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Biomedical subjects

S Shafi

Publications and source records attributed to S Shafi.

29 records · Page 2Linked to original sources
PubMed1993

Acute myeloid leukemia-FAB classification and its correlation with clinico-haematological features.

The French-American and British (FAB) classification of 62 consecutive cases of acute myeloid leukemia was undertaken. AML-M2 was the commonest FAB type (32.26%), followed by M1 and M4 (22.58% each), M5 (8.6%) and M6 and M7 (1.61% each), respectively. One of the patients was diagnosed as AML-MO (not a FAB type). The mean age of M1, M2, M3 and M5 cases was between 25 and 29 years, whereas in M4 patients it was 45.6 years. AML-M2, M4 and M5 were commoner in males, M1 in females and M3 equal in both sexes. Feeling of weakness, easy fatiguability and pallor were invariably present in all FAB types. All the patients of M1 and M5, 85% of M2, 64% of M4 and 50% of M3 presented with fever. Bleeding manifestations were most frequent in M3 cases followed by M5, M1, M4 and M2, respectively. Hepatomegaly and splenomegaly were relatively less prominent features in M3 as compared to other FAB types. Amongst the haematological parameters, anaemia was more severe in M1, leucocytosis in M2 and thrombocytopenia in M3 cases as compared to other FAB types.

Acute Disease↗
PubMed1990

Determinants of the atherogenic flux of low-density lipoprotein into arteries.

Evidence is provided that in anaesthetized rabbits the atherogenic uptake of low-density lipoprotein (LDL) by arterial walls is accelerated by norepinephrine at its physiological concentrations in rabbit and human blood. The principle of the experiments was to compare the uptake of intravenously injected, radioactively labelled LDL, methylated to prevent removal by high-affinity receptors, in the two carotid arteries of anaesthetized rabbits after infusing low concentrations of norepinephrine noradrenaline into one carotid and saline as control into the other, the volume rates of infusion being about 1% of the carotid blood flows. The results thus obtained may contribute towards an explanation for the accelerated atherosclerosis and the increased incidence of its clinical manifestation in conditions associated with elevated blood norepinephrine concentrations, including the episodic increases associated with stress and cigarette smoking as well as the more persistent increases caused by phaeochromocytoma.

Arteries↗
PubMed1989

Increased uptake of methylated low-density lipoprotein induced by noradrenaline in carotid arteries of anaesthetized rabbits.

Atherosclerosis is accelerated in hyperlipidaemias but, apart from the concentration of low-density lipoprotein (LDL) in the blood, very little is known about other influences on the disease process. We now provide evidence that in anaesthetized rabbits the atherogenic uptake of LDL by arterial walls is accelerated by noradrenaline at its physiological concentrations in rabbit and human blood. The principle of the experiments was to compare the uptake of intravenously injected, radioactively labelled LDL, methylated to prevent removal by high-affinity receptors, in the two carotid arteries of anaesthetized rabbits after infusing low concentrations of noradrenaline into one carotid and saline as control into the other, the volume rates of infusion being about 1% of the carotid blood flows. Human LDL, which behaves sufficiently like rabbit LDL for these purposes, was prepared, methylated and radio-iodinated by standard methods. At the end of the infusions, the arteries were excised and their radioactivities determined. Noradrenaline infused for 2 h to produce local blood concentrations of nominally 1, 10, 50 and 100 nM significantly increased the LDL radioactivities of the walls of the noradrenaline-infused carotids. Concentrations of nominally 100 nM also increased the LDL radioactivities of the walls of the saline-infused carotids; this was associated with significant increases in their blood noradrenaline concentrations. These results may contribute towards an explanation for the accelerated atherosclerosis and the increased incidence of its clinical manifestations in conditions associated with elevated blood noradrenaline concentrations, including the episodic increases associated with stress and cigarette smoking as well as the more persistent increases caused by phaeochromocytoma.

Animals↗
PubMed1987

Comparison of uptake and degradation of low density lipoproteins by arteries and veins of rabbits.

The uptake and degradation of low density lipoproteins were compared in arteries and veins of rabbits in vivo. Rabbits were injected with low density lipoproteins labelled singly with 125I (125I-LDL) or doubly with 131I and with [125I]tyramine cellobiose (TC-LDL) which remains trapped intracellularly. After increasing times up to 24 h the largest vessels were perfused to remove blood, fixed in situ and excised. When the uptake of 125I-LDL by arteries and veins was compared on the basis of luminal surface area, there were no significant differences up to 3.5 h. When degradation rates of double labelled LDL were compared after 24 h on the same basis, the arteries contained significantly more TC label than the veins, but when the comparison was based on dry weights there were no significant differences. These results show that veins, like arteries, take up LDL from the circulating blood; and they suggest that the preferential accumulation of LDL in arteries susceptible to atherosclerosis may be accounted for, at least in part, by more degradation of LDL in arteries than in veins.

Animals↗
PubMed1985

Increased accumulation of lipoprotein and cholesterol in re-endothelialized rat carotid artery after laser damage.

The permeability characteristics of acute endothelial lesions and completely regenerated endothelium were investigated. The endothelium of rat carotid arteries was selectively damaged by laser irradiation. When [125I]LDL was injected 24 h later, the average [125I]LDL uptake in the damaged arteries was about 13 times the uptake by the non-irradiated, contralateral control arteries. Fourteen weeks after the irradiation, the vessel walls with regenerated endothelium had taken up twice as much [125I]LDL as the controls. Sixteen weeks after the irradiation, orally administered [3H]cholesterol was accumulated 5 times more by the irradiated than by the control vessel wall. These findings show that the adherent platelets contribute importantly to the LDL cholesterol accumulation by the vessel wall with acute endothelial lesion and that the regenerated endothelium promotes the accumulation of LDL cholesterol.

Animals↗
PubMed1984

Delay in primary haemostasis produced by a fish diet without change in local thromboxane A2.

Twelve apparently healthy male volunteers were maintained for 6 weeks on a fish diet, the haemostatic effects of which were determined as standardized skin bleeding times; thromboxane A2 formation in vivo in the bleeding time blood and in vitro in clotting venous blood; platelet aggregability; and platelet phospholipids. Within 1 week the fish diet changed the fatty acid composition of platelet membrane phospholipids, with increases in omega-3 and decreases in omega-6 fatty acids; described platelet aggregability by ADP and collagen; but the bleeding time was unchanged. Not until 6 weeks on the diet did the bleeding time increase (by 37%: P less than 0.01) and it was still increased 3 weeks after the end of the diet, when the fatty acid composition of the platelets had returned to normal. The effect of the diet on decreased aggregability of platelets also failed to follow the changes in their fatty acid composition and in the bleeding time. Aggregation by ADP and by the highest dose of collagen was decreased throughout the diet and for several weeks thereafter, i.e. even when the fatty acid composition had reverted to the pre-dietary pattern and long after the normalization of the bleeding time. The diet caused no change in the in vivo appearance of thromboxane A2 in the bleeding time blood, contrasting with its effect in decreasing the in vitro formation of thromboxane A2 in clotting venous blood. These observations suggest that such fish diets do not delay haemostasis by diminishing the formation of thromboxane A2 locally nor directly by decreasing the aggregability of platelets or directly by the induced changes in their omega-3 fatty acids.

Adult↗
PubMed1983

Thromboxane A2 in skin-bleeding-time blood and in clotted venous blood before and after administration of acetylsalicylic acid.

The 'Simplate' technique for measuring skin bleeding time was adapted to quantify thromboxane A2 in the emerging blood as the stable degradation product thromboxane B2 in twelve Swedish and ten English volunteers. During the bleeding time thromboxane B2 concentrations increased, but as the rate of blood loss fell the rate of production of thromboxane A2 was constant. The English subjects had shorter bleeding times and produced more thromboxane A2 than the Swedish subjects. When the Swedish subjects were grouped according to bleeding times those with the shortest had more thromboxane A2 than those with longer bleeding times. Clotting venous blood in vitro produced much more thromboxane A2 than bleeding-time blood and there was no correlation with bleeding time. Determination of the capacity of clotting blood to form thromboxane A2 is therefore irrelevant to in-vivo haemostasis. Acetylsalicylic acid greatly diminished the appearance of thromboxane A2 in the bleeding time and prevented the increase of thromboxane A2 concentration with time.

Adenosine Diphosphate↗
PubMed1983

Quantification of blood from skin bleeding time determinations: effects of fish diet or acetylsalicylic acid.

The Simplate II technique for measuring bleeding time was adapted to quantify the volume of blood as a function of time and for determining how this parameter was affected by either acetylsalicylic acid (ASA) or a dietary supplement of fish. Both increased the bleeding time significantly. Irrespective of the final bleeding time, the rate of blood loss increased for about the first 2 min and then decreased almost linearly until bleeding stopped. This time course was not affected by either ASA or the fish diet. The lack of effect by ASA suggests that the initial increase in bleeding time, presumably due to reversal of vasoconstriction, does not involve prostaglandin derivatives. After ASA the rate of blood loss was significantly greater throughout, probably caused by deceleration of platelet aggregation. During the fish diet, when bleeding time was increased, there was no change in the rate of blood loss until the last 2-3 min during which bleeding continued at a very low rate. The results support the conclusion that the delay in primary haemostasis produced by a fish diet is due to a different mechanism than that produced by ASA.

Adult↗