A microscopic study of kidney tissue in Familial Mediterranean Fever patients.

Familial Mediterranean Fever (FMF) is an autosomal recessive hereditary disease leading mostly to renal failure and nephrotic syndrome. The ultrastructure of kidney has not been fully investigated in FMF associated renal disease. The aim of this study is to provide further evidence on the ultrastructure of kidney in patients with FMF who suffer from renal disease. Renal biopsies obtained from two patients who were diagnosed with FMF renal disease complications were examined. Examination of renal tissue by light and electron microscopy identified degenerations both in tubules and the filtration barrier. Foot processes were partly effaced. Amorphous material was found in thickened glomerular basement membranes. Fibrous material deposits in thick Bowman's capsule wall were also seen. Finally, degeneration in the form of folding of plasma membrane and vacuolization as well as fusion in mitochondria cristae, was observed. Accumulation of tissue remnants in the lumen was also found in tubules.

Ultrastructural determination of gingival Langerhans cells in alloxan-induced diabetic rats.

The ultrastructure of Langerhans cells has not been fully investigated in diabetes-associated gingival tissues. The present study was carried out to investigate the ultrastructure of gingival Langerhans cells in alloxan-induced diabetic rats. Gingival biopsies were obtained from 22 diabetic and 18 control rats. Langerhans cells were observed by transmission electron microscopy (TEM) in the basal layers of healthy oral epithelium. On rare occasions, Langerhans cells were found in the suprabasal layers of the oral epithelium. Langerhans cells in the oral epithelium of diabetic rats were seen in the basal and suprabasal layers. Usually, Langerhans cells had clear cytoplasm and convoluted or indented nuclei and few or no specific granules. The clear cytoplasm contained mitochondria, lysosomes and a small number of rough-surfaced endoplasmic reticulum regions, but it lacked tonofilament. Occasionally, centrioles were also observed in the cytoplasm. The membrane of Langerhans cells had no junctional complexes such as desmosomes. In diabetic rats, Langerhans cell precursors were developed into specific granule-bearing cells. Both Langerhans cells and their granules were more frequent in the gingiva of diabetic rats than in the control group. These data suggest that Langerhans cells play an important role in explaining the pathogenesis and development of diabetic gingivitis.

The investigation of the ultrastructural neutrophil changes in alloxan-induced diabetes in rats: response to a chemotactic challenge.

Experimental diabetes is one of the most popular conditions in which to study the relation between neutrophil leukocyte activity and periodontal destruction. The aetiology of neutrophil dysfunction in the gingival tissue associated with diabetes has yet to be clarified. Diabetes in rats decreases neutrophil chemotactic activity in proportion to the severity of this systemic disorder. The present study was carried out to evaluate the relationship between the severity of diabetes and the neutrophil response to two chemotactic agents, and to correlate the observed neutrophil defects with the degree of diabetes. In this study two chemotactic agents, casein (0.2 microl, 2 mg ml(-1)) or N-formylmethionylleucylphenylalanine (FMLP; 0.2 microl, 10(-4) M), were placed into the gingival crevices of alloxan-induced diabetic rats. Gingival biopsies were taken 15 min later and then at 5-min intervals up to 45 min and investigated by electron microscopy. Adherence and migration were observed in the rats with moderate diabetes 30 min after the application of casein. There was chemotaxis after 35 min of administration of the peptide FMLP. By 40 min neutrophils with pyknotic nuclei were observed. At 45 min neutrophils with a decreased number of granules were present. As the severity of the diabetes increased, the neutrophils degenerated and were structurally distorted. In the rats which had alloxan-induced diabetes there was abnormal periodontal damage. This damage is thought to be related to dysfunctional neutrophils. These findings many contribute to an answer to the following question: why is there an apparent variability in the susceptibility of periodontal breakdown in diabetics?

Effects of chronic alcohol consumption on myocardial ischemia in rats.

The effects of chronic alcohol consumption on myocardial ischemia and gas perfusion with 95% O(2)-5% CO(2) were investigated in isolated rat heart. Eighteen adult male Wistar rats were used. Rats were assigned into six groups for each group to contain three rats: normal, alcoholic, normal ischemic, alcoholic ischemic, normal ischemic and 95% O(2)-5% CO(2) perfused, alcoholic ischemic and 95% O(2)-5% CO(2) perfused, respectively. Alcohol (7.2%, v/v) was given to rats by a modified liquid diet for 21 days. Rats were anaesthetized with ketamine (1-2mg kg(-1)). Hearts were quickly isolated. Normal and alcoholic rat hearts were directly sent to the electron microscopic preparation. The other hearts were cut into small pieces and put into Krebs solution. The solution was continuously bubbled using 95% N(2)-5% CO(2) 20 min for ischemia. After removal of normal ischemic and alcoholic ischemic heart specimens for electron microscopic examination, the remaining hearts of the last two groups were bubbled with 95% O(2)-5% CO(2) for another 20 min for the purpose of reperfusion and then were also prepared for electron microscopic examination. The hearts were investigated with a transmission electron microscope (Jeol 100 CXII TEM). Twenty-one days of chronic alcohol consumption was found to have no significant effect on myocardial ischemia determined by transmission electron microscopic examination. Our results suggest that there is no significant relationship between 21 days of alcohol consumption by a liquid diet and myocardial protection.