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Biomedical subjects

I Takei

Publications and source records attributed to I Takei.

At least 55 records · Page 3Linked to original sources
PubMed1993

Detection of heat shock protein in patients with insulin-dependent diabetes mellitus.

We have investigated whether antibodies to heat shock protein (hsp) 65 are present in sera from patients with insulin-dependent diabetes mellitus by using Mycobacterium leprae hsp65. Fifty-two sera from patients with IDDM, 36 from patients with unclassified insulin-treated diabetes mellitus and 41 from normal healthy controls were examined by ELISA assay. Seventeen (32.7%) out of 52 IDDM sera and 10 (27.8%) out of unclassified insulin-treated diabetic sera were positive for anti-Mycobacterium (anti-M. leprae) hsp65 antibodies while none of the healthy control sera were positive. Based on western blot analysis, 12 of the 17 IDDM sera and 1 of 2 sera from the unclassified insulin-treated diabetics were positive for anti-M.leprae hsp65 antibodies while all normal control sera were negative. These results support the idea that hsp65 may play a role in the pathogenesis of IDDM. Future studies are necessary to elucidate the role of hsp65 in the pathogenesis of IDDM.

Antibodies, Bacterial↗
PubMed1993

Thyrotropin-producing microadenoma associated with pituitary resistance to thyroid hormone.

A 21-yr-old female with hyperthyroidism is described. Though her serum-free T3 was 17.8 pmol/L and free T4 was 60.2 pmol/L, TSH was as high as 10.7 mU/L. TRH stimulated an increase in TSH from 10.7-91.7 mU/L. T3 administration in gradually increasing doses of 100, 200, and 400 mg/day resulted in gradual reduction in serum TSH. Cranial computed tomography and magnetic resonance imaging revealed a microadenoma of the pituitary gland. Histology of the surgical specimen showed a TSH-producing adenoma with TSH cell cluster islets and decreased numbers of TSH cells in the nonneoplastic pituitary. Cultured cells from the adenoma secreted TSH spontaneously and in response to TRH. This TRH-stimulated TSH secretion was suppressed by T3 in a dose-dependent manner. One year postoperatively, neither residual tumor nor recurrence were seen by computed tomography and magnetic resonance imaging. However TSH, as well as free T3 or T4, was still high and overresponsive to TRH.

Adenoma↗
PubMed1993

A case of aldosterone producing adenoma associated with high PRA after long-term angiotensin converting enzyme inhibitor treatment.

A 62-year-old patient with non-insulin dependent diabetes (NIDDM) was admitted to our hospital for blood pressure control. He had been treated with angiotensin converting enzyme inhibitor (ACEI) for 7 years and showed marked hypokalemia with increased urinary potassium excretion. Hormonal examination revealed a normal plasma aldosterone concentration and increased plasma renin activity (PRA, 13.4 ng/ml/h), so potassium losing nephropathy was suspected. After discontinuation of the ACEI, PRA decreased to normal. An adrenal adenoma was found on abdominal magnetic resonance imaging (MRI) and adrenalectomy was performed to confirm aldosterone producing adenoma (APA). Although ACEIs are said not to alter PRA in APA, this drug was primarily responsible for the increased PRA in this case. This is a rare case of APA, which showed markedly increased PRA during ACEI treatment.

Adenoma↗
PubMed1992

Suppression of development of diabetes in NOD mice by lactate dehydrogenase virus infection.

It has been reported that lactate dehydrogenase virus (LDV) selectively infects a subpopulation of macrophages, thereby affecting the immune system. We studied the effects of LDV infection on the development of diabetes in non-obese diabetic (NOD) mice. Five-week-old female NOD mice were infected with LDV (10(8) ID50/mouse) and observed until 23 weeks of age. None of the 21-LDV-infected mice developed diabetes, whereas 10/14 (71.4%) uninfected mice did. Although the subpopulations of T cells and the percentage of Mac1-positive cells in the NOD murine spleen and the number of harvested peritoneal macrophages were unaffected by LDV infection, the proportions of Ia-positive peritoneal macrophages were significantly decreased in LDV-infected compared with uninfected mice (1.1 +/- 0.2%, 6.5 +/- 2.9%; P < 0.01). In LDV-infected NOD mice, insulitis of the same grade as that seen in uninfected NOD mice was observed. In another experiment, 3, 5, 10 or 16-week-old female NOD mice were infected with LDV. None of the mice infected with LDV at 3, 5 or 10 weeks of age developed diabetes and only one of six infected at 16 weeks of age did. These findings indicate that LDV infection suppresses the development of diabetes in female NOD mice by reducing the capacity of Ia-positive macrophages, and suggest that the development of human type 1 diabetes may be suppressed by certain viral infections.

Animals↗
PubMed1992

Prolonged QT interval in alcoholic autonomic nervous dysfunction.

QT prolongation on electrocardiography is related to sudden cardiac death and is frequently found in alcoholics. We studied QT prolongation in relation to the function of cardiac autonomic nerves assessed by the coefficient of variation of the R-R interval (CVRR) in three age-matched groups of men: 32 alcoholics with autonomic nervous dysfunction (AN), 32 alcoholics without AN, and 32 healthy controls. The QTc interval and CVRR were measured at rest on the 30th day of abstinence, when electrolyte imbalance had disappeared. Subjects with arrhythmia, conduction abnormality, cardiomegaly, ischemic heart disease or diabetes mellitus were excluded. A CVRR of less than 80% of standard predicted value was judged to represent AN. In alcoholics, QTc correlated negatively with the ratio of CVRR to its standard value (r = -0.49, p < 0.0001). The incidence of QTc prolongation was higher in alcoholics with AN (46.9%) than in alcoholics without AN (21.9%, p < 0.05). QTc prolongation was not observed in healthy controls. The QTc interval was significantly (p < 0.01) longer in alcoholics with AN (444 +/- 20 msec) than in alcoholics without AN (426 +/- 17) and in healthy controls (398 +/- 18). These results suggest that alcoholism causes dysfunction of the autonomic nerves as well as worsening QT prolongation, and this may predispose such patients to sudden cardiac death.

Adult↗
PubMed1991

Effect of alpha-adrenergic blockade on blood pressure, glucose, and lipid metabolism in hypertensive patients with non-insulin-dependent diabetes mellitus.

To clarify the long-term effects of alpha-adrenergic blockade on blood pressure, glucose, and lipid metabolism, a selective alpha 1-adrenergic inhibitor (prazosin, 1.0 to 2.0 mg/day in divided doses) was administered as a single antihypertensive agent to 10 (four men and six women, aged 52 to 76 years) hypertensive patients (systolic blood pressure [SBP] greater than or equal to 150 mm Hg or diastolic blood pressure [DBP] greater than or equal to 90 mm Hg) with non-insulin-dependent diabetes mellitus (NIDDM) for up to 20 weeks. Blood pressure, glucose tolerance and immunoreactive insulin (IRI) response to 75 gm oral glucose load, hemoglobin A1 (Hb A1), serum lipid profile, and serum apolipoprotein were examined before and after treatment. SBP and DBP were significantly reduced at 20 weeks after treatment with the selective alpha 1-adrenergic inhibitor (SBP 167 +/- 6 mm Hg versus 152 +/- 7 mm Hg; DBP 81 +/- 3 mm Hg versus 76 +/- 3 mm Hg, (p less than 0.05 and p less than 0.01, respectively). Glucose tolerance and IRI response to glucose load were not significantly changed at 4 and 12 to 20 weeks after selective alpha 1-inhibitor treatment compared with the baseline data before treatment; the level of Hb A1 was not significantly changed at 4 and 20 weeks after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1991

The suppressive effect of anti-asialo GM1 antibody on low-dose streptozotocin-induced diabetes in CD-1 mice.

To elucidate the role of natural killer (NK) cells in the pathogenesis of diabetes in streptozotocin-induced diabetes, we examined whether treatment with anti-asialo GM1 antibody prevents the occurrence of diabetes in CD-1 mouse model. Anti-asialo GM1 antibody was injected intraperitoneally 2-3 times a week starting three days before the first streptozotocin injection. In controls, rabbit immunoglobulin or saline was injected instead of anti-asialo GM1 antibody. Three of twelve anti-asialo GM1 antibody-treated mice developed diabetes, however eight of eight (100%) rabbit immunoglobulin injected mice and 20 of 23 saline-injected mice developed diabetes. The incidence of diabetes in the anti-asialo GM1 antibody-injected group was significantly higher than in the two control groups (p less than 0.01, p less than 0.01, respectively). The NK-cell activities of spleen cells from anti-asialo GM1 antibody-treated mice were significantly lower than in control mice. Flow-cytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from spleens of anti-asialo GM1 antibody-injected mice but no suppression of T-lymphocytes could be demonstrated. These results suggest that NK cells play a role in the pathogenesis of streptozotocin-induced diabetes in CD-1 mice.

Animals↗
PubMed1991

Anti-asialo GM1 antibody suppression of cyclophosphamide-induced diabetes in NOD mice.

To elucidate the role of natural killer (NK) cells in the pathogenesis of diabetes in the non-obese diabetic (NOD) mouse, we examined whether or not cyclophosphamide-induced diabetes occurs in NOD mice intraperitoneally (i.p.) injected with anti-asialo GM1 antibody. Two weeks after a single intraperitoneal injection of cyclophosphamide, none of the 24 NOD mice which had previously been treated with antiasialo GM1 antibody, 2-3 times per week for either 2 or 3 weeks, had developed indications of diabetes such as glycosuria or a high plasma glucose level. On the other hand, signs of diabetes were found in 10 of 24 control NOD mice injected with normal rabbit Ig instead of anti-asialo GM1 antibody (p less than 0.01). The NK cell activities of spleen cells from anti-asialo GM1 antibody-treated mice were significantly lower than those of control mice (p less than 0.01). Flowcytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from the spleens of anti-asialo GM1 antibody-injected mice but no suppression of CD8+ and CD4+ cells could be demonstrated. These observations suggest that NK cells are involved in the development of diabetes in NOD mice.

Animals↗
PubMed1990

Cytophagic histiocytic panniculitis evolving into total lipodystrophy.

A 15-year-old boy had persistent fever with severe neutropenia, thrombocytopenia, coagulation disorder, and marked elevation of lactate dehydrogenase values. A diagnosis of cytophagic histiocytic panniculitis was made after repeated skin biopsies. Three years after onset, he gradually lost 20 kg in body weight, and both skin and bone marrow specimens revealed degenerative changes of fatty tissue without any inflammatory cells. These findings suggest that total lipodystrophy syndrome results from the inflammatory destructive process of adipose tissue. To our knowledge, our report is the first to show, in a series of histologic studies, that an inflammatory destructive process may be involved in some cases of total lipodystrophy syndrome.

Adolescent↗
PubMed1989

Insulin autoantibodies in mouse models of insulin-dependent diabetes.

To clarify the significance of insulin autoantibodies (IAA) in insulin-dependent diabetes mellitus, we measured the IAA longitudinally in non-obese diabetic (NOD) mice, and in high-dose streptozotocin-induced diabetes (high-SZ) and EMC virus-induced diabetes (EMC) in mice, and compared the data with the occurrence of insulitis. The IAA were detected by the polyethylene glycol (PEG) method using 125I-(Tyr A14) human insulin. The IAA were found in 38% of NOD mice and correlated with the occurrence of insulitis. The prevalence of IAA was 0% before the appearance of insulitis, 80% at 12-14 weeks of age and 30% after 20 weeks of age in female NOD mice. In male NOD mice, IAA were found in 45% at 12-14 weeks of age and 20% after 20 weeks. In high-SZ mice, IAA were detected in several mice while insulitis was not present. In EMC-virus induced diabetic mice, IAA and lymphocytic infiltration into the islets were detected 4-14 days after EMC virus infection. These results suggest that (a) IAA are markers for islet autoimmunity in NOD mice, (b) the presence of IAA does not always reflect insulitis, (c) the presence of IAA is not sufficient for the development of overt diabetes and (d) the appearance of IAA may reflect a difference of the immune response genotype.

Animals↗
PubMed1989

[Klebsiella pneumoniae meningitis associated with liver abscess: a case report].

We report a rare case of Klebsiella pneumoniae meningitis associated with liver abscess, which was successfully treated with cefotaxime (CTX), one of the third-generation cephalosporins. A 53-year-old man was admitted to Keio University Hospital on June 13, 1988, because of a fever and a headache. On June 3, he suddenly started shivering and his temperature rose to 39 degrees C. He then began to complain of polydipsia, polyuria, and a weight loss of 4 kg a week. On June 11, he developed a severe headache. Four years prior to this incident, he had been diagnosed as having diabetes after a routine medical examination, but had neglected to undergo medical treatment. On admission, laboratory data showed leukocytosis, hyperglycemia (394 mg/dl) and ketonuria (4+). A lumbar puncture yielded cloudy cerebrospinal fluid (CSF) containing 500/3 cells/mm8, of which about 70% were neutrophils. A diagnosis of diabetic ketoacidosis and purulent meningitis was made. A treatment with ampicillin (ABPC) and CTX, (12 g/day, each) was begun. On the third day, cultures of a blood specimen and CSF yielded both K. pneumoniae. The MICs of CTX to K. pneumoniae isolated from blood and CSF were both 0.05 microgram/ml. ABPC was discontinued, gentamicin was administered for 2 days, CTX was continued at the same dosage level and an administration of prednisolone 40 mg daily was begun.(ABSTRACT TRUNCATED AT 250 WORDS)

Cefotaxime↗
PubMed1989

The suppressive effect of cyclophosphamide on low-dose streptozotocin-induced diabetes in mice.

We found that low-dose streptozotocin (SZ)-induced diabetes in mice is suppressed by cyclophosphamide (CY) and studied the mechanisms of this suppression. Male CD-1 mice were injected intraperitoneally with SZ (40 mg/kg) for five consecutive days (group SZ). In addition, CY (200 mg/kg) was injected on the first day (group CY-1) or on days 1 and 5 (group CY-2). In group SZ, all mice developed diabetes within nine days after the first injection of SZ. Group CY-1 did not develop hyperglycemia for 14 days and group CY-2 did not develop it throughout the experimental period (40 days). Insulitis was suppressed slightly in group CY-1 and completely in group CY-2. The number of spleen cells did not change in group SZ compared with that before cyclophosphamide treatment. They decreased significantly on days 3 and 7 in both groups CY-1 and CY-2 (p less than 0.01 or p less than 0.05), but then increased significantly on days 14 and/or 21 (p less than 0.01 or p less than 0.05) compared with those before cyclophosphamide treatment. The Thy 1.2- and L3T4-positive cells increased significantly in group SZ but they decreased on days 3 and 7 in both groups CY-1 and CY-2 (p less than 0.01) compared with the controls. These results suggest that (1) this large reduction of lymphocytes at the beginning of SZ treatment may lead to the prevention of hyperglycemia and insulitis, and (2) T-cells, especially L3T4-positive cells may play an important role in the pathogenesis of this type of diabetes.

Animals↗
PubMed1988

Insulin autoantibodies in non-obese diabetic (NOD) mice and streptozotocin-induced diabetic mice.

Similar to Insulin-dependent diabetes mellitus (IDDM) in man, diabetes in the non-obese diabetic (NOD) mouse and that induced by low-dose of multiple injections of streptozotocin (low-dose SZ) develop in conjunction with the presence of insulitis. We measured insulin autoantibodies (IAA) in NOD and low-dose SZ mice and compared the levels with mice given a single diabetogenic dose of streptozotocin (high-dose SZ) as well as control CD-1 mice. The mean insulin binding in female NOD mice was 3.08 +/- 1.49 (mean + SD)% and that in male NOD mice was 2.86 +/- 3.70%, as compared with 1.10 +/- 0.35% in the control CD-1 mice (p less than 0.01, p less than 0.05). Sera from low-dose SZ and high-dose SZ mice showed 1.07 +/- 0.23% and 0.93 +/- 0.45% of IAA which did not differ from controls. The number of mice with IAA above the mean + 2SD value of CD-1 mice were 8/9 female NOD mice and 9/20 male NOD mice. Insulitis was found in all NOD and low-dose SZ mice but not in any high-dose SZ mice and control CD-1 mice. These results suggest that (a) IAA are markers for islet autoimmunity in the NOD mouse, (b) presence of IAA does not reflect insulitis, and (c) the appearance of IAA may reflect a difference of the immune response genotype.

Animals↗
PubMed1984

Cell-mediated cytotoxic islet cell surface antibodies to human pancreatic beta cells.

Sera containing islet cell surface antibodies show a complement-dependent cytotoxic reaction against islet cells, but it has not yet been clarified whether islet cell surface antibodies exhibit cell-mediated cytotoxicity to these cells. By 51Cr release assay we investigated whether islet cell surface antibodies showed a cytotoxic reaction to human pancreatic B cells (JHPI-1 clone) in the presence of normal human lymphocytes. The sera from 14 islet cell surface antibody-positive, 16 islet cell surface antibody-negative Type 1 (insulin-dependent) diabetic patients and 18 islet cell surface antibody-negative healthy subjects were studied. Four sera containing islet cell surface antibodies showed specific cytotoxicity above the mean +3SD value of healthy subjects, and the mean specific cytotoxicity of islet cell surface antibody-positive sera differed significantly from that of both islet cell surface antibody-negative groups. These results suggest that this cell-mediated cytotoxic mechanism may play an important role in the pathogenesis of Type 1 diabetes.

Adolescent↗
PubMed1984

Immunological aspect of non-obese diabetic mice: immune islet cell-killing mechanism and cell-mediated immunity.

The non-obese diabetic mouse is thought to be one of the best available animal models for human Type 1 (insulin-dependent) diabetes. By 51Cr release assay we investigated cell-mediated cytotoxicity to the islet cell of Balb/C mice, natural killer activity, and antibody-dependent cell-mediated cytotoxicity activity of spleen lymphocytes from pre-diabetic non-obese diabetic mice. The cell-mediated cytotoxicity to islet cells of non-obese diabetic mice was significantly higher than that of control ICR mice. In contrast, natural killer and antibody-dependent cell-mediated cytotoxicity activities of the spleen cells from the non-obese diabetic mice were significantly lower than those of ICR mice spleen cells. These results suggest that lymphocytes from non-obese diabetic mice were sensitized to the antigen of islet cells and that the non-specific cellular immunity of non-obese mice was reduced. They suggest also that this immune islet cell-killing mechanism may play an important role in the pathogenesis of diabetes in non-obese diabetic mice.

Animals↗