Oxalate has been reported to have a toxic effect on endothelial cells in culture [2], leading to suggestions that hyperoxalaemia may contribute to endothelial damage and thus to arterial disease in patients receiving dialysis. We studied this possibility during a study of the effects of ascorbate supplementation on plasma oxalate in patients receiving dialysis

Rats given a low-fibre diet based on boiled white rice developed symptoms of severe vitamin K deficiency within 23 d. Inclusion of autoclaved black-eye beans (Vigna unguiculata) in the diet prevented the bleeding syndrome. To test the hypothesis that deficiency resulted from low phylloquinone intake exacerbated by inadequate production of menaquinones by the enteric bacteria, a follow-up experiment was carried out in which groups of rats were given an all-rice diet, a rice+beans diet or a stock diet. Rats on the allrice diet had significantly lower faecal concentrations of the main menaquinone-producing bacterial species (Bacteroides fragilisandBacteroides vulgutus) than animals on either of the other two diets. This coupled with the much lower faecal output on this diet suggests that total menaquinone production was low for the all-rice diet. The alterations in faecal flora were associated with several significant changes in caecal metabolism. Rats given the stock diet had much shorter caecal transit times and a considerably greater proportion of butyric acid in volatile fatty acid end-products than did rats on either of the other two diets.

The effect of neuropeptide Y on platelet-rich citrated human plasma has been studied both before and after addition of adrenaline. The peptide has no aggregatory properties of its own, but in the concentrations tested it does slow and inhibit the aggregatory responses of platelets to adrenaline. This effect is dose-dependent. The implications of this finding are discussed.

In a proposed study of fibrinolytic therapy in experimental streptococcal endocarditis, this disease was induced in pigs by preinoculation damage to the aortic valve; the technique of this is described. If untreated, the disease runs a protracted course, similar to that in man. Fibrinolytic activity, normally low in the pig, can be increased by stress, by urokinase, by plasmin and briefly by streptokinase if supplemented by human plasminogen. The proposed experiments were abandoned in pigs, chiefly because of technical difficulties in obtaining frequent samples of blood and maintaining infusions. In experiments on the response of ADP-induced aggregation of pig platelets to prostacyclin, they were found to be about 10 times more resistant than human platelets. It is suggested that this resistance to prostacyclin, together with their usually low state of systemic fibrinolytic activity, may explain the susceptibility of pigs to bacterial endocarditis.

Using standard one stage clotting assays the concentrations of factors II, VII, IX and X were determined in 37 patients stabilised on warfarin for between three months and 17 years. Contrary to popular belief, the concentrations were not equally depressed, with factor X the lowest, factor II at intermediate value, factors VII and IX the highest. Some 71% of the variance of the British corrected ratio (BCR) could be accounted for by measurement of the factors assayed. Analysis of this variance showed 91% of the explained variance attributable to factor II, 7% to factor VII, 1.6% to factor IX and 0.4% to factor X. With the sudden and recent withdrawal of human thromboplastin, investigation of the sensitivities of the animal thromboplastins to changes in vitamin K dependent factors in orally anticoagulated patients is needed to ensure that the potentially alarming falls in factors II and X in these patients are being adequately detected.

One hundred and forty three multitransfused patients with hereditary haemostatic disorders were examined for evidence of disease related to the acquired immune deficiency syndrome (AIDS). Ninety nine patients with severe haemophilia A were tested for anti-HTLV-III and 76 were found to be positive. All except one of these seropositive patients had received commercial factor VIII concentrates at some time. Eighteen patients with haemophilia B were tested and all were anti-HTLV-III negative. Three out of 36 sexual partners of patients with haemophilia A positive for anti-HTLV-III were also seropositive. One, who had recently received blood transfusions, had AIDS with Pneumocystis carinii pneumonia. Three patients with severe haemophilia A died from AIDS. A further 30 haemophiliacs had AIDS Newcastle Haemophilia Reference Centre and Department of Haematology, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP PETER JONES, MD, FRCP, director P J HAMILTON, MRCPATH, FRCP, consultant haematologist MAUREEN FEARNS, RGN, clinical nurse specialist ALAN OXLEY, FIMLS, chief medical laboratory scientific officer Department of Immunology, Newcastle General Hospital, Newcastle upon Tyne NE4 GRAHAM BIRD, MD, MRCPATH, consultant immunologist Virology Section, Department of Microbiology, Middlesex Hospital and University College Medical School, London RICHARD TEDDER, MRCP, MRCPATHI, senior lecturer Institute of Cancer Research, Chester Beatty Laboratories, London RACHANEE CHEINGSONG-POPOV, PHD, research scientist Public Health Laboratory Service, Newcastle General Hospital, Newcastle upon Tyne ARTHUR CODD, Ms, MD, consultant microbiologist Correspondence to: Dr Jones. related complex or lymphadenopathy that could be related to HTLV-III infection. There was a significant correlation between lymphadenopathy and anti-HTLV-HI seropositivity. No evidence of casual spread of AIDS was found since all 68 health care stafftested were anti-HTLVIII negative, including three surgeons who regularly worked with patients positive for anti-HTLV-III. The resources devoted to counselling and laboratory support in centres treating people at risk and their families need to be urgently reassessed.

One hundred and forty-three multitransfused patients with hereditary haemostatic disorders were examined for evidence of disease related to the acquired immune deficiency syndrome (AIDS). Ninety-nine patients with severe haemophilia A were tested for anti-HTLV-III and 76 were found to be positive. All except one of these seropositive patients had received commercial factor VIII concentrates at some time. Eighteen patients with haemophilia B were tested and all were anti-HTLV-III negative. Three out of 36 sexual partners of patients with haemophilia A positive for anti-HTLV-III were also seropositive. One, who had recently received blood transfusions, had AIDS with Pneumocystis carinii pneumonia. Three patients with severe haemophilia A died from Aids. A further 30 haemophiliacs had AIDS related complex or lymphadenopathy that could be related to HTLV-III infection. There was a significant correlation between lymphadenopathy and anti-HTLV-III seropositivity. No evidence of casual spread of AIDS was found since all 68 health care staff tested were anti-HTLV-III negative, including three surgeons who regularly worked with patients positive for anti-HTLV-III. The resources devoted to counselling and laboratory support in centres treating people at risk and their families need to be urgently reassessed.

In a double blind, randomised trial, the effects of 1 g aspirin and 1 g paracetamol were compared on bleeding time and platelet aggregation in 40 volunteers (20 females). Also investigated was the relationship between plasma aspirin esterase activity and both bleeding time and platelet aggregation after aspirin. Following 1 g aspirin there was a significant increase in bleeding time at 24 h (p<0.01). A significant reduction (P<0.01) in platelet aggregation with collagen was observed at 1, 6 and 24 h after aspirin, but no significant reduction (P>0.05) was observed with ADP. Paracetamol had no effect on bleeding time or platelet aggregation. Plasma aspirin esterase activity ranged from 0.26–0.6 µmol/ml/min. A significant negative correlation (R=−0.55, P<0.001) was observed between percentage increase in bleeding time (24 h) and plasma aspirin esterase activity. Further significant correlations were observed between plasma aspirin esterase activity and change in platelet aggregation with collagen at 1 h (R=0.68, P<0.001), 6 h (R=−0.73, P<0.001) and 24 h (R=−0.67, P<0.001). These results suggest that it might be possible to predict an individual's haemostatic response to aspirin from knowledge of their plasma aspirin esterase activity.

The effect of 1 mg of intravenous glucagon on platelet aggregation has been investigated in 12 normal subjects pre-treated with salicylate. All subjects demonstrated the expected inhibition of collagen-induced secondary aggregation but retained the normal adenosine diphosphate (ADP)-induced primary aggregation phase 18 h after the salicylate therapy (600-1,200 mg). Subsequent administration of glucagon caused a significant increase in the ADP-induced primary aggregation phase in the 12 subjects. This data indicates that glucagon increases the reactivity of platelets to ADP and may help to explain the common clinical association of raised plasma glucagon, increased platelet aggregation and vascular disease.

SummaryThis study was undertaken to investigate the effect of various forms of hormone replacement therapy (HRT) upon postmenopausal women while controlling as many variables as possible. It was felt that the age, duration of amenorrhoea and the general health of the patients should be as comparable as possible and that each patient should provide her own pretherapy and posttherapy control data. In addition, it was felt that any placebo effect should be investigated and the patients were therefore randomly allocated to placebo tablets or one of six available forms of HRT. The age/sex registers of two large general practices were scrutinized and all women between 49 and 54 years of age were asked to cooperate; for a variety of reasons only 56 women were suitable and willing to take part in the project, yielding 8 women for each of the seven possible therapy groups. Blood samples were taken at 7‐day intervals three times before therapy was given and the mean of the three values was used as the control value. The women returned on day 21 of each subsequent therapy cycle for six consecutive months and finally three months after discontinuing therapy. From the data the following broad conclusions can be drawn: (i) some women have classic symptoms of hot flushes and sweating despite high endogenous oestrogen concentrations; (ii) vaginal cytology is a relatively poor indicator of endogenous oestrogen status; (iii) while follicle stimulating hormone (FSH) and luteinizing hormone (LH) concentrations are reduced on HRT neither is decreased to anywhere near premenopausal values while prolactin is unaffected; (iv) plasma cholesterol levels are reduced on HRT, the pulse rate is slower and both systolic and diastolic blood pressure are reduced to a small but significant extent; (v) there is no adverse effect upon blood clotting; and (vi) most women experience significant or complete relief of symptoms on all forms of HRT as do some women taking a placebo. The combined preparations containing an oestrogen and progestogen produced vaginal bleeding in only 80 per cent of the women. Thus protection by regular endometrical shedding may not be afforded to all women. As vaginal bleeding is unacceptable to most women if they can achieve the same symptomatic relief without inducing menstruation, it is suggested that women have a low dose oestrogen preparation prescribed cyclically for 6 to 12 months. If therapy is to be maintained for a longer time, uterine curretage should be undertaken at regular intervals to exclude the possibility of endometrial carcinoma developing.

Changes in coagulation tests (fibrin/ fibrinogen degradation products, factor-VIII activity, and platelet-count) and in renal function (creatinine clearance and serum concentration, clearance, and fractional reabsorption of urate) were measured in late pregnancy. 10 patients with severe pre-eclampsia showed changes in both coagulation and renal function when compared with 13 normotensive controls. 18 patients with mild pre-eclampsia had changes in renal function only. Results from 5 patients with essential hypertension did not differ from those of the normotensive group. When results from the patients with severe pre-eclampsia were arranged in order of decreasing protein excretion, only renal-function tests correlated significantly with this ranking. It is suggested that, in the management of patients with established pre-eclampsia, assessment of renal function may be of greater practical value than measurement of the degree of coagulopathy.

SummaryThe technique of isoelectric focusing in polyacrylamide gel was used to investigate the protein patterns of amniotic fluid obtained from women with rhesus isoimmunization. There were no specific changes in protein pattern which could be related to the severity of haemolytic disease. Qualitative changes in the electrophoretic mobility of transferrin were demonstrated. Serial investigations showed that these changes were related to gestational age and were probably a feature of normal pregnancy. The phenomenon appears to be due to alteration in the sialic acid content of the transferrin, presumably the result of alteration in neuraminidase activity.

The relation between maternal and cord blood folate activity was investigated in a group of 110 primigravidae and their infants. Approximately half of these mothers had received folic acid supplements during their pregnancy, and the effects of this on infant blood folate levels at birth and at 6 weeks were also studied. In unsupplemented pregnancies there was a significant relation between infant and maternal blood folate levels at delivery. The results of folic acid supplementation during pregnancy were reflected by higher cord blood values, but 6 weeks after delivery infant plasma folate levels were essentially the same in both groups and independent of maternal supplies before delivery.

Two series of cases of Rh isoimmunization were subjected to liquor examination for bilirubin and protein level. Series 1 comprised 298 cases for the years 1962 and 1963. Series 2 comprised 179 consecutive cases for 1967 in which preliminary selection for liquor examination had been made on the basis of previous history and maternal antibody titre.Bilirubin was measured as the liquor bilirubin ratio, and protein levels were estimated in series 1 by the Folin and Ciocalteau technique and in series 2 by a modified biuret method.Correlations with severity of haemolytic disease in the foetus was made, taking into account the stage of gestation of liquor examination. Both bilirubin and protein levels correlate with severity, but bilirubin is superior to protein. Interrelation of these measurements as bilirubin/protein ratio was inferior to bilirubin level as a method of forecasting severity.

Comparison of Chemical and Spectrophotometric Methods of Estimating Bilirubin in Amniotic Fluid Get access A. McNay, B.Sc, A. McNay, B.Sc Department of Child Health, University of Newcaslle-upon-Tyne, Newcastle-upon-Tyne, 1, England Search for other works by this author on: Oxford Academic Google Scholar A. Oxley, F.I.M.L.T., A. Oxley, F.I.M.L.T. Department of Child Health, University of Newcaslle-upon-Tyne, Newcastle-upon-Tyne, 1, England Search for other works by this author on: Oxford Academic Google Scholar W. Walker, M.D. W. Walker, M.D. Department of Child Health, University of Newcaslle-upon-Tyne, Newcastle-upon-Tyne, 1, England Search for other works by this author on: Oxford Academic Google Scholar American Journal of Clinical Pathology, Volume 50, Issue 1_ts, July 1968, Pages 122–125, https://doi.org/10.1093/ajcp/50.1_ts.122 Published: 01 July 1968 Article history Received: 21 August 1967 Published: 01 July 1968