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Biomedical subjects

Takayuki Okada

Publications and source records attributed to Takayuki Okada.

At least 19 recordsLinked to original sources
PubMed2006

Deliberate self-harm and childhood hyperactivity in junior high school students.

The present study aimed to explore the status of deliberate self-harm (DSH) among junior high-school students, and investigate the relationship between DSH and substance use and childhood hyperactivity. Subjects were 239 boys (mean age = 14.16 years, SD = 0.67) and 238 girls (14.22, 0.68) from a junior high-school in Kanagawa, Japan. A self-reporting questionnaire consisting of original questions on self-cutting, self-hitting, and tobacco and alcohol use was employed with the Wender Utah Rating Scale (WURS) for assessing childhood hyperactivity. Overall, 8.00% and 27.70% of males and 9.30% and 12.20% of females reported self-cutting and self-hitting, respectively. Regarding substance use, 33.10% and 74.10% of males and 14.30% and 63.40% of females reported tobacco and alcohol use, respectively. Comparisons of WURS scores between those with and without experience of problematic behaviors revealed that with all problematic behaviors in both genders, scores of those with experience were significantly higher than those without (P < 0.01 except for self-cutting in females, P < 0.05). The present study indicated that DSH is an important problem, even among children as young as junior high-school age. An association between DSH and childhood hyperactivity was also suggested.

Attention Deficit Disorder with Hyperactivity↗
PubMed2006

[Association between substance abuse problems and antisocial tendencies in male juvenile delinquents: A study using the Psychopathy Checklist, Youth Version].

AIMS: We examined an association between substance abuse problems and antisocial tendencies in male juvenile delinquents. METHODS: Subjects were 57 male adolescents consecutively incarcerated between December 2004 and February 2005 in a juvenile classification home. A self-reporting questionnaire was used to assess substance abuse problems in the subjects: Drug abuse problems were assessed by the Drug Abuse Screening Test (DAST-20), and alcohol abuse problems were assessed by the Quantities-Frequencies Scale (QFS). A semi-structured interview was also preformed according to the Psychopathy Checklist, Youth Version (PCL: YV). Associations between questionnaire responses and interview findings were examined using Pearson's correlation or Spearman's rank correlation test. RESULTS: Of our subjects, the 17.5% were recognized as a problematic drug abuser, and the 52.6% as a problematic drinker. Neither of the total DAST-20 nor QFS score was significantly correlated with the total PCL: YV score, and also with each score of the four PCL: YV subfactors. However, significant correlations were found between some items on the PCL: YV and the DAST-20 or QFS score. The DAST score was significant correlated with the PCL: YV item, "impression management" (rs=0.35, p<0.001), and the QFS score was significant correlated with "serious violations of conditional release" (rs=0.33, p<0.05) and "criminal versatility" (rs=0.48, p<0.001). CONCLUSION: More than a half of male juvenile delinquents had alcohol abuse problems. Alcohol intake may be considered to promote repetition and diversification of their antisocial behaviors, although overall antisocial tendencies were not associated with drug and alcohol abuse problems in male juvenile delinquents.

Adolescent↗
PubMed2005

Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation.

Activation of p38 mitogen-activated protein (MAP) kinase (MAPK) has been implicated in the mechanism of cardiomyocyte (CMC) protection and injury. The p38 MAPK controversy may be related to differential effects of this kinase on apoptosis and necrosis. We have hypothesized that p38 MAPK-mediated F-actin reorganization promotes apoptotic cell death, whereas it protects from osmotic stress-induced necrotic cell death. Cultured neonatal rat CMCs were subjected to 2 h of simulated ischemia followed by reoxygenation. p38 MAPK activity measured by phosphorylation of MAP kinase-activated protein (MAPKAP) kinase 2 was increased during simulated ischemia and reoxygenation. This was associated with translocation of heat shock protein 27 (HSP27) from the cytosolic to the cytoskeletal fraction and F-actin reorganization. Cytochrome c release from mitochondria, caspase-3 activation, and DNA fragmentation were increased during reoxygenation. Robust lactate dehydrogenase (LDH) release was observed under hyposmotic (140 mosM) reoxygenation. The p38 MAPK inhibitor SB-203580 abrogated activation of p38 MAPK, translocation of HSP27, and F-actin reorganization and prevented cytochrome c release, caspase-3 activation, and DNA fragmentation. Conversely, SB-203580 enhanced LDH release during hyposmotic reoxygenation. The F-actin disrupting agent cytochalasin D inhibited F-actin reorganization and prevented cytochrome c release, caspase-3 activation, and DNA fragmentation, whereas it enhanced LDH release during hyposmotic reoxygenation. When CMCs were incubated under the isosmotic condition for the first 15 min of reoxygenation, SB-203580 and cytochalasin D increased ATP content of CMCs and prevented LDH release after the conversion to the hyposmotic condition. These results suggest that F-actin reorganization mediated by activation of p38 MAPK plays a differential role in apoptosis and protection against osmotic stress-induced necrosis during reoxygenation in neonatal rat CMCs; however, the sarcolemmal fragility caused by p38 MAPK inhibition can be reversed during temporary blockade of physical stress during reoxygenation.

Actins↗
PubMed2005

Integrated pharmacological preconditioning and memory of cardioprotection: role of protein kinase C and phosphatidylinositol 3-kinase.

Although protein kinase C (PKC) and phosphatidylinositol 3 (PI3)-kinase are implicated in cardioprotective signal transduction mediated by ischemic preconditioning, their role in pharmacological preconditioning (PPC) has not been determined. Cultured neonatal rat cardiomyocytes (CMCs) were subjected to simulated ischemia for 2 h followed by 15 min of reoxygenation. PPC of CMCs consisted of administration of 50 microM adenosine, 50 microM diazoxide, and 50 microM S-nitroso-N-acetylpenicillamine (SNAP), each alone or in combination, for 15 min followed by 30 min of washout before simulated ischemia. Although PKC-epsilon and PI3-kinase were significantly activated during treatment with adenosine, activation of these kinases dissipated after washout. In contrast, PPC combined with adenosine, diazoxide, and SNAP elicited sustained activation of PKC-epsilon and PI-3 kinase after washout. The combined-PPC, but not the single-PPC, protocol conferred antiapoptotic and antinecrotic effects after reoxygenation. The PKC inhibitor chelerythrine (5 microM) or the PI3-kinase inhibitor LY-294002 (10 microM) given during the washout period partially blocked the activation of PKC-epsilon and PI3-kinase mediated by the combined-PPC protocol, whereas combined addition of chelerythrine and LY-294002 completely inhibited activation of PKC-epsilon and PI3-kinase. Chelerythrine or LY-294002 partially blocked antiapoptotic and antinecrotic effects mediated by the combined-PPC protocol, whereas combined addition of chelerythrine and LY-294002 completely abrogated antiapoptotic and antinecrotic effects. These results suggest that the combined-PPC protocol confers cardioprotective memory through sustained and interdependent activation of PKC and PI3-kinase.

Adenosine↗
PubMed2005

[Personal exposures of benzene treated workers and a simple biological monitoring].

A simple method of biological monitoring has been developed for occupational benzene exposure. Personal benzene exposure monitoring using a passive sampler and GC/FID was carried out on 74 workers from a benzene-treated company. Their urines were collected before and after work-shift. After treatment of urine samples using solid phase extraction (SPE), trans, trans-muconic acid(t, t-MA) concentration in the elute was analysed by HPLC. Correlation between benzene exposure (X: ppm) and urinary t, t-MA concentration (Y: mg/g x creatinine) for non-smokers was Y = 0.948X + 0.586 (r = 0.798, P < 0.01) and Y = 0.885X + 0.894 (r = 0.871, P < 0.01) for smokers, respectively. The t, t-MA concentration on 1 ppm TLV exposure to benzene was estimated as 1.5 and 1.8 (mg/g creatinine) for non-smokers and smokers, respectively. These values are in agreement with some investigators. This indicates that our simple method for biological monitoring of benzene exposure can be of great service.

Acetylcysteine↗
PubMed2005

Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.

p38 MAP kinase activation is known to be deleterious not only to mitochondria but also to contractile function. Therefore, p38 MAP kinase inhibition therapy represents a promising approach in preventing reperfusion injury in the heart. However, reversal of p38 MAP kinase-mediated contractile dysfunction may disrupt the fragile sarcolemma of ischemic-reperfused myocytes. We, therefore, hypothesized that the beneficial effect of p38 MAP kinase inhibition during reperfusion can be enhanced when contractility is simultaneously blocked. Isolated and perfused rat hearts were paced at 330 rpm and subjected to 20 min of ischemia followed by reperfusion. p38 MAP kinase was activated after ischemia and early during reperfusion (<30 min). Treatment with the p38 MAP kinase inhibitor SB-203580 (10 microM) for 30 min during reperfusion, but not the c-Jun NH(2)-terminal kinase inhibitor SP-600125 (10 microM), improved contractility but increased creatine kinase release and infarct size. Cotreatment with SB-203580 and the contractile blocker 2,3-butanedione monoxime (BDM, 20 mM) or the ultra-short-acting beta-blocker esmorol (0.15 mM) for the first 30 min during reperfusion significantly reduced creatine kinase release and infarct size. In vitro mitochondrial ATP generation and myocardial ATP content were significantly increased in the heart cotreated with SB-203580 and BDM during reperfusion. Dystrophin was translocated from the sarcolemma during ischemia and reperfusion. SB-203580 increased accumulation of Evans blue dye in myocytes depleted of sarcolemmal dystrophin during reperfusion, whereas cotreatment with BDM facilitated restoration of sarcolemmal dystrophin and mitigated sarcolemmal damage after withdrawal of BDM. These results suggest that treatment with SB-203580 during reperfusion aggravates myocyte necrosis but concomitant blockade of contractile force unmasks cardioprotective effects of SB-203580.

Animals↗
PubMed2005

Characteristics of self-cutters among male inmates: association with bulimia and dissociation.

It was examined whether bulimia and dissociation are common in male self-cutters, as has been found in female self-cutters. The subjects were 796 male inmates of a juvenile prison. A self-reporting questionnaire was used to assess self-cutting, histories of psychoactive substance use, problem behaviors, and traumatic life events in the subjects. The Adolescent Dissociative Experience Scale and the Bulimia Investigatory Test of Edinburgh were also used. Subjects were divided into two groups: self-cutting and non-cutting. Questionnaire responses and dissociation and bulimia assessments were compared between the groups. Self-cutters began smoking (P < 0.001) and drinking (P < 0.001) earlier, and more frequently used illicit psychoactive drugs (P < 0.001), experienced childhood physical abuse (P < 0.001), and reported suicide attempts (P < 0.001), suicidal ideation (P < 0.001), and outward violence toward a person (P < 0.001) or object (P < 0.001) than non-cutters. Self-cutters also scored significantly higher on the bulimia (P < 0.001) and dissociation tests (P < 0.001). Logistic regression analysis demonstrated that suicide attempt (odds ratio, 4.311) and suicidal ideation (odds ratio, 2.336) could discriminate between male inmates with and without self-cutting. Male self-cutters showed 'multi-impulsive bulimic' tendencies resembling those of female self-cutters, although to a lesser extent. Clinical features of male as opposed to female self-cutters were influenced by gender differences.

Adolescent↗
PubMed2005

[Rethinking criminal responsibility: practical application of operational diagnosis and gnostic into expert testimony].

There had been argument concerning the difference between the agnostic approach and the gnostic approach to the psychiatric perspective of criminal responsibility until the landmark ruling by the 3rd court of the Japanese Supreme Court in 1984. The decision upheld the gnostic approach and affirmed that the defendant's criminal responsibility should be based on such factors as psychopathology, motive, modus operandi, situation surrounding the crime, and pre-morbid personality, as long as the offense was not directly motivated by the delusion or hallucination. The gnostic explanation includes so many various factors that the psychiatric testimony cannot easily be objective, while agnostic experts can find a conclusion about criminal responsibility only by psychiatric diagnosis. To establish a standard, the authors summarized the means of determination of criminal responsibility. The authors also discussed various topics related to criminal responsibility including Asperger's syndrome, illicit drug intoxication, and prescribed drug intoxication.

Amphetamine-Related Disorders↗
PubMed2004

Ischemic preconditioning-mediated restoration of membrane dystrophin during reperfusion correlates with protection against contraction-induced myocardial injury.

Dystrophin is an integral membrane protein involved in the stabilization of the sarcolemmal membrane in cardiac muscle. We hypothesized that the loss of membrane dystrophin during ischemia and reperfusion is responsible for contractile force-induced myocardial injury and that cardioprotection afforded by ischemic preconditioning (IPC) is related to the preservation of membrane dystrophin. Isolated and perfused rat hearts were subjected to 30 min of global ischemia, followed by reperfusion with or without the contractile blocker 2,3-butanedione monoxime (BDM). IPC was introduced by three cycles of 5-min ischemia and 5-min reperfusion before the global ischemia. Dystrophin was distributed exclusively in the membrane of myocytes in the normally perfused heart but was redistributed to the myofibril fraction after 30 min of ischemia and was lost from both of these compartments during reperfusion in the presence or absence of BDM. The loss of dystrophin preceded uptake of the membrane-impermeable Evans blue dye by myocytes that occurred after the withdrawal of BDM and was associated with creatine kinase release and the development of contracture. Although IPC did not alter the redistribution of membrane dystrophin induced by 30 min of ischemia, it facilitated the restoration of membrane dystrophin during reperfusion. Also, myocyte necrosis was not observed when BDM was withdrawn after complete restoration of membrane dystrophin. These results demonstrate that IPC-mediated restoration of membrane dystrophin during reperfusion correlates with protection against contractile force-induced myocardial injury and suggest that the cardioprotection conferred by IPC can be enhanced by the temporary blockade of contractile activity until restoration of membrane dystrophin during reperfusion.

Animals↗
PubMed2004

New tubular bioabsorbable knitted airway stent: feasibility assessment for delivery and deployment in a dog model.

PURPOSE: The aim of this study was to determine whether it is possible to deliver and deploy a new device, a poly-L-lactic acid (PLLA) tubular knitted airway stent, under bronchoscopic guidance in a dog model. DESCRIPTION: The delivery system consisted of a flexible balloon catheter (controlled radial expansion balloon dilator, M00558440, Boston Scientific Corporation, MA, USA) preloaded with a stent. A delivery catheter preloaded with a stent was advanced to a target point in the trachea under bronchoscopic guidance. Once the stent was positioned, the balloon was inflated for sixty seconds. The stent was in full contact with the tracheal wall upon deflation of the balloon. EVALUATION: The stents were successfully delivered into the tracheal lumen and successfully deployed in all dogs. CONCLUSIONS: This is the first study to prove the feasibility of delivering and deploying the PLLA stents in a dog model, using a balloon expansion technique. Further investigation with large numbers of subjects and long-term follow-up will be necessary to assess the utility of the bioabsorbable knitted tubular stent before clinical applications begin.

Absorbable Implants↗
PubMed2003

SCA8 repeat expansion: large CTA/CTG repeat alleles are more common in ataxic patients, including those with SCA6.

We analyzed the SCA8 CTA/CTG repeat in a large group of Japanese subjects. The frequency of large alleles (85-399 CTA/CTG repeats) was 1.9% in spinocerebellar ataxia (SCA), 0.4% in Parkinson disease, 0.3% in Alzheimer disease, and 0% in a healthy control group; the frequency was significantly higher in the group with SCA than in the control group. Homozygotes for large alleles were observed only in the group with SCA. In five patients with SCA from two families, a large SCA8 CTA/CTG repeat and a large SCA6 CAG repeat coexisted. Age at onset was correlated with SCA8 repeats rather than SCA6 repeats in these five patients. In one of these families, at least one patient showed only a large SCA8 CTA/CTG repeat allele, with no large SCA6 CAG repeat allele. We speculate that the presence of a large SCA8 CTA/CTG repeat allele influences the function of channels such as alpha(1A)-voltage-dependent calcium channel through changing or aberrant splicing, resulting in the development of cerebellar ataxia, especially in homozygous patients.

Asian People↗
PubMed2003

Integrated pharmacological preconditioning in combination with adenosine, a mitochondrial KATP channel opener and a nitric oxide donor.

BACKGROUND: Mitochondrial K(ATP) channel activation is an essential component of ischemic preconditioning. These channels are selectively opened by diazoxide and may be up-regulated by adenosine and nitric oxide. Therefore, pharmacological preconditioning with diazoxide in combination with adenosine and a nitric oxide donor (triple-combination pharmacological preconditioning) may enhance cardioprotection. METHODS AND RESULTS: Isolated and perfused rat hearts underwent ischemic preconditioning with 3 cycles of 5 minutes of ischemia and 5 minutes of reperfusion before 5 minutes of oxygenated potassium cardioplegia and 35 minutes of ischemia. Pharmacological preconditioning was performed by adding adenosine, diazoxide, and a nitric oxide donor S-nitroso-N-acetyl-penicillamine each alone or in combinations for 25 minutes followed by 10 minutes washout before cardioplegic arrest. Only triple-combination pharmacological preconditioning conferred significant cardioprotection as documented by highly improved left ventricular function and limited creatine kinase release during reperfusion that was comparable to that afforded by ischemic preconditioning. Mitochondrial K(ATP) channel activity assessed by flavoprotein oxidation was increased by diazoxide, but no further increase in flavoprotein oxidation was obtained by ischemic preconditioning and triple-combination pharmacological preconditioning. Significant activation of protein kinase C-epsilon was observed in only ischemic preconditioning and triple-combination pharmacological preconditioning. Pretreatment with the mitochondrial K(ATP) channel inhibitor 5-hydroxydecanoate or the protein kinase C inhibitor chelerythrine abrogated activation of protein kinase C-epsilon and cardioprotection afforded by ischemic preconditioning and triple-combination pharmacological preconditioning. CONCLUSIONS: Integrated pharmacological preconditioning is not simply mediated by enhanced mitochondrial K(ATP) channel activation, but is presumably mediated through amplified protein kinase C signaling promoted by coordinated interaction of adenosine, mitochondrial K(ATP) channel activation, and nitric oxide.

Adenosine↗
PubMed2003

Combined pharmacological preconditioning with a G-protein-coupled receptor agonist, a mitochondrial KATP channel opener and a nitric oxide donor mimics ischaemic preconditioning.

1. Although pharmacological preconditioning (PPC) has emerged as an alternative to ischaemic preconditioning (IPC) in cardioprotection, the efficacy of PPC compared with IPC has not been investigated. Because IPC is mediated by complex signalling cascades arising from multiple triggers, we have hypothesized that combined PPC is necessary to mimic IPC. 2. Isolated and perfused rat hearts underwent IPC by three cycles of 5 min ischaemia and 5 min reperfusion before 30 min global ischaemia followed by 120 min reperfusion. Adenosine (30 micromol/L), diazoxide (50 micromol/L) and s-nitroso-N-acetylpenicillamine (SNAP; 50 micromol/L) were added for 25 min just before (pretreatment modality) or 45 min before (PPC modality) the index ischaemia. 3. Ischaemic preconditioning significantly improved isovolumic left ventricular (LV) function and reduced infarct size. Although pretreatment with adenosine, diazoxide or SNAP alone was capable of reducing infarct size, PPC with each drug alone or in a combination of two drugs except for diazoxide plus SNAP failed to reduce infarct size. In contrast, PPC in combination with adenosine, diazoxide and SNAP (triple combination PPC) conferred significant improvement of LV function and reduction of infarct size that was as effective as IPC. 4. Cardioprotection afforded by triple combination PPC was abolished by the Gi/o-protein inhibitor pertussis toxin, the mitochondiral KATP channel inhibitor 5-hydroxydecanoate or the nitric oxide (NO) scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide (carboxy-PTIO). 5. Protein kinase C (PKC)-epsilon in the particulate fraction was activated throughout preconditioning ischaemia and reperfusion. Although PKC-epsilon was activated during treatment with adenosine, diazoxide or SNAP alone, it was inactivated after washout. In contrast, PKC-epsilon remained activated after triple combination PPC. The PKC inhibitor chelerythrine abolished activation of PKC-epsilon and cardioprotection afforded by IPC and triple combination PPC. 6. These results demonstrate that combined PPC with a G-protein-coupled receptor agonist, a mitochondrial KATP channel opener and an NO donor is necessary to mimic IPC and such synergistic cardioprotection is associated with enhanced and sustained activation of PKC-epsilon.

Adenosine Triphosphate↗
PubMed2003

Loss of intracellular dystrophin: a potential mechanism for myocardial reperfusion injury.

Because the absence of sarcolemmal dystrophin renders cardiomyocytes vulnerable to mechanical force, the present study investigated whether sarcolemmal membrane fragility upon reperfusion is associated with the loss of membrane dystrophin. Dystrophin was distributed exclusively in the sarcolemmal membrane of buffer-perfused rat cardiomyocytes, but was translocated to the myofibrils during 30 min of ischemia and then lost during reperfusion. Upon reperfusion, the membrane impermeable dye, Evans blue (EB), accumulated in cardiomyocytes depleted of dystrophin. Reperfusion with the contractile blocker 2,3-butanedione monoxime (BDM) resulted in no accumulation of EB in cardiomyocytes despite the loss of dystrophin. Upon withdrawal of BDM, however, EB accumulated in dystrophin-depleted cardiomyocytes. Loss of sarcolemmal dystrophin may be involved in the mechanism of contractile force-induced reperfusion injury.

Animals↗