In three children with haemolytic uraemic syndrome (HUS), evidence of red cell polyagglutinability due to Thomsen Friedenreich antigen (T-antigen) exposure was demonstrated. This was suspected after difficulties in ABO typing and was confirmed using specific antisera. Further supportive evidence included elevation of plasma sialic acid, alteration in red cell surface charge and evidence of T-antigen exposure in the renal biopsy specimen of one patient. Although involvement of this antigen in the pathogenesis of HUS has been associated with a high mortality, all three children have made a complete recovery. With early recognition and subsequent avoidance of plasma products, prognosis of this condition may be improved.

Antigens, Tumor-Associated, Carbohydrate↗

PubMed1989

Immunologic therapy for hemolytic-uremic syndrome.

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Child↗

PubMed1989

Endothelial cell-stimulating angiogenesis factor in vitreous from extraretinal neovascularizations.

The presence of endothelial cell-stimulating angiogenic factor (ESAF) in diseased human vitreous humour has been established. The molecular mass and chromatographic behavior of this material and its property of activating procollagenase indicate it to be identical to the ESAF isolated from other sources. The biological activity of ESAF from human vitreous was demonstrated by its ability to induce positive responses in the rabbit corneal pocket, and in the chick chorioallantoic membrane and yolk sac membrane tests.

Angiogenesis Inducing Agents↗

PubMed1988

Pathogenesis of haemolytic uraemic syndrome.

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Bacterial Toxins↗

PubMed1988

Bovine and human pineal glands contain substantial quantities of endothelial cell stimulating angiogenic factor.

Using a quantitative assay the amount of a low Mr endothelial cell stimulating angiogenesis factor (ESAF) has been determined in human pineal glands and bovine brain, retina, pineal gland, liver and kidney. Pineal glands contain approximately ten times as much ESAF as the retina or grey and white matter from the cerebral cortex and a hundred times as much as highly vascular tissues such as liver and kidney. The relevance of these findings to the highly vascular nature of the pineal gland is discussed.

Angiogenesis Inducing Agents↗

PubMed1988

Hormonal modulation of guanyl nucleotide binding to rat luteal membranes.

Guanyl nucleotides are known to play a dual role in the activation of the adenylate cyclase system of the rat corpus luteum, being required for human choriogonadotropin (hCG) stimulation of the enzyme and modulating hCG binding to some hormone receptors. Current models of adenylate cyclase activation require that guanyl nucleotide binding be enhanced by hormones, and we have examined this binding in rat luteal membrane preparations known to contain guanyl nucleotide-modulated hCG receptors. [3H] Guanylyl-imidodiphosphate (GMPPnP), a nonhydrolyzable analog of guanosine triphosphate (GTP), was used to investigate binding to urea-washed, heavy rat luteal membranes. Binding was found to be linear, with respect to the amount of membranes added, in the range of 2-10 mg wet wt. tissue equivalents, and equilibrium was reached after a 30-min incubation at 30 degrees C. Analysis of equilibrium binding experiments gave a Ka of 1.2.10(7) +/- 0.9.10(7) M-1, with 460 +/- 430 fmol binding sites per mg tissue in the absence of hormone, Kinetic experiments showed an association rate constant of 2.6.10(5) +/- 0.5.10(5) M-1 min-1 and a dissociation rate constant of 1.8.10(-2) +/- 0.9.10(-2) min-1. In the presence of hCG, the Ka was unchanged; however, the number of binding sites increased by 50-120%. Competitive binding assays utilizing other nucleotides revealed that a hierarchy of GMPPnP = GTP greater than guanosine diphosphate (GDP) greater than inosine triphosphate (ITP) in displacing labeled GMPPnP. A similar hierarchy was also found for hCG-stimulated adenylate cyclase activity (GMPPnP = GTP greater than ITP) and for modulation of hCG binding (GMPPnP greater than GTP greater than ITP).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗

PubMed1988

Increased procollagenase activating angiogenic factor in the vitreous humour of oxygen treated kittens.

Previous studies have demonstrated an increase in a low molecular weight angiogenic factor (ESAF) present in the retinae of kittens with oxygen induced retinopathy. The present paper describes differences in the quantity of ESAF extracted from the vitreous humour of control and oxygen treated animals and proposes a mechanism for the induction of intravitreal neovascularisation.

Angiogenesis Inducing Agents↗

PubMed1988

Parathyroid hormone-independent regulation of 1,25(OH)2D in response to inhibition of bone resorption.

Both plasma level of 1,25-dihydroxyvitamin D [1,25(OH)2D] and intestinal Ca absorption increase after biphosphonate-induced inhibition of bone resorption. Parathyroid hormone (PTH) has been considered a key mediating element of this homeostatic response. In the present work, the role of PTH was assessed by studying the influence of 1-hydroxypentane-1,1-bisphosphonate (HPeBP) on vitamin D and Ca metabolism in both intact and thyroparathyroidectomized (TPTX) rats. In intact rats, HPeBP given at 0.1 mg P/kg body wt sc for 10 days strongly inhibited bone resorption without affecting bone formation. This effect was associated with a marked stimulation of intestinal Ca absorption and Ca balance. In this condition, HPeBP caused a marked rise in plasma 1.25(OH)2D without affecting the level of 25-hydroxyvitamin D. In TPTX rats, HPeBP given at same dose also inhibited bone resorption and enhanced plasma 1,25(OH)2D, intestinal Ca absorption and Ca balance. In summary, this study shows that bisphosphonates such as HPeBP with prevailing inhibitory activity on bone resorption induce a marked stimulation of both 1,25(OH)2D production and intestinal Ca absorption. This homeostatic response is not attenuated after PTH removal. Thus, as previously shown for the response to low Ca diet, PTH does not appear to be an essential mediating factor for stimulating 1,25(OH)2D production in response to an increase in bone mineral retention.

Animals↗

PubMed1988

Simplified quantification of urinary protein excretion in children.

The protein/creatinine ratio (Up/Uc) measured in 71 early morning urine samples (EMU) correlated closely with timed overnight urine (ONU) protein excretion rates (r = 0.96). The relationship was linear throughout the entire range of normal and abnormal protein excretion, an ONU rate of 1 mg/h/m2 body surface area being proportional to an EMU Up/Uc of 5 mg/mmol. Using the Coomassie Blue dye-binding method the upper limit of Up/Uc in 377 apparently healthy children and adolescents aged 3-19 years was shown to be 20 mg/mmol. Albumin/creatinine ratios (Ua/Uc) were also determined in the 377 healthy subjects, yielding a normal working upper limit of 3 mg/mmol. Although in normal individuals studied longitudinally the day-to-day variation of both Up/Uc and Ua/Uc was appreciable, all measurements remained within the cross-sectional normal range. While the determination of Ua/Uc has a role in the study of "microproteinuria", it is comparatively costly for routine use. The measurement of the EMU Up/Uc avoids errors and difficulties associated with timed urine collection, simplifies sample handling by the laboratory and is inexpensive. In clinical practice this is the method of choice for the quantification of proteinuria in patients with renal disease.

Adolescent↗

PubMed1988

Juvenile nephronophthisis with calcification of basal ganglia and pancreatic insufficiency.

Juvenile nephronophthisis is a major cause of progressive renal failure in children. Its manifestations are varied and protean. It is a multisystem syndrome, encompassing and overlapping related disorders. We treated a 4-year-old girl who presented with various manifestations of progressive renal failure characteristic of juvenile nephronophthisis, in addition to calcification of the basal ganglia and pancreatic lipomatosis, two associated conditions hitherto undescribed. It is hoped that further reports of other associated conditions may help to clarify further the nature of this complex syndrome.

Basal Ganglia Diseases↗

PubMed1987

Dilated cardiomyopathy associated with haemolytic uraemic syndrome.

In two children with the haemolytic uraemic syndrome dilated cardiomyopathy occurred in the absence of hypertension, or fluid or electrolyte disturbance. These cases presented with acute left ventricular failure. Echocardiography showed left ventricular dilatation and reduced contractility. There was also ventricular wall thickening, which persisted. Twelve other children with haemolytic uraemic syndrome had prospective echocardiography. Eleven of them showed no evidence of cardiomyopathy and in one transient dilatation and reduced contractility developed without clinical signs. Dilated cardiomyopathy is a rare but important extrarenal manifestation of the haemolytic uraemic syndrome and is best demonstrated by echocardiography.

Cardiomyopathy, Dilated↗

PubMed1987

Trends in physician availability in 10 urban areas from 1963 to 1980.

The overall growth in the physician supply has so dominated the public policy agenda that issues of physician distribution within urban areas have received little attention. In this study, we examined the changes in physician availability in the poverty and nonpoverty areas of 10 U.S. cities between 1963 and 1980. We found that the overall availability of patient care physicians increased in both poverty and nonpoverty areas, with greater growth in the nonpoverty areas. For office-based primary care physicians, however, there was a 45% decline in availability in the poverty areas and a 27% decline in the nonpoverty areas. We conclude that the overall increase in the physician supply may not adequately correct geographic and specialty maldistribution in urban areas. We suggest that special educational, service delivery, and financing strategies within urban areas continue to be needed to address problems of inequitable physician availability.

Adult↗

PubMed1986

Haemolytic-uraemic syndrome: clinical experience of an outbreak in the West Midlands.

In 1982-3, 35 children from the West Midlands developed the haemolytic-uraemic syndrome. This was a higher incidence than expected and included an epidemic localised to the Wolverhampton area in July 1983 which comprised 11 cases in two weeks. Twenty three children were treated with dialysis, of whom three died. Six patients developed chronic renal failure, four of them from Wolverhampton. Extrarenal manifestations included neurological sequelae in four, two of whom also developed insulin dependent diabetes mellitus and chronic renal failure. Cardiomyopathy occurred in one child, who also had chronic renal failure. The outcome of these 35 patients was not predictable from prognostic criteria derived from previous experience in Britain. This, together with the high prevalence of extrarenal disease and the geographical localisation of the 1983 outbreak, suggested an aetiological agent new to the region. Faeces from 10 patients were examined for verotoxin producing Escherichia coli, and positive strains of serotype O157.H7 were found in three patients during the Wolverhampton outbreak.

Child↗

PubMed1986

The effects of retinoid treatment and antiestrogens on the growth of T47D human breast cancer cells.

The ability of all-trans-retinoic acid, 13-cis-retinoic acid, the free acid of etretinate (RO 10-1670), the 'arotinoid' RO 13-6298 and its free acid RO 13-7410 to affect the growth of T47D human breast cancer cells in vitro was investigated. The growth of T47D cells was inhibited by all of the retinoids tested, with the arotinoids being up to 100 times more effective than all-trans-retinoic acid. The presence of cellular retinoic acid binding protein (cRABP) was indicated by the cellular uptake of [3H]all-trans-retinoic acid. Maximum binding was 460 fmol/micrograms DNA. All of the retinoids with a polar terminal free carboxyl group readily competed for the binding sites, but none of the retinoids competed for the estrogen or progesterone receptor. Co-treatment of the T47D cells with 0.1 microM all-trans-retinoic acid and either tamoxifen (1 microM) or hydroxytamoxifen (10 nM or 0.1 microM) produced an additive effect on growth inhibition. No such additive effect was observed when T47D cells were co-treated with arotinoids and antiestrogens. The results showed that the T47D cells can serve as a useful model in vitro to test the effects of the synthetic retinoids and antiestrogens on steroid receptor-positive human breast cancer.

Binding, Competitive↗