Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is presented for the occurrence of a locus for schizotaxia on the short arm of chromosome 6. This derives from study of 63 informative members of seven pedigrees in which the proband and a parent (or a sib of parent) suffered with schizophrenia and other kin were either normal or fell within a spectrum of conditions related to schizophrenia. For linkage of HLA and schizotaxia a Lod score, 2.57, at recombination frequency 0.15 is reported, which gives p = 0.008. This is in contrast to data on 54 informative members of six pedigrees with atypical (schizo-affective or mixed) psychoses in two generations. Glyoxalase isoenzymes were of value in linkage analysis in two pedigrees. No evidence for linkage was found for any erythrocyte surface antigen nor for 15 other genetic markers. Details for each pedigree are provided.
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PMID:Genetic markers for schizotaxia. 42 Sep

Autoimmune mechanisms have been postulated to play a role in the pathogenesis of schizophrenia. Recently, increased numbers of B lymphocytes expressing the CD5 (Leu-1) surface antigen have been observed in patients with certain autoimmune diseases. In the present study, approximately 30% of schizophrenic patients (11/34) were found by cytofluorometric methods to have similarly increased levels of circulating CD5+ B cells compared with 6% (2/33) of healthy individuals and 5% (1/20) of patients with bipolar affective disorder. In schizophrenic patients with a "high" CD5+ B-cell phenotype, the percentage of B cells expressing the CD5 surface marker (mean +/- SEM, 52.4% +/- 3.5%) was comparable to that reported for patients with rheumatoid arthritis and significantly greater than that reported for patients with bipolar affective disorder (25.7% +/- 2.5%) and healthy controls (31.0% +/- 1.8%). Schizophrenic patients with high levels of CD5+ B cells had increased numbers of total B cells compared with control subjects and patients with low levels of CD5+ B cells. An elevation in CD5+ B cells may delineate a subgroup of schizophrenic patients whose disease has an underlying autoimmune and/or genetic cause.
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PMID:Increased numbers of CD5+ B lymphocytes in schizophrenic patients. 247 93

Approximately 5% of 8-10-year-olds experience exceptional difficulties learning to read (developmental dyslexia). This usually has a congenital basis; it runs in families, and affects 4 times as many boys as girls. Dyslexics typically show impairment both in phonemic segmentation (the subdivision of speech beyond the natural syllabic level) and in sequencing small visual symbols. Both these skills draw upon the ability of the nervous system to time sensory events precisely. A specific magnocellular cell type which expresses a distinctive surface antigen plays a crucial role in these functions. The development of this cell line is probably congenitally impaired in dyslexics. Visually they have lowered flicker and motion sensitivity, and disorder of the magnocellular layers of the Lateral Geniculate Nucleus can be seen post mortem. Likewise they have lowered sensitivity to changes in frequency and amplitude of sounds, hence impaired discrimination of speech sounds. These disorders are associated with abnormal hemispheric lateralisation in these subjects, e.g. dyslexics show reduction or reversal of the usual left > right asymmetry of the planum temporale. Many of these characteristics of impaired magnocellular function and reversed hemispheric asymmetry are found not only in dyslexic children but also in developmental dysphasics, autistics, high schizotypes and schizophrenics. I will speculate therefore that normal magnocellular development promotes normal hemispheric asymmetry and that impaired magnocellular development is responsible for a spectrum of problems associated with impaired hemispheric specialisation, ranging from the mildest, dyslexia, to the most severe, schizophrenia.
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PMID:Developmental dyslexia, neural timing and hemispheric lateralisation. 777 21

Genetic linkage, molecular analysis, and in situ hybridization have identified TYR and D11S388 as markers flanking the chromosome 11 breakpoint in a large pedigree where a balanced translocation, t(1;11)(q43;q21), segregates with schizophrenia and related affective disorders. Somatic cell hybrids, separating the two translocation chromosomes from each other and from the normal homologues, have been produced with the aid of immunomagnetic sorting for chromosome 1- and chromosome 11-encoded cell-surface antigens. The genes for two of these antigens map on either side of the 11q breakpoint. Immunomagnetic bead sorting was also used to isolate two stable X-irradiation hybrids for each cell-surface antigen. Each hybrid carries only chromosome 11 fragments. Translocation and X-irradiation hybrids were analyzed, mainly by PCR, for the presence of 19 chromosome 11 and 4 chromosome 1 markers. Ten newly designed primers are reported. The X-irradiation hybrids were also studied cytogenetically, for human DNA content, by in situ Cot1 DNA hybridization and by painting the Alu-PCR products from these four lines back onto normal human metaphases. The generation of the translocation hybrids and of the chromosome 11q fragment hybrids is a necessary preliminary to determining whether a schizophrenia-predisposition gene SCZD2 is encoded at this site.
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PMID:Schizophrenia-associated chromosome 11q21 translocation: identification of flanking markers and development of chromosome 11q fragment hybrids as cloning and mapping resources. 838 24

We aimed to determine the prevalence of hepatitis B surface antigen (HBsAg) among chronic schizophrenia patients in Jordan. Over a period of 12 months, 192 patients (106 male and 86 female) were tested for hepatitis B virus (HBV) by enzyme immunoassay. An equal number of age- and sex-matched healthy controls was also tested. Of the schizophrenia patients, 14 (10 male and 4 female) were positive for HBsAg while only 5 (4 male and 1 female) of the control subjects tested positive. The difference was not statistically significant but it indicates that chronic schizophrenia patients are a risk group for HBV infection and likely to benefit from preventive measures (health education and immunization against HBV).
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PMID:Prevalence of hepatitis B virus among chronic schizophrenia patients. 1269 Jul 75

Thromboxane A2 (TxA2) and the activation of its receptor have been shown to modulate vasoconstriction and platelet aggregation as well as dopaminergic and serotonergic signalling. Dopaminergic and serotonergic systems play a crucial role in the pathophysiology of schizophrenia and these systems are the main targets of antipsychotics (APs). As the first antipsychotic (AP) chlorpromazine (CPZ) has already been shown to reduce TxA2, we hypothesized that the AP clozapine and its metabolite N-desmethylclozapine (NDMC) might also influence TxA2 production. We measured levels of thromboxane B2 (TxB2), the metabolite of the very unstable molecule TxA2, in unstimulated and stimulated blood samples of 10 healthy female subjects in a whole blood assay using toxic shock syndrome toxin-1 (TSST-1) and monoclonal antibody against surface antigen CD3 combined with protein CD40 (OKT3/CD40) as stimulants. Blood was supplemented with the APs CPZ, clozapine or NDMC in one of four different concentrations. Additionally, thromboxane levels were measured in blood without the addition of APs under different stimulation conditions. Under TSST-1 as well as OKT3/CD40 stimulation, mean TxB2 concentrations were significantly (p < 0.05) decreased by clozapine over all applied concentrations. NDMC led to a decrease in TxB2 levels under unstimulated conditions as well as under TSST-1 stimulation. CPZ reduced TxB2 production at low concentrations under unstimulated and TSST-1- stimulated conditions. Clozapine, NDMC and CPZ possibly act on neurotransmitter systems via modulation of TxA2 or TxB2 production. Additionally, known side effects of APs such as orthostatic hypotension may be a result of changes in the concentrations of TxA2 or TxB2.
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PMID:Impact of clozapine, N-desmethylclozapine and chlorpromazine on thromboxane production in vitro. 2275 58