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Biomedical subjects

R Komatsu

Publications and source records attributed to R Komatsu.

At least 37 records · Page 2Linked to original sources
PubMed1998

Idiopathic retroperitoneal fibrosis with duodenal obstruction successfully treated with corticosteroids.

We report a case of idiopathic retroperitoneal fibrosis presenting with duodenal obstruction. A 55-year-old man suddenly developed severe epigastric pain and was admitted to our hospital. On abdominal computed tomography (CT), a large retroperitoneal mass was found. Hypotonic duodenography showed obstruction of the third portion of the duodenum. He was diagnosed as idiopathic retroperitoneal fibrosis and was treated with prednisolone. The patient improved dramatically. He has been well for twelve months without any further treatment.

Duodenal Obstruction↗
PubMed1998

Effects of trifluoperazine and promethazine on the release of transmitter quanta at the mouse neuromuscular junction.

The present experiments examined the effects of phenothiazine derivatives, such as trifluoperazine and promethazine, on the release of transmitter quanta in preparations of the mouse diaphragm. The frequency (F, s-1) of miniature end-plate potentials and the quantal content (m) of endplate potentials were measured intracellularly at the same endplate in a bathing solution that contained 0.5-0.8 mM Ca2+ ions and 5 mM Mg2+ ions. Trifluoperazine (4 microM) significantly reduced both F and m. The inhibitory effect on m, but not on F, was subject to competition by Ca2+ ions. Promethazine at 48 microM, but not at 16 microM, reduced the quantal release. It was apparent that the effect of trifluoperazine was competitively antagonized by Ca2+ ions at motor nerve terminals.

Animals↗
PubMed1998

[Plaque progression and destabilization in human coronary arteries].

To verify the roles of angiotensin-converting enzyme (ACE) and vascular endothelial growth factor (VEGF) in the progression and destabilization of coronary atherosclerosis in humans, we have studied the expression of ACE and VEGF in coronary arterial segments, using immunohistochemical techniques. Our results strongly suggest that enhanced ACE expression in atheromatous plaques and ruptured plaques contributes greatly to the further progression of atherosclerosis via an increase in vascular angiotensin II formation. Our findings also suggest that distinct expression of VEGF play a role in the progression and destabilization of human coronary atherosclerosis.

Acute Disease↗
PubMed1993

[Changes in plasma and urinary calcium levels during cardiopulmonary bypass].

Plasma total protein, total calcium, ionized calcium and urinary calcium were measured in six patients scheduled for open heart surgery, and the effect of the administration of calcium during and after cardiopulmonary bypass (CPB) was studied. After the initiation of CPB, plasma total protein decreased significantly from 5.47 +/- 0.50 g.dl-1 to 2.55 +/- 0.23 g.dl-1 (P < 0.01). Total calcium also decreased from 2.14 +/- 0.29 mmol.l-1 to 1.38 +/- 0.07 mmol.l-1 (P < 0.01), and remained depressed during CPB. However, ionized calcium was not decreased and showed normal value during CPB because total protein concentration was decreased by hemodilution. Urinary calcium excretion increased gradually during CPB from 0.18 +/- 0.17 mmol.h-1 to 0.87 +/- 0.38 mmol.h-1 (P < 0.01) and the increase continued after CPB. Fractional excretion of filtered calcium increased from 0.85 +/- 0.63% to 54.16 +/- 36.52% (P < 0.05) accompanied with hypothermia. From these findings, reabsorption of the calcium in the kidney was thought to be inhibited by the influence of hypothermia at the early phases after weaning from CPB. When total protein returned to normal value after weaning from CPB, percentage of ionized calcium is predicted to diminish. We conclude that after weaning from CPB, administration of calcium is required because of the prolonged increase of urinary calcium excretion, particularly if blood containing citrate is given.

Aged↗
PubMed1992

Glucagonlike peptide-1(7-36)amide suppresses glucagon secretion and decreases cyclic AMP concentration in cultured In-R1-G9 cells.

We previously reported that GLP-1(7-36)amide had glucagonostatic action as well as insulinotropic action in the perfused rat pancreas. In this study, we examined the effect of GLP-1(7-36)amide on glucagon secretion and cAMP concentration in glucagon-secreting cell line, In-R1-G9. GLP-1(7-36)amide (1nM) significantly suppressed glucagon secretion and decreased cAMP concentration in the cells. GLP-1(1-37) did not affect glucagon secretion. It is suggested that inhibitory effect of GLP-1(7-36)amide on glucagon secretion is at least partly mediated by adenylate cyclase system.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Glucagon-glucose (GG) test for the estimation of the insulin reserve in diabetes.

The residual B-cell function was examined by means of the plasma C-peptide response 6 min after a combined injection of glucagon and glucose (GG test) or conventional glucagon test (G test) in four insulin-dependent diabetic patients (IDDM group), in 18 diabetic patients treated with insulin (Insulin group), 31 treated with oral hypoglycemic agents (SU group) and 27 treated with diet only (Diet group) and in 22 borderline cases. By GG test, 6-min C-peptide values of the IDDM group were 0.27 +/- 0.05 nM (n = 4) and were significantly lower than those of the Insulin group (0.89 +/- 0.09 nM, n = 12), the SU group (1.42 +/- 0.10 nM, n = 13), the Diet group (2.47 +/- 0.22 nM, n = 11) and the borderline cases (3.38 +/- 0.22 nM, n = 11). Patients with a 6-min C-peptide concentration below 0.75 nM by GG test appeared to be insulin-requiring patients. In the G test, plasma C-peptide concentrations at 6 min were 0.35 +/- 0.08 nM in the IDDM group (n = 2), 0.72 +/- 0.20 nM in the Insulin group (n = 7), 1.08 +/- 0.09 nM in the SU group (n = 20), 1.40 +/- 0.19 nM in the Diet group (n = 17) and 2.05 +/- 0.21 nM in the borderline cases (n = 12). Some of the Diet group patients showed extremely low C-peptide responses. When comparing the GG test and G test in individual cases, a greater C-peptide response was seen with the GG test in all cases except for IDDM patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Factors associated with development of tuberculosis among children and young adults: a study of newly registered cases].

In order to elucidate the factors relevant to the management and prevention of tuberculosis among children and young adults, a total of 191 tuberculosis cases who were newly registered at Health Centers in Saitama Prefecture and were aged less than 30 years were interviewed, and case-finding processes, treatment course and risk factors for clinical development were studied. Analyses of the time course from the patients' becoming aware of the clinical symptoms through the establishment of the diagnosis showed that the bacteriologically positive patients and the patients with cavitary lesion took a longer time before initiating medical action and before being finally diagnosed as tuberculous. Follow-up observation of patients' course of treatment revealed that 13% of the patients took prescribed medication irregularly or were lost to treatment. A case-control study was performed to determine the relationship between life style and disease risk. The control group was selected to match the patients for age and sex and also roughly with occupation. The risk factors found to be associated with the development of tuberculosis in this study included; family members' present or past history of tuberculosis, working night shift every week, eating at home less than once a day, diet not well balanced, indifference to personal health, lack of knowledge about tuberculosis and not attending 'cram' school. Also, patients were more likely to be taller and slimmer than controls.

Adolescent↗
PubMed1989

Presence of glucagon-(1-21)-Like immunoreactive substance in the dog small intestinal mucosa.

By using an antiserum (K291) specifically directed to the C-terminal of glucagon-(1-21)-peptide, we demonstrated the presence of glucagon-(1-21)-like immunoreactivity (G21-IR) in the dog intestine. G21-IR was found to be widely distributed throughout the small intestine and colon in parallel with the distribution of glucagon-like immunoreactivity (GLI), measured by N-terminal glucagon antiserum (OAL196). The subsequent analyses by gel filtration and three HPLC columns (reverse phase, ion exchange and further reverse phase columns) showed that G21-IR consisted of three main peaks, and the smallest molecular form of G21-IR is identical to glucagon-(1-21)-peptide.

Amino Acid Sequence↗
PubMed1989

Effect of glucagon-(1-21)-peptide on secretin-stimulated pancreatic exocrine secretion in anesthetized dogs.

The effects of glucagon-(1-21)-peptide on pancreatic exocrine secretion and plasma glucose levels were studied and compared with those of native glucagon in anesthetized dogs. Intravenous bolus administration of 1 nmol or 10 nmol/kg of glucagon-(1-21)-peptide evoked a significant inhibition of secretin-stimulated pancreatic juice secretion and protein output in a dose-dependent manner, as equimolar doses of glucagon did. Native glucagon induced an immediate and transient increase in pancreatic juice volume, which was followed by a significant inhibition. However, glucagon-(1-21)-peptide showed only the inhibitory action. Glucagon-(1-21)-peptide had no effect on plasma glucose levels even when a dose of 10 nmol/kg was given. The results suggest that the N-terminal amino-acid residues of glucagon play an important role in the inhibition of pancreatic exocrine secretion.

Animals↗
PubMed1989

Glucagonostatic and insulinotropic action of glucagonlike peptide I-(7-36)-amide.

We examined the effect of glucagonlike peptides (GLPs), which are cleaved from preproglucagon in the enteroglucagon cells, on rat endocrine pancreas with the isolated perfused system. GLP-I-(7-36)-amide, a truncated form of full-sequence GLP-I-(1-37), showed a potent inhibitory effect on glucagon secretion. This inhibitory effect of GLP-I-(7-36)-amide was demonstrated at concentrations of 0.25, 2.5, and 25 nM in 11.2 and 2.8 mM glucose. In contrast, insulin release was significantly stimulated by GLP-I-(7-36)-amide at its concentration from 0.025 to 25 nM in a high glucose concentration, whereas in a low glucose concentration, the stimulation was seen only at the highest concentration (25 nM). Neither GLP-I-(1-37) nor GLP-II showed any effect on glucagon and insulin release. Although several gastrointestinal hormones have been nominated as incretins, none of them may suppress the glucagon secretion. A truncated form of GLP-I, GLP-I-(7-36)-amide thus seems to be a unique incretin that exerts glucagonostatic action.

Animals↗
PubMed1988

Glucagon-like peptide-1 (7-36 amide): a potent glucagonostatic and insulinotropic hormone.

Glucagon-like peptide-1 (GLP-1) (1-37) and the fraction derived from it, GLP-1 (7-36 amide), are peptides encoded by the preproglucagon gene and possibly co-secreted with enteroglucagon. When added at a 25-nM concentration, GLP-1 (7-36 amide) decreased the release of glucagon from the perfused rat pancreas from 68.5 +/- 9.0 pg/ml to 41.5 +/- 11.5 pg/ml at 2 min in the presence of 11.2 mM glucose (P less than 0.01), and from 196.0 +/- 32.5 pg/ml to 87.0 +/- 23.5 pg/ml at 5 min in the presence of 2.8 mM glucose (P less than 0.05). Insulin levels increased from 12.6 +/- 3.0 microU/ml to 48.9 +/- 14.0 microU/ml at 10 min in the presence of 11.2 mM glucose (P less than 0.05) and from 2.0 +/- 0.4 microU/ml to 8.2 +/- 2.3 microU/ml at 2 min in the presence of 2.8 mM glucose (P less than 0.05). Glucagon and insulin release were not affected significantly by GLP-1 (1-37), irrespective of glucose concentration. We suggest that GLP-1 (7-36 amide) rather than enteroglucagon may be the true physiologic gut hormone and that it may act as 'incretin' in the enteroinsular axis. We suggest further that the glucagonostatic and insulinotropic activities of this peptide are unique and might be important in islet-cell function.

Animals↗