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Knowledge gaps about smoking cessation in hospitalized patients and their doctors.BACKGROUND: Hospitalization is an opportune time for smoking cessation support; cessation interventions delivered by hospital physicians are effective. While general practitioners' and outpatients' knowledge and attitudes towards smoking cessation have been studied in great detail, in-patient cessation programmes have received less attention.
 DESIGN: Questionnaire-based survey of a convenience sample of hospital physicians and in-patients at Göttingen University Hospital, Germany.
 METHODS: All 159 physicians directly involved in bedside care on medical and surgical wards received a three-page questionnaire examining smoking status, knowledge of smoking-attributable morbidity and mortality, and their understanding of the effectiveness of methods to achieve long-term smoking cessation. Perceived barriers to the delivery of counselling and cessation services to smoking patients were identified. One thousand randomly selected patients on medical (N = 400) and surgical (N = 600) wards were invited to complete a similar questionnaire.
 RESULTS: Seventy-seven physicians (response rate 48.4%) and 675 patients (67.5%) completed the questionnaire. Patients and physicians alike underestimated the smoking-attributable risk of developing smoking-related cancers and chronic obstructive lung disease. In addition, severe misperceptions regarding the effectiveness of cessation methods were noted in both populations with 'willpower' being thought to be most effective in achieving abstinence. Only one-third of smoking patients recalled having been counselled to quit. Physicians identified lack of time as a central barrier to counselling smoking patients.
 CONCLUSIONS: These findings suggest that hospitalized smokers in a large German university hospital might not be treated according to international guidelines.
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Association of the brain-derived neurotrophic factor val66met polymorphism with magnetic resonance spectroscopic markers in the human hippocampus: in vivo evidence for effects on the glutamate system.The brain-derived neurotrophic factor (BDNF) is a key regulator of synaptic plasticity and has been suggested to be involved in the pathophysiology and pathogenesis of psychotic disorders, with particular emphasis on dysfunctions of the hippocampus. The aim of the present study was to replicate and to extend prior findings of BDNF val66met genotype effects on hippocampal volume and N-acetyl aspartate (NAA) levels. Hundred and fifty-eight caucasians (66 schizophrenic, 45 bipolar, and 47 healthy subjects; 105 subjects underwent MRI and 103 MRS scanning) participated in the study and were genotyped with regard to the val66met polymorphism (rs6265) of the BDNF gene. Hippocampal volumes were determined using structural magnetic resonance imaging (MRI), and measures of biochemical markers were taken using proton magnetic resonance spectroscopy ((1)H-MRS) in the hippocampus and other brain regions. Verbal memory was assessed as a behavioral index of hippocampal function. BDNF genotype did not impact hippocampal volumes. Significant genotype effects were found on metabolic markers specifically in the left hippocampus. In particular, homozygous carriers of the met-allele exhibited significantly lower NAA/Cre and (Glu + Gln)/Cre metabolic ratios compared with val/val homozygotes, independently of psychiatric diagnoses. BDNF genotype had a numerical, but nonsignificant effect on verbal memory performance. These findings provide first in vivo evidence for an effect of the functional BDNF val66met polymorphism on the glutamate system in human hippocampus.
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Interrelated neuropsychological and anatomical evidence of hippocampal pathology in the at-risk mental state.BACKGROUND: Verbal learning and memory deficits are frequent among patients with schizophrenia and correlate with reduced magnetic resonance imaging (MRI) volumes of the hippocampus in these patients. A crucial question is the extent to which interrelated structural-functional deficits of the hippocampus reflect a vulnerability to schizophrenia, as opposed to the disorder per se.
 METHOD: We combined brain structural measures and the Rey Auditory Verbal Learning Test (RAVLT) to assess hippocampal structure and function in 36 never-medicated individuals suspected to be in early (EPS) or late prodromal states (LPS) of schizophrenia relative to 30 healthy controls.
 RESULTS: Group comparisons revealed bilaterally reduced MRI hippocampal volumes in both EPS and LPS subjects. In LPS subjects but not in EPS subjects, these reductions were correlated with poorer performance in RAVLT delayed recall.
 CONCLUSIONS: Our findings suggest progressive and interrelated structural-functional pathology of the hippocampus, as prodromal symptoms and behaviours accumulate, and the level of risk for psychosis increases. Given the inverse correlation of learning and memory deficits with social and vocational functioning in established schizophrenia, our findings substantiate the rationale for developing preventive treatment strategies that maintain cognitive capacities in the at-risk mental state.