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Biomedical subjects

M Melissari

Publications and source records attributed to M Melissari.

35 records · Page 2Linked to original sources
PubMed1988

Prospective rheumatological study of muscle and joint symptoms during Trichinella nelsoni infection.

One hundred and fifty patients were assessed during an outbreak of Trichinella infection in Northern Italy. The aetiological agent was proved to be T. nelsoni. A detailed prospective rheumatological study was carried out. Myalgia was observed in 88 per cent, muscle weakness in 60 per cent, myositis in 62 per cent and arthralgia in 20 per cent of the patients. The arthralgia score was strictly related to myalgias-myositis. The degree of myositis correlated with the degree of hypereosinophilia. Muscle damage in tissue samples was often observed in areas where eosinophils were the major cell population infiltrating the tissue. No relationship was seen between IgG antibody titers against Trichinella or IgE levels and clinical manifestations. Steroids, thiabendazole or mebendazole were not administered. We observed no CNS or heart involvement nor did we see vasculitis. After six months 18 patients, with the highest degree of myositis and hypereosinophilia had all improved. None showed abnormalities in laboratory tests and only four were still complaining of muscle aches. T. nelsoni-related infection appears to induce musculoskeletal symptoms in the majority of patients, but the long term course and prognosis is favourable.

Adolescent↗
PubMed1985

Cutaneous hyperpigmentation induced by amiodarone hydrochloride.

Amiodarone (Cordarone) is an iodinated compound widely used in the treatment of cardiac arrhythmias for more than a decade. A patient who developed a persistent blue-gray skin pigmentation of the light-exposed areas following long-term amiodarone hydrochloride administration is reported. The cutaneous signs and the ultrastructural findings are described. This rare iatrogenic hyperpigmentation is peculiarly due to lipofuscin and not melanin deposits. Its pathogenesis may be related to the basic action of the drug on the lysosome and to the extra phototoxic-induced lysosomal damage, which accounts for the specific location of the hyperpigmentation over the light-exposed areas.

Aged↗
PubMed1984

Structural compensatory mechanisms in rat heart in early spontaneous hypertension.

The response of the left ventricle (LV) during the development of spontaneous hypertension (SH) in rats was studied morphometrically at 21, 28, 35, and 45 days after birth and compared with that of normotensive (WK) controls. LV hypertrophy, varying from 24 to 27%, was characterized by the preservation of the volume fraction of capillary lumen and capillary luminal surface in the myocardium, as a result of capillary proliferation. From 21 to 45 days the number of capillaries per unit area of myocardium increased 68% in SH rats by the insertion in parallel of new capillary elements among the myocytes. This estimation was obtained by correcting the value of capillary density at 45 days for the amount of spreading produced by myocyte growth during this interval. On a similar basis capillary proliferation was only 24% in WK rats. Myocyte growth in experimental animals (151%) was achieved by a 77% enlargement in myocyte cross-sectional area (MCSA) and by a 42% lengthening of the cells. In controls myocyte expansion (124%) was the result of comparable increments in MCSA (47%) and myocyte length (53%).

Aging↗
PubMed1984

Squamous cell carcinoma arising in a dermoid cyst of the ovary. Clinical and pathological report of a case.

A case of squamous cell carcinoma arising in a dermoid cyst of the ovary of a 38 year-old woman is reported. Its frequency is nearly 1%; nevertheless it is opinion that the real frequency could be higher if the hystological examination of the cyst would be made more accurately. Clinical and pathological findings of this case are presented in this brief note. The importance to always make an intraoperatively frozen-section examination is emphasized. The patient is alive and well after six months after surgery.

Adult↗
PubMed1982

Quantitative structural changes of the rat thoracic aorta in early spontaneous hypertension. Tissue composition, and hypertrophy and hyperplasia of smooth muscle cells.

The thoracic aorta of 21-, 28-, 35-, and 45-day-old spontaneously hypertensive (SH) and Wistar Kyoto (WK) rats was analyzed morphometrically to evaluate the cellular hypertrophy and proliferation of medial smooth muscle cells during the development of genetically determined hypertension. The absolute increase in volume of collagen and ground substance, and elastic tissue was also measured. In SH animals, cellular hypertrophy was found to be the dominant mechanism of muscle growth in the 21- to 28-day and 35- to 45-day intervals, resulting in an overall 68% enlargement of the mean cell volume from 21 to 45 days. The total number of smooth muscle cells increased only 21% (not statistically significant) and the tendency toward hyperplasia was restricted to the 28- to 35-day period. Normotensive controls showed cell proliferation mainly from 21 to 28 days and cellular hypertrophy from 35 to 45 days with an absolute 33% increase in the number of cells and a 26% larger volume of the mean smooth muscle cell at 45 days of age. from 21 to 45 days, the above changes in cell size and number provoked an overall 104% and 67% growth of the muscle mass in SH and WK rats, respectively. The initial response phase of spontaneous hypertension was also characterized by an increase of collagen and ground substance, 184%, which was slightly greater than that of the elastic component, 168%. Changes in mural concentration of fibrous proteins that were similar to but of less magnitude than those of controls, were seen. These results demonstrate that short-term spontaneous hypertension determines a simultaneous growth adaptation in every component structure of the media of the thoracic aorta leading to a disproportionate accumulation of scleroproteins that markedly exceeds that of the contractile component of the vessel wall. At a cellular level, smooth muscle cell hypertrophy is the prevailing process that underlies the tissue response of the aorta in early hypertension.

Aging↗
PubMed1980

Morphometry of the renal corpuscle during postnatal growth and compensatory hypertrophy.

Morphometry was used to measure the growth changes in renal corpuscle and glomerular size and composition in outer, middle, and inner cortical layers during postnatal development in normal and mononephrectomized rats. Glomerular growth was 4.16-fold in normal rats and 6.12-fold after nephrectomy. The cell populations in glomeruli showed distinctly different growth patterns. Cellular hypertrophy and hyperplasia during normal growth were 2.72 and 1.52 for epithelial cells, 0.93 and 3.70 for endothelial cells, and 1.28 and 2.65 for mesangial cells; corresponding values during stimulated growth were 2.75 and 1.92, 1.19 and 4.11, and 1.65 and 3.09. A linear transcortical gradient of corpuscle diameters was found in young animals and normal adults, with the mean volume of juxtamedullary renal corpuscles two times greater than that of subcapsular corpuscles in all animal groups. Despite their size variation, a striking transcortical uniformity was evident in the composition of glomeruli in each group with respect to the volume fractions and mean cell volume in each cell population, the volume and surface density of basement membrane, the volume and length density of capillary loops, the volume fraction of mesangial matrix, and the division of basement membrane into peripheral and axial portions.

Animals↗
PubMed1980

Morphometric study of early postnatal development of the thoracic aorta in the rat.

Tissue, cellular, and subcellular morphometry of the thoracic aorta in 1-, 5- and 11-day-old rats was used to quantify the cellular hypertrophy and proliferation of smooth muscle cells and the absolute increases in volume of elastic laminase and collagen during the early postnatal period. In the 1- to 5-day interval, total wall volume increased 2.9-fold, wall thickness and the number of smooth muscle cells doubled, mean cell volume increased by 40%, and the volumes of elastic laminae and collagen increased 3.7- and 3.3-fold, respectively. From 5 to 11 days, circumferential growth of the aortic wall, without further thickening, produced smaller and unequal growth increments of each of its component structures, with increases in collagen (3.2-fold) > elastic laminae (2.3-fold) > muscle cells (1.6-fold). In the overall growth of smooth muscle cells (4.6-fold) from 1 to 11 days, only the cytoplasmic volume fractions of glycogen aggregates and rough endoplasmic reticulum were altered significantly (-76%, +32%). Certain aspects of normal postnatal aortic growth paralleled the response of adult aorta to experimentally induced hypertension.

Animals↗
PubMed1980

Morphometry of medial hypertrophy in the rat thoracic aorta.

Surgical constriction of the subdiaphragmatic aorta in young adult male rats induced a 54 per cent hypertrophy (39 per cent thickening) of the wall of the thoracic aorta in 8 days, with no increase in the number of elastic lamellae. Morphometric analysis of the aorta wall showed volume increases of its component smooth muscle cells (57 per cent) elastic laminae (30 per cent), collagen (136 per cent), and endothelium plus subendothelial space (40 per cent). Mean cell volume of smooth muscle cells increased 55 per cent from 272 +/- 11 to 421 +/- 21 cu. mum. (p less than 0.005). The number of smooth muscle cells per centimeter of length of thoracic aorta was 4.2 +/- 0.3 x 10(6) in both control and experimental animals. Thus, aortic medial hypertrophy following aortic stenosis included enlargement but no proliferation of smooth muscle cells. Absolute volume increases in the average smooth muscle cell included the nucleus (27 per cent), myofilaments (47 per cent), mitochondria (62 per cent), rough endoplasmic reticulum (246 per cent), smooth endoplasmic reticulum (23 per cent), and caveolae (37 per cent).

Animals↗
PubMedDate not supplied

Connective tissue accumulation in the left coronary artery of young SHR.

The left coronary artery of 21-, 28-, and 45-day-old spontaneously hypertensive rats and Wistar-Kyoto rats was analyzed morphometrically to evaluate the structural alterations of the vessel wall during the development of genetically determined hypertension. In 45-day-old rats, hypertension was associated with a significant expansion of the partial volume of collagen and ground substance (119%) within the arterial wall. This change exceeded the concurrent accumulation of elastin (77%) and smooth muscle cell mass (34%). The growth of the muscle compartment was also characterized by a marked increment of rough endoplasmic reticulum (103%). The increase in the mural concentration of fibrous proteins at this early age may be viewed as the initial adverse effect of hypertension on muscular arteries.

Aging↗