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Biomedical subjects

T Kusano

Publications and source records attributed to T Kusano.

At least 181 records · Page 10Linked to original sources

Degradation of phospholipid in Pseudomonas aeruginosa induced by polymyxin B.

Effects of polymyxin B on the synthesis and degradation of lipid, ribonucleic acid (RNA) and protein in Pseudomonas aeruginosa were investigated. It was found that polymyxin B caused a marked degradation of the lipid fraction which was prelabeled with (3H-2)-glycerol. Thin-layer chromatographic analysis indicated that the main degraded lipids were phosphatidylethanolamine and phosphatidylglycerol, which constituted 80% and 15% of the total phospholipids of this organism, respectively. Polymyxin B also inhibited synthesis of RNA and protein in vivo. The severe inhibition of the uptake of labeled amino acids by polymyxin B indicated that the observed inhibition of RNA and protein synthesis possibly occurred at the level of substrate transports. The degradation of phospholipid might account for the defective membrane activities.

Bacterial Proteins↗

A new reduced human-mouse somatic cell hybrid containing the human gene for adenine phosphoribosyltransferase.

A system that selects for the gene directing synthesis of the enzyme adenine phosphoribosyltransferase (APRT) uses the antibiotic alanosine to prevent endogenous synthesis of adenylic acid. With the aid of this system, a new series of human-mouse hybrids has been prepared between wild type human diploid fibroblasts and an enzyme-deficient mouse line. Survival of the hybrids depended upon the presence of the APRT, which was shown to have the isoelectric pH characteristic of the human enzyme and not that of the mouse. Reduced hybrids containing the enzyme lacked all human biarmed chromosomes, so that unless a rearrangement had occurred, the aprt gene must be located on an acrocentric chromosome. The hybrid cells became APRT(-) with a frequency of 2 x 10(-3), probably by loss of the human aprt chromosome. The APRT(-) progeny could be obtained selectively by growth in medium containing fluoroadenine.

Adenine↗

Human-mouse hybrid cell lines and susceptibility to poliovirus. I. Conversion from polio sensitivity to polio resistance accompanying loss of human gene-dependent polio receptors.

A number of human-mouse somatic hybrid cell lines have been prepared, containing from 3 to 12 human biarmed chromosomes. These lines were susceptible to poliovirus type 1, producing viral yields comparable to those of the human parental cells. A small proportion of the cells of these lines survived the polio infection, and their progeny were solidly resistant to reinfection with the virus. Both sensitive and resistant hybrids produced virus following infection with viral ribonucleic acid, indicating that the cytoplasm of the resistant hybrids was able to support viral multiplication. Viral adsorption studies carried out at 4 C showed that the resistant sublines had negligible ability to adsorb the virus. It was concluded that the hybrid cells became resistant to polio through loss of the human chromosome bearing the gene for the receptor substance.

Adsorption↗

Human-mouse hybrid cell lines and susceptibility to polio virus. II. Polio sensitivity and the chromosome constitution of the hybrids.

A number of human-mouse hybrid cell lines with partial human chromosome complements were sensitive to poliovirus because the cells contained the viral receptor substance of human origin. Infection of the lines with one type of poliovirus regularly led to the survival of a few cells, whose progeny were found to be resistant to all types of poliovirus. Comparison of the chromosomes of sensitive hybrids and their resistant sublines showed no consistent difference in the number of biarmed human chromosomes of any group. The number of acrocentrics was always lower in the resistant hybrids than in the corresponding sensitive lines. It is suggested that the human chromosome bearing the polio receptor gene is an acrocentric.

Animals↗

Percutaneous transhepatic cholangioscopic lithotripsy and change of biliary manometry patterns.

BACKGROUND/AIMS: Percutaneous transhepatic cholangioscopic lithotripsy (PTCSL) is used to remove bile duct stones. This work aims to evaluate the clinical usefulness of PTCSL and the reversibility of the terminal bile duct dysfunctions after PTCSL. METHODOLOGY: Thirty patients who underwent PTCSL using mechanical and/or electrohydraulic lithotripsy over the past 10 years (20 patients with common bile duct stones and 10 with intrahepatic bile duct stones) were evaluated. Terminal bile ductal pressure was measured using the percutaneous transhepatic biliary drainage (PTBD) tube prior to and after lithotripsy by means of variable-load cholangiomanometry. RESULTS: Complete stone extraction was possible in 26 patients (86.7%). The other 4 patients had intrahepatic stones. Complications included 2 cases of hemobilia, one of pneumonia, and 3 of localized peritonitis. Of 26 patients without residual stones, only 4 patients had a linear pressure flow (P-F) pattern which indicates normal biliary tract function prior to lithotripsy. In 17 of 22 patients with other type P-F patterns, however, these types also changed to a linear pattern after complete removal of stones. The P-F pattern of the other 5 patients remained unchanged. CONCLUSIONS: PTCSL is a safe and efficient method treating biliary tract lesions while preserving the function of the sphincter of Oddi. The terminal biliary tract function normalized after stone removal. Thus, PTCSL was useful for patients with complicated bile duct stones not accessible to endoscopic retrograde management.

Bile Ducts↗

Vascular reconstruction of the hepatic artery using the gastroepiploic artery: a case report.

A 59 year-old woman with obstructive jaundice secondary to proximal bile duct carcinoma underwent percutaneous transhepatic biliary drainage (PTDB). This revealed complete obstruction of the bifurcation of the hilar hepatic duct and encasement of the right hepatic artery. Wedged hilar hepatectomy with combined resection of the extrahepatic bile duct, gallbladder, and the encased right hepatic artery was performed. The hepatic artery was reconstructed using an in situ right gastroepiploic artery (GEA) pedicle graft. The anastomosis was protected with fatty tissue from the greater omentum. This technique can be used to reconstruct the hepatic artery after radical surgery for malignant hepatobiliary and pancreatic disease.

Arteries↗