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Receptors abnormalities

A large number of glucocorticoid-resistant subclones of the lymphoid cell lines S49.1, WEHI-7 and CEM-7 have been isolated in the way described above. Receptor defects of different types were found to be the prevailing cause for resistance. For classifying the receptor abnormalities a whole-cell hormone-binding assay followed by crude cell fractionation has been employed [20,57],... [Pg.220]

In two other types of receptor abnormalities discovered in resistant S49.1 variants the binding of hormone is normal or almost normal but the subcellular receptor distribution differs from the wild-type. In the phenotype called nt" the receptors are nuclear transfer deficient in the sense of diminished nuclear binding and decreased affinity for chromatin and general DNA. In the nt1 ( increased nuclear transfer ) type the receptors show increased binding to nuclei or chromatin and abnormally high affinity for DNA [12,20,23]. This latter phenotype is quite rare it has only been recovered in two instances in S49.1 subclones and in glucocorticoid-re-... [Pg.220]

Despite these findings, some literature still maintains that schizophrenia or psychosis is associated with dopamine receptor abnormalities. A meta-analysis of post-mortem and imaging studies of dopamine receptors failed to mention the confounding effects of drugs, even though the analysis revealed a substantial and statistically significant correlation between the medication status of subjects and D2-receptor density compared with controls across studies (r=0.63,p<.05) (Zakzanis Hansen 1998). [Pg.92]

GABAa- and GABAB-type receptors abnormalities in thalamus in schizophrenia... [Pg.461]

Scarr E, Pavey G, Copolov D, Dean B. 2004. Hippocampal 5-hydroxytryptamine receptors Abnormalities in postmortem brain from schizophrenic subjects. Schizophr Res 71 383-392. [Pg.488]

Reynolds GP, Brown JE, McCall JC, Mackay AVP (1992) Dopamine receptor abnormalities in the striatum and pallidum in Tardive Dyskinesia. A post mortem study. J Neural Transm 87 225-230. [Pg.568]

Lee M, Martin-Ruiz C, Graham A, Court J, Jaros E, Petty R, Iversen P, Baumtm M, Perry E 2002) Nicotinic receptor abnormalities in the cerebellar cortex in autism. Brain 125 1483-1495 Lerer E, Levi S, Salomon S, Darvasi A, Yitmiya N, Ebstein RP (2008) Association between the oxytocin receptor (OXTR) gene and autism relationship to Vineland adaptive behavior scales and cognition. Mol Psychiatry 13 980-988... [Pg.395]

Nordberg, A., Nicotinic receptor abnormalities of Alzheimer s disease therapeutic implications, Biol. Psychiatry, 49, 200, 2001. [Pg.231]

Gonadotropin and gonadotropin-receptor abnormalities signal defects Enzyme deficiencies cho/esfero/c/esmo/ase, 17a-hydroxylase, 17, 20-desmolase Galactosemia... [Pg.1508]

Lee M, Martin-Ruiz CM, Graham AJ, Court JA, Jaros E, Perry RH, Iverson P, Bauman ML, Perry EK (2002) Nicotinic receptor abnormalities in the cerebellar cortex in autism. Brain 125 1483-1495. [Pg.157]

Manganese at micromolar concentrations has long been recognized as essential for the proper development and normal function of the nervous system [1,5,8,188]. Recent reports add to the already abundant knowledge of the role of Mn(II) in neurochemistry of the whole organism. A deficiency or an excess of Mn(II) causes severe neurotoxic developmental and functional effects [188-190]. Exposure to abnormal levels of Mn(II) in the developmental stages of life may cause the mature animal to exhibit ataxia or startle responses [191], susceptibility to seizures or epilepsy [192-194]. In these reports most of the effects have been shown to correlate with or interrelate to levels of neurotransmitters or hormones, specific binding to receptors, abnormal diet, or stress [195-198]. [Pg.98]


See other pages where Receptors abnormalities is mentioned: [Pg.269]    [Pg.188]    [Pg.390]    [Pg.446]    [Pg.447]    [Pg.456]    [Pg.458]    [Pg.464]    [Pg.468]    [Pg.150]    [Pg.777]    [Pg.2314]    [Pg.2317]    [Pg.1790]    [Pg.2849]    [Pg.466]    [Pg.2664]    [Pg.424]    [Pg.500]    [Pg.154]    [Pg.222]    [Pg.32]   
See also in sourсe #XX -- [ Pg.69 ]




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