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Biomedical subjects

H Tamai

Publications and source records attributed to H Tamai.

At least 19 recordsLinked to original sources

9-cis beta-carotene in human plasma and blood cells after ingestion of beta-carotene.

For 44 wk, thirty male volunteers were given daily either 60 mg of synthesized all-trans beta-carotene, a naturally-occurring beta-carotene derived from Dunaliella bardawil, or a placebo. Basal levels of 9-cis beta-carotene in plasma, platelets, and mononuclear cells were 10, 20, and 25% of those of the all-trans form, respectively. The plasma levels reached a maximum after two weeks of administration and plateaued thereafter in the subjects who took the beta-carotene preparations. The all-trans beta-carotene level in the subjects given the synthesized all-trans form was almost twice that for the Dunaliella preparation. The plasma 9-cis level was found to be higher in the all-trans beta-carotene group than in the Dunaliella group, despite no intake of the 9-cis form in the all-trans group and the higher intake of the 9-cis form in the Dunaliella group. This finding suggests that isomerization of the all-trans form to the 9-cis form may occur in the body either during or after absorption.

Adult

Beneficial effect of fructose-1,6-bisphosphate on mitochondrial function during ischemia-reperfusion of rat liver.

BACKGROUND/AIMS: Several groups have reported that administration of fructose-1,6-bisphosphate (FBP) reduces ischemic injury. The aim of this study was to determine the protective effect of FBP on the impairment of mitochondrial oxidative phosphorylation by ischemia-reperfusion injury in the rat liver. METHODS: The respiratory control ratio (RCR) and the adenine nucleotide content of mitochondria isolated from ischemic and reperfused livers with or without FBP treatment were measured. RESULTS: In FBP-treated livers, the cellular adenosine triphosphate level was restored to more than 50% of normal after 120 minutes of reperfusion following 120 minutes of ischemia, whereas that of control livers only reached 15% of normal. The RCR and the adenine nucleotide content of mitochondria isolated from FBP-treated livers were significantly higher than those of mitochondria from control livers after ischemia and reperfusion. FBP strongly suppressed the formation of lipid peroxides during reperfusion. In vitamin E-deficient rats, the RCR decreased markedly during reperfusion, but FBP protected the mitochondria against reperfusion injury. CONCLUSIONS: FBP has a protective effect against ischemia-reperfusion injury on the liver and especially preserves the oxidative phosphorylation capacity of hepatic mitochondria.

Adenosine Triphosphate

HLA-A and -DRB4 genes in controlling the susceptibility to Hashimoto's thyroiditis.

HLA-linked genetic factors involved in the pathogenesis of HT were studied in 71 patients with HT by serologic typing for HLA-A, -B, -C, -DR, and -DQ specificities and by DNA typing for HLA-DRB1, -DRB3, -DRB4, -DRB5, -DQA1, -DQB1, AND -DPB1 genes using the PCR-SSOP method. Typing results demonstrated significant positive associations of HT with HLA-A2 and -DRB4*0101 (DR53) (p < 0.01, RR = 2.03, EF = 0.61 and p < 0.0001, RR = 4.48, EF = 0.69, respectively). Although HLA-DR8, -DRB1*0403, -DQA*03, and -DQB1*0303 were statistically more prevalent in the patient group than in the controls, these associations were presumably due to the strong linkage disequilibria of these alleles with HLA-A2 or -DRB4*0101 in the Japanese population. Ninety-seven percent of the patients (69 out of 71) were positive for HLA-A2 or -DRB4*0101 compared to 79% in controls (RR = 8.7, p < 0.0005). The combination of HLA-A2 and -DRB4*0101 showed higher OR of risk for HT (OR = 12.8) than HLA-A2 (OR = 7.3) or DRB4*0101 (OR = 7.5) alone. These observations suggest that at least two loci, HLA-A and HLA-DRB4 together, may control the susceptibility to HT. On the other hand, the frequency of DQA1*0102 was significantly decreased in the patient group, suggesting that DQA1*0102 might confer resistance to HT.

Genetic Predisposition to Disease

Effects of monoclonal antibody against CD45RB on peripheral blood mononuclear cell proliferation and on HLA-DR and adhesion molecule expression on thyrocytes of patients with autoimmune thyroid disease.

To evaluate the role of CD45 (especially that of the ectodomain region B) on immunocyte-thyrocyte signaling in patients with autoimmune thyroid disease (AITD), we have examined the in vitro and in vivo effects of a monoclonal antibody (mAb) against with CD45RB, termed MT3. MT3 was added to cultured peripheral blood mononuclear cells (PBMC) from patients with AITD and was additionally injected into severe combined immunodeficient (SCID) mice to which Graves' thyroid cells and intrathyroidal lymphocytes were engrafted. MT3 stimulated proliferation of PBMC when cultured for 2 to 3 days in patients with Hashimoto's thyroiditis (HT) and Graves' disease (GD) and in normal controls (NC). However, when cultured for 7 days, the stimulation index [SI: counts per minute (cpm) with mAb/cpm without mAb] was lowered by MT3 in NC and GD patients. However, the mean SI was not lowered in patients with HT. In SCID mice, the concentrations of human immunoglobulin G, antithyroglobulin and antithyroperoxidase antibodies in sera were not significantly changed by injecting MT3. The expression of human leukocyte antigen (HLA)-DR and intercellular adhesion molecule (ICAM)-1 on engrafted human thyrocytes decreased after the tissues were engrafted into the control mice to which vehicle alone was injected. However, in the mice injected with MT3, HLA-DR and ICAM-1 expression remained high or up-regulated by the injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Case report: intraglomerular metastasis with neoplastic cell interposition.

A case is described of an 88-year-old man with lung cancer, nephrotic syndrome, and renal dysfunction who died suddenly of an acute myocardial infarction and whose autopsy revealed many adenocarcinoma cells stacked within glomerular capillary lumina of his kidney, entering into basement membrane zones (ie, neoplastic cell interposition). In addition, glomeruli showed a lobular transformation, doubling of glomerular basement membrane, and electron dense deposits along the glomerular basement membrane. These changes were similar to those of membraneoproliferative glomerulonephritis. The association of intraglomerular metastasis and membranoproliferative glomerulonephritis-like lesions led the authors to speculate that the latter glomerular change might have provided an attractive opportunity for circulating tumor cells to be trapped and grow within the glomerular lumina. This mode of metastasis has not been well-recognized. The authors describe the experience, review the literature, and discuss its possible pathogenesis.

Adenocarcinoma

Pharmacokinetics of all-trans retinoic acid in pediatric patients with leukemia.

Since all-trans retinoic acid (ATRA) induces complete remission in a high proportion of patients with acute promyelocytic leukemia (APL), and its effectiveness appears to be related to the plasma or serum level, a pharmacokinetic study of ATRA was undertaken in nine patients with various leukemias. After oral administration at a dose of 30 mg/m2, the time required to reach the peak plasma level of ATRA (20-1198 ng/ml) was between 120 and 240 min and the apparent plasma elimination half life was 21-51 min. In addition, 13-cis retinoic acid was detected in the plasma of seven patients, indicating the occurrence of ATRA isomerization in vivo. ATRA therapy did not induce complete remission in all patients, even when high plasma levels were achieved. Among the six APL patients given ATRA therapy, one who failed to respond had a very low plasma ATRA level. These findings suggest that it may be useful to monitor plasma levels during oral ATRA therapy in order to achieve an appropriate treatment regimen.

Adolescent

Lack of effect of thyroxine administration on elevated thyroid stimulating hormone receptor antibody levels in treated Graves' disease patients.

Increased levels of antibodies to TSH receptors are thought to be a major cause of active Graves' disease or recurrence following therapy. It was recently reported that T4 administration during antithyroid drug treatment for Graves' disease resulted in a significant decrease of TSH receptor antibodies compared to drug therapy alone. It is known that these antibodies may remain elevated long after patients become euthyroid, so a large number of patients whose antibodies remained significantly elevated after 1 year of methimazole therapy were evaluated in the study. A total of 330 Graves' disease patients were treated with methimazole for 1 year. TSH receptor antibody titers remained persistently elevated in 195 patients. Thirty-five randomly selected patients were continued on maintenance doses of methimazole for a second year, and 160 patients were treated with a combination of methimazole and thyroxine for a second year. T4 doses needed ranged from 75-100 micrograms/day to maintain serum-free T4 and free T3 within the normal range. After 6 months of combined therapy, 35 patients were found to have suppressed serum TSH levels. The patients were divided after 18 months into three groups: A, B, and C. Group C, consisting of 35 randomly selected patients (8 males and 27 females) whose ages ranged from 12-62 years and who had been maintained on methimazole alone, served as controls. Group B, whose serum TSH levels were suppressed after 6 months of combined therapy, consisted of 9 males and 26 females whose ages were 15-66 years. Group A, 35 randomly selected patients with normal serum TSH levels after methimazole and thyroxine therapy for 6 months, consisted of 8 males and 27 females whose ages were 10-63 years. TSH receptor antibody titers gradually decreased in all three groups with drug therapy, and there was no significant difference in the titers at corresponding times, i.e. 0, 1.0, 1.5, and 2.0 years. After treatment for 2.0 years, all patients of the three groups were followed for a further 12 months. Rates of recurrence among the above three groups were not significantly different during the observation period. In the present study, T4 administration in combination with antithyroidal drugs had no effect on levels of antibodies to TSH receptors and no effect on rates of recurrence. The reason for the discrepant results in the present study from previous reports is not known.

Adolescent

[Anesthesia for SUMO wrestlers].

We anesthetized 34 sumo wrestlers. All patients were male. Average age was 21.1. Their height was 181.9 +/- 4.5 (mean +/- SD) cm, and they weighted 135.2 +/- 16.9 kg. Anesthetic methods used were spinal anesthesia alone in 17 patients, general anesthesia alone in 9, general anesthesia + epidural anesthesia/or spinal anesthesia/or axillary block in 8. The preoperative data showed findings common to obese patients; liver dysfunction, abnormal blood sugar, and abnormal ECG such as ST depression or left ventricular hypertrophy. For intubation, fiberscopy was required in one patient, and almost all patients required high FIO2, otherwise SaO2 decreased. For spinal anesthesia or epidural anesthesia, we needed long needles of 8 to 15 cm.

Adult

Effect of long-term administration of beta-carotene on lymphocyte subsets in humans.

To examine whether or not beta-carotene alters immune indexes, we performed a single-blind trial in healthy male nonsmokers. Lymphocyte subsets were assessed by double labeling with monoclonal antibodies before and after 44 wk of administration of either beta-carotene (60 mg/d; n = 10) or placebo (n = 10). In addition, we measured the beta-carotene concentrations in plasma, mononuclear cells (MNC), platelets, and red blood cells (RBCs), as well as the plasma alpha-tocopherol concentration. An increase of plasma and MNC beta-carotene concentrations to four and three times the baseline value was noted after 2 and 4 wk, respectively. The CD4-CD8 ratio increased after 9 mo of beta-carotene administration whereas natural killer cells, virgin T cells, memory T cells, and cytotoxic T cells remained unaltered throughout the study. No side effects or toxicities were detected by a questionnaire survey and routine laboratory tests.

Adult

Immunological findings and thyroid function of untreated Graves' disease patients with undetectable TSH-binding inhibitor immunoglobulin.

OBJECTIVE: TSH-binding inhibitory immunoglobulin (TBII) is undetectable in about 10% of untreated Graves' disease patients, but the clinical characteristics and immunological significance of this finding are unknown. In this study we evaluated the clinical characteristics of TBII negative Graves' disease. PATIENTS: We examined TBII in 1048 untreated patients at Kuma hospital from 1986 to 1990 and found 69 TBII undetectable patients (12 men and 57 women, mean age +/- SEM 35 +/- 2 years, group A). MEASUREMENTS: We compared the clinical characteristics and immunological findings of group A with 57 untreated TBII detectable Graves' patients who were selected randomly (11 men and 46 women, mean age +/- SEM 40 +/- 2 years, group B). T4, TSH, FT4, FT3, 123I thyroid uptake, TBII, thyroid stimulating antibodies (TSAb) and the volume of the thyroid using ultrasonography were measured at the first visit. RESULTS: Serum T4, FT4 and FT3 levels in group A were significantly lower than those in group B (P < 0.001). The values of TSAb in group A were significantly lower than those in group B (593 +/- 67 (mean +/- SE) vs 2143 +/- 280%, respectively, P < 0.001). The 123I thyroid uptake in group A was significantly lower than that in group B (53.1 +/- 1.1 vs 61.4 +/- 1.4%, respectively, P < 0.01). The thyroid volume in group A was significantly smaller than that in group B (39.1 +/- 3.0 vs 51.3 +/- 3.3 ml, respectively, P < 0.01). TSAb was undetectable in about 10% (6) of the TBII negative untreated Graves' patients at their first visit. CONCLUSION: In the present study, untreated TBII negative patients with Graves' disease were characterized by mild elevation of thyroid hormones, mildly elevated 123I uptake, weak TSAb activities and small goitres. The finding of both TBII and TSAb negative titres in untreated Graves' disease patients was also confirmed.

Adult

A case of tetrasomy 9p.

A case of mosaic 9p tetrasomy (46,XX/47,XX, + dic[9] [q21]) is reported. Clinical manifestations of the patient were generalized hypotonia, severe mental retardation and characteristic dysmorphic features of 9p tetrasomy. A brief review of the literature is also included.

Chromosome Aberrations

Insulin response to intravenous glucose in patients with anorexia nervosa showing low insulin response to oral glucose.

To investigate the cause of a low insulin secretory response to an oral glucose tolerance test (OGTT) in patients with anorexia nervosa (AN), we performed iv glucose tolerance tests (IVGTT) before and after treatment in 36 anorectic patients who showed low insulin secretion in response to the OGTT. These patients were subdivided into 3 groups by glucose tolerance curves during the OGTT: normal type, blood glucose level peaking 60 min or earlier after oral glucose ingestion; delayed type, blood glucose level peaking 90 min or later after oral glucose; and flat type, peak blood glucose level of 5.56 mmol/L or less after oral glucose. The results showed that the normal and flat type groups had normal glucose and insulin responses to iv glucose. In the delayed type group, in which the longest duration of AN before therapy was found, initial insulin secretion was decreased in response to both oral and iv glucose, indicating diminished pancreatic beta-cell function. After weight gain, this parameter improved significantly in both tests. The rate of glucose disappearance for the IVGTT was lower both before and after weight gain in this subgroup compared to that in normal controls, suggesting insulin resistance. In conclusion, the low insulin response to oral glucose seen in the flat type group may be due to the disturbance of gastrointestinal factors, such as motility. In contrast, the observations suggest that the delayed type group has beta-cell failure corrected by weight gain and has insulin resistance requiring a longer recovery time; these abnormalities are related to the duration of AN.

Administration, Oral

Severe depression associated with ACTH, PRL, and GH deficiency: a case report.

A 68-year-old man was hospitalized in August, 1990 with general malaise, loss of energy, poor appetite and severe depression. He had experienced depressed moods, markedly diminished interest, feelings of worthlessness, diminished ability to think, general malaise and muscle weakness beginning in November, 1989. He was treated for depression at another hospital until his emergent admission to our hospital because of difficulty in walking. Laboratory studies disclosed hyponatremia, low plasma ACTH level (4.2 pmol/L), and a low cortisol level (27.6 nmol/L). Rapid ACTH test elicited an increase in serum cortisol from 75.6 nmol/L to 361.2 nmol/L at 30 min. Ovine corticotropin releasing hormone (CRH) did not stimulate secretion of either ACTH or cortisol. Human growth hormone releasing hormone (GRH) together with thyrotropin releasing hormone (TRH) elicited a normal response of TSH and low responses of GH and PRL. The patient's serum autoantibodies to anterior pituitary cell membranes using GH3 rat pituitary cells and AtT-20 mouse pituitary cells were positive. On the basis of these data, the diagnosis of selective ACTH, GH and PRL deficiency was made and thought to have been caused by lymphocytic adenohypophysitis. Following cortisol replacement therapy, he quickly regained his appetite and was restored to a normal mental state of being.

Adrenocorticotropic Hormone

Homocysteine induces iron-catalyzed lipid peroxidation of low-density lipoprotein that is prevented by alpha-tocopherol.

Homocystinuria is an inborn error of methionine metabolism that is characterized by the premature development of arteriosclerosis. As one of the major factors in the pathogenesis of arteriosclerosis, modification of low-density lipoprotein (LDL) has received widespread attention by many investigators. In this study, to elucidate the relationship between elevated homocysteine levels and premature arteriosclerosis, we investigated the role of homocysteine in the iron-catalyzed oxidative modification of LDL. When LDL isolated from a healthy subject was incubated with homocysteine and ferric ion, a gradual decrease of polyunsaturated fatty acids (PUFA), formation of thiobarbituric acid-reactive substances (TBARS) and fluorescent substances, and the fragmentation of apoprotein B (apoB) were observed. The extent of oxidative modification was dependent on the concentration of homocysteine. Modification of LDL was suppressed until the remaining alpha-tocopherol concentration reached a critical level. When the alpha-tocopherol content of LDL was increased by 2.6-fold, both the formation of TBARS and the fragmentation of apoB were suppressed. These results suggest that homocysteine might promote iron-catalyzed oxidation of LDL and imply its role for the development of premature arteriosclerosis.

Adult

Changes in beta-carotene levels by long-term administration of natural beta-carotene derived from Dunaliella bardawil in humans.

Long-term administration of a beta-carotene preparation derived from Dunaliella bardawil, a beta-carotene-rich algae, was studied in healthy young male volunteers. The daily administration of 60 mg of the beta-carotene preparation (30 mg of all-trans beta-carotene and 30 mg of 9-cis beta-carotene) was performed and beta-carotene concentrations were determined in the plasma, red blood cells (RBC), platelets (PLT), and mononuclear cells (MN). The all-trans beta-carotene level increased four-, two-, and threefold the baseline in plasma, PLT, and MN, respectively. Basal levels of 9-cis beta-carotene in plasma, PLT, and MN were low and found as one-tenth, one-fifth, and one-fifth of all-trans beta-carotene, which increased three-, two-, and 1.5-fold the baseline, respectively. Plasma and RBC alpha-tocopherol levels were not changed by the intake of beta-carotene. No side effects or toxicities were documented in any of the subjects during the administration period. In conclusion, the bioavailability of beta-carotene derived from Dunaliella bardawil was preferential for all-trans beta-carotene, although a small amount of the 9-cis form was detected in the plasma and blood cells.

Adult

[Effects of inorganic fluoride, inhalation time and dosage of sevoflurane on renal function during sevoflurane anesthesia of long duration].

In sevoflurane anesthesia of long duration, we studied correlations with renal function of the area under the curve (AUC), rate of decrease and maximum level of serum inorganic fluoride (F), sevoflurane dosage, and duration of administration. In 15 neurosurgical patients, we measured serum and urine levels of F, blood urea nitrogen (BUN), creatinine, serum and urine beta 2-microglobulin (BMG), and urine N-acetyl-beta-D-glucosaminidase (NAG). AUC and the rate of decrease of serum F were calculated. There were no correlations among the maximum level, AUC, the rate of decrease of serum F, sevoflurane dosage, duration of administration, BUN, creatinine, BMG, and NAG. It is concluded that in sevoflurane anesthesia of long duration, F, sevoflurane dosage and duration of administration do not affect renal function.

Adult

[Anesthetic management of a patient with adrenocorticotropic hormone (ACTH) deficiency].

A 73 year old woman with ACTH deficiency was admitted to our hospital for gastrectomy. She had taken corticosteroid for 3 years. The day before surgery, she took 25 mg of hydrocortisone per os. Hydrocortisone 100 mg was administered intravenously 30 minutes before surgery, during and after surgery, and on the next day after surgery. Serum concentrations of ACTH and cortisol were measured 1 hour after the first administration of hydrocortisone 100 mg, 2 hours after the second and 15 hours after the third administration. The ACTH concentration was always lower than the lowest limit of detection. Cortisol concentrations were 140.0, 180.0 and 14.5 micrograms.dl-1 at each measurement. Serum concentration of aldosterone after the induction of anesthesia was lower than the normal range. Her hemodynamics were very stable and electrolytes balance was not disturbed with corticosteroid treatment during and after surgery.

Adrenocorticotropic Hormone