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Biomedical subjects

A Noda

Publications and source records attributed to A Noda.

At least 217 records · Page 12Linked to original sources

Pancreatic endocrine function in experimental pancreatolithiasis in dogs.

In attempt to clarify changes of pancreatic endocrine function in human calcified pancreatitis at its earlier stages, an experimental model of pancreatolithiasis comparable to the human disease was produced in six dogs after incomplete ligation of the major pancreatic duct. Endocrine function was serially examined by intravenous glucose (0.5 g/kg) tolerance test and insulin (0.5 U/kg) tolerance test before and 3, 6, and 12 months after the duct ligation. Neither alpha nor beta cell dysfunction became apparent until 12 months after the ligation. The disappearance rate of glucose in an intravenous glucose tolerance test decreased from 2.92 +/- 0.41 (mean +/- SE) of the preligation value to 1.58 +/- 0.17%/min at the end of the 12 months period (p less than 0.02). Plasma insulin response to glucose was also reduced significantly. Although hypoglycemia induced during an intravenous insulin tolerance test was maximal in the 12th month, distinct response of plasma pancreatic glucagon to the hypoglycemia disappeared. Endocrine insufficiency of the pancreas observed in this experimental model was similar to that reported in human pancreatolithiasis, although the severity is less.

Animals↗

Follow-up study of chronic pancreatitis.

The general profile of pain in the evolution of pancreatitis was analysed in relation to exocrine and endocrine pancreatic function in 127 patients with primary chronic pancreatitis followed up over 3 years. Pain decreased or disappeared in 67.8% and 55.9% of calcifying pancreatitis, respectively. While pancreatic exocrine function remained abnormal in spite of an improvement of pain in 72% of 18 patients with calcifying pancreatitis, it improved with the amelioration of pain in 64% of 25 patients with non-calcifying pancreatitis during the follow-up period. Alcohol abstinence seems most important for pain relief in patients with non-calcifying pancreatitis but not calcifying pancreatitis. Changes in glucose tolerance test were not related with those in pain. In calcifying pancreatitis, 69.2% of patients with calcifying pancreatitis were diabetic or became so, while 66.7% of patients with non-calcifying pancreatitis remained non-diabetic during the observation period.

Adult↗

Metabolism of isoniazid and free hydrazine formation in isolated rat hepatocytes.

Isoniazid (INH) was incubated with isolated rat hepatocytes, and the amounts of acetyl-INH, monoacetylhydrazine, diacetylhydrazine and hydrazine formed were determined by gas chromatography-mass spectrometry (GC-MS). Subsequent analyses of kinetic parameters of metabolic pathways and enzymological study of rat liver homogenate revealed that hydrazine was formed preferentially from INH, catalyzed by soluble hydrolytic enzymes.

Animals↗

Characteristic biotransformation of aminopyrine in rat when administered with barbital.

After the administration of aminopyrine with or without barbital to rats, aminopyrine and its main metabolites were detected in plasma and the brain by means of gas chromatography-mass spectrometry. It was clarified that a marked increase of 4-monomethylaminoantipyrine was observed in the case of coadministration of aminopyrine and barbital, while the plasma level of aminopyrine decreased significantly compared with single administration.

Aminopyrine↗

Tissue distribution of isoniazid and its metabolites in rats.

Distribution of isoniazid and its metabolites was observed in the liver, kidney, lung and plasma after the subcutaneous administration of isoniazid to rats. The tissue levels of isoniazid, acetylisoniazid, acetylhydrazine, 1,2-diacetylhydrazine and hydrazine were determined by mass fragmentography using a gas chromatograph-mass spectrometer equipped with a multiple ion detector-peak matcher. Using the compounds labeled with a stable isotope as an internal standard, namely the isotope dilution method, made it possible to estimate trace amounts of these metabolites in the tissues. The amount of hydrazine was much less than the other hydrazines, but the metabolite which is well known as a mutagen, could be successfully detected in the tissues and plasma. The greater part of free hydrazine is formed through a direct hydrolysis of isoniazid. The isoniazid-hydrolyzing activity was found to be significantly higher in the liver homogenate. This suggested that hydrazine formation is mainly caused by hepatic hydrolysis.

Absorption↗

Microbial adjuvant and autoimmunity. IV. Production of lesions in the exocrine pancreas of mice by repeated injection of syngeneic pancreatic extract together with the capsular polysaccharide of Klebsiella pneumoniae.

Definite lesions in the exocrine pancreas were produced when SMA mice were immunized eight times at intervals of 30 days with a mixture of extract of pooled pancreas from syngeneic mice and the capsular polysaccharide of Klebsiella pneumoniae type I Kasuya strain (CPS-K), whereas no pancreatic lesions were produced in mice given CPS-K alone or pancreatic extract alone. The typical histological changes were characterized by infiltration with lymphocytes, plasma cells, and other mononuclear cells, degeneration and lysis of the acinar cells, destruction of the lobular architecture, and replacement of fatty tissue and fibrous connective tissue. The endocrine islets were well preserved. No specific histological changes were produced in the organs other than the pancreas in these mice. Most of mice immunized with pancreatic extract mixed with CPS-K produced serum precipitins to syngeneic pancreatic antigens. However, severe pancreatic lesions were also produced in mice showing no definite precipitin production.

Adjuvants, Immunologic↗