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Aims: The means of suicide vary, but in cases of impaired consciousness, it is often difficult to determine the initial treatment because it is not known whether a patient has overdosed or used pesticides or poisons. Therefore, we investigated the clinical characteristics of suicide by medication in patients with suicide attempts who were brought to the emergency department, especially the influence of age. Methods: Patients with suicide attempts were transported to the two hospitals. There were 96 males (38.4%) and 154 females (61.6%). The mean age was 43.5 ± 20 years, and both males and females were most often in their 20s. Data on sex, age, motive for suicide, means of suicide attempt, psychiatric diagnosis, length of hospital stay, and place of discharge were retrospectively analyzed. Results: The average age of the patients by means of suicide attempt was 40.5 years for "prescription drugs," 30.2 years for "over‐the‐counter drugs," and 63.5 years for "pesticide/poison." For each means of suicide attempt, there was a significant difference in age among patients with suicide attempts using "prescription drugs," "over‐the‐counter drugs" and "pesticides/poisons." There was a statistical bias in the means and reasons for each suicide attempt. Conclusion: The results showed that the age of patients who used over‐the‐counter medicines and pesticides and poisons varied significantly. It was thought that pesticide use should be considered first, especially when patients aged 50 years and over are brought to the hospital with impaired consciousness due to suicide attempts. [ABSTRACT FROM AUTHOR]

The article discusses research which aimed to determine the characteristics of severe bereavement-related depression (BRD) in the elderly population in Japan. Topics covered include the clinical features of individuals with BRD, the rates of hospitalization for severe deterioration of social functioning, and a comparison of their hospitalization rates with that in individuals with non-bereavement related depression (NBRD).

In Japan, the cognitive behavioral approach with behavioral limitation (CBBL), which is based on operant and cognitive behavioral therapy, is a commonly practiced approach for inpatients with anorexia nervosa (AN).[1] The CBBL treatment procedure has a system of rewarding the patient for gaining bodyweight in order to encourage normalized eating behaviors. Although the outcomes of CBBL for adult patients have been shown to be consistent in previous studies,[[2]] no studies have been conducted to clarify the benefits or dropout rate among adolescents with AN treated with the CBBL approach. The DO group was defined as the patients who made a patient- or family-initiated decision to discontinue treatment at any point before achieving full remission. [Extracted from the article]

Aims The aim of this study was to evaluate differences in vulnerability to traumatic stress and the 1-year course of post-traumatic stress symptoms among patients with pre-existing psychiatric disorders after the Great East Japan Earthquake. Methods The Impact of Event Scale-Revised ( IES-R) was used to assess post-traumatic stress symptoms in 612 patients with schizophrenic ( ICD-10 F2; n = 163), mood ( F3; n = 299), or neurotic disorders ( F4; n = 150) at 1-4 months and again at 13-16 months after the disaster (retention rate: 68%). Results The mean IES-R total score for all diagnostic groups was 18.6 at index and 13.4 at follow up. The mean IES-R total score for patients with neurotic disorders (22.5) was significantly higher than that of patients with mood disorders (18.1) and schizophrenic disorders (15.9). At follow up, these scores decreased for all groups and inter-group differences were not observed. Conclusions Vulnerability to traumatic stress after a disaster was most severe in patients with neurotic disorders, followed by mood disorders, and, lastly, schizophrenic disorders. This difference among the three diagnostic groups was not found 1 year after the disaster. [ABSTRACT FROM AUTHOR]

To clarify whether reelin signaling is involved in dopaminergic neurotransmission in the adult mouse brain, we investigated dopamine function in mice lacking reelin (reeler). We found that methamphetamine-induced locomotor activity is significantly attenuated in reeler mice. To elucidate the mechanism of this phenomenon, we first investigated presynaptic dopamine release; however, there were no significant differences in wildtype, heterozygous reeler and homozygous reeler mice. Next, we examined the locomotor response to intra-accumbens injection of dopamine D1 and D2 receptor agonists, and found that lack of reelin signaling results in decreases in both D1 and D2 receptor-mediated dopaminergic functions. In addition, we measured dopamine receptor binding in the striatum, and found that both D1 and D2 classes of dopamine receptors are reduced in reeler mice. Furthermore, we found that the phosphorylation levels of DARPP-32 are also changed by lack of reelin signaling. Finally, to distinguish between a developmental role of reelin or an acute role of reelin in adult mouse, we intraventricularly infused CR-50, a monoclonal antibody against reelin. Interestingly, infusion of CR-50 also significantly reduced methamphetamine-induced hyperlocomotion in wildtype mice, showing that reelin has an acute role in the dopaminergic system. These results indicate that reelin signaling plays a pivotal role in the dopaminergic system in adult mice, especially in postsynaptic levels. [ABSTRACT FROM AUTHOR]

Neonatal hypoxic ischemic encephalopathy is a brain injury caused by oxygen deprivation due to perinatal asphyxia and is a leading cause of neonatal mortality and chronic neurological disability. Parasagittal cerebral injury (PCI) is a relatively mild form of hypoxic ischemic encephalopathy involving intravascular watershed zones of three major vessels.[1] PCI symptoms are usually subtle and sometimes PCI is asymptomatic; however, the long-term outcomes of the disorder are unclear. PCI affects full-term infants and sometimes newborns with PCI have normal perinatal stages and normal Apgar scores.[4] Thus, early PCI diagnosis is difficult without MRI and is often overlooked. [Extracted from the article]

The FXYD domain-containing ion transport regulator 6 (FXYD6) gene encodes phosphohippolin that regulates cellular ion transport by altering the kinetic properties of Na,K-ATPase. Phosphohippolin is highly expressed in brain regions that are relevant to schizophrenia. The FXYD6 gene is located at chromosome 11q22-24, one of the most established linkage regions for schizophrenia. Therefore, it may be possible that genetic variants in FXYD6, including the regulatory genomic elements could cause abnormal function or expression of phosphohippolin and increase the genetic risk for schizophrenia. A previous study suggested that polymorphisms in FXYD6 are associated with schizophrenia in UK samples. However, conflicting results have been reported in the Japanese population. In this study, we aimed to test the prior genetic association findings using different samples from the ethnically homogeneous Japanese population (1,060 schizophrenic patients and 1,060 age- and sex-matched controls). From the FXYD6 gene, we examined six single nucleotide polymorphisms (rs11216573, rs555577, rs1815774, rs4938445, rs4938446, and rs497768), all of which were previously analyzed for association. We did not detect any significant allelic, genotypic or haplotypic association in our Japanese samples. Meta-analysis incorporating previous and the present studies also showed that the FXYD6 gene is not associated with schizophrenia. We conclude that the FXYD6 gene does not have a major influence on susceptibility to schizophrenia across populations., ((c) 2010 Wiley-Liss, Inc.)

Autism is a pervasive developmental disorder diagnosed in early childhood. Abnormalities of serotonergic neurotransmission have been reported in autism. Serotonin transporter (SERT) modulates serotonin levels, and is a major therapeutic target in autism. Factors that regulate SERT expression might be implicated in the pathophysiology of autism. One candidate SERT regulatory protein is the roundabout axon guidance molecule, ROBO. SerT expression in Drosophila is regulated by robo; it plays a vital role in mammalian neurodevelopment also. Here, we examined the associations of ROBO3 and ROBO4 with autism, in a trio association study using DNA from 252 families recruited to AGRE. Four SNPs of ROBO3 (rs3923890, P = 0.023; rs7925879, P = 0.017; rs4606490, P = 0.033; and rs3802905, P = 0.049) and a single SNP of ROBO4 (rs6590109, P = 0.009) showed associations with autism; the A/A genotype of rs3923890 showed lower ADI-R_A scores, which reflect social interaction. Significant haplotype associations were also observed for ROBO3 and ROBO4. We further compared the mRNA expressions of ROBO1, ROBO2, ROBO3, and ROBO4 in the lymphocytes of 19 drug-naïve autistic patients and 20 age- and sex-matched controls. Expressions of ROBO1 (P = 0.018) and ROBO2 (P = 0.023) were significantly reduced in the autistic group; the possibility of using the altered expressions of ROBO as peripheral markers for autism, may be explored. In conclusion, we suggest a possible role of ROBO in the pathogenesis of autism. Abnormalities of ROBO may lead to autism either by interfering with serotonergic system, or by disrupting neurodevelopment. To the best of our knowledge, this is the first report relating ROBO with autism.