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Biomedical subjects

H Tamai

Publications and source records attributed to H Tamai.

At least 217 records · Page 12Linked to original sources
PubMed1991

Monochloramine, a neutrophil-derived oxidant, stimulates rat colonic secretion.

Neutrophil-derived oxidants may be involved in inflammatory bowel disease. Stable oxidants formed by halogenation of primary amines (e.g., monochloramine, NH2Cl) are extremely potent and may be of major importance in the pathophysiological response in inflammatory bowel disease. We tested the effects of NH2Cl relative to other oxidants on muscle-stripped rat colon under short-circuit conditions. Serosal addition of the oxidants evoked a concentration-dependent increase in short-circuit current (Isc). The EC50 values were 3.2 microM for NH2Cl, 6.5 microM for HOCl and 6.5 microM for H2O2. Responses to NH2Cl and H2O2 were abolished by removal of Cl- or Ca++. Unidirectional 36Cl- flux measurements showed that both oxidants (50 microM) evoked significant decreases in net chloride absorption. Tetrodotoxin (0.5 microM) and atropine (0.5 microM) partially inhibited the initial phase of the response to 50 microM NH2Cl; tetrodotoxin completely inhibited and atropine partially inhibited the response to 50 microM H2O2. Piroxicam (5 microM) inhibited the increase in Isc to 50 microM NH2Cl and H2O2 by 20-45% and 90%, respectively. Serosal prostaglandin E2 levels were significantly increased after the addition of 50 microM NH2Cl and H2O2. The morphological response to NH2Cl consisted of changes in mucosal depth and crypt architecture. In conclusion, at concentrations found in inflamed tissue, both NH2Cl and H2O2 increase Isc probably by stimulating release of arachidonate metabolites and neurotransmitter(s). NH2Cl also may act directly on the epithelial cell to stimulate Isc and evoke Cl- secretion.

Animals↗
PubMed1990

Effects of neutrophil-derived oxidants on intestinal permeability, electrolyte transport, and epithelial cell viability.

There are several pathophysiologic conditions in which intestinal inflammation is associated with enhanced mucosal permeability, fluid loss, and epithelial cell injury. The objective of this study was to determine the effects of polymorphonuclear leukocyte (PMN)-derived oxidants on ileal mucosal permeability in vivo as well as electrolyte transport and epithelial cell viability in vitro. Using blood-to-lumen clearance of [51Cr]EDTA as a measure of mucosal permeability, we found that luminal perfusion with hydrogen peroxide (H2O2), hypochlorous acid (HOCl), or monochloramine (NH2Cl) produced a dose-dependent increase in mucosal permeability. Perfusion with 0.1 mM, 0.5 mM, and 1.0 mM oxidant produced a 2 +/- 1, 5 +/- 2, and 11 +/- 5-fold increase in mucosal permeability for H2O2, a 2 +/- 1, 8 +/- 3, and 36 +/- 12-fold increase for HOCl, and a 3 +/- 1, 11 +/- 2, and 30 +/- 7-fold increase for NH2Cl. Taurine monochloramine (TauNHCl) was ineffective in enhancing the blood-to-lumen clearance of [51Cr]EDTA. Furthermore, 0.01 mM and 0.1 mM NH2Cl and H2O2 produced significant increases in short-circuit current across rat ileum in vitro, whereas HOCl and TauNHCl were without effect. Tissue resistance and potential difference were not altered, suggesting that NH2Cl, HOCl, and H2O2 were not cytotoxic under these conditions. Cultured intestinal epithelial cells exposed to NH2Cl and HOCl were injured in a dose-dependent manner in vitro, whereas H2O2 and Tau NHCl were nontoxic. Taken together, our data suggest that PMN-derived oxidants may mediate the enhanced mucosal permeability, electrolyte transport, and epithelial cell injury associated with acute inflammation of the bowel.

Animals↗
PubMed1990

Small bowel transit time measured by hydrogen breath test in patients with anorexia nervosa.

The gastrocecal transit time was measured in 10 patients suffering from anorexia nervosa, using a lactulose hydrogen breath test, and was compared with the orocecal transit time in 11 healthy controls. One of the 10 patients and one of the 11 controls were excluded from this study because of no discernible increase in hydrogen excretion. The transit time was significantly prolonged in patients with anorexia nervosa compared with controls (117 min +/- 31 SD vs 81 min +/- 33 SD, P less than 0.02). In addition to delayed gastric emptying, which has hitherto been well known, the small bowel transit time was considered to be prolonged in patients with anorexia nervosa. Both these abnormalities seem to contribute to the development of various gastrointestinal symptoms in patients with anorexia nervosa.

Adolescent↗
PubMed1990

Sensitivity of thyroids to endogenous thyrotrophin in patients with Graves' disease.

T3 nonsuppressibility and TSH nonresponsiveness to TRH are characteristics of untreated hyperthyroid Graves' disease. Although the tests are commonly restored to normal during antithyroidal drug therapy, dissociation of TRH and T3 suppression tests have been observed in euthyroid Graves' disease and during drug therapy. Abnormalities of pituitary-thyroidal regulation and persistence of thyroid autoimmune disease have been found in Graves' patients following various modalities of therapy. The present study investigated in vivo sensitivity to endogenous TSH of thyroids in 144 Graves' disease patients following treatment with subtotal thyroidectomy, 131I, or antithyroidal drugs. After administration of TRH, thyroidal sensitivity to TSH was determined by the following: delta T3 (peak T3 minus basal T3), % increase in T3 (peak over basal), and the ratio of delta T3 to delta TSH. Significant differences in sensitivity to TSH in T3 nonsuppressible patients were found compared to suppressible patients regardless of their TSH responses to TRH or modality of therapy. These data suggest that measurements of serum T3 and TSH following TRH administration to determine in vivo thyroidal sensitivity may be substituted for the T3 suppression test as a confirmatory test for Graves' disease or as a prognosticator of relapse following therapy.

Adolescent↗
PubMed1990

Unusual thyroid scintigrams in Plummer's disease during methimazole therapy. Conversion of hot to hypofunctional nodules.

Thyroid scintigrams of two women (aged 48 and 58) with Plummer's disease showed unusual radioiodine accumulation during treatment with methimazole (MMI). Before MMI therapy, the scintigrams revealed most of the radioiodine uptake only in the nodules of the patients and very little uptake in the non-nodular portions of the thyroid. After initiation of MMI therapy, scintigrams performed at three and eight months revealed that the hot nodules had become hypofunctional and that the surrounding tissues had normal radioiodine accumulation. The findings indicate that the nodules in Plummer's disease continue to concentrate MMI selectively compared with normal surrounding thyroid tissue during therapy.

Adenoma↗
PubMed1990

Hashimoto's thyroiditis manifesting monoclonal lymphocytic infiltration.

Hashimoto's thyroiditis (HT) and lymphoma are sometimes difficult to distinguish between. Moreover, lymphoma sometimes develops in a thyroid gland from pre-existing HT. Open- or large-needle biopsy usually distinguishes between them; the specimen may be examined histologically and subjected to immunohistochemistry. Another possible method of examination is fine-needle aspiration biopsy (FNAB). The cells obtained may be evaluated cytologically, and subjected to flow cytometry, using various antibodies. In this study, anti-kappa and anti-lambda antibodies are especially important, as a gross predominance of kappa or lambda B lymphocytes infiltrating the thyroid is evidence for a B cell monoclone. In this study, 15 patients were selected because of their rapidly growing goitres. They all underwent FNAB. Five had cytology typical of HT, and no evidence of monoclonality on flow cytometry. They were diagnosed as HT without further histopathology. The remaining 10 patients had cytology suspected of lymphoma, or evidence of monoclonality on flow cytometry, or both. These patients underwent open- or large-needle biopsy. Only three of them were diagnosed histopathologically as lymphoma; the other seven were diagnosed histopathologically as HT, making 12 cases of HT in all. Five of these 12 cases, and one of the three cases of lymphoma showed flow cytometrical evidence of monoclonality; thus evidence of monoclonality from FNAB, while interesting, does not necessarily serve to differentiate between HT and lymphoma. Furthermore, the immunohistochemical assessment of monoclonality did not correlate with the flow cytometrical assessment. Follow-up evidence will be required to discover whether those patients with a B cell monoclone in their HT are the ones who develop a lymphoma.

Aged↗
PubMed1990

Follow-up study of thyroid stimulating-blocking antibodies in hypothyroid patients.

It has been shown that hypothyroidism of some patients may be associated with increased activity of thyroid stimulating-blocking antibodies (TSBAb). The present study was undertaken to follow the course of thyroid blocking, stimulating immunoglobulins and TSH-binding inhibitor immunoglobulins (TBII) in six hypothyroid patients who had elevated TSBAb and were treated with T4. Four of the six had Graves' disease previously treated with antithyroidal drugs, one had Graves' disease treated with 131I and one had subacute thyroiditis and subsequently became hypothyroid. The patients were followed for 1-5 years. Blocking activity and TBII normalized in four of the six during T4 therapy, so T4 was discontinued and they remained euthyroid. These data indicate that it is important to monitor carefully thyroid function in hypothyroid patients treated with a fixed amount of T4 to avoid subclinical hyperthyroidism and its consequence, e.g. osteoporosis.

Adolescent↗
PubMed1990

Prolactin responses in dexamethasone suppression test in patients with anorexia nervosa.

In anorexia nervosa (AN), abnormalities are present in the hypothalamic-pituitary-adrenal axis, but the prolactin (PRL) response to dexamethasone suppression test (DST) has not yet been studied. In order to study the interrelationships between the various endocrine abnormalities, we investigated the responses of PRL and cortisol to DST (1 mg of dexamethasone at 2300) in AN patients. The subjects were 12 female inpatients with AN and 8 age- and sex-matched healthy controls. The percentage suppression and absolute change in PRL levels before and after dexamethasone administration were significantly different in the 2 groups. In the control group PRL levels suppressed to 36.5 +/- 3.7% of basal, while AN levels declined to 79.4 +/- 8.9% of basal. When the percentage suppression of PRL was compared between patients with and without cortisol suppression, the mean PRL level was 68.9 +/- 7.8% of the basal level for the cortisol-suppressed patients and 100.4 +/- 19.1% for the nonsuppressed patients. Hence in both groups, the percentage PRL suppression was significantly reduced compared with the control group, and indeed nonexistent in cortisol-nonsuppressed patients. The finding that there was less PRL suppression in the cortisol-suppressed patients than in the controls suggests that, in AN, there may be an abnormality in PRL secretion not related to the hypothalamic-pituitary-adrenal axis. Further work is needed to distinguish between the PRL response to stress and potential hypothalamic abnormality.

Adult↗
PubMed1990

Human pancreatic polypeptide responsiveness to insulin-induced hypoglycemia in anorexia nervosa.

Patients with anorexia nervosa occasionally suffer from hypoglycemic comas. We investigated the role of human pancreatic polypeptide (HPP) in insulin-induced hypoglycemia (0.1 U/kg of regular insulin). Ten female patients with anorexia nervosa (20.7 +/- 2.0 years, mean +/- SEM; 34.9 +/- 1.7 kg, mean +/- SEM) and 8 age-matched female controls (20.9 +/- 0.6 years, 51.5 +/- 0.8 kg) were tested. In the patients with anorexia nervosa, testing was performed before and after the restoration of body weight (45.0 +/- 0.8 kg). There was no significant difference in glucose nadir between patients with anorexia nervosa and the control subjects. However, glucose recovery from nadir was delayed in patients with anorexia nervosa. In anorexia nervosa patients, the plasma pancreatic glucagon responses to insulin-induced hypoglycemia did not differ from those of the controls. Results also showed, however, that HPP responses to insulin-induced hypoglycemia were significantly higher in patients with anorexia nervosa than in controls (p less than 0.01). The increased HPP responses were still present after the restoration of body weight in anorexia nervosa patients. A complete body weight recovery or a longer period of time may be required to normalize the HPP response to insulin-induced hypoglycemia in patients with anorexia nervosa, after the restoration of body weight.

Adolescent↗
PubMed1990

Plasma beta-endorphin during fasting in man.

To identify the effects of acute starvation on endogenous opioids in man, plasma beta-endorphin (beta-EP) was measured in 17 patients before, during and after fasting. Patients were assigned a posteriori into two groups: group A, comprised of 11 patients able to tolerate 5-7 days of fasting, and group B, comprised of 6 patients able to tolerate 10 days of fasting. Changes in plasma beta-EP, serum cortisol, circulating nutritional markers, and their relative levels were assessed on the 5th and 10th days of fasting, and on the 5th and 10th days of the refeeding period. Beta-EP had increased by the 5th day (group A: 4.74 +/- 0.42 to 6.91 +/- 0.65 pmol/l, p less than 0.01; group B: 3.60 +/- 0.48 to 5.14 +/- 0.22 pmol/l, p less than 0.05, and remained at 5.05 +/- 0.65 pmol/l on the 10th day (group B: 0.05 less than p less than 0.1) during fasting. Group B had lower levels of plasma beta-EP on the 5th day of fasting than group A (p less than 0.05). However, serum cortisol levels changed similarly in both groups. Plasma beta-EP showed no significant correlation with either the percentage of body weight lost or the body mass index (kg/m2) over this study period. These findings indicate that plasma beta-EP is elevated in the early phase of fasting, while not directly being associated with body weight changes. Plasma beta-EP is lower and less activated in subjects who are able to tolerate fasting for longer periods.

Adolescent↗
PubMed1990

Effect of cholinergic muscarinic receptor blockade on human growth hormone (GH)-releasing hormone-(1-44)-induced GH secretion in anorexia nervosa.

The presence of hypothalamic disturbances affecting GH secretion in anorexia nervosa has been suggested, although a normal GH response to GH-releasing hormone (GHRH) administration has been shown in these patients. The present study was performed to investigate the role of acetylcholine in regulating GH secretion by using pirenzepine, which selectively blocks muscarinic cholinergic receptors. Paired tests were performed in nine anorexia nervosa patients (age +/- SEM, 19.1 +/- 1.2 yr; percent ideal body weight, -32.7 +/- 2.2%) and in six normal controls (20.1 +/- 0.3 yr; -3.1 +/- 1.8%). GHRH-(1-44) (1 microgram/kg) was infused iv with and without pirenzepine pretreatment (0.6 mg/kg, iv). Basal levels of GH were not different in anorexia nervosa compared to normal controls, whereas, somatomedin-C levels were significantly lower in anorexia nervosa patients. However, after pirenzepine administration, the GHRH-stimulated GH responses were completely blocked in normal controls, but not in anorexia nervosa patients. These results suggested that altered muscarinic cholinergic mechanism are involved in the modulation of GH secretion in patients with anorexia nervosa.

Acetylcholine↗
PubMed1990

Thyroid response, especially to thyrotropin-binding inhibitory immunoglobulins, in euthyroid relatives of patients with Graves' disease: a clinical follow-up.

Three hundred and fifty-three euthyroid relatives of Graves' disease patients were tested for TSH binding inhibitory immunoglobulins (TBII). Eighteen had elevated levels of TBII, and 232 who had negative TBII levels also agreed to be followed for a period of 6-30 months. TBII was chosen as the critical screening measurement for this study, rather than thyroid-stimulating antibodies (TSAb) and thyroid-stimulating blocking antibodies (TSBAb), because of the availability and ease of use of TBII RIA kits. Eleven of the 18 subjects with elevated TBII were T3 nonsuppressible (group I), and 10 of the 11 were TRH unresponsive. Nine of these 10 subjects showed TSH levels below 0.05 mU/L. The remaining 7 subjects were T3 suppressible and TRH responsive (group II). Alterations in thyroid status occurred in 8 of the 11 subjects in group I during follow-up. One developed hypothyroidism, and 7 became hyperthyroid. The hypothyroid subject had initial titers of TBII, TSAb, and TSBAb that were markedly elevated, and TSAb disappeared when she became hypothyroid. Six of the 7 subjects who developed hyperthyroidism had elevated TSAb and negative TSBAb titers while they were euthyroid. All 7 subjects in group II remained euthyroid during the follow-up period. Only 2 of the 232 relatives who initially had negative TBII titers became hyperthyroid during the follow-up period. The results indicate that euthyroid relatives with a family history of Graves' disease who have elevated TBII levels and suppressed basal serum TSH concentrations have a much higher potential to develop hyperthyroidism than those who have normal or negative TBII levels.

Adolescent↗
PubMed1990

The occurrence of thyrotropin binding-inhibiting immunoglobulins and thyroid-stimulating antibodies in patients with silent thyroiditis.

Silent (painless) thyroiditis has been recognized as a clinical entity for over a decade and is characterized by spontaneously resolving thyrotoxicosis. Its etiology is uncertain; however, a few reports have indicated the occurrence of TSH binding-inhibiting immunoglobulins (TBII) and thyroid-stimulating antibodies (TSAb) in some of the patients. The present study was undertaken to evaluate thyroid function and the occurrence of TBII and TSAb and thyroid autoantibodies (antithyroglobulin and antimicrosomal) in 53 patients with silent thyroiditis during the course of their disease. The patients were divided into 2 major groups: I) those who developed transient hypothyroidism and II) those who did not. All patients initially had significantly increased concentrations of serum T4, free T4, and free T3, suppressed TSH levels, and decreased thyroid radioiodine uptake. TBII and TSAb were initially positive in 8 (15.1%) and 10 patients (18.9%), respectively. Forty patients were available for follow-up. TBII was positive in 6 of 24 (25.0%), and TSAb was positive in 8 of 24 (33.3%) of the patients who developed transient hypothyroidism during the course of their disease. Among the patients who did not become hypothyroid at any time, TBII was positive in only 2 of 16 (12.5%), and none of the patients became TSAb positive. The findings indicate that increased TSAb and TBII activity may be detected in patients with silent thyroiditis and, when present, are associated with transient hypothyroidism during the course of the disease.

Adolescent↗
PubMed1990

Thyroid-stimulating antibody and thyrotropin-binding inhibitory immunoglobulin activity in hypothyroid patients who subsequently developed thyrotoxicosis.

Although abnormal thyroid-stimulating and -blocking antibodies have been demonstrated in hyperthyroid and hypothyroid patients with autoimmune thyroid disorders, a direct correlation is not always observed. Thyroid-stimulating antibody, thyrotropin-binding inhibitory immunoglobulin, and thyroid-stimulating blocking antibody levels were determined in three hypothyroid patients who subsequently developed hyperthyroidism. Thyroid-stimulating antibodies levels were normal in one, elevated in another, and unmeasured in the third hypothyroid patient, but became elevated in all patients with the onset of hyperthyroidism. There was discordance, however, in one patient who had markedly elevated thyroid-stimulating antibodies and TSH-binding inhibitory immunoglobulin levels when she was hypothyroid. The data indicate that thyroidal responses to the abnormal stimulating antibodies may differ among patients with autoimmune thyroid disease.

Adult↗
PubMed1990

Effects of supernatants of peripheral blood mononuclear cells stimulated by thyroid microsomal antigen on thyrocyte HLA-dr expression in vitro.

Supernatants of 5 day cultures of peripheral blood mononuclear cells (PBMC) stimulated by thyroid microsomal antigens (TMA), and liver microsomal antigens (LMA) have been utilized to induce HLA-DR expression on human thyroid epithelial cells (TEC). The PBMC were obtained from 8 normal control persons and 13 patients with autoimmune thyroid disease (AITD) (7 Graves' disease and 6 Hashimoto's thyroiditis). The TEC HLA-DR expression was measured by an enzyme-linked immunosorbent assay (ELISA) technique. TEC HLA-DR expression was calculated as follows: (experimental optical density-control optical density) x 10(3): TEC HLA-DR index: % HLA-DR expression of IFN gamma 100 U/ml stimulation; and stimulation index (SI): TEC HLA-DR expression index induced by PBMC supernatants with antigen stimulation/TEC HLA-DR expression index induced by PBMC supernatants without antigen stimulation x 100. Supernatants without antigen stimulation from both normal control subjects and patients were able to induce TEC HLA-DR expression only minimally: 36.7 +/- 32.6 (mean +/- SD) TEC HLA-DR index for normal controls and 21.3 +/- 15.5 TEC HLA-DR index for AITD (not significant). The SI curves of both TMA and LMA were significantly different between control and AITD using two-way ANOVA test (p less than 0.01). TMA-stimulated PBMC supernatants from the patients increased TEC HLA-DR expression when compared to basal level using paired t-test; TMA 1 ng/ml, SI 179 +/- 99, less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Adipose tissues and vitamin E.

1. Vitamin E content in the adipose tissue was examined in rats with and without vitamin E deficiency. With the progression of vitamin E depletion, the more rapid decrease in tocopherol concentration was observed in brown adipose tissue (BAT) than in white adipose tissue (WAT), and the rate of decrease of tocopherol was approximately three times faster in BAT than in WAT. After the intramuscular administration of 10 mg/kg of all-rac-tocopheryl acetate twice a week for two weeks to vitamin E-deficient rats, a similar pattern of increase was observed in the tocopherol concentrations of BAT and WAT, although the rate of increase was slower in WAT than in BAT. 2. Changes of tocopherol concentration in BAT and WAT were investigated in normo-nourished rats with hyperlipemia produced by the intramuscular injection of Triton WR-1339 for 7 days. A marked increase in tocopherol concentration was observed in both BAT and WAT in the late period of hyperlipemia, with the increase being greater in WAT. 3. The fatty acid composition of adipose tissue was compared between rats with and without vitamin E deficiency. No significant differences were observed in BAT and WAT between the two groups. 4. The glucose uptake of WAT was not altered in vitamin E-deficient rats when compared with control rats.

Adipose Tissue↗
PubMed1990

Clinical evaluation of alpha-tocopherol in buccal mucosal cells of children.

1. Tocopherol concentrations in plasma, red blood cells (RBCs), and buccal mucosal cells were examined in newborn infants (before feeding), children (2-15 years old), and adults. Tocopherol concentrations in adults and newborn infants showed the greatest difference in plasma and the smallest difference in RBC. Buccal cell tocopherol concentrations in adults were 2.3 times higher than those in infants. The majority of newborn infants had RBC tocopherol levels below the normal limit (115 micrograms/100 ml of packed cells). Also, more than one third of buccal cell tocopherol levels determined in newborn infants were below a level of 15 ng/mg protein, which was determined as the lower limit of normal in healthy children on the basis of the testing of 97 samples. 2. After administration of a daily dose of 600 mg of RRR-alpha-tocopherol for three months to young adults, tocopherol levels in buccal mucosal cells reached a level of more than 4 times the basal level after rising throughout the 3-month period, while levels in RBC and plasma showed less than a 3-fold increase and reached a maximum within one month. Buccal cell tocopherol levels showed a poor correlation to the RBC and plasma tocopherol levels, while the tocopherol/lipid ratio was closely correlated with RBC and plasma tocopherol levels. After a single dose of 600 mg of RRR-alpha-tocopherol, RBC and plasma tocopherol concentrations reached a maximum within 24 hours, while buccal cell tocopherol did so 4 to 6 days later. 3. Very obese children and hyperlipemic obese children showed lower buccal cell tocopherol levels, accompanied by lower RBC tocopherol levels and higher plasma tocopherol levels, when compared with non-obese children and normolipemic obese children.

Adolescent↗