,11-dihydro-6-H-pyrido-[2,3-b]-benzodiazep ine-6 one¿ (AF-DX 116), an M2 receptor antagonist, and HHSiD. The decrease by ACh of isoporterenol stimulated cAMP accumulation was minimized by AF-DX 116 but not by HHSiD or pirenzipine. Pertussis toxin treatment minimized ACh induced decrease in isoproterenol stimulated rise in cAMP and ATP release, but not ACh induced 6-keto-PGF1 alpha synthesis. These data suggest that ACh stimulates prostacyclin production in coronary endothelial cells via M3 mAChR and in ventricular myocytes M2 and M3 mAChR. Moreover, ACh induced decrease in cAMP, but not the increase in 6-keto-PGF1 alpha production, is mediated by pertussis toxin sensitive G alpha i proteins in these cells.

6-Ketoprostaglandin F1 alpha↗