Search PubMed⌕ Search

Biomedical subjects

T Maeda

Publications and source records attributed to T Maeda.

At least 1,207 records · Page 67Linked to original sources
PubMed1985

Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy.

Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. Ten patients (group 1) had retinopathy corresponding to stage III-V (Scott's classification), and the remaining seven patients (group 2) had no retinopathy despite longer duration of diabetes in comparison with the patients in group 1. There were no differences in age, percent of ideal body weight, and serum HbA1 levels between the two groups. Basal serum GH levels were 1.9 +/- 0.4 ng/ml (mean +/- SEM) in group 1, and not different from the values in group 2 (1.6 +/- 0.7 ng/ml). However, GH responses to synthetic human GRH-44 (1 micrograms/kg body wt, i.v. bolus) were significantly greater in group 1, as judged by the maximal response or integrated GH secretion after the administration of GRH. There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. Paradoxical GH responses to TRH (500 micrograms, i.v. bolus) were found in only one patient in each group. We have thus demonstrated that GH responses to GRH are more pronounced in diabetic patients with retinopathy than in patients without this complication, although it remains to be determined whether or not greater GH responses to GRH are causally related to the development of diabetic retinopathy.

Blood Glucose↗
PubMed1985

Urinary excretions of kininase I and kininase II activities in essential hypertension. A sensitive and simple method for its kinin-destroying capacity.

To further clarify the role of the renal kallikrein-kinin system in essential hypertension, a sensitive and simple method for the determination of both human urinary kininase I and kininase II was established, and the system components were determined in patients. In the measurement of kininase activity, desalted urine samples were incubated with synthetic bradykinin, and the reaction was terminated with kininase inhibitors, ethylene diamine tetraacetic acid and phenanthroline. Thus, kininase activity was determined as the kinin-destroying capacity. Moreover, the specific inhibitor for kininase II, SQ14225, was applied for the separation of kininase I and kininase II activities. Daily urinary excretions of total kininase and kininase I activities were significantly higher in essential hypertensive patients than those in normotensive subjects, whereas no difference was observed in kininase II activity. As reported previously, daily excretions of urinary kallikrein and kinin simultaneously determined in these patients were significantly lower than excretions in normotensive subjects. From these results, it was suggested that not only decreased renal kallikrein, but also increased kininase activity, may play an important role in the suppression of the renal kallikrein-kinin system through the reduction of active kinin level in essential hypertension.

Adolescent↗
PubMed1985

[Immunological monitoring of brain tumors--prognosis based on T-lymphocyte subpopulations and skin testing for delayed hypersensitivity].

We have already reported on the usefulness of the phytohemagglutinin (PHA) skin test and the purified protein derivative (PPD) skin test in predicting the prognosis of brain tumor patients. This paper outlines our investigation of T-lymphocyte subpopulations and analysis of their utilization. The cellular immunological states of brain tumor patients were examined by means of PHA and PPD skin tests, the blastogenic response of T-lymphocytes to PHA and the T-lymphocyte subpopulations. Our subjects consisted of 10 cases of glioma (8 astrocytoma, 2 ependymoma), 2 cases of meningioma, one of teratoma, one of hemangioblastoma and 4 of metastatic brain tumor. These were divided into 2 groups: the benign group, which included low grade astrocytoma, meningioma, teratoma and hamangioblstoma, and the malignant group which included malignant glioma and metastatic brain tumor. The T-lymphocytes were counted by monoclonal antibody assay using Ortho-mune T-lymphocyte monoclonal antibody (OK series). We then counted an analysis to determine metastatic brain tumor. The T-lymphocytes were counted by monoclonal antibody assay using Ortho-mune T-lymphocyte monoclonal antibody (OK series). We then conducted an analysis to determine whether or not the T-lymphocyte subpopulations could be of value in the prediction of the possible prognosis of patients. The results were as described below. Ratio of helper/inducer T-lymphocytes (OKT 4 positive cells: Th) to suppressor/cytotoxic T-lymphocytes (OKT 8 positive cells: Ts) were 1.78 +/- 0.18 in the benign group and 1.00 +/- 0.49 in the malignant group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The effects of d-propranolol and captopril on post-ischaemic acute renal failure in rats.

The effect of the combined therapy of d-propranolol and captopril was evaluated in post-ischaemic acute renal failure in rats. The glomerular filtration rate measured 24 hours after ischaemic insult in the animals receiving no drugs was 54 +/- 11 microliter/min/100g body weight while in animals treated with the combination of d-propranolol and captopril it was 305 +/- 35 microliter/min/100g body weight (p less than 0.05). The precise mechanism of protection afforded by the combination therapy is not clear, but this approach could be useful in protecting the kidney from ischaemic damage.

Acute Kidney Injury↗