Gotowa bibliografia na temat „Schizophrenia – Genetic aspects”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Schizophrenia – Genetic aspects”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Schizophrenia – Genetic aspects"
Morozova, A. Yu, E. A. Zubkov, Ya A. Zorkina, A. M. Reznik, G. P. Kostyuk i V. P. Chekhonin. "Genetic aspects of schizophrenia". Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 117, nr 6 (2017): 126. http://dx.doi.org/10.17116/jnevro201711761126-132.
Pełny tekst źródłaKarayiorgou, Maria. "Genetic aspects of schizophrenia". Clinical Neuroscience Research 1, nr 1-2 (styczeń 2001): 158–63. http://dx.doi.org/10.1016/s1566-2772(00)00015-3.
Pełny tekst źródłaBöök, Jan A. "Genetic aspects of schizophrenia". Clinical Genetics 19, nr 5 (23.04.2008): 357. http://dx.doi.org/10.1111/j.1399-0004.1981.tb00726.x.
Pełny tekst źródłaBellivier, F. "Schizophrenia, antipsychotics and diabetes: Genetic aspects". European Psychiatry 20, S4 (grudzień 2005): S335—S339. http://dx.doi.org/10.1016/s0924-9338(05)80187-7.
Pełny tekst źródłaMuir, Walter J. "Genetic aspects of the biology of schizophrenia". Current Opinion in Psychiatry 5, nr 1 (luty 1992): 2–5. http://dx.doi.org/10.1097/00001504-199202000-00002.
Pełny tekst źródłaTrifu, Simona Corina, Anca Vlăduţi i Antonia Ioana Trifu. "Genetic aspects in schizophrenia. Receptoral theories. Metabolic theories". Romanian Journal of Morphology and Embryology 61, nr 1 (2020): 25–32. http://dx.doi.org/10.47162/rjme.61.1.03.
Pełny tekst źródłaKambarova, D. K., i A. G. Golubev. "Biochemical and genetic aspects of pathogenesis of schizophrenia". Journal of Evolutionary Biochemistry and Physiology 47, nr 5 (październik 2011): 407–19. http://dx.doi.org/10.1134/s0022093011050021.
Pełny tekst źródłaGalderisi, S., i M. Maj. "Deficit schizophrenia: An overview of clinical, biological and treatment aspects". European Psychiatry 24, nr 8 (grudzień 2009): 493–500. http://dx.doi.org/10.1016/j.eurpsy.2009.03.001.
Pełny tekst źródłaPopov, Nikolay T., Vili K. Stoyanova, Nadezhda P. Madzhirova i Tihomir I. Vachev. "Epigenetic aspects in schizophrenia etiology and pathogenesis". Folia Medica 54, nr 2 (1.10.2012): 12–16. http://dx.doi.org/10.2478/v10153-011-0082-x.
Pełny tekst źródłaSyvälahti, E. K. G. "Biological Factors in Schizophrenia Structural and Functional Aspects". British Journal of Psychiatry 164, S23 (kwiecień 1994): 9–14. http://dx.doi.org/10.1192/s0007125000292672.
Pełny tekst źródłaRozprawy doktorskie na temat "Schizophrenia – Genetic aspects"
Zhang, Xiaowei, i 张晓薇. "Twin studies on childhood externalizing behavior and schizophrenia". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208003.
Pełny tekst źródłaWycoff, Jeffrey M. L. "Neuropsychological patterns in RISC identified schizotypic subjects". Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/864928.
Pełny tekst źródłaDepartment of Psychological Science
Wong, Nai-kei, i 黃乃淇. "Expression of myelin-related genes in an immune-precipitated mouse model of schizophrenia". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4378026X.
Pełny tekst źródłaWong, Hoi-man Emily, i 黃凱敏. "Genome-wide association analyses on complex diseases: from single-nucleotide polymorphism to copy numbervariation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hub.hku.hk/bib/B50534099.
Pełny tekst źródłapublished_or_final_version
Psychiatry
Doctoral
Doctor of Philosophy
Truter, Erika. "Genetic association analysis of polymorphisms in four cytochrome P450 genes, the MDR1 gene and treatment-outcome in Xhosa schizophrenia patients". Thesis, Link to online version, 2007. http://hdl.handle.net/10019/350.
Pełny tekst źródłaWright, Galen Egan Buckley. "Molecular genetic analysis of two genes, CYP2D6 and COMT, in the schizophrenia-susceptibility locus on chromosome 22q in the Xhosa population". Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20366.
Pełny tekst źródłaWolff, Anne-Lise. "A kinematic investigation of oculomotor and skeletomotor performance in schizotypy /". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85104.
Pełny tekst źródłaThis thesis investigates oculomotor and skeletomotor function in clinically unaffected individuals who are at elevated risk for schizophrenia based on their scores on either a positive-symptom schizotypy questionnaire (Perceptual Aberration Scale) (n = 21) or a negative-symptom schizotypy questionnaire (Physical Anhedonia) (n = 20), and in Controls (n = 29).
In Manuscript 1, we review the evidence suggesting that skeletomotor deficits are present in neuroleptic-naive schizophrenia patients and high-risk populations. The review supports the notion of skeletomotor dysfunction in these groups and underscores the lack of studies using instrumentation to characterize the deficits. In Manuscript 2, we compare the oculomotor performance of positive-symptom and negative-symptom schizotypes to that of controls. Results suggest that smooth pursuit deficits identify high-risk individuals with either positive or negative symptomatology, while antisaccade deficits identify primarily individuals with positive symptoms. In Manuscript 3, we use high-speed instrumentation and kinematic measures to evaluate skeletomotor function, and to assess the relationship between oculomotor and skeletomotor deficits in positive and negative-symptom schizotypes. This study revealed differential patterns of skeletomotor deficits in positive- and negative-symptom schizotypy, with both patterns suggestive of frontal-striatal dysfunction. In general, oculomotor and skeletomotor deficits were not associated.
Together these results support the notion of motor deficits across domains in risk for schizophrenia. In addition, they highlight the importance of distinguishing between positive and negative symptomatology when investigating the pathophysiology of risk for schizophrenia.
Morgan, Vera Anne. "Intellectual disability co-occurring with schizophrenia and other psychiatric illness : epidemiology, risk factors and outcome". University of Western Australia. School of Psychiatry and Clinical Neurosciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0209.
Pełny tekst źródłaHitzeroth, Angelika. "Association of genetic variants and the susceptibility to abnormal involuntary movements and tardive dyskinesia (TD) in Xhosa schizophrenia patients". Thesis, Stellenbosch : University of Stellenbosch, 2007. http://hdl.handle.net/10019.1/2147.
Pełny tekst źródłaNo obvious explanations exist for the development of abnormal involuntary movements (AIM), but several hypotheses have been proposed for tardive dyskinesia (TD) development. Since TD seems to have a genetic basis, several genetic variants have been investigated in TD development in various populations. Few studies have focused on African populations. This study focused on genetic variants (previously investigated in other populations) and the development and severity of AIM and TD in a Xhosa schizophrenia population. Genotype and allele frequencies determined were compared to those described in the literature for other populations. Following a report of an association between Ala-9Val and schizophrenia in a Turkish population, this study subsequently investigated this association in the Xhosa population. MnSOD Ala-9Val was genotyped using HEX-SSCP analysis and the DRD3 Ser9Gly variant was genotyped using restriction enzyme digestion by MscI. Genotyping was followed by statistical comparisons of the various groups, as well as association analyses between the variant and schizophrenia (only for MnSOD), AIM, or TD development and severity. The groups included a Xhosa schizophrenia group, a subgroup of the Xhosa schizophrenia group that had AIM (AIM+) and did not have AIM (AIM-), a subgroup of the AIM+ group that had TD (TD+), and a healthy Xhosa control group. A possible interaction between Ala-9Val and Ser9Gly in the development of AIM and TD was also investigated. Lastly, it was attempted to genotype CYP2D6*4, CYP2D6*10 and CYP2D6*17 using various PCR methods followed by restriction enzyme analysis. MnSOD Ala-9Val genotype and allele frequencies were similar to those of the Turkish population, but differed to those of the Asian populations. No association between Ala-9Val and the development and severity of schizophrenia was found. However, a relationship between genotype and AIM or TD development was observed, as well as an association between TD severity and Ala- 9Val genotype. DRD3 Ser9Gly genotype and allele frequencies were similar to those of the African American population, but differed from other populations. No significant association between Ser9Gly and the development and severity of AIM or TD was detected, nor was an interactive effect between Ala-9Val and Ser9Gly in AIM or TD development observed. The genotyping of CYP2D6 proved difficult and these variants could therefore not be analysed. The CYP2D6*4 genotype and allele frequencies that could be determined from some samples, were similar to the frequencies described previously for African populations. While we did not find an association between Ser9Gly in TD or AIM development and severity, nor an interaction between Ala-9Val and Ser9Gly, we did observe a relationship between Ala-9Val and AIM or TD development and TD severity. The effect of this variant is probably small and other variants, specifically those in genes involved in free radical removal should be investigated in combination with Ala-9Val. With regard to CYP2D6 it is suggested that high-throughput genotyping methods (e.g. microarray technology) should be used in the future. This will enable simultaneous genotyping of several variants and can be used in various populations. This study is the first of its kind by focusing on the unique South African Xhosa population and TD or AIM development.
Koen, Liezl. "Chromosomal aberrations in the Xhosa schizophrenia population". Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/1189.
Pełny tekst źródłaBACKGROUND: Schizophrenia is a heterogeneous illness resulting from complex gene-environment interplay. The majority of molecular genetic work done has involved Caucasian populations, with studies in these and Asian populations showing 2-32% of sufferers to have chromosomal aberrations. So far the discovery of a specific susceptibility mechanism or gene still eludes us, but the use of endophenotypes is advocated as a useful tool in this search. No cytogenetic studies of this nature have been reported in any African schizophrenia population. AIM: The aim of the study was to combine genotypic and phenotypic data, collected in a homogenous population in a structured manner, with the hope of characterising an endophenotype that could be used for more accurate identification of individuals with possible chromosomal abnormalities. METHODOLOGY: A structured clinical interview was conducted on 112 Xhosa schizophrenia patients. (Diagnostic Interview for Genetic Studies, including Schedules for the Assessment of Negative and Positive Symptoms.) Blood samples (karyotyping and/or FISH analysis) as well as urine samples (drug screening) were obtained and nine head and facial measurements were performed. Descriptive statistics were compiled with reference to demographic, clinical and morphological variables. Comparisons between mean differences for these variables were made.
Książki na temat "Schizophrenia – Genetic aspects"
Genetic models of schizophrenia. Amsterdam, Netherlands: Elsevier, 2009.
Znajdź pełny tekst źródłaSearching for the causes of schizophrenia. Oxford: Oxford University Press, 1994.
Znajdź pełny tekst źródłaCortical deficits in schizophrenia: From genes to function. New York: Springer, 2008.
Znajdź pełny tekst źródłaTorrey, E. Fuller. Schizophrenia and manic-depressive disorder: The biological roots of mental illness as revealed by the landmark study of identical twins. New York: Basic Books, 1994.
Znajdź pełny tekst źródłaDahlem Workshop on Biological Perspectives of Schizophrenia (1986 Berlin, Germany). Biological perspectives of schizophrenia: Report of the Dahlem Workshop on Biological Perspectives of Schizophrenia, Berlin 1986, October 26-31. Chichester: Wiley, 1987.
Znajdź pełny tekst źródłaBoklage, Charles E. How new humans are made: Cells and embryos, twins and chimeras, left and right, mind/self\soul, sex, and schizophrenia. Singapore: World Scientific, 2010.
Znajdź pełny tekst źródłaHunter, Beatrice Trum, i Beatrice Trum Hunter. Gluten intolerance: The widespread genetic defect that can cause arthritis, enteritis, schizophrenia and other health problems. New Canaan, CT: Keats, 1987.
Znajdź pełny tekst źródłaBoklage, Charles E. How new humans are made: Cells and embryos, twins and chimeras, left and right, mind/self/soul sex, and schizophrenia. New Jersey: World Scientific, 2009.
Znajdź pełny tekst źródłaBoklage, Charles E. How new humans are made: Cells and embryos, twins and chimeras, left and right, mind/self/soul, sex, and schizophrenia. New Jersey: World Scientific, 2010.
Znajdź pełny tekst źródłaLang, Mary V. Trends In Schizophrenia Research. Nova Biomedical Books, 2004.
Znajdź pełny tekst źródłaCzęści książek na temat "Schizophrenia – Genetic aspects"
Scourfield, Jane, i Peter McGuffin. "Genetic aspects". W Schizophrenia in Children and Adolescents, 119–34. Cambridge University Press, 2000. http://dx.doi.org/10.1017/cbo9780511526800.007.
Pełny tekst źródłaKinney, D. K. "Schizophrenia and Bipolar Disorder: Genetic Aspects". W International Encyclopedia of the Social & Behavioral Sciences, 13537–43. Elsevier, 2001. http://dx.doi.org/10.1016/b0-08-043076-7/03366-0.
Pełny tekst źródłaKwon, Ester J., Takahiro Soda i Li-Huei Tsai. "Neurodevelopment and Schizophrenia". W Neurobiology of Mental Illness, redaktor Pamela Sklar, 327–37. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0025.
Pełny tekst źródłaBrüne, Martin. "Schizophrenia spectrum and other psychotic disorders". W Textbook of Evolutionary Psychiatry and Psychosomatic Medicine, 159–76. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780198717942.003.0008.
Pełny tekst źródłaAndreasen, Nancy C. "The core dimensions of schizophrenia". W New Oxford Textbook of Psychiatry, redaktorzy John R. Geddes, Nancy C. Andreasen i Guy M. Goodwin, 565–73. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0057.
Pełny tekst źródłaJablensky, Assen, Hannah E. Jongsma, James B. Kirkbride i Peter B. Jones. "Epidemiology of schizophrenia and related disorders". W Oxford Textbook of Neurologic and Neuropsychiatric Epidemiology, redaktorzy Carol Brayne, Valery L. Feigin, Lenore J. Launer i Giancarlo Logroscino, 277–92. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749493.003.0028.
Pełny tekst źródłaLarge, Charles H. "Genetic association of voltage-gated ion channels with psychotic disorders". W Psychotic Disorders, redaktorzy Michael A. P. Bloomfield i Oliver D. Howes, 335–40. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190653279.003.0037.
Pełny tekst źródłaTsuang, Ming T., William S. Stone i Stephen V. Faraone. "Schizoaffective and schizotypal disorders". W New Oxford Textbook of Psychiatry, 595–602. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0080.
Pełny tekst źródłaGhaemi, S. Nassir. "Fundamentals of Neurobiology". W Clinical Psychopharmacology, redaktor S. Nassir Ghaemi, 17–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199995486.003.0002.
Pełny tekst źródła