Analysis of a representative sample of natural family planning users in England and Wales, 1984-1985.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Flynn.
Explore the source record for details and available documents.
The relationship between dietary sodium intake (as assessed by the 24-h urinary excretion of sodium) and urinary calcium excretion was examined in a selected group of free-living Irish individuals (n = 94), under conditions in which the completeness of urine collections was assessed. Results indicated that there was a significant positive correlation between 24-h urinary sodium and calcium excretion for males (r = 0.56, P less than 0.001) and females (r = 0.35, P less than 0.01). In addition, linear regression analysis indicated that mean 24-h urinary calcium excretion increased by 39 mg and 26 mg for a 1 g increment in sodium intake for males and females, respectively. The relationship between dietary sodium intake and urinary calcium excretion was also examined in 12 healthy young adults under controlled dietary conditions. Urinary sodium and calcium excretion values over 24 h were positively correlated for males (r = 0.44, P less than 0.05) and females (r = 0.80, P less than 0.001). However, the relationship was only statistically significant for 5 of the 12 subjects when the data were analysed on an individual basis. Results of this study suggest that salt intake may be an important determinant of urinary calcium loss in certain individuals and, as such, may be a risk factor in the development of osteoporosis. However, further studies are required to establish whether low salt intakes have a beneficial effect on calcium balance in free-living individuals.
The sodium, potassium and creatinine contents of three non-consecutive 24-h urine samples collected by 34 selected adult individuals (10 m; 24 f) living in Cork City were determined. The pooled mean 24-h excretion of sodium and potassium in collections adjudged to be complete were 152 mmol and 78 mmol, respectively. There was no significant difference between group average weekday and weekend-day excretion of Na or K, for either males or females. This suggests that weekend 24-h urinary collections, which most subjects find more convenient, are suitable for studies of sodium and potassium intakes of groups. The ratios of intra- to inter-individual variation for 24-h urinary sodium were 1.4 and 2.1 for males and females, respectively. The corresponding ratios for 24-h urinary potassium were 6.6 for males and 4.9 for females. These ratios indicated that there were large individual day-to-day variations in urinary sodium and potassium excretion in this group. It was estimated that a sample size of 35-60 individuals would be required to estimate group mean sodium and potassium intakes by means of single 24-h urine collections.
A functional antithrombin III (AT III) deficiency has been identified in two generations of a family with a high incidence of thrombosis. The deficiency presented as approximately 50% reduction in heparin cofactor activity compared to its antigen concentration. No abnormality was detected by crossed immunoelectrophoresis in the presence or absence of heparin. Plasma from the propositus was precipitated with dextran sulphate, applied to heparin-Sepharose and the AT III stepwise eluted with NaCl. The AT III had a reduced ability to inactivate thrombin, when this was monitored by substrate hydrolysis or by SDS polyacrylamide gel electrophoresis. Its mobility was normal by the latter technique using 10-20% gradient gels under reducing and non-reducing conditions. AT III from the patient was reapplied to heparin-Sepharose and eluted with a NaCl gradient. An active pool eluted in the same NaCl concentration range used to purify normal AT III, while predominantly inactive AT III eluted at higher NaCl concentrations. It is concluded that this variant, designated AT III Glasgow, has increased affinity for heparin but reduced ability to inactivate thrombin.
It has been shown previously that antithrombin III Northwick Park has reduced ability to inactivate thrombin and is characterized by an additional anodal component on crossed immunoelectrophoresis (Howarth et al, 1985). We have applied plasma from an affected family member to heparin-Sepharose and eluted the antithrombin III with a salt gradient. Evidence is presented that a variant component has slightly higher affinity for heparin than normal antithrombin III. Furthermore, this variant component is present in plasma as an approximately 120,000 MW inactive antithrombin III complex that can be reduced with dithiothreitol to MW approximately 60,000, indicating disulphide bridging. Using ion-exchange chromatography, the inactive complex has been isolated and shown to migrate in the same position as the anodal peak on crossed immunoelectrophoresis.
The in vivo stimulatory potential of estrogens and progestogens on monocytes/macrophages was examined in peritoneal exudate cells from Balb/cBy mice treated with continuous infusions for 15 days. Mice received a daily dose of 6.6 X 10(-10) M of one of the following compounds: prednisone, testosterone, estrogens--17 beta-estradiol and diethylstilbesterol, progestogens--progesterone and ethisterone and the bile acid lithocholic acid. Although total numbers of peritoneal exudate cells and the percentage of macrophages within those populations did not change with any of the treatments, the number of Ia-positive cells did significantly increase with the two estrogens, the two progestogens and the bile acid given the mice. The production of interleukin 1 was also stimulated by the treatment of the animals with the two estrogens, the two progestogens, and the bile acid, but not the glucocorticoid or testosterone. The activation of Ia expression, therefore, correlated with the production of IL-1. Estrogens and progestogens appear to have a marked effect on in vivo activation of monocytes/macrophages and may relate to differences in females and males in developing immune responses related to the actions of monocytes/macrophages.
The heparinoid of natural origin Org 10172 has anti-factor Xa activity but minimal anti-thrombin activity, and little effect upon broad spectrum assays such as the KCCT in vitro. Its anticoagulant effects have been compared to those of commercial heparin in 7 patients undergoing haemodialysis for chronic renal failure. Commercial heparin was administered in a dose (5,000 iu bolus + 1,500 iu/hour continuous iv infusion) previously shown to inhibit fibrin formation during haemodialysis. This produced mean anti-factor Xa levels in plasma between 0.7-1.0 iu/ml and largely suppressed fibrin formation for 5 h dialysis measured as mean FPA levels in plasma. Administration of Org 10172 as a bolus of 1,350 anti-factor Xa u or 2,000-2,400 anti-factor Xa u produced plasma anti-factor Xa levels of less than 0.5 u/ml and allowed fibrin clot and FPA generation during dialysis. Org 10172 administered as a bolus dose of 4,000-4,800 anti-factor Xa u produced mean anti-factor Xa levels of greater than 0.5 u/ml, allowed dialysis of 6 patients for 5 h and appreciably suppressed FPA generation during dialysis, with little effect on the KCCT. It is concluded that the anti-factor Xa activity of Org 10172 may reflect its ability to inhibit fibrin during dialysis and that single bolus injection of Org 10172 may be a useful alternative method of achieving anticoagulation.
Anticoagulation during haemodialysis for chronic renal failure can be assessed by measurement of plasma fibrinopeptide A (FPA) levels as an objective method of monitoring the initial step in fibrin formation, in conjunction with visual inspection of the dialyser circuit for fibrin clot deposition. Employing this approach, unfractionated commercial heparin administered as an intravenous bolus followed by an intravenous maintenance dose (5,000 IU + 1,500 IU/h) was found to suppress almost completely fibrin formation and deposition during prolonged dialysis. Comparison of a low molecular weight heparin, Kabi 2165, revealed that it can inhibit fibrin formation in the extracorporeal circulation, that this property is largely reflected in its anti-factor Xa activity in plasma, and that a useful and effective dose of Kabi 2165 for haemodialysis may be 4,000 anti-factor Xa U intravenous bolus + 750 anti-factor Xa U/h intravenous maintenance infusion. This dose only minimally alters the KCCT and corresponds to approximately 60% of that of unfractionated heparin, which may be important in the long-term use of heparin in these patients.
We have performed a dose ranging study of a low MW heparin, Kabi 2165, during haemodialysis in humans (n = 16) and compared it to a dose of unfractionated commercial heparin that has already been shown to inhibit fibrin formation. Low MW heparin administered as 5000 or 10,000 anti-factor Xa units, s.c., half an hour prior to the initiation of dialysis was unable to prevent fibrin formation in the dialyser circuit. A single bolus injection of 5000 anti-factor Xa units of low MW heparin given i.v. inhibited fibrin formation, as determined by FPA generation, for up to 4 h and permitted dialysis for 6 h. Such a bolus injection may be useful for short frequent dialyses. Infusion of low MW heparin in the same dosage regimen as unfractionated heparin, 5000 anti-factor Xa units bolus plus 1500 anti-factor Xa units/h, resulted in a progressive rise in heparin, caused by its longer half-life of elimination from the circulation, and almost completely suppressed both FPA generation and fibrin clot formation for 6 h dialysis. From these studies we calculate that infusion of this low MW heparin at a dose of approximately 4000 anti-factor Xa units bolus plus 750 anti-factor Xa units/h should be a useful regimen that will be effective in suppressing fibrin formation during prolonged dialysis, and the plasma anti-factor Xa level of low MW heparin may reflect its ability to inhibit fibrin formation, although exactly comparable anti-factor Xa levels of unfractionated commercial heparin and low MW heparins may not have identical inhibitory effects.
This report consists of two separate studies. Study I was a prospective one in which 23 pregnant women ultrasonically diagnosed as having small fetuses were compared with 22 women with large fetuses. Maternal plasma zinc concentrations pre- and post-35 weeks gestation were significantly higher in mothers of small than in mothers of large infants. Twelve women with normal pregnancies participated in study II. Biochemical data obtained in maternal plasma during the third trimester of pregnancy, including total, albumin-bound and alpha 2-macroglobulin-bound plasma zinc concentrations and plasma copper concentration were compared with infant anthropometric data at birth. The results indicated significant negative correlations between maternal plasma zinc and albumin-bound zinc concentrations and plasma copper concentration in the third trimester of pregnancy and mid-arm circumference and ponderal index. The results of these studies, in the light of other data reported for primates and humans, suggest the need for a more extensive investigation of the relationship between maternal circulating zinc and copper concentrations and fetal growth.
We have studied the within-person variability in the excretion of sodium, potassium, calcium, magnesium and creatinine in 20-60-year old men and women from 8 European centres. Only the data from people who reported that their collections were complete were entered in the analysis. The within-person coefficients of variation for the electrolytes ranged from 28 to 38 and that for creatinine from 21 to 24. The corresponding number of days required to estimate the excretion of electrolytes and creatinine to within 20 per cent of the habitual excretion (95 per cent confidence interval) varied between 4 for creatinine in men to 14 for magnesium in both men and women. The results of this study demonstrate once more that creatinine is unsuitable as a marker of completeness of urine collection for the individual.
Monocytes/macrophages from placenta have been reported to produce the immunological factor interleukin 1. In the present study both isolated adherent cells and tissue pieces produced interleukin 1, but the tissue piece culture supernatants also had colony stimulating activity. None of the following active factors were found in either culture supernatants: interleukin 2, interferon, erythropoietin and platelet-derived growth factor. Lysates of isolated placental cells contained interleukin 1, indicating that the factor was being produced in utero. Placentas from caesarean deliveries were likewise found to produce more interleukin 1 than placentas from normal term deliveries. The role(s) of placental-produced interleukin 1 is yet to be defined.
Three incidents are reported, from different radiotherapy centres, in which an implanted iridium-192 wire remained in the tissues of a patient after withdrawal of the plastic tubing in which it was contained. In each case the instrument used to cut the wire had probably formed a hook on the end of the wire which caused it to catch in the tissues. Detailed recommendations are made for avoiding such incidents in the future, the most important of which is that the patient should be effectively monitored after the supposed removal of all radioactive sources.
Plant lectin-induced proliferation of lymphocytes in vitro in both whole-spleen cell and T cell-enriched cultures was markedly effected by depletion of media copper, magnesium or zinc. The T lymphocyte-oriented mitogens concanavalin A and phytohemagglutinin and the B lymphocyte-oriented mitogen lipopolysaccharide were used to study variations in [3H]thymidine incorporation in lymphocytes cultured in media deficient in one mineral element. Since the stimulatory action of these mitogens also relates to the interaction of lymphocytes with accessory cells, we looked at the phagocytic ability of accessory cells cultured in the depleted media. In addition, we determined the variations in cell surface markers for B lymphocytes (Ia), T lymphocytes (Thy 1.2, Lyt 1 and Lyt 2) and accessory cells (Ia). Media depleted of copper, magnesium or zinc did not support normal T-lymphocyte proliferation but did support normal B-lymphocyte proliferation. The phagocytic ability of magnesium-deficient and zinc-deficient accessory cells was also depressed. This was related to depressed Ia expressions in the magnesium-deficient and zinc-deficient whole-spleen cell cultures. Total T-lymphocyte numbers, as well as Lyt 1+ cell percentages, were unchanged by media depletion, whereas Lyt 2+ cell percentages were depressed in both copper-deficient and magnesium-deficient splenocyte cultures.
Explore the source record for details and available documents.
The interaction of low doses of alcohol and marginal zinc deficiency during gestation was studied in pregnant mice and their fetuses. The combination of the two agents at subteratogenic doses was related to increased external and internal defects. Pregnant mice fed a diet containing 10 micrograms/g zinc were orally dosed with 2.0 micrograms/g of 50% ethanol for 18 days of pregnancy. Fetuses from these dams presented with more fetal defects than fetuses from control dams. Analysis of maternal livers showed a significant effect of alcohol on liver magnesium and zinc. Changes in fetal heart zinc levels were the only significant tissue effect of alcohol in the fetus.
The roles of zinc in immune responses continue to be defined and its impact on a broadening list of immune functions reported. Fundamental to the operation of zinc-dependent processes may be shifts in tissue zinc. Since the spleen is a site of activation, proliferation, and differentiation of lymphocytes, we examined changes in copper and zinc levels in spleens of antigen-stimulated A/J mice. Antigen stimulation with human immunoglobulin G and heat killed Staphylococcus aureus was compared with the actions of a nonantigenic inflammatory agent CaCl2. Between-group variations in copper and zinc with antigen treatment were compared in heart, liver, and spleen tissues. The zinc contents of spleens from antigen-treated mice were elevated, as were liver levels of the essential trace element. There were no significant increases in copper levels associated with antigen treatment. CaCl2-treated animal spleens demonstrated decreases in spleen copper and zinc content that were related to weight changes in the spleens, but not to specific treatment effects. Changes were suggestive of Interleukin-1 (IL-1) actions, which led to direct studies of IL-1 actions on splenic zinc. Partially purified IL-1 was injected into the tail vein and heart of A/J mice; liver and spleen zinc levels were determined 16 and 40 hours after injection. Significant increases in liver and splenic zinc concentrations were measured at both time intervals after IL-1 treatment. Antigen stimulation and, more directly IL-1, were related to stimulated increases in splenic zinc.(ABSTRACT TRUNCATED AT 250 WORDS)
Mouse and human placental tissue contains a large number of mononuclear phagocytes. These cells, isolated from placenta, were shown to produce the multifaceted immune factor interleukin-1. Activity in the supernatants of 48-hour mononuclear phagocyte cultures was associated with a 12,000- to 18,000-dalton protein, consistent with known interleukin-1 characteristics. Stimulation of phagocytosis with latex beads increased the production and release of interleukin-1 from these placental cells, which may be a useful source of this protein.