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There exist clinical characteristics of methamphetamine (MAP) psychosis in the Japanese population. MAP psychosis involves paranoid-hallucinatory states indistinguishable from paranoid schizophrenia, with residual volitional disturbances (e.g., loss of spontaneity and idleness). Paranoid-hallucinatory states persist after the pharmacological effects of MAP have worn off and readily reappear upon a reinjection of MAP. Individuals with a history of MAP psychosis further undergo spontaneous recurrence of their paranoid-hallucinatory states in response to stress. The development of MAP psychosis might therefore be related to persisting brain damage or changes in brain metabolism induced by repeated MAP use, and thus studies of the clinical course and neurological basis of MAP psychosis could provide insights into the pathophysiology of schizophrenia. Accordingly, psychiatrists have studied the clinical characteristics of MAP psychosis and examined the neurobiological basis of MAP-induced behavioral sensitization, using animals. MAP-induced behavioral sensitization might well be related to dopamine supersensitivity; however, the contribution of presynaptic autoreceptors remains controversial, and other hypotheses should be considered. Recently, the process that triggers spontaneous recurrence of MAP psychosis (flashbacks) and corresponding peripheral neurotransmitter functions has been studied. Stress sensitization associated with noradrenergic hyperactivity, involving increased dopamine release, appears to be crucial in the development of flashbacks. Overall, MAP-induced susceptibility to paranoid-hallucinatory states and to abnormal behavior (e.g., stereotyped behavior) in animals is examined as a model for predicting relapses of paranoid schizophrenia. Further extensive studies on the neurobiological and molecular mechanisms of this susceptibility are required.

A number of consistent clinical observations provide direction for the hypothesis that pathological sensitization of neuronal systems may be an important factor for relapse or the onset of stimulant-induced psychosis (eg, methamphetamine or amphetamine psychosis, cocaine psychosis and phencyclidine psychosis) and schizophrenia. First, psychotic symptoms can be produced in normal subjects by stimulants. Secondly, a large portion of schizophrenic patients exhibit exacerbation of psychotic symptoms in response to stimulants at doses which would not be psychotogenic in normal subjects. Lastly, the ability of stress to precipitate the onset and relapse of schizophrenia is well documented. In this regard, acute responses to stimulants provide useful information for relapse prediction of schizophrenia and substance abuse. This paper addresses the nature and role of pathological sensitization in relapse of stimulant-and phencyclidine-induced psychosis and schizophrenia, and its relation to pathophysiology of schizophrenia.

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Aldol reaction of 4-nitrobenzaldehyde with acetone gives 4-(4-nitrophenyl)-4-hydroxy-2-butanone in high yield in the presence of both secondary amine and mesoporous silica, whereas the yield is low in the absence of the mesoporous silica.

Approximately 300 microbial natural products in our library were screened for insecticidal activities against three species of agricultural pests, including aphids. Among the several compounds that showed insecticidal activities, pyripyropene A had high aphicidal activity in vivo. Furthermore, in advanced tests, pyripyropene A applications with foliar sprays and soil drenching controlled aphids on cabbage. On the basis of its unique and promising activities, we selected pyripyropene A as the active component of potential insecticides.

The occurrence of preeclampsia before 20 weeks of gestation is rare and usually associated with trophoblastic diseases or antiphospholipid syndrome. Here, we report a case of preeclampsia before 20 weeks of gestation in the absence of the aforementioned disorders. A healthy 30-year-old nulliparous woman presented with new onset of hypertension and proteinuria at 18 weeks of gestation. Fetal ultrasound did not reveal any abnormalities. Empirical steroid treatment was initiated based on a tentative diagnosis of underlying renal disease. The clinical course of the disease was progressive despite steroid treatment and the fetus died in utero 8 days after the initiation of treatment. Following delivery, a renal biopsy was performed and provided a diagnosis of preeclampsia. All symptoms resolved postpartum. This report demonstrates that preeclampsia may occur before 20 weeks of gestation and should always be considered in the differential diagnosis of pregnant women with new onset of hypertension with proteinuria. Previous published cases are summarized briefly.

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