No abstract

Quality of life (QOL) was assessed in three groups of patients, consisting of 30 schizophrenic patients with duration of illness <2 years, 30 schizophrenic patients with duration of illness > or = 2 years and 30 dysthymic patients. The diagnoses were made according to ICD-10. Two scales of quality of life were used, one of which was specific for schizophrenia, while the other was generic for all patients. On inter-group comparison the two schizophrenia groups did not show significant differences in quality of life, but on comparing schizophrenic and dysthymic patients, significant differences emerged. Dysthymic patients were significantly less satisfied than schizophrenic patients with duration of illness <2 years in the domain of physical health. In the domains of satisfaction with medication and leisure-time activities, both schizophrenic groups were significantly more satisfied than the dysthymic group. Comparison of the quality of life ratings of our patients with those of a well-known study from Sweden revealed some significant differences which relate to the domains of work, contacts, inner experience and leisure-time activities. Cultural factors are invoked to account for these differences. The need for refinement of assessment of quality of life in multi-racial and multi-ethnic contexts is stressed.

Cellular effects of ionizing radiation include oxidative damage to macromolecules, unfolded protein response (UPR) and metabolic imbalances. Oxidative stress and UPR have been shown to induce macroautophagy/autophagy in a context-dependent manner and are crucial factors in determining the fate of irradiated cells. However, an in-depth analysis of the relationship between radiation-induced damage and autophagy has not been explored. In the present study, we investigated the relationship between radiationinduced oxidative stress, UPR and autophagy in murine macrophage cells. A close association was observed between radiation-induced oxidative burst, UPR and induction of autophagy, with the possible involvement of EIF2AK3/PERK (eukaryotic translation initiation factor 2 alpha kinase 3) and ERN1/IRE1 (endoplasmic reticulum [ER] to nucleus signaling 1). Inhibitors of either UPR or autophagy reduced the cell survival indicating the importance of these processes after radiation exposure. Moreover, modulation of autophagy affected lethality in the whole body irradiated C57BL/6 mouse. These findings indicate that radiation-induced autophagy is a pro-survival response initiated by oxidative stress and mediated by EIF2AK3 and ERN1.

The etiology of schizophrenia has been the focus of intensive research for a long time. Perspectives have changed drastically with the development of new investigative techniques. Clinical observations made by Kraepelin, Clouston, Bender, and Watt are now being complemented by neuroimaging and genetic studies to prove the neurodevelopmental hypothesis. At the same time, neuropathological and longitudinal studies of schizophrenia often support a neurodegenerative hypothesis. To provide a theoretical basis to the available evidence, another hypothesis called the progressive neurodevelopmental model has also emerged. This review presents some key evidence supporting each of these theories followed by a critical analysis of each.

There is growing interest in the relationship between cannabis and psychosis. The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication, acute psychosis that lasts beyond the period of acute intoxication, and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case-studies indicate that cannabinoids can induce acute psychosis which lasts beyond the period of acute intoxication and persisting as long as a month. Exposure to cannabis in adolescence is associated with an increased risk for later psychotic disorder in adulthood; this association is consistent, somewhat specific, shows a dose-response, and is biologically plausible. The link between cannabinoids and psychosis is greater with earlier age of exposure to cannabinoids, childhood abuse and genetic vulnerability. However, cannabinoids are neither necessary nor sufficient to cause a persistent psychotic disorder. More likely cannabinoids are a 'component cause' interacting with other known (family history) and unknown factors to result in psychosis outcomes. While more research is needed to better understand the relationship between cannabinoid use and psychosis, and the neural underpinnings of this link, clinicians should be mindful of the potential risk of psychosis especially in vulnerable populations, including adolescents and those with a psychosis diathesis.