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Patients with β-thalassaemia major frequently suffer from hypersiderosis which leads to hemochromatosis of major organs such as the heart and liver. Little information exists about the ultrastructural pathology of the human heart in β-thalassaemia patients. Five Cypriot patients with elevated blood ferritin and intractable heart failure were investigated. Cardiac biopsies from these patients were studied by light and electron microscopy, as well as by X-ray microanalysis. Ultrastructural examination revealed the presence of disrupted myocytes showing loss of myofibers, dense nuclei, and a variable number of pleomorphic electron dense granules. These cytoplasmic granules or siderosomes consisted of iron-containing particles as confirmed by X-ray microanalysis. It is likely that the ultrastructural changes observed in myocytes of patients with β-thalassaemia are largely due to iron deposition. [ABSTRACT FROM AUTHOR]

Background: Ras GTPase isoforms have been implicated in proliferative renal disease and are known to have differential cellular expression in kidney. However, their exact subcellular location in various cells is unknown., Methods: Immunogold labelling for Ras isoforms (Harvey, Kirsten and Neural) was performed for subcellular localization under electron microscopy in fresh normal kidney specimens, obtained from the opposite pole of kidneys removed for renal cell cancer., Results: There was prominent staining shown by Ha-Ras only on the glomerular foot processes as compared with basement membrane or the endothelial cells. Mesangial cells showed intense staining in the cytosol with Ha-Ras (absent in the nucleus), minimal staining with Ki-Ras and none with N-Ras. In both the proximal and distal convoluted tubules, there was a clear staining of the mitochondria with Ha-Ras, with mild cytosolic staining with all of the isoforms., Conclusions: Ras isoforms have distinct and separate subcellular distributions in normal kidney cells. Understanding the functional aspects of this distribution pattern is essential if Ras is to be targeted by genetic or molecular therapeutic tools.

Background: Ki-Ras is well studied in its oncogenic form in relation to pancreatic pathologies. However, the individual contribution of each of the wild-type Ras isoforms (Ha-, Ki-, and N-) in pancreatic cells in health and disease is unknown., Methods: Archival formalin-fixed, paraffin-embedded specimens of normal (n = 6) and malignant pancreas (n = 35) were used for immuno-histochemical detection of Ras isoforms using a modified polymer system. In addition, immunogold labelling for Ras isoforms was done for subcellular localisation under electron microscopy., Results: Pancreatic ductal cells expressed Ha-Ras in the cytoplasm, with Ki-Ras in the apical region and N-Ras (50% of cases) in a supranuclear distribution. Pancreatic acinar cells express all three isoforms with some nuclear expression of Ki-Ras and supranuclear expression of N-Ras. Islets show Ki- and Ha-Ras mainly with differential expression of Ha-Ras (beta cells showing less Ha-Ras and more Ki-Ras than alpha cells). Electron microscopy shows that Ha-Ras is mainly localised in the endoplasmic reticulum and Golgi apparatus of the acinar cells with some plasma membrane localisation of Ki-Ras in the ductal cells. There was no change in any of the Ras isoform expression in the ductal or acinar cells in various malignancies studied (Mann-Whitney U test, p > 0.1)., Conclusions: Ras isoforms have distinct and separate cellular and subcellular distribution that may persist even in the malignantly transformed state. Understanding this distinct functional distribution patterns in detail is an essential step if mutant Ki-Ras is to be targeted in the pancreas by genetic or molecular therapeutic tools.

The surface ultrastructure of normal and abnormal endometrial cells from patients receiving oestrogen therapy for the climacteric syndrome was studied by scanning electron microscopy. Patients with endometrial pathology were treated with oral progestogens. Excessive oestrogen stimulation caused proliferation of cilia and microvilli. Cystic hyperplasia was characterised by a proliferation of cilia until they covered more than one-third of the surface area of the endometrium; further proliferation occurred in cases of adenomatous hyperplasia when the surface was almost completely covered with cilia. Cell morphology remained apparently normal until atypical hyperplasia, when occasional cells appeared large and irregular, or adenocarcinoma occurred, when the surface cells appeared large, pleomorphic and sometimes wrinkled, being mostly devoid of cilia. Although cystic hyperplasia was converted to a normal histological picture of atrophic or pseudo-decidual endometrium by courses of progestogen, the deciliated endometrial cells showed persisting abnormal ultrastructural characteristics.