A 2011 publication in World Psychiatry thoughtfully, but somewhat pessimistically, addressed the question of how schizophrenia might be prevented.1 A review of causal evidence2 a decade later offers little further hop...A 2011 publication in World Psychiatry thoughtfully, but somewhat pessimistically, addressed the question of how schizophrenia might be prevented.1 A review of causal evidence2 a decade later offers little further hope. We hypothesise that an emergent increase in syndromal schizophrenia in New Zealand, particularly in Maori (descendants of the indigenous Polynesian population), may present opportunities for prevention.展开更多
Background Recently,publications have hypothesised that the demonstrated increase in the incidence of schizophrenia in New Zealand is a side effect of the increased strength of available cannabis derivatives over the ...Background Recently,publications have hypothesised that the demonstrated increase in the incidence of schizophrenia in New Zealand is a side effect of the increased strength of available cannabis derivatives over the last 25+years and the much more recent increase in the population's use of methamphetamine.Aim To compare the rates of later schizophrenia between age-matched mental health service users with initial diagnoses as alcohol abusers or illicit drug users.Method From the PRIMHD comprehensive national database,all users of the mental health services over a 5-year period who received an ICD-10 presenting diagnosis of alcohol or substance use/abuse were identified.For each person identified,the database was examined for the following 3 years to determine the numbers later diagnosed with schizophrenia.Results For the initial alcohol problem people in their twenties,1.7%were diagnosed as suffering from schizophrenia in the subsequent 3 years.For the initial drug problem people,the rate was 10.9%.Within that drug-using population,the indigenous Maori developed schizophrenia at a higher rate than did the remainder of the population.Conclusion These findings in New Zealand require further research into their generalisability,context and explanation.展开更多
Despite their ubiquitous use for rendering patients unconscious for surgery, our understanding of how general anesthetics cause hypnosis remains rudimentary at best. Recent years have seen increased interest in ＂top-...Despite their ubiquitous use for rendering patients unconscious for surgery, our understanding of how general anesthetics cause hypnosis remains rudimentary at best. Recent years have seen increased interest in ＂top-down＂ cortico-centric theories of anesthetic action. The aim of this study was to explore this by investigating direct cortical effects of anesthetics on cerebrocortical evoked potentials in isolated mouse brain slices. Evoked potentials were elicited in cortical layer IV by electrical stimulation of the underlying white matter. The effects of three anesthetics （ketamine, etomidate, and isoflurane） on the amplitude, latency, and slope of short-latency evoked potentials were quantified. The N2/P3/N4 potentials - which represent the early cortical response - were enhanced by etomidate （increased P3-N4 slope, P 〈0.01）, maintained by ketamine, and reduced by isoflurane （lower N2/P3 amplitude, P 〈0.01）. These effects closely resemble those seen in vivo for the same drugs and point to a cortical mechanism independent of effects on subcortical structures such as the thalamus.展开更多
文摘A 2011 publication in World Psychiatry thoughtfully, but somewhat pessimistically, addressed the question of how schizophrenia might be prevented.1 A review of causal evidence2 a decade later offers little further hope. We hypothesise that an emergent increase in syndromal schizophrenia in New Zealand, particularly in Maori (descendants of the indigenous Polynesian population), may present opportunities for prevention.
文摘Background Recently,publications have hypothesised that the demonstrated increase in the incidence of schizophrenia in New Zealand is a side effect of the increased strength of available cannabis derivatives over the last 25+years and the much more recent increase in the population's use of methamphetamine.Aim To compare the rates of later schizophrenia between age-matched mental health service users with initial diagnoses as alcohol abusers or illicit drug users.Method From the PRIMHD comprehensive national database,all users of the mental health services over a 5-year period who received an ICD-10 presenting diagnosis of alcohol or substance use/abuse were identified.For each person identified,the database was examined for the following 3 years to determine the numbers later diagnosed with schizophrenia.Results For the initial alcohol problem people in their twenties,1.7%were diagnosed as suffering from schizophrenia in the subsequent 3 years.For the initial drug problem people,the rate was 10.9%.Within that drug-using population,the indigenous Maori developed schizophrenia at a higher rate than did the remainder of the population.Conclusion These findings in New Zealand require further research into their generalisability,context and explanation.
基金supported in part by the Waikato Medical Research Foundation
文摘Despite their ubiquitous use for rendering patients unconscious for surgery, our understanding of how general anesthetics cause hypnosis remains rudimentary at best. Recent years have seen increased interest in ＂top-down＂ cortico-centric theories of anesthetic action. The aim of this study was to explore this by investigating direct cortical effects of anesthetics on cerebrocortical evoked potentials in isolated mouse brain slices. Evoked potentials were elicited in cortical layer IV by electrical stimulation of the underlying white matter. The effects of three anesthetics （ketamine, etomidate, and isoflurane） on the amplitude, latency, and slope of short-latency evoked potentials were quantified. The N2/P3/N4 potentials - which represent the early cortical response - were enhanced by etomidate （increased P3-N4 slope, P 〈0.01）, maintained by ketamine, and reduced by isoflurane （lower N2/P3 amplitude, P 〈0.01）. These effects closely resemble those seen in vivo for the same drugs and point to a cortical mechanism independent of effects on subcortical structures such as the thalamus.
