The purpose of the present study was to evaluate the relationship between sleep disturbances and depression in the Japanese elderly. Methods: These investigations in the Japanese elderly were carried out with the Geriatric Depression Scale, the Pittsburgh Sleep Quality Index, and questions on restless legs syndrome and nocturnal eating disorder. A total of 2023 people (male: 1008; female: 1015; average age: 74.2 ± 6.3 years) were analyzed by c 2 test and simple and multiple logistic regression. The prevalence of sleep disturbance was 37.3% and that of depression was 31.3%. Female gender and/or older ( ≥ 75 years) age were significantly associated with depression. Characteristics in depressive elderly were poor sleep efficiency, sleep disturbances due to difficulty of initiating sleep (DIS), breathing discomfort, coldness and pain, poor subjective sleep quality and lack of enthusiasm for activities. Sleep disturbances due to using the bathroom, breathing discomfort and coldness and long sleep latency were associated with depression in younger (65-74 years) men. Sleep disturbance due to DIS was associated with depression in older ( ≥ 75 years) men. Sleep disturbance due to pain was associated with depression in younger and older women. Poor sleep efficiency was associated with depression in older women. Poor subjective sleep quality was associated with depression in younger and older men and younger women. Lack of enthusiasm was associated with depression in younger and older men and older women. Restless legs syndrome was statistically significantly associated with depression in younger men. It is concluded that sleep disturbance and depression among the Japanese elderly are closely related symptoms. The features of sleep disturbance with depression differed with sex and age.

As an addendum to our list of 1999 reviewers, 1 I extend special gratitude to the following reviewers whose service rendered on our behalf last year will bear fruit in our Journal this year. The commitment and expertise of these devoted individuals are the foundations upon which our scholarly and scientific excellence rests. Schizophrenia-Associated Idiopathic UnconjugatedHyperbilirubinemia (Gilbert's Syndrome): 3 Case Reports Sir: Idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome) is a relatively common congenital hyperbilirubinemia occurring in 3% to 7% of the population. [1][2][3] Recently, it was reported that schizophrenic patients showed a significantly higher frequency of hyperbilirubinemia relative to patients with other psychiatric disorders and the general healthy population. 4 However, there has been only one previous case report of Gilbert's syndrome occurring in a schizophrenic patient. 5 We report 3 cases in which patients developed schizophrenia and Gilbert's syndrome and discuss clinical aspects of Gilbert's syndrome in schizophrenic patients and the relationship between hyperbilirubinemia and schizophrenia. Case 1. Mr. A, a 26-year-old single man, was diagnosed with schizophrenia at age 23 and admitted to the Shimane Medical University Hospital (Izumo, Japan). At that time, mild hyperbilirubinemia (total bilirubin level = 2.8 mg/dL, direct bilirubin level = 0.3 mg/dL), predominantly unconjugated, was first diagnosed on a routine laboratory test at admission and led us to suspect Gilbert's syndrome. After admission, Mr. A's psychiatric symptoms were well controlled by neuroleptic treatment. Laboratory tests of blood bilirubin levels showed an improvement 2 weeks after admission (total bilirubin level = 0.5 mg/dL, direct bilirubin level = 0.2 mg/dL). At the age of 26, coincident with discontinuation of antipsychotic medication, Mr. A experienced exacerbation of the psychotic condition and recurrent hyperbilirubinemia (total bilirubin level = 3.4 mg/dL, direct bilirubin level = 0.4 mg/dL) with a diagnosis of Gilbert's syndrome. He was readmitted to the Shimane Medical University Hospital in a severely psychotic state. Mr. A's psychotic condition has improved during the past 6 months with the administration of neuroleptics. Laboratory tests of blood bilirubin levels also showed improvement (total bilirubin level = 0.5 mg/dL, irect bilirubin level = 0.2 mg/dL). Mr. A experienced no relapse of psychotic condition with concomitant re-increase of unconjugated bilirubin levels.Case 2. Mr. B, a 33-year-old single man, was diagnosed with schizophrenia at age 25, at which time treatment with neuroleptics was started. Coincident with the onset of psychosis, hyperbilirubinemia (total bilirubin level = 2.3 mg/dL, direct bilirubin level = 0.3 mg/dL), predominantly unconjugated, was first diagnosed on a routine laboratory test and led us to suspect Gilbert's syndrome. At the age of 30 years, Mr. B experienced exacerbation of the psychotic condition. He was admitted to the Shimane Medical Unive...

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One biological effect of nitric oxide (NO) has been believed to be exerted through induction of the ADP-ribosyltransferase activity of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Though this notion is based on the finding that NO increases the auto-ADP-ribosylation of GAPDH, controversial data have also been reported. To determine whether or not NO really activates ADP-ribosylation, we re-examined the NO-induced modification of GAPDH with NAD+. GAPDH was modified equally with [adenosine-14C]NAD+ and [carbonyl-14C]NAD+, indicating that the glycoside bond of NAD+ between ADP-ribose and nicotinamide is intact. The release of nicotinamide from NAD+ was not evident during incubation of GAPDH with [carbonyl-14C]NAD+. Thus, the modification of GAPDH is apparently not ADP-ribosylation. In addition, we found that basal and glyceraldehyde-3-phosphate-induced modifications of GAPDH, both of which have also been explained as ADP-ribosylation, were not ADP-ribosylation, and that the modification of GAPDH in the absence and presence of NO or GA3P was distinct in the dithiothreitol effect or resistance to HgCl2.

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We report the case of a 62-year-old man who was administered sodium valproate (VPA) and who subsequently developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). He had been taking VPA for treatment of idiopathic generalized tonic-clonic convulsions since he was 56 years old. After substituting VPA with zonisamide, the serum sodium level returned to normal. We consider this episode of SIADH to be the result of a combination of factors including a weakness of the central nervous system and the long-term administration of VPA.

A case of schizophrenia-like psychosis (psychotic disorder not otherwise specified according to the DSM-IV criteria) with pericentric inversion on chromosome 9 [inv.(9) (p11; q13)] is reported. In this case, a minor brain anomaly, a small cyst in the left subcortex, was observed on magnetic resonance imaging of the brain. In the clinical course, prominent chronic hallucinations were observed; however, there was no evidence of the disorganization of personality, delusion, and deterioration in level of functioning that are usually seen in schizophrenia. This case and a review of the literature indicate that the pericentric region of chromosome 9 might be a potential areas of interest for the aetiology of psychiatric disorders. The phenotype-karyotype relationship of pericentric inversion on chromosome 9 and its relationship to psychosis are discussed.