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Biomedical subjects

K Shima

Publications and source records attributed to K Shima.

At least 325 records · Page 18Linked to original sources
PubMed1988

Correlation between minimal secretory capacity of pancreatic beta-cells and stability of diabetic control.

The significance of the minimal secretory capacity of pancreatic beta-cells for the stability of the plasma glucose level was studied in 20 patients with insulin-dependent diabetes mellitus. Changes in plasma concentrations of major counterregulatory hormones in response to hypoglycemia were also investigated in these patients to clarify their contribution to diabetic brittleness. beta-Cell function was evaluated on the basis of elevation of plasma C-peptide immunoreactivity (CPR) during the intravenous glucagon test with a highly sensitive assay for plasma CPR that could detect as little as 0.03 ng/ml. After stimulation with glucagon, a significant increase in plasma CPR was observed in 10 of the patients whose beta-cell function had been evaluated as completely depleted by a conventional assay for plasma CPR. A clear inverse correlation was found between the secretory capacity of pancreatic beta-cells measured in this way and the degree of glycemic instability (r = -.74, P less than .01). Infusion of insulin at a rate of 0.15 U.kg-1.h-1 for 60 min caused a continuous decrease in the plasma glucose level, resulting in neuroglycopenia in 7 of the 10 CPR nonresponders but only 2 of the CPR responders. During insulin-induced hypoglycemia, plasma glucagon immunoreactivity did not increase in the CPR nonresponders but increased significantly in the CPR responders. A positive correlation was found between the minimal residual beta-cell capacity and the responsiveness of alpha-cells to hypoglycemia (r = .65, P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Asymptomatic hyperbromidaemia detected as pseudohyperchloridaemia measured with an ion selective electrode meter.

Six patients were found to have increased serum chloride concentrations when these concentrations were determined with an ion-selective electrode, but not when determined by continuous flow mercuric thiocyanate colorimetry or amperometric-coulometric titration. Their serum bromide levels of 1.8-8.0 mmol/l were much higher than those of 0.07-0.13 mmol/l in normal controls. The urinary bromide excretion, measured in two of these patients, was higher than that in normal subjects. No common symptoms or abnormalities in laboratory findings except hyperbromidaemia were found in these patients, who claimed not to have taken any drugs containing bromide. For determination of the incidence of subclinical hyperbromidaemia, the serum bromide concentrations were measured in sera of 1,323 outpatients sent to Tokushima University Hospital for routine measurements of blood chemistry over a one-month period. Five samples showed abnormally high bromide levels. It is concluded that subclinical hyperbromidaemia is not as rare as generally thought, though the aetiology of this state is unknown. Chloride determination with an ion-selective electrode can be used to screen for hyperbromidaemia, since increased levels of bromide ion result in apparently high chloride values.

Adult↗
PubMed1988

[Benefits of cisplatin-based polychemotherapy in non-small cell bronchogenic carcinoma. Kyushu Lung Cancer Chemotherapy Study Group].

We studied the efficacy of cisplatin-based polychemotherapy for non-small-cell lung cancer. One hundred nineteen patients with adenocarcinoma or large cell carcinoma were randomized to receive cyclophosphamide, adriamycin, cisplatin and mitomycin C (CAPM) or mitomycin C, cytosine arabinoside and tegafur (MCT), and 48 patients with squamous cell carcinoma were randomized to receive cisplatin, adriamycin and peplomycin (PAP) or mitomycin C, cyclophosphamide, tespamine, toyomycin and tegafur (MCTTT). Radiation was given to the chest in patients with stage I-III disease. The response rates were CAPM, 34.5%; MCT, 13.1% (p less than 0.01) and PAP, 63.3%; MCTTT, 42.3%. A significant difference in response rate between the CAPM and MCT regimens was observed only in stage IV patients and not in stage I-III patients. The median survival was 9.5 months in the CAPM arm vs. 6.5 months in the MCT arm (p less than 0.007), and 8.5 months in the PAP arm vs. 6.5 months in the MCTTT arm. Improved median survival for the CAPM regimen was noted only in stage IV patients and not in stage I-III patients when compared to patients given the MCT regimen, respectively. Nausea and vomiting were significantly increased in patients with cisplatin-based polychemotherapy. Myelosuppression was more severe with the CAPM regimen than with the other chemotherapy regimens. We concluded that cisplatin-based polychemotherapy, CAPM and PAP therapy were of more benefit to patients with disseminated non-small-cell lung cancer than MCT and MCTTT therapy.

Adult↗
PubMed1988

[Clinical analysis of trigeminal neuropathy as initial manifestations--an etiological study].

The differential diagnosis of trigeminal neuropathy is quite challenging because there is a significant variety of causes for the disorder. We reviewed our cases of trigeminal neuropathy by studying first the initial manifestations in order to evaluate their underlying disorders. Sixty-four patients with trigeminal neuropathy came to our Out-Patients clinic. We have excluded from our analysis any patients with atypical pain, facial migraine, nasal sinusitis, pain from inflammation of dental pulp or facial bones, and pretrigeminal neuralgia. In 53 cases (83%) we identified the causes; 35 of them were cases of symptomatic trigeminal neuritis and 18 were trigeminal neuralgia while, in the remaining 11 cases, no definitive causative disorder was identified. Among the 35 patients with symptomatic neuritis, 10 cases were found to have malignant neoplasms including 5 cases of squamous cell carcinoma, 6 had a virus infection, 5 had traumatic origin, 4 had multiple sclerosis, 2 exhibited Tolosa-Hunt syndrome, 2 had MCTD, and there were single cases of sarcoidosis, serpentine aneurysm, cavernous sinus thrombosis, maxillary cyst and trigeminal neurinoma. The remaining 11 cases of neuritis whose causes were undetermined showed clinical features similar to trigeminal sensory neuropathy, an analogue of Bell's palsy, a benign self-limiting condition. Since the cases shared symptoms of impairment of taste, and, occasionally, of facial palsy, vestibular insufficiency, hearing disturbance, hypoglossal palsy or signs of cerebellar lesion, we strongly suspected a virus origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Discrepancy of fasting plasma glucagon levels measured by different glucagon antisera.

To investigate the possible discrepancy between immunoreactive glucagon (IRG) levels measured by two glucagon-specific antisera, OAL-123 and 30K, fasting plasma IRG levels were measured in 30 diabetics (DM group), 56 patients with impaired glucose tolerance (IGT group) and 96 normal subjects (normal group). The fasting plasma IRG measured by OAL-123 (OAL-IRG) in DM, IGT and normal groups were 121 +/- 53, 125 +/- 43 and 119 +/- 57 pg/ml, whereas the fasting plasma IRG measured by 30K (30K-IRG) were 109 +/- 92, 92 +/- 44 and 91 +/- 68 pg/ml, respectively. There was no significant difference in the distribution of the fasting IRG levels among DM, IGT and normal groups. Although there was a statistically significant correlation between OAL- and 30K-IRG, their correlation coefficient was as small as 0.29, and 31 of 182 cases showed a large discrepancy exceeding 100 pg/ml between the two IRG values. The OAL- and 30K-IRG measured again six months later did not show a significant change, where the first and second IRG levels showed a good correlation (0.72 and 0.83 for OAL- and 30K-IRG, both p less than 0.001). The gel chromatography of the 14 plasma with fasting OAL-IRG higher than 200 pg/ml showed that the main contributor to the fasting IRG was the component of big plasma glucagon (BPG). These data suggest that there is a significant discrepancy in the fasting plasma IRG levels measured by the different glucagon antisera and that the discrepancy is caused by the different immunoreactivity of BPG to the different glucagon antisera.

Blood Glucose↗
PubMed1987

Radioimmunoassay of glycosylated albumin with monoclonal antibody to glucitol-lysine.

An immunoassay specific for glycosylated albumin was developed by the use of beads coated with antibody to human serum albumin (beads) and 125I-labelled monoclonal antibody to reduced bovine glucosylated low density lipoprotein. One bead was capable of binding 100 ng of serum albumin which had been treated with sodium borohydride (NaBH4) to reduce the Schiff base in the protein. The monoclonal antibody reaction with glucitol-lysine epitopes on the reduced glucosylated proteins and amino acids studied, including human serum albumin (HSA), bovine serum albumin and hippuryl-L-lysine. The detection limit of this assay was 100 pmol/mg HSA, which was sensitive enough for clinical use. The mean serum reduced glycosylated albumin concentration measured by this new method was significantly higher in diabetic patients (2.63 +/- 0.35 nmol/mg HSA, n = 32) than in healthy subjects (0.53 +/- 0.05 nmol/mg HSA, n = 38). The serum reduced glycosylated albumin concentration correlated with both hemoglobin A1c (r = 0.69, p less than 0.005) and the fasting blood glucose level (r = 0.51, p less than 0.005) in diabetic patients.

Aged↗
PubMed1987

A large molecular form of glucagon-like peptide-1 (GLP-1) immunoreactivity is co-released with glucagon from pancreas by arginine in normal subjects.

Plasma immunoreactivities of glucagon-like peptide-1 (GLP-1IR) in normal subjects were measured with a specific radioimmunoassay during the arginine tolerance test. Plasma GLP-1IR after arginine infusion showed a 3-fold increase in parallel to plasma glucagon immunoreactivity and plasma glucagon-like immunoreactivity, measured with a glucagon C-terminal specific antiserum (OAL 123) and an N-terminal and/or central region specific glucagon antiserum (OAL 196), respectively. This finding suggested that the increased immunoreactivities of GLP-1 as well as that of glucagon were of pancreatic origin. Upon gel chromatography, plasma at the basal state showed three GLP-1 immunoreactive peaks, eluted in the position of void volume, synthetic GLP-1(72-108), and a smaller molecular fraction. Gel chromatography of plasma after an arginine load showed an additional peak (Mr 13,000-15,000) with little change in other GLP-1 immunoreactive peaks. This large molecular form of GLP-1IR was also shown to exist in the human pancreatic extract. Moreover, the free GLP-1 concentrations in plasma before and after an arginine load were shown to be about equal by reverse phase HPLC. These data suggested that in normal subjects arginine stimulation co-releases GLP-1IR, predominantly large molecular form, with glucogen from the pancreas.

Adult↗
PubMed1987

Synthesis of 7a-substituted benzoylaminoalkyl-hexahydro-1H-pyrrolizines and evaluation of their antiarrhythmic activity.

Several 7a-substituted benzoylaminoalkyl-hexahydro-1 H-pyrrolizines were synthesized by acylations of 7a-aminoalkyl-hexahydro-1 H-pyrrolizines. All compounds synthesized were evaluated for their antiarrhythmic activities using the chloroform-mouse method, and some of them were found to have significant antiarrhythmic activities, comparable to that of procainamide.

Animals↗
PubMed1987

Effect of the enteroinsular axis on both the A- and B-cell response to arginine after oral glucose in man.

Studies were made on the effect of the enteroinsular axis on amino acid-induced insulin and glucagon secretion during hyperglycaemia in man. The responses of plasma immunoreactive insulin, C-peptide, and immunoreactive glucagon to arginine infusion were investigated in nine healthy subjects after induction of hyperglycaemia by an oral glucose load and by intravenous glucose infusion to produce similar glucose concentrations in the arterialised blood. The plasma immunoreactive insulin and C-peptide levels increased to higher levels after an oral glucose load than after an intravenous infusion of glucose. The incremental areas under the immunoreactive insulin and C-peptide curves during arginine infusion were significantly greater (p less than 0.01) after oral than after intravenous glucose administration. The plasma immunoreactive glucagon level was suppressed equally after oral and intravenous glucose loads. However, during subsequent arginine infusion, the plasma immunoreactive glucagon level rose more in the presence of hyperglycaemia induced by oral than intravenous glucose. The incremental area under the plasma immunoreactive glucagon curve during arginine infusion was 1.6-fold greater after glucose ingestion than after intravenous glucose infusion. These results suggest that the enteroinsular axis has a stimulatory effect on the responses of pancreatic A and B cells to arginine after oral glucose administration.

Administration, Oral↗
PubMed1987

Effects of gut hormones on bile acid uptake and release in cultured rat hepatocytes.

In cultured rat hepatocytes, the effects of gut hormones on bile acid uptake and release were studied. It was found that cultured hepatocytes continued to secrete bile acids into the culture medium and incorporated them effectively as a function of incubation time. Gut hormones such as secretin, glucagon, vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), gastric inhibitory polypeptide (GIP), tetragastrin, cholecystokinin-octapeptide (CCK-8), pancreatic polypeptide (PP), neurotensin substance P, beta-endorphin (beta-End), methionine-enkephalin (Met-enk), motilin, bombesin and somatostatin (SS) had no effect on bile acid uptake by cultured hepatocytes. In bile acid release studies, only secretin caused a dose-dependent stimulation of bile acid release, while other gut hormones had no effect on bile acid release into medium. These results indicate that secretin acts directly on cultured rat hepatocytes and/or bile canaliculi, besides its effect on the bile duct, and influences bile acid metabolism.

Animals↗