Search PubMed⌕ Search

Biomedical subjects

G J Chader

Publications and source records attributed to G J Chader.

At least 253 records · Page 14Linked to original sources
PubMed1970

Uptake of oestradiol by the rabbit hypothalamus. Specificity of binding by nuclei in vitro.

The binding of [6,7-(3)H]oestradiol-17beta to subcellular fractions of the hypothalamus and the cerebellum of the rabbit was studied in vitro. Uptake of steroid was higher in hypothalamic nuclei than in cerebellar nuclei. Lower binding was observed in other fractions of both tissues. After dialysis of the fractions, hypothalamic nuclei retained a high percentage of oestradiol whereas cerebellar nuclei lost most of the bound steroid. Supernatant fractions of both tissues retained a significant proportion of label after dialysis and after gel filtration on Sephadex G-200. No specific binding was observed in these fractions when subjected to sucrose-density-gradient centrifugation. Purification of nuclei followed by incubation with labelled oestradiol in the absence of the supernatant fraction resulted in loss of binding of steroid by hypothalamic nuclei. Incubation of the purified hypothalamic nuclei with supernatant fraction maintained the binding specificity of hormone retention.

Animals↗
PubMedDate not supplied

Retinoblastoma--origin from a primitive neuroectodermal cell?

The histogenesis of retinoblastoma, the most common intraocular neoplasm of childhood, remains controversial. Previous studies have attributed the origin of the tumour to neuronal, glial or primitive stem cells of retina. In the study described here we have used immunofluorescence to search for the presence of a neuronal marker, neurone-specific enolase (NSE) and a glial marker, glial fibrillary acidic protein (GFAP), in the cells of the human retinoblastoma line Y-79 (ref. 4), before and after successful differentiation into neuronal and glial-like cells. We found that all undifferentiated cells contain both NSE and GFAP, whereas the differentiating neuronal and glial-like cells gradually lose one marker and selectively express the marker that correlates with their morphology. Our results support the notion that retinoblastoma originates from a primitive bipotential (or multipotential) neuroectodermal cell.

Cell Differentiation↗
PubMedDate not supplied

Increased TRPM-2/clusterin mRNA levels during the time of retinal degeneration in mouse models of retinitis pigmentosa.

Retinitis pigmentosa (RP) is a genetically and clinically heterogeneous group of human disorders that is characterized by diminished retinal function, visual cell loss, and blindness. Elevated levels of TRPM-2/clusterin mRNA, a marker for the apoptotic process, have been reported in retinas from patients with advanced stage RP. In the present study we examine TRPM-2/clusterin expression in two genetically distinct mouse models of RP, the rd (retinal degeneration) and rds (retinal degeneration slow) mice. We establish that in advanced postretinal degenerative stages of the rd mutant the retinal TRPM-2/clusterin mRNA levels are highly elevated, as is seen in the case of human RP. Examination of TRPM-2/clusterin mRNA levels in retina and whole eyes from the rd mouse and morphologically normal controls during the period of retinal degeneration (postnatal days 8-21) in the rd phenotype shows that TRPM-2/clusterin mRNA levels are elevated in the rd animal, and this increase begins just after postnatal day 10 and remains high for the remainder of the time course examined. Northern analysis of rds retina and whole eyes shows a delayed increase in TRPM-2/clusterin mRNA levels relative to the rd profile, coinciding with the known period of rds retinal degeneration (postnatal day 14 to 1 year). In each case, the onset of increased TRPM-2/clusterin mRNA levels coincides with the time of photoreceptor cell death.

Animals↗