Biomedical subjects

T Uehara

Publications and source records attributed to T Uehara.

At least 109 records · Page 6Linked to original sources

PubMed1998

Myocardial glucose metabolism in patients with hypertrophic cardiomyopathy: assessment by F-18-FDG PET study.

In an investigation of myocardial metabolic abnormalities in hypertrophic myocardium, the myocardial glucose metabolism was evaluated with F-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) in 32 patients with hypertrophic cardiomyopathy, and the results were compared with those in 9 patients with hypertensive heart disease. F-18-FDG PET study was performed in the fasting and glucose-loading states. The myocardial regional %dose uptake was calculated quantitatively. The average regional %dose uptake in the fasting state in the patients with asymmetric septal hypertrophy and dilated-phase hypertrophic cardiomyopathy was significantly higher than that in the patients with hypertensive heart disease (0.75 +/- 0.34%, 0.65 +/- 0.25%, and 0.43 +/- 0.22%/100 g myocardium, respectively). In contrast, the average %dose uptake in the glucose-loading state in the patients with asymmetric septal hypertrophy and dilated-phase hypertrophic cardiomyopathy was not significantly different from that in patients with hypertensive heart disease (1.17 +/- 0.49%, 0.80 +/- 0.44% and 0.99 +/- 0.45%, respectively). The patients with apical hypertrophy had also low %dose uptake in the fasting state (0.38 +/- 0.21%) as in the hypertensive heart disease patients, so that the characteristics of asymmetric septal hypertrophy and dilated-phase hypertrophic cardiomyopathy are considered to be high FDG uptake throughout the myocardium in the fasting state. Patients with apical hypertrophy are considered to belong to other disease categories metabolically. F-18-FDG PET study is useful in the evaluation of the pathophysiologic diagnosis of patients with hypertrophic cardiomyopathy.

Blood Glucose↗

PubMed1998

Glucose tolerance and myocardial F-18 fluorodeoxyglucose uptake in normal regions in coronary heart disease patients.

To elucidate the relation between glucose tolerance and myocardial uptake of F-18 fluorodeoxyglucose (FDG), FDG-PET with 75 g oral glucose loading was performed on 43 coronary artery disease patients (twice in 2 patients). The patients were divided into 4 groups based on the blood glucose level (BS) and the insulinogenic index (II): group 1, normal (n = 9); group 2, impaired glucose tolerance (IGT, n = 12); group 3, mild diabetes mellitus (DM) (II > 0.4, n = 12); and group 4, severe DM (II < or = 0.4, n = 12). Percent (%) dose uptake of FDG in the normal regions of the myocardium was not significantly different in groups 1, 2, and 3, but it was much lower in group 4 than in groups 1 and 2. In groups 2, 3, and 4, % dose uptake showed a definite negative correlation with BS 60 min after glucose loading (r = -0.450, p < 0.05), and a close positive correlation with II (r = 0.363, p < 0.05). These findings indicate that myocardial FDG uptake in normal regions is not greatly impaired in patients with IGT or mild DM. Myocardial viability can be assessed by oral glucose loading in patients with IGT and mild DM as well as in patients with normal glucose tolerance.

Aged↗

PubMed1998

Long-term survivors with pN2 non-small cell lung cancer after a complete resection with a systematic mediastinal node dissection.

OBJECTIVE: A substantial number of surgical patients with pN2 disease have survived longer than 5 years without any evidence of recurrence, although the surgical indications for those patients remain controversial. The present study was performed in order to clarify the clinical characteristics of the long-term survivors with pN2 disease. METHODS: We retrospectively reviewed the cases of 111 patients with pN2 disease who had undergone a complete resection with a systematic mediastinal lymph node dissection from 1974 through 1991. RESULTS: Of the 111 patients with pN2 disease, 20 survived longer than 5 years after a surgical resection. When both the pre- and post-operative conditions were compared between the long-term survivors and the others, the long-term survivors were characterized by significantly higher proportions of cN0 disease (P = 0.031), pT1 disease (P = 0.004), skip metastasis without hilar node metastasis (P = 0.028), and metastasis of a single mediastinal station (0.044). Of those characteristics, only the likelihood of having cN0 disease could be pre-operatively determined. The survival rate of such a population with cN0-pN2 disease was 34.5% at 5 years and 29.6% at 10 years after a complete resection, respectively. CONCLUSIONS: Pathologic N2 patients with some favorable prognostic factors can survive long-term after a complete resection combined with a systematic mediastinal lymph node dissection. At present, due to the lack of any effective adjuvant therapy, a systematic mediastinal node dissection should be routinely performed even in patients with cN0 disease.

Carcinoma, Non-Small-Cell Lung↗

PubMed1998

Dysfunctional parenting as a risk factor to lifetime depression in a sample of employed Japanese adults: evidence for the 'affectionless control' hypothesis.

BACKGROUND: Although many case-control studies have replicated an association between dysfunctional parenting and a lifetime diagnosis of depression, few epidemiological studies have explored the association. In addition, little is known about the association in non-western countries. METHODS: Using logistic regression analyses, additive and interactive contributions of parental child-rearing behaviours, as measured by the Parental Bonding Instrument (PBI), toward the risk for having a lifetime diagnosis of major depressive disorder were explored in 418 employed Japanese adults. The diagnosis was provided by using the Inventory to Diagnose Depression, lifetime version. The analyses were conducted for male and female subjects separately. RESULTS: Parental care rather than parental protection was primary in predicting lifetime depression in both male and female subjects. An interactive combination of low care and high protection ('affectionless control') was a significant risk factor for lifetime depression in male respondents' reporting child-rearing behaviours of both parents and female respondents' reporting paternal child-rearing behaviours. Model improvements when entering the PBI scores were larger in male subjects than in female subjects. CONCLUSIONS: The results suggested that a combination of low care and over-protection increases a risk to lifetime depression even in a non-clinical sample; that an association between dysfunctional parenting (particularly low care) and the development of depression is independent of culture; and that Japanese boys are more sensitive than Japanese girls to dysfunctional parenting as regards the development of depression.

Adolescent↗

PubMed1998

Personality differences in the Munich Personality Test between patients with major depression and panic disorder.

This study attempted to determine whether patients with major depression and panic disorder could be differentiated by personality features, measured by the Munich Personality Test (MPT). One of the six MPT personality dimensions, 'rigidity', was developed in relation to the 'melancholic type of personality', which may be a specific personality feature of depressive subjects. We therefore hypothesized that the MPT might be sensitive to possible personality differences between patients with major depression and panic disorder. Sixty-six patients with major depression and 27 patients with panic disorder, taken from consecutive intakes at an outpatient unit, were compared in terms of six personality dimensions of the MPT. The results demonstrated that rigidity could significantly differentiate the two patient groups, even after the possible confounding effects on the personality assessments were statistically partialled out. The MPT was suggested to be powerful for describing distinctive personality features of depressive subjects from anxiety subjects.

Adult↗

PubMed1998

Dramatic effect of ethosuximide on epileptic negative myoclonus: implications for the neurophysiological mechanism.

Epileptic negative myoclonus (ENM) is a recently defined epileptic seizure type seen in various epileptic syndromes. Although the long-term prognosis appears to be favorable, the treatment of localization-related epilepsy (LRE) with ENM in childhood is sometimes difficult due to the apparently pharmaco-resistant nature of ENM. We evaluated the effects of antiepileptic drugs (AEDs) in 10 patients with ENM. Carbamazepine was administered to eight patients, none of whom improved. Responses to clonazepam and valproic acid were unpredictable, whereas ethosuximide (ESM) achieved complete control of ENM in all six cases treated with this drug as adjunctive therapy. The pharmacological responses of ENM to CBZ and ESM were quite similar to those of absence seizures. According to the SPECT and ictal EEG findings in addition to the pharmacological responses from this study, we favor to postulate that ENM is produced by a direct inhibitory action on the motor cortex resulting in the interruption of voluntary muscle contraction as generated by sharp-slow wave complexes, compatible with the mechanism considered to underlie absence seizures. ENM are refractory to treatment and persisting if the wrong AEDs, such as PHT or CBZ, are selected at the diagnosis of LRE. We recommended a trial of ESM when ENM develops during the clinical course of LRE regardless of etiology.

Adolescent↗

PubMed1998

Comparison of dual-isotope acquisition of 201Tl and 99Tcm-tetrofosmin for the detection of ischaemic heart disease and determination of the optimal imaging time of 99Tcm-tetrofosmin.

Comparative studies of thallium-201 (201Tl) and 99Tcm-tetrofosmin for the detection of ischaemic heart disease (IHD) have previously been reported. These 201Tl and 99Tcm-tetrofosmin studies were usually performed separately with different exercise loads at an interval of several days. Here, we used a dual-isotope technique with exercise myocardial SPET (single photon emission tomography) in 17 patients with IHD and 10 patients with normal coronary arteries. The triple-energy window (TEW) method was applied for cross-talk correction. SPET imaging was performed at 10 and 70 min (S1 and S2) after the injection of 99Tcm-tetrofosmin (222 MBq) and 201Tl (74 MBq) at peak exercise to determine the optimal imaging time of 99Tcm-tetrofosmin. The S2 value was obtained 35 min after the subject drank a glass of milk to accelerate hepatobiliary clearance. Twenty-five minutes after S2, 37 MBq of 201Tl were reinjected at rest and SPET imaging (S3) was performed. Immediately after S3, 666 MBq of 99Tcm-tetrofosmin were reinjected and SPET imaging (S4) was performed 50 min later. Representative short and vertical long axis tomograms were divided into 17 segments. Each segment was assessed using a 4-point scoring system. The defect score was defined as the sum of each segmental score. The defect scores for imaging at exercise were 14.3 +/- 11.4 for 201Tl at S1, 11.4 +/- 8 for 99Tcm-tetrofosmin at S1 and 9.7 +/-9.8 for 99Tcm-tetrofosmin at S2 (P < 0.01), respectively. The washout rate of 99Tcm-tetrofosmin for the first hour was 15.5 +/- 7.3% and 11.8 +/- 7.7% (P < 0.01), respectively, for the normal and ischaemic segments. The image quality of 201Tl at S1 was almost equivalent to that of 99Tcm-tetrofosmin at S1/S2. The overall sensitivity and specificity for the detection of ischaemia was 94% and 82% for 201Tl at S1, 89% and 86% for 99Tcm-tetrofosmin at S1, and 88% and 95% for 99Tcm-tetrofosmin at S2, respectively. The overall accuracy was 86%, 88% and 92%, respectively. The myocardial viability score was 7.4 +/- 7.1 for 201Tl at S3 and 5.8 +/- 7.0 for 99Tcm-tetrofosmin at S4 (P < 0.01). The results indicate that the diagnostic accuracy of 99Tcm-tetrofosmin for myocardial ischaemia is almost equivalent to that of 201Tl as assessed by dual SPET imaging, and that the optimal imaging time for 99Tcm-tetrofosmin is within 10-35 min (S1) after exercise.

Coronary Disease↗

PubMed1998

High frequency of unruptured intracranial aneurysms in female patients with ischaemic heart disease.

OBJECTIVES: Concurrence of coronary atherosclerotic lesions and intracranial aneurysms has been pointed out in several postmortem and clinical studies. However, the relative risk for intracranial aneurysms in patients with ischaemic heart disease remains uncertain. The aim of this study is to elucidate clinically whether ischaemic heart disease is a risk factor for intracranial aneurysms. METHODS: Between October 1993 and May 1995, 84 patients with ischaemic heart disease with angiographically established coronary artery stenoses who had no history of stroke (ischaemic heart disease group; men:women=58:26, mean (SD) age=61.1 (9.6) years) and 200 age matched subjects with minor neurological disorders who had no history of ischaemic heart disease (control group; men:women=117:83, mean (SD) age=62.0 (9.2) years) were screened with magnetic resonance angiography (MRA) for the presence of unruptured intracranial aneurysms. For all MRA positive patients, selective angiography was then undertaken. RESULTS: In the ischaemic heart disease group, the frequency of unruptured intracranial aneurysms established angiographically was 3.4% for men and 15.4% for women, compared with 2.6% and 3.6% respectively in the control group. Multiple logistic regression analyses disclosed that ischaemic heart disease was a significant and independent predictor for intracranial aneurysms in women. CONCLUSIONS: These results suggest that in women ischaemic heart disease is a risk factor for intracranial aneurysms. Coexistence of intracranial aneurysms should be suspected in women patients with ischaemic heart disease.

Aged↗

PubMed1998

Spontaneous dural carotid cavernous sinus fistula presenting isolated ophthalmoplegia: evaluation with MR angiography.

We describe three patients with spontaneous dural carotid cavernous sinus fistula presenting an isolated ophthalmoplegia where magnetic resonance angiography demonstrated abnormal flow-related enhancements in the cavernous sinus with extension into the inferior petrosal sinus. Magnetic resonance angiography is of value in evaluation of patients with isolated ophthalmoplegia.

Arteriovenous Fistula↗

PubMed1998

[The involvement of cytokines, chemokines and inducible nitric oxide synthase (iNOS) induced by a transient ischemia in neuronal survival/death in rat brain].

Inflammatory/immunological processes underlie the survival/damage of neurons after brain ischemia. In glial cells, cytokines such as IL-1 beta and TNF-alpha are produced following ischemic stresses. On the other hand, it is suggested that NO/iNOS is involved in neuronal apoptosis. We here review the ischemia-induced production of cytokine/iNOS and the neurotrophic/neurotoxic effects. It is not clear whether or not the neuronal death after brain ischemia is apoptosis or necrosis. Under the condition of transient forebrain ischemia, however, we obtained results suggesting apoptosis in the delayed neuronal death of the CA1 pyramidal neurons. The time course and cellular localization of postischemic iNOS expression depend on the properties of the ischemic insult. The iNOS induction is detected primarily in astrocytes after the transient forebrain ischemia when the neuronal apoptosis is observed. We discuss a variety of cytokines with neurotrophic/neurotoxic actions that are produced by ischemia or environmental stresses in glial cells. From the neurotoxicological aspect of the neuro-glial interaction, we also review recent findings on signalling pathways of the iNOS induction in glial cells and the mechanisms of the cytotoxic actions of NO.

Animals↗

PubMed1998

[The precise characterization and the crucial mechanism of NO-induced cytotoxicity].

NO is believed to be involved in neurotoxicity after various neuronal stresses. NO donors are toxic and cause changes in cellular morphology such as condensed and fragmented chromatin, shriveled nuclei, apoptotic bodies and membrane blebbing. These observations are consistent with the overall description of apoptosis. The crucial mechanism of NO-induced cytotoxicity is still unclear. Several mechanisms for NO-induced cytotoxicity in neurons have been proposed. It has been reported that NO enhances ADP-ribosylation or S-nitrosylation of an increasing number of proteins, and two of these proteins were identified as NO-target proteins. One is glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a key enzyme of glycolytic conversion, which is S-nitrosylated by NO inhibiting the enzyme activity. Hence, inhibition of GAPDH activity by NO would decrease the amount of ATP. NO also activates poly (ADP-ribose) polymerase (PARP) in the presence of DNA damage. The activation of PARP results in depletion of NAD and ATP. The energy depletion by NO could cause cell death. Recently, several factors such as Fas, the caspases (interleukin-1 beta-converting enzyme (ICE)-like proteases), Bcl-2 and the tumor suppressor gene product p53 have been shown to be involved in apoptotic cell death. We here discuss the crucial mechanisms of NO-induced cytotoxicity and also discuss recent findings about the protective effect of NO on cell death.

Animals↗

PubMed1998

[Possible involvement of caspase activation in nitric oxide-induced neuronal apoptosis in SH-SY5Y cells].

We here report involvement of caspases in NO-induced neuronal apoptosis. Our experiments were designed to elucidate how NO induces neuronal cell death using NOC18, a new type of NO donor that spontaneously releases NO alone, without enzymatic metabolization. NOC18 induced apoptosis in human neuroblastoma SH-SY5Y cells in a concentration- and time-dependent manner estimated with DNA fragmentation assay, FACScan analysis, and nuclear morphology. In this study, oxyhemoglobin, an NO trapper, suppressed NOC18-triggered DNA fragmentation, indicating that NO from NOC18 is an apoptosis-inducer. An increase in caspase-3-like protease activity was observed in parallel with the induction of apoptosis, but no caspase-1-like protease activity was detected. The level of pro-caspase-2 protein, a precursor of caspase-2, was decreased dramatically. In addition, NOC18 also caused the cleavage of PARP, yielding an 85 kDa protein, a typical fragment of the caspases reaction. Oxyhemoglobin blocked the decrease in pro-caspase-2 and the cleavage of PARP by NOC18. Moreover, NO elicited the release of cytochrome c into the cytosol from mitochondria during apoptosis. These results suggest that activation of caspases by cytochrome c released from mitochondria is involved in neuronal apoptosis induced by NO.

Apoptosis↗

PubMed1998

Bremazocine recognizes the difference in four amino acid residues to discriminate between a nociceptin/orphanin FQ receptor and opioid receptors.

We investigated the molecular basis of the discrimination between nociceptin/orphanin FQ receptor (NociR) and opioid receptors (OPRs) by bremazocine, a non-type-selective opioid ligand. Construction of several chimeric receptors between NociR and kappa-opioid receptor (KOPR) and mutant NociRs followed by binding experiments with [3H]bremazocine showed that the mutation of only four amino acid residues of NociR, Ala216, Val279, Gln280 and Val281, to the amino acid residues located at the corresponding position of KOPR, Lys227, Ile290, His291 and Ile292, made it possible for the resultant mutant NociR to bind bremazocine with high affinity. Considering that these four amino acid residues are conserved among mu-, delta- and kappa-OPRs, the present result suggests that bremazocine recognizes the difference in these four amino acid residues to discriminate between NociR and OPRs.

Amino Acid Sequence↗

PubMed1998

Efficacy and limitation of F-18-fluorodeoxyglucose positron emission tomography during fasting to assess myocardial viability in the acute phase of myocardial infarction.

OBJECTIVE: The present study was designed to determine the ability of positron emission tomography (PET) to assess myocardial viability and ischemia in acute myocardial infarction (MI) after reperfusion therapy (thrombolysis and/or coronary angioplasty). METHODS: PET with fluorine-18-labeled fluorodeoxyglucose (FDG) under fasting conditions and thallium-201 single-photon emission computed tomography (TL) were analyzed in 21 patients one week following MI. Myocardial viability was also assessed by regional wall motion using serial analysis of 2-D echocardiography or left ventriculography. RESULTS: Marked uptake of FDG together with a residual perfusion defect were observed in the infarct region in all patients one week post MI. However, in 9 of the 21 patients, the infarct-related coronary artery had no significant stenosis after reperfusion therapy and remained patent in one month post MI suggesting no myocardial ischemia. In contrast, in 4 of the 21 patients the regional wall motion was akinetic and there was a complete defect observed with TL imaging at one month post MI, indicating no viability in the infarct region. CONCLUSIONS: PET using fasting FDG at one week post MI had a limitation to predict myocardial viability or ischemia.

Acute Disease↗

PubMed1998

SPECT findings in mitochondrial encephalomyopathy.

UNLABELLED: We investigated the alterations in regional cerebral blood flow (rCBF) in mitochondrial encephalomyopathy (MEM), using [123I]N-isopropyl-p-iodoamphetamine (IMP) or 99mTc-hexamethyl propyleneamine oxime SPECT in 10 MEM patients. METHODS: Four of the patients had MEM with lactic acidosis and strokelike episodes (MELAS), 2 had Kearns-Sayre syndrome (KSS), 1 had myoclonic epilepsy with ragged red fibers (MERRF) and 3 had cytochrome C oxidase deficiency (CCOD). Cerebral perfusion reserve was obtained from 6 patients (3 MELAS, 1 MERRF, 1 KSS, 1 CCOD) for a comparative analysis using the split-dose 123I-IMP SPECT method before and after the injection of acetazolamide. RESULTS: All patients with MELAS showed focal hypoperfusion in the parietal and/or occipital lobes. Follow-up studies (3 MELAS patients) revealed extension or improvement in the abnormal perfusion. The hypoperfused lesions were correlated with abnormal CT/MRI findings. Perfusion was normal in 1 MERRF, 2 KSS and 3 CCOD patients, whereas CT/MRI findings in 1 MERRF, 1 KSS and 1 CCOD patient were abnormal. The cerebral perfusion reserve in 3 MELAS patients was decreased significantly compared with that in patients with other types of MEM (MELAS 7.4%, other MEM 33.8%; p < 0.05). CONCLUSION: The rCBF was altered specifically in patients with MELAS, suggesting that brain perfusion SPECT will be useful in diagnosing and assessing such patients. The decreased cerebral perfusion reserve in patients with MELAS may represent an important feature of the pathogenesis of the strokelike episodes. The SPECT findings of patients with other types of MEM (MERRF, KSS and CCOD) were normal.

Adolescent↗

PubMed1998

[A case of primary Sjögren's syndrome accompanied by transverse myelitis].

Here we report a case of Sjögren's syndrome (SS) accompanied by transverse myelitis. A 46-year-old woman with 7-year history of primary SS was admitted to Tokyo Metropolitan Ohtsuka Hospital in September 1997 because of muscular weakness in lower extremities. She had had a low grade fever, numbness, and pain in bilateral lower extremities since July 1992. Neurological examination revealed transverse myelopathy at the level of Th 4, and peripheral neuropathy in lower extremities. Cerebrospinal fluid analysis showed slight elevation of protein and the cell count. A diagnosis of transverse myelitis and peripheral neuropathy presenting as neurologic manifestations of SS was made. Treatment was initiated with 30 mg of prednisolone, followed by improvement of fever and neurological findings. Although central nervous system complications of SS have been presented in Western countries, little information is available about Japanese patients. To our knowledge, this is the second case report which describes the occurrence of transverse myelitis in Japanese patients with SS.

Anti-Inflammatory Agents↗

PubMed1997

Discriminant validity of the Inventory to Diagnose Depression between patients with major depression and pure anxiety disorders.

We examined the discriminant validity of the Inventory to Diagnose Depression (IDD), a self-report instrument designed to diagnose major depressive disorder as defined in DSM-III-R. Forty patients with major depression (MD), 20 patients with anxiety disorders, who had not had a lifetime history of depression (ADs), and 40 control subjects completed the IDD. The IDD results were compared in the three contrasting groups (MD vs. AD+control subjects, MD vs. AD, and MD vs. control subjects). The concordance between the IDD and clinical diagnoses, using a structured interview, was significantly high in the three groups (k = 0.81, 0.66, 0.90, respectively). The IDD total score in the MD group was the highest among the three groups and was distinguished from the AD group or control group (P < 0.001, F = 139.9, d.f. = 2,97). However, the IDD occasionally diagnosed subjects with AD as having MD.

Adult↗

PubMed1997

Activation of Stat1 and subsequent transcription of inducible nitric oxide synthase gene in C6 glioma cells is independent of interferon-gamma-induced MAPK activation that is mediated by p21ras.

Rat C6 glioma cells have been used to characterize molecular events involved in the regulation of inducible nitric oxide synthase (iNOS) gene expression stimulated by interferon-gamma (IFN-gamma) plus lipopolysaccharide (LPS). IFNs induce a signaling event which involves activation of Stat1 transcription factor. Previous studies have shown that IFNs also induce extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) activation. However, the mechanisms by which IFNs stimulate MAPK activation remain elusive. Here we show that in C6 glioma cells, transiently expressing the dominant-negative form of c-Ha-Ras (Asn-17) abrogated IFN-gamma-induced ERK1 and ERK2 activation. Furthermore, PD98059, a specific MEK1 inhibitor, also blocked this activation. These results indicate that p21ras and MEK1 are required for IFN-gamma-induced ERK1 and ERK2 activation. Recent studies have reported that MAPK is responsible for serine phosphorylation of Stat1 which is required for Stat1's DNA binding and maximal transcriptional activity. Thus, we examined the role of the Ras-MAPK pathway in Stat1 activation and subsequent iNOS induction in C6 glioma cells. Further experiments showed that neither Asn-17 Ras expression nor concentrations of PD98059, which completely abrogated IFN-gamma-induced ERK1 and ERK2 activation, affected Stat1 DNA binding activity or iNOS induction, indicating that the Ras-MAPK pathway does not appear to be involved in the activation of Stat1 and subsequent iNOS induction in C6 glioma cells.

Animals↗