Schizophrenia is a severe psychiatric disease with a strong genetic component. Brain-derived neurotrophic factor (BDNF) has been implicated in the pathogenesis of schizophrenia and bipolar (BP) disorders. The present study has examined two polymorphisms in linkage disequilibrium in the BDNF gene, which have been variously reported as associated with schizophrenia and BP. In our study, 321 probands with a primary diagnosis of schizophrenia or schizoaffective disorder, and 263 with a diagnosis of bipolar affective disorder, were examined together with 350 controls drawn from the same geographical region of Scotland. The val66met single-nucleotide polymorphism (SNP) showed significant (P ¼ 0.005) association for valine (allele G) with schizophrenia but not bipolar disorder. Haplotype analysis of val/ met SNP and a dinucleotide repeat polymorphism in the putative promoter region revealed highly significant (Po1 Â 10 À8 ) under-representation of the methionine or met-1 haplotype in the schizophrenic but not the BP population. We conclude that, although the val66met polymorphism has been reported to alter gene function, the risk may depend upon the haplotypic background on which the val/met variant is carried.

We have found that the enzyme activity previously reported as plasma PO actually comprises two enzymes, PO and ZIP. This study shows a statistically significant decrease of both enzymes in BD patients undergoing lithium treatment. No statistically significant change in PO or ZIP activity is observed in schizophrenic patients.

Findings suggest that the human dysbindin gene may play a role in the susceptibility to bipolar affective disorder, which underscores a potentially important area of etiological overlap with schizophrenia. The existence of shared genetic risk factors will, in time, lead to changes in the current nosology of major psychoses.

unexpected that mutations in different populations have a different haplotype background. 14 Likewise, different haplotypes were found to be associated for dysbindin (DTNBP1), another schizophrenia susceptibility gene. 15 Additional fine-mapping studies are required to identify the causative variation(s) and to establish if NRG1 or a nearby gene is involved. 9 In conclusion, our results further support the evidence for NRG1 as a schizophrenia susceptibility gene across populations, and suggest that the course of illness in schizophrenia is influenced by different sets of genes.

In order to evaluate the modulatory effects of manganese, high fat diet fed and alloxan diabetic rats were taken and the changes in the glucose oxidation, glycerol release and effects of manganese on these parameters were measured from adipose tissue. An insulin-mimetic effect of manganese was observed in the adipose tissue in the controls and an additive effect of insulin and manganese on glucose oxidation was seen when Mn2+ was added in vitro. The flux of glucose through the pentose phosphate pathway and glycolysis was significantly decreased in high fat fed animals. Although the in vitro addition of Mn2+ was additive with insulin when 14CO2 was measured from control animals, it was found neither in young diabetic animals (6-8 weeks old) nor in the old (16 weeks old). Both insulin and manganese caused an increased oxidation of carbon-1 of glucose and an increase of its incorporation into 14C-lipids in the young control animals; the additive effect of insulin and manganese suggests separate site of action. This effect was decreased in fat fed animals, diabetic animals and old animals. Manganese alone was found to decrease glycerol in both the control and diabetic adipose tissue in in vitro incubations. The results of the effects of glucose oxidation, lipogenesis, and glycerol release in adipose tissue of control and diabetic animals of different ages are presented together with the effect of manganese on adipose tissue from high fat milk diet fed animals.

979hypotension, nausea, dryness of the mouth, and rashes. The ward staff are familiar with the routine postoperative checks of blood pressure, pulse, and temperature, these being done hourly for the first six hours and four-hourly thereafter. After six hours enough time has elapsed for any abnormal response to the drug to be noticed. The most important value is the respiratory rate. This must be checked hourly and a clear indication given to the nursing staff of the minimum rate acceptable before action should be taken. The time taken to recharge the microdrop dispenser and count the respiration rate is just over a minute, but the routine of intramuscular injections is also time-consuming. Furthermore, a patient with no pain can help himself in bed more readily than one in pain, who may require constant nursing attention for minor nursing details; thus more time may be spent attending to the general well-being of the patients rather than complying with the stringent rules associated with the administration of intramuscular narcotics.Almost undoubtedly the success of a continuous narcotic infusion rests on its management, and in wards in which the nursing staff are interested and involved the results are much better than in those where the staff are too busy or preoccupied to allow such treatment to work. Ideally a pain team should administer the postoperative analgesia: this could consist of a small group of interested and experienced nursing sisters under the direction of an anaesthetist. The team would be responsible not only for organising the narcotic infusion regimen but also for topping up epidural catheters on the wards. Glycosylated haemoglobin concentrations in newly diagnosed diabetics before and during treatment Journal, 1979, 1, 979-981 Summary and conclusions Concentrations of total glycosylated haemoglobins (Hb A1) were measured in 40 diabetics at diagnosis and at monthly intervals after treatment with chlorpropamide, insulin, or diet alone was begun. The mean Hb A1 concentration at presentation in 16 patients treated with chlorpropamide was significantly higher than that in 12 patients treated with insulin, and the duration of glycaemic symptoms was much longer in the chlorpropamidetreated group. In contrast, the mean plasma glucose concentration was similar in both groups. The mean concentrations of Hb A1 and plasma glucose at diagnosis in the 12 patients treated by diet alone were lower than those in the other two groups, and most of these patients were free of symptoms.

Although current psychiatric nosology separates bipolar disorder and schizophrenia into non-overlapping categories, there is growing evidence of a partial aetiological overlap between them from linkage, genetic epidemiology and molecular genetics studies. Thus, it is important to determine whether genes implicated in the aetiology of schizophrenia play a role in bipolar disorder, and vice versa. In this study we investigated a total of 15 single nucleotide polymorphisms (SNPs), and all possible haplotypes, of genes that have been previously implicated in schizophrenia or bipolar disorder - RGS4, PRODH, COMT and GRK3 - in a sample of 213 cases with bipolar affective disorder type 1 and 197 controls from Scotland. We analysed the polymorphisms allele-wise, genotype-wise and, for each gene, haplotype-wise but obtained no result that reached nominal significance (p<0.05) for an association with the disease status. In conclusion, we could not find evidence of association between RGS4, PRODH, COMT and GRK3 genes and bipolar affective disorder 1 in the Scottish population.

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