34 research outputs found

    The ultrastructure of alcoholic liver disease: A review and analysis of 100 biopsies

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    Liver biopsies from 100 patients with alcoholic liver disease of various grades of severity were examined by light and electron microscopy. A comprehensive account of ultrastructural morphology is presented. The organellar changes were variable both in nature and intensity. The most consistent ultrastructural changes, irrespective of disease severity, were dilatation of endoplasmic reticulum and fat accumulation. The former is the EM counterpart of hepatocyte swelling at the light microscope level. Collagen deposition was detected earlier and more accurately by electron microscopy. A physical relationship between Mallory bodies and intermediate filament was also detected. As is the case with light microscopy, if cellular, stromal and organellar changes are considered independently, some may be regarded as typical, but none as pathognomonic of alcoholic liver disease

    Loss of heterozygosity occurs at the D11S29 locus on chromosome 11q23 in invasive cervical carcinoma

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    Allelotypic detection of loss of heterozygosity (LOH) has been used to identify putative tumour-suppressor genes. Loci on human chromosome 11q23 are frequently altered in malignant disease, and LOH has been reported at an anonymous D11S29 locus at 11q23 in a proportion of breast and ovarian cancers and malignant melanomas. Previous studies have reported a high frequency of LOH in cervical carcinoma mapping to 11q23. Using polymerase chain reaction techniques employing probes for a recently described polymorphic dinucleotide microsatellite within this locus, we have searched for LOH in 69 cases of invasive cervical carcinoma. Genomic material was microdissected from sections cut from archival paraffin-embedded material, using the patients' constitutional genotype as a control Sixty-two (90%) of the cases were informative, and LOH occurred in 25/62 (40%) of tumours. Loss of an arm or single chromosome 11 is a well-recognised event in cervical carcinoma, and by employing other microsatellite polymorphisms mapping to 11q13 and 11p11-p12 we excluded those cases with widespread allelic loss. By doing so, LOH at D11S29 was found in 16/53 (30%) of tumours. The findings suggest a putative tumour-suppressor gene on 11q involved in cervical carcinogenesis
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