Biomedical subjects
Publications and source records attributed to E Mathews.
Perinatal mortality rate was assessed for 13964 consecutive births in SAT Hospital, Trivandrum, South India, during a period of one year. The overall perinatal mortality rate was 42.75, stillbirth rate 24.41 and early neonatal mortality rate 18.79. The perinatal mortality rate in multiple pregnancy was 156.65. Preventable causes of perinatal mortality still make a major contribution to perinatal deaths in developing countries.
We have examined the relationships among activation of blood coagulation, generation of monocyte procoagulant activity, and clinical activity in patients with Crohn's disease. Subclinical activation of blood coagulation was measured using a radioimmunoassay for fibrinopeptide A. Fibrinopeptide A levels were strongly correlated with the level of disease activity as measured by the Crohn's disease activity index. Patients with active disease who were successfully treated either medically or surgically demonstrated a reduction of fibrinopeptide A levels. Failure of fibrinopeptide A to return to the normal range predicted an early relapse. Monocyte tissue factor generation was assessed in both unstimulated and lipopolysaccharide-stimulated mononuclear cell cultures obtained from the peripheral blood of patients with Crohn's disease. A strong correlation (r = 0.89) was observed between plasma fibrinopeptide A levels and monocyte tissue factor generation. These results suggest that monocyte procoagulant generation may contribute to the activation of blood coagulation in this inflammatory bowel disease. Moreover, fibrinopeptide A levels in Crohn's disease may provide a useful quantitative measure of inflammatory activity.
Dietary supplements with safflower oil, linseed oil, cod liver oil and hydrogenated coconut oil were given to rats at levels of 5, 20 and 40 energy % to simultaneously assess the effects of both type and level of dietary fat on tissue fatty acid composition and prostanoid synthesis. There was no significant change in weight gain or blood pressure between the dietary groups after the 4-week dietary regimen. The liver oil and linseed oil diets depressed the arachidonic acid content of kidney phospholipids at all levels of supplementation. The arachidonic acid content of plasma lipids was significantly elevated in animals on the safflower oil diet at 20 and 40 energy % while those on the same level of liver oil diet showed a marked reduction in arachidonic acid. Whole blood synthesis of thromboxane B2 varied significantly at all levels of fat supplementation, with the 20 energy % safflower oil fed group showing maximally enhanced thromboxane B2 production compared to the coconut oil group (P less than 0.001). Conversely, the liver oil groups showed depressed thromboxane B2 synthesis at 20 and 40 energy % (P less than 0.01) compared to the coconut oil group and at 5 energy % compared to the safflower oil group (P less than 0.05). Production of 6-ketoprostaglandin F1 alpha and prostaglandin E2 by incubated kidney homogenates only differed significantly between the dietary groups at 40 energy %. Urinary excretion of 6-ketoprostaglandin F1 alpha was increased by 45% and 55% in rats fed the safflower oil diet at 20 and 40 energy %, respectively compared to the saturated fat diet, while in the liver oil groups excretion was reduced by 20% and 32%. Dietary suppression of prostanoid synthesis is explained in part by changes in available arachidonic acid and competitive inhibition of cyclooxygenase by (n - 3) fatty acids. Thus, minor changes in dietary fat can readily alter tissue fatty acid composition, but both the extent and nature of changes in phospholipid and prostanoid metabolism vary markedly according to the tissue site.
The influence of dietary modification of polyunsaturated fatty acids (PUFA) on renin secretion, renal vascular tone and prostanoid excretion was studied in isolated perfused rat kidneys under basal conditions and in response to angiotensin II. After a four-week regimen of diets enriched with safflower oil, linseed oil or saturated fat, providing 20% of total energy intake (20 energy %), the animals which were fed linseed oil showed a significant fall in the proportion of arachidonic acid in renal phospholipids and a reduction in urinary prostaglandin excretion. In comparison with the other dietary groups, linseed oil feeding also resulted in a consistently lower renal vascular tone with increasing doses of angiotensin II. Under basal conditions both the PUFA-fed groups had significantly lower renal venous renin secretion rates relative to the saturated fat-fed control group. Infusion of angiotensin II (10 ng/min) suppressed renin secretion and abolished significant differences between the groups. As both the control group and the safflower oil group excreted similar levels of urinary prostaglandins, these results suggest that dietary enrichment with 20 energy % PUFA alters renin secretion by a prostaglandin-independent mechanism and that this may contribute to the lower blood pressures observed in these animals compared with the saturated fat-fed control group.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Functional proteins coded by genes 46 and 47 are required for (i) continuation of deoxyribonucleic acid (DNA) synthesis in the late period of T4 infection and (ii) production of normal, late replicating DNA which contains strands with a sedimentation coefficient in alkaline sucrose greater than that of mature DNA (73S). Continued DNA synthesis in the late period in the absence of functional genes 46 or 47 can be achieved by inhibiting late protein synthesis either by using bacterio-phage with a second mutation in gene 55 or by adding chloramphenicol to the culture before the decline in the rate of DNA synthesis. However, when functional 46/47 proteins are absent throughout infection, no strands with a sedimentation coefficient greater than 73S (in alkaline sucrose) are produced. This is the case even when DNA synthesis is allowed to continue. DNA arrest is accompanied by conversion of rapidly sedimenting, replicating DNA to slower sedimenting forms. When 46/47 is absent from the beginning of infection, the conversion product has a smaller sedimentation coefficient than mature DNA both in neutral and alkaline sucrose. When DNA arrest occurs midway in infection by heat-inactivating the ts46 enzyme, the conversion product has a sedimentation coefficient (i) the same as mature DNA in both neutral (63S) and alkaline sucrose if capsid assembly is allowed to take place and (ii) close to 63S in neutral sucrose but heterogenous and relatively greater (up to 100S) in alkaline sucrose if capsid assembly is inhibited. The structure of this DNA is unknown.
Explore the source record for details and available documents.
Explore the source record for details and available documents.