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Biomedical subjects

Y T Kishk

Publications and source records attributed to Y T Kishk.

10 recordsLinked to original sources
PubMed1993

Identification of cardiovascular abnormalities in children with empyema thoracis by two-dimensional and Doppler echocardiography.

To our knowledge, echocardiographic assessment of children with empyema has not been reported previously in the literature. Two-dimensional and Doppler echocardiography were performed in 47 children with acute (n = 23) and chronic (n = 24) empyema and 34 control subjects. Echocardiography demonstrated pericardial effusion in 11 of 47 patients (23 percent). Those with acute empyema had significantly thicker pericardium (p < 0.009) than control subjects. Tricuspid regurgitation was present in 21 of 47 patients (45 percent). The mean right ventricular internal dimension in diastole was significantly larger in patients with acute (p < 0.00002) and chronic (p < 0.006) empyema than that of control subjects. The mean tricuspid pressure gradients indicated an elevated mean right ventricular systolic pressure with increased calculated mean pulmonary arterial systolic pressures of children with acute empyema (38.5 +/- 6.4 mm Hg) and chronic (39.8 +/- 5.6 mm Hg) empyema than the normal mean (20 +/- 4 mm Hg). Children with chronic empyema had significantly less mean left ventricular internal dimension in diastole (p < 0.005) and left ventricular internal dimension in systole (p < 0.02) than control subjects. Strikingly, their mean left ventricular mass was also significantly less (p < 0.05) than that of subjects with either acute empyema or control subjects. These results provide baseline data for follow-up of children with acute and chronic empyema.

Acute Disease↗
PubMed1990

Accelerated atherogenesis occurs following platelet destruction and increases in megakaryocyte size and DNA content.

Platelets and megakaryocytes have a role in atherogenesis. In this study the effect of platelet destruction, caused by injection of serum containing anti-platelet antibodies, on the development of atheroma and on megakaryocyte size and DNA content was studied in rabbits on a high cholesterol diet. Seven days after destruction of the circulating platelets a significant (150% and 300% in two separate studies) increase in the area of atheroma in the aorta was demonstrated. Histological examination revealed that large quantities of extracellular lipid and connective tissue were present in these plaques. The acceleration of atherogenesis in this model was found to be preceded by a significant increase in megakaryocyte size and in the frequency of megakaryocytes with a high DNA content. Platelets derived from large, high ploidy megakaryocytes may be of importance for the development of the atherosclerotic lesion. Neither the endothelial permeability as assessed by injection of Evans blue nor the prostacyclin production by the aorta of animals injected with anti-platelet serum were significantly different from the aortas of control animals.

Animals↗
PubMed1985

Platelet volume subpopulations in acute myocardial infarction: an investigation of their homogeneity for smoking, infarct size and site.

Mean platelet volume and count were measured in three groups: patients with acute myocardial infarction, a control group with myocardial ischaemia but no infarction and an asymptomatic group of young males. Mean platelet volume was significantly larger in the myocardial infarction group compared with the ischaemic heart disease group or the asymptomatic group. Two subpopulations were present within the myocardial infarction group. One subgroup had a large mean platelet volume and low count. The other subpopulation was indistinguishable, with regard to platelet count and mean volume, from the ischaemic heart disease group. Over 60% of the myocardial infarction group lay in the area of high platelet volume and low count compared with 13% of the ischaemic heart disease control group and 38% of the asymptomatic group. Acute myocardial infarction is likely to be associated with a large mean platelet volume and low count compared with the ischaemic heart disease group. There is no statistical evidence that this condition is related to smoking or size and site of infarct. This evidence suggests that large mean platelet volume and low platelet count could be a major risk factor for myocardial infarction.

Blood Platelets↗
PubMed1984

Platelet production in myocardial infarction and sudden cardiac death.

Megakaryocyte cytoplasmic volumes were studied in 13 subjects 18 +/- 2 days after admittance to the coronary care unit. Seven had suffered a myocardial infarction (MI group) while six had chest pain but no recent infarction. Megakaryocytes were also studied in 10 subjects suffering coronary sudden unexpected death (CSD group) and 11 subjects suffering sudden unexpected un-natural death. There was no significant difference between the megakaryocyte cytoplasmic volume distributions of the MI and CSD groups, although they had a significantly greater mean (p less than 0.01) and range (p less than 0.001) than their respective control groups. There was no significant difference in platelet volumes observed within 24 hr of the infarct and 18 +/- 2 days later. Mean platelet volume was significantly correlated (r = 0.89, p less than 0.006) to mean megakaryocyte cytoplasmic volume in the MI group. A computer simulation of platelet production showed no significant difference between platelet volumes observed in the MI group and those estimated to be circulating before death in the CSD group.

Adult↗
PubMed1984

The origin of platelet count and volume.

Platelet count and volume were measured in man (n = 51) and rat (n = 9). Bone marrow megakaryocyte nuclear and megakaryocyte planimetric areas were measured in man (n = 11) and rat (n = 9). Megakaryocyte cytoplasmic volumes were computed from the planimetric areas. Rat had a significantly higher (p less than 0.001) mean megakaryocyte cytoplasmic volume than man and a significantly wider range (p less than 0.01). Rat mean platelet volume was significantly lower (p less than 0.001) than man while the rat platelet count was significantly higher (p less than 0.001) than man. A computer simulation of the random binary sequential division of megakaryocyte cytoplasm was used to explain these observations. Transmission electron microscopy shows that the site of this binary sequential division is probably the pulmonary circulation. The number of circulating megakaryocytes ml-1 of blood which would maintain the observed platelet counts was computed. The ellipses of constant density associated with the bivariate Gaussian distribution of platelet count and mean volume were computed. Platelet volume distributions of 13 men within two standard deviations of the composite mean of platelet count and mean volume were used to construct the platelet volume distribution signature in normal man. A similar platelet volume distribution signature for rat was constructed. The two distributions were significantly different. Neither rat nor man had a log Gaussian platelet volume distribution, however the measured volume distributions tended towards a log Gaussian curve.

Adult↗
PubMed1983

Changes in volume and density of platelets in myocardial infarction.

The distributions of platelet volume and density were measured in 15 men suffering myocardial infarction and in 22 healthy controls. The method used separated 93% of the total platelet population from whole blood. Mean platelet volume of the study group compared with that of controls was increased by a mean of 0.98 fl (p less than 0.001) in the first 12 hours after myocardial infarction, and by 1.24 fl six weeks later (p less than 0.001). Distribution of platelet volume remained log normal after myocardial infarction. Modal platelet density was increased by a mean of 25 g/l (p less than 0.05) after myocardial infarction. Platelet volume is probably chronically large in men suffering myocardial infarction and may be related to changes in megakaryocytes. It is suggested that the increase in platelet volume occurs before infarction.

Adult↗
PubMed1983

Platelet production: a computer based biological interpretation.

The platelet volume distribution was measured in rat and rabbit in normal steady state platelet production. The animals were then sacrificed and the planimetric megakaryocyte and nuclear areas in each animal were measured using histological techniques. These areas were used to obtain an estimate of the megakaryocyte, megakaryocyte cytoplasm and nuclear volume distributions. The production, by physical fragmentation, of the platelet population from the measured megakaryocyte cytoplasm volume distribution was simulated on a computer. The platelet volume distribution predicted by physical fragmentation was then compared with the measured circulating platelet volume distribution from each animal. The physical fragmentation theory gave an accurate quantitative prediction of the observed platelet volume distribution over the whole volume range. Furthermore fragmentation theory predicted the mean platelet volume, the mode, the maximum frequency of the platelet volume distribution and the range of this distribution. Autopsy studies of megakaryocytes volume distributions in healthy man were fragmented to obtain predicted normal platelet volume distributions from the computer simulation. These distributions were compared with measured circulating platelet volume distributions from apparently healthy men who had a similar mean platelet volume. The platelet volume distribution predicted by physical fragmentation was again in quantitative agreement with the measured distribution over the whole volume range. This study provides further evidence that platelet production from megakaryocyte cytoplasm is by physical fragmentation. Furthermore the computer simulation suggests that the mode of production has a specific form. It also explains why different mammals have different mean platelet volumes.

Animals↗
PubMedDate not supplied

Platelet and megakaryocyte changes in cholesterol-induced experimental atherosclerosis.

Rabbits were fed either 2 g cholesterol in 10 ml olive oil daily with normal diet (n = 5) or normal diet alone (n = 5). After 12 weeks, the cholesterol-fed animals had developed fatty plaques involving 24% +/- 4% of the surface area of the aorta; the control animals had none. Mean platelet volume was significantly smaller (p less than 0.04) in the cholesterol-fed animals (4.1 +/- 0.3 fl) compared with the controls (4.8 +/- 0.4 fl). The heterogeneity of the average volume distributions of the two groups, characterized by the statistical parameters of the coefficient of variation, skewness, and kurtosis, was also significantly different. Platelet count was significantly higher (p less than 0.001) in the cholesterol-fed group (7.48 +/- 1.06 x 10(11) platelets/liter blood) compared to the control group (4.86 +/- 0.60 x 10(11) platelets/liter blood). Mean megakaryocyte cytoplasmic volume was significantly larger (p less than 0.001) in the cholesterol-fed rabbits (12,262 +/- 1485 fl) compared with controls (6,814 +/- 761 fl). The range of cytoplasmic volumes was also significantly increased in the cholesterol-fed rabbits. A significant (p less than 0.01) increase in mean megakaryocyte nuclear volume in the cholesterol-fed animals was accompanied by a nonsignificant increase in mean nuclear DNA content: 30.2 +/- 3.7 N compared with a control value of 23.6 +/- 4.0 N. This evidence indicates that a high cholesterol diet in rabbits is associated with changes in platelet production from megakaryocytes as well with as the development of atherosclerosis.

Animals↗