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Biomedical subjects

T Taminato

Publications and source records attributed to T Taminato.

At least 19 recordsLinked to original sources
PubMed2004

Constitutively activated phosphatidylinositol 3-kinase primes platelets from patients with chronic myelogenous leukemia for thrombopoietin-induced aggregation.

In this study, we examined the effect of thrombopoietin (TPO) on the aggregation of platelets from 40 patients with myeloproliferative disorders (MPDs), including 17 patients with chronic myelogenous leukemia in the chronic phase (CML-CP), 10 with polycythemia vera, 10 with essential thrombocythemia, and three with myelofibrosis. TPO by itself dose-dependently induced the aggregation of platelets from patients with CML-CP but not from those with other MPDs or with CML-CP in cytogenetical complete remission. The expression of CD63 in CML-CP platelets was induced by TPO treatment. Phosphatidylinositol 3-kinase (PI3-kinase) was constitutively activated in CML-CP platelets. Pretreatment with PI3-kinase inhibitors (wortmannin and LY294002) dose-dependently inhibited TPO-induced aggregation of CML-CP platelets. The Abl kinase inhibitor imatinib mesylate and the Jak inhibitor AG490 suppressed TPO-induced aggregation of CML-CP platelets. Pretreatment with imatinib mesylate, but not with AG490, inhibited the activity of PI3-kinase in CML-CP platelets. In addition, tyrosine phosphorylation of Jak2 was undetected in CML-CP platelets before TPO treatment. These findings indicate that the constitutive activation of PI3-kinase primes CML-CP platelets for the aggregation induced by TPO, and that Bcr-Abl, but not Jak family protein tyrosine kinases, are involved in the constitutive activation of PI3-kinase in CML-CP platelets.

Androstadienes↗
PubMed2003

Hypoglycaemia in patients with liver diseases administered levothyroxine.

OBJECTIVE: Experience of a few hypoglycaemic patients with liver disease and receiving levothyroxine suggested to us that the prevalence of hypoglycaemia might be higher in such patients. The purpose of this study was to ascertain whether the prevalence of hypoglycaemia this was actually the case. METHODS: This study was a retrospective, cross-sectional analysis of a medical computerized database and/or written reports from our university hospital. Patients with primary liver disease who were admitted to our hospital between April 1998 and August 2000 were divided into two groups; the first group received levothyroxine and the second group did not. The patients in the second group were selected from three different time periods within the period shown. The prevalence of hypoglycaemia (blood glucose level <70 mg/dL) was compared between the two groups. RESULTS: The prevalence of hypoglycaemia was significantly higher in the group receiving levothyroxine compared with the group not receiving levothyroxine (four of eight patients (50.0%) vs. three of 59 (5.1%), P = 0.003, Fisher's exact test). CONCLUSIONS: The results suggest that levothyroxine may be a risk factor for hypoglycaemia in patients with liver disease. While a larger study, perhaps with an alternative study design is needed to confirm this, and to investigate possible mechanisms of effect, it would be prudent to monitor the blood glucose level of such patients closely.

Aged↗
PubMed2002

Nosocomial contamination by Mycobacterium gordonae in hospital water supply and super-oxidized water.

We experienced contamination by Mycobacterium gordonae of the hospital water of our surgical ward. The contamination was discovered following detection of the organism in operative lung samples, washed with super-oxidized water. Repeated examination of water demonstrated contamination by M. gordonae occurred only in the surgical ward, related to the apparatus for making super-oxidized water. No patients were infected by M. gordonae. After changing the water supply equipment and cleaning the water tubes, M. gordonae in the water disappeared.

Cross Infection↗
PubMed2001

Bezafibrate attenuates the overexpression of plasminogen activator inhibitor-1 messenger RNA by a combination of mono-unsaturated fatty acid and insulin in hepG2 cells.

The effects of bezafibrate (PPAR alpha activator) and troglitazone (PPAR gamma activator) on the expression of plasminogen activator inhibitor type-1 (PAI-1) in HepG2 cells were investigated. Exposure of the cells for 24 hours to either oleic acid or insulin showed no obvious effects on PAI-1 synthesis, whereas the combination of the two agents induced a 2.3-fold increase in PAI-1 synthesis, which was accompanied by a 3-fold increase in both the 2.2 kb and 3.2 kb forms of PAI-1 mRNA. This up-regulation of PAI-1 synthesis was attenuated by bezafibrate in a dose-dependent manner (1-100 microM) with 30% reversal at 100 microM. In contrast, troglitazone further stimulated PAI-1 synthesis to 140% of the level obtained in the presence of both oleic acid and insulin. This attenuation by bezafibrate and enhancement by troglitazone required the presence of both oleic acid and insulin. It is interesting that PAI-1 expression was affected so differently by these two PPAR activators.

Bezafibrate↗
PubMed2001

Neuropeptide Y in central control of feeding and interactions with orexin and leptin.

Neuropeptide (NPY) increases feeding when injected into the brain. In this study, we tested the hypothesis that its action might be related to feeding regulation of the orexin and leptin systems in rats. Intracerebroventricular administration of NPY (1 nmol/5 microL) stimulated feeding in rats. Injection of an antibody to orexin-A inhibited feeding, suggesting that endogenous orexin exerts a stimulatory tone on feeding. Intracerebroventricular injection of orexin antiserum before injection of NPY significantly attenuated the feeding response to NPY. On the other hand, ip pretreatment with leptin (2 mg/kg) significantly decreased food intake and inhibited NPY-induced feeding. We then examined whether orexin-containing neurons are activated under the stimulation of feeding in response to intracerebroventricular NPY or suppression of feeding in response to ip leptin, using Fos-like immunoreactivity (FLI) as a marker of neural activation. We observed that FLI was induced in the paraventricular, supraoptic, and dorsomedial nuclei as well as the lateral hypothalamic area (LHA) following administration of NPY. Double staining with anti-Fos and antiorexin antibodies revealed that 23.4% of the orexin-containing neurons in the LHA expressed FLI after NPY injection. Approximately 7.8% of the orexin-positive neurons in the LHA coexpressed Fos after leptin plus NPY. Our data indicate that a functional interaction among NPY, orexin, and leptin exists that may contribute to the central regulation of appetite.

Animals↗
PubMed2001

Central administration of neuromedin U activates neurons in ventrobasal hypothalamus and brainstem.

Neuromedin U (NMU) is a peptide isolated from the porcine spinal cord. Recently, two receptors for NMU have been identified and characterized. A recent study indicated that NMU is an anorectic chemical in the brain. The present study shows that NMU has an action in the brain to inhibit food intake in rats. Intracerebroventricular injection of NMU inhibited dark-phase feeding. Animals injected with NMU showed a strong increase in Fos-immunoreactive nuclei in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus, and in the parabrachial nucleus of the brain stem. Double immunohistochemistry revealed that a high number of oxytocin-immunoreactive neurons in the PVN and SON contained Fos after intracerebroventricular injection of NMU. In addition, a small proportion of vasopressinergic cells within the PVN and SON were found to contain Fos. The effect of NMU on the hypothalamus and brain stem contributes to the inhibitory effects of NMU on feeding behavior.

Animals↗
PubMed1999

Impairment of ventilatory response to metabolic acidosis in insulin-dependent diabetic patients with advanced nephropathy.

Sudden cardiopulmonary arrest due to a defective respiratory reflex is observed in diabetic patients. Impaired ventilatory response in diabetic patients to acute hypoxia or hypercapnia induced by the inhalation of an artificial gas has been reported. Little is known regarding the respiratory compensatory ability for mild to moderate metabolic acidosis due to renal failure in insulin-dependent diabetic subjects. Arterial blood pH, HCO3-, PaCO2 and PaO2 were measured in 13 insulin-dependent diabetic subjects with advanced nephropathy and in 33 non-diabetic subjects with end-stage renal failure. The diabetic group consisted of six predialysis patients and seven on regular hemodialysis (HD) and the non-diabetic group, ten predialysis patients and 23 on HD. Differences between measured partial arterial pressure of carbon dioxide (PaCO2) and predicted PaCO2 determined from HCO3- were examined. PaCO2 was significantly higher in the diabetic than in non-diabetic group (40.0 +/- 7.4 versus 31.1 +/- 5.1 mmHg, p < 0.05 in predialysis, 42.0 +/- 6.4 versus 36.0 +/- 2.6 mmHg, p < 0.05 in HD), though plasma pH was essentially the same for either. Differences in measured PaCO2 and predicted PaCO2 were significantly larger in the diabetic group than in non-diabetic group. Ventilatory response to uremic acidosis may thus be considered impaired in subjects with advanced diabetic nephropathy.

Acidosis↗
PubMed1996

Alterations in basal and glucose-stimulated voltage-dependent Ca2+ channel activities in pancreatic beta cells of non-insulin-dependent diabetes mellitus GK rats.

In genetically occurring non-insulin-dependent diabetes mellitus (NIDDM) model rats (GK rats), the activities of L- and T-type Ca2+ channels in pancreatic beta cells are found to be augmented, by measuring the Ba2+ currents via these channels using whole-cell patch-clamp technique, while the patterns of the current-voltage curves are indistinguishable. The hyper-responsiveness of insulin secretion to nonglucose depolarizing stimuli observed in NIDDM beta cells could be the result, therefore, of increased voltage-dependent Ca2+ channel activity. Perforated patch-clamp recordings reveal that the augmentation of L-type Ca2+ channel activity by glucose is markedly less pronounced in GK beta cells than in control beta cells, while glucose-induced augmentation of T-type Ca2+ channel activity is observed neither in the control nor in the GK beta cells. This lack of glucose-induced augmentation of L-type Ca2+ channel activity in GK beta cells might be causatively related to the selective impairment of glucose-induced insulin secretion in NIDDM beta cells, in conjunction with an insufficient plasma membrane depolarization due to impaired closure of the ATP-sensitive K+ channels caused by the disturbed intracellular glucose metabolism in NIDDM beta cells.

Animals↗
PubMed1996

Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects.

Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). We have identified two missense mutations, Gly198-->Cys (Gly198Cys) in exon 7 and Glu354-->Gln (Glu354Gln) in exon 12. Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. Association studies show no relationship between NIDDM and either of the two mutations.

Alleles↗
PubMed1995

Daily variation of serum lipids in relation to the circadian rhythm of platelet aggregation in healthy male persons.

The circadian rhythm of platelet aggregation was compared with that of serum lipids in seven healthy male persons. Daily variations of remnant lipoprotein-cholesterol and of remnant lipoprotein-triglycerides were related to those of arachidonic acid-, ADP (adenosine diphosphate)-, and collagen-induced aggregation in platelet-rich plasma and to ADP-induced aggregation in whole blood, respectively. Statistical analyses indicate that the time course of remnant-cholesterol was correlated to that of ADP-induced aggregation in platelet-rich plasma and the time courses of blood cholesterol and triglyceride were correlated to arachidonic acid- and serotonin-induced platelet aggregation in platelet-rich plasma, respectively. In whole blood, the time course of remnant lipoprotein-triglyceride was correlated only to ADP-induced platelet aggregation. In contrast, the daily variation of HDL (high density lipoprotein)-cholesterol did not influence either that of platelet aggregation in platelet-rich plasma or that in whole blood. Our findings are of clinical interest regarding the development of atherosclerosis and thrombotic events in persons with an elevated level of serum lipids.

Adolescent↗
PubMed1994

[The mechanism of thyroid hormone abnormalities in patients with diabetes mellitus].

In order to clarify the mechanism of impaired thyroid hormone levels in patients with diabetes mellitus, thyroid hormone, thyroid hormone binding inhibitor (THBI), inhibitor of extrathyroidal conversion of T4 to T3 (IEC) and free fatty acid (FFA) were examined. In addition, TRH test was performed on 9 diabetic patients showing poor control of plasma glucose before and after glycemic control. Before glycemic control, fasting plasma glucose and HbA1c were significantly higher than after glycemic control (P < 0.05). T3 and the T3/T4 ratio significantly increased and rT3 significantly decreased after glycemic control (P < 0.05). THBI index and plasma FFA level significantly decreased and %T3 production (IEC) significantly increased after glycemic control (P < 0.05). The response of TSH to TRH significantly increased after glycemic control. In conclusion, (1) the presence of THBI, (2) the presence of IEC, and (3) dysfunction of the hypothalamo-hypophysial-thyroid axis are considered to be involved in abnormal thyroid function in diabetic patients.

Blood Glucose↗
PubMed1993

Selective impairment of the cytoplasmic Ca2+ response to glucose in pancreatic beta cells of streptozocin-induced non-insulin-dependent diabetic rats.

Pancreatic islets from the streptozocin-induced non-insulin-dependent diabetes mellitus (NIDDM) rat model showed a diminished insulin response to 16.7 mmol/L glucose, but the insulin response to arginine remained intact. To evaluate the importance of intracellular calcium concentration ([Ca2+]i) in the diminished insulin response to glucose, the [Ca2+]i of pancreatic beta cells was investigated using fura-2. Glucose produced heterogeneous responses of [Ca2+]i, which were in beta-cell clusters of both the control and NIDDM groups. Many cells showed initial slight decreases of [Ca2+]i, which were followed by gradual and large increments of [Ca2+]i after glucose stimulation of beta cells in the control group. On the other hand, the increase of [Ca2+]i in response to glucose was markedly diminished in beta cells of the NIDDM group compared with controls. The average lag time to [Ca2+]i elevation of beta cells in the NIDDM group was significantly longer than that of the control group. Arginine produced marked increases of [Ca2+]i, in contrast to the effect of glucose stimulation in the NIDDM group. These results suggest that the diminished and delayed [Ca2+]i increases in beta cells of NIDDM rats in response to glucose stimulation are responsible for the selectively impaired insulin response to glucose in the rat model of NIDDM.

Animals↗