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Biomedical subjects

S C Robson

Publications and source records attributed to S C Robson.

At least 127 records · Page 7Linked to original sources
PubMed1996

Hepatitis E in South Africa: evidence for sporadic spread and increased seroprevalence in rural areas.

Hepatitis E virus (HEV) is a major cause of non-A, non-B hepatitis in developing countries. Factors influencing sporadic spread of hepatitis E are unclear. We examined anti-HEV seroprevalence and demographic data from 407 urban and 360 rural black South African adults living in formal housing, squatter camps, or mud huts. Anti-HEV sero-prevalence ranged from 5.8% to 19.1% (mean 10.7%) in the different regions. Mean urban and rural rates were 6.6% and 15.3%, respectively (P = 0.0001). Rural mud hut dwellers, using unchlorinated river water, were at greater risk (17.4%) than rural villagers (5.3%; P = 0.008). A linear relation was found between seroprevalence and age, suggesting sporadic spread. The high prevalence in mud hut dwellers suggests that contaminated water plays a major role in HEV spread in South Africa. Routine chlorination or boiling of river drinking water before consumption may reduce HEV infection.

Adult↗
PubMed1996

Fetal hepatic necrosis following blood sampling from the intrahepatic vein.

Previous reports have suggested that fetal blood sampling from the intrahepatic vein is not associated with significant fetal hepatic injury. We report a case of fetal liver necrosis occurring 24 h following blood sampling from the intrahepatic vein of a fetus with severe growth retardation at 34 weeks. The placenta was in a posterior position, precluding either blood sampling from the placental insertion or placental biopsy. Fetal death occurred in utero within 24 h of the procedure, which was carried out by an experienced operator. At post-mortem the liver appeared normally formed, but the right lobe was diffusely congested, with a well-defined demarcation line between the right and left lobes. Liver histology revealed extensive recent haemorrhagic necrosis of the right lobe.

Adult↗
PubMed1996

Maternal uniparental disomy for chromosome 2 in association with confined placental mosaicism for trisomy 2 and severe intrauterine growth retardation.

We report a liveborn infant with severe intrauterine growth retardation and renal failure, delivered following detection of non-mosaic trisomy 2 by chorionic villus biopsy in the first trimester. Detailed analysis post-delivery indicated apparent complete trisomy 2 of the chorionic tissues, with a chromosomally normal infant demonstrating maternal uniparental disomy for chromosome 2.

Adult↗
PubMed1996

Delayed xenograft rejection.

Despite considerable progress in understanding the mechanisms of discordant xenograft rejection, and overcoming hyperacute rejection through targeting of complement or antibody, vascularized xenografts are typically rejected within days. Here, Fritz Bach and colleagues discuss the importance of endothelial cell activation, platelet aggregation and other aspects of thrombosis, as well as the contribution of host natural killer cell and monocyte activation in overcoming this next barrier to prolonged xenograft survival.

Animals↗
PubMed1996

Inhibition of T cell mitogenesis by a novel anti-CD45R monoclonal antibody.

CD45 consists of a major family of membrane glycoproteins which have protein tyrosine phosphatase activity and regulate early activation events, progression and maturation signals in leucocytes. Various isoforms of CD45 (Mr 180-240 kDa) regulate sets of intermolecular associations between different surface receptors, and appear to be differentially expressed on B and T cells (namely CD45RA, B or CD45RO). We describe a novel IgG2a mAb directed against restricted and unique CD45R modified epitopes expressed preferentially on peripheral blood T cells. This anti-CD45R antibody (I(2)4c) at concentrations of 50 and 200 ng/mL inhibited mitogenic T cell lectin and anti-CD3-stimulated lymphocyte proliferation and blocked associated IL-2 secretion in vitro. Phorbol ester-stimulated mitogenesis was unaltered suggesting that the inhibition occurs independent of protein kinase C-mediated pathways. Western blotting and immunoprecipitation of purified cell lysates reveals that I(2)4c preferentially binds the higher Mr bands of CD45 expressed on T cells. Following T cell activation in vitro, the 190 kDa band became more predominant and an additional 130 kDa protein, possibly a proteolytic fragment was recognized. I(2)4c may inhibit T cell mitogenesis by direct effects on CD45R alone or by preventing interaction with other membrane-associated proteins and hence adhesive interactions with monocytes. Such interactions may however inhibit the initiation of signal transduction and, as a consequence, alter cellular activation by mitogenic lectins and anti-CD3 in vitro.

Animals↗
PubMed1996

Superficial hand vein responses to NG-monomethyl-L-arginine in post-partum and non-pregnant women.

1. During human pregnancy marked vasodilatation occurs in arterial and venous vascular beds. The mechanisms responsible for this change remain unclear. The contribution of increased nitric oxide activity to vasodilatation associated with pregnancy was determined by examining superficial hand vein responses to NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthase, in post-partum women 24-48 h after delivery when vasodilatation remains at levels present during the third trimester. 2. Seventeen healthy women, 24-48 h post partum, and 13 healthy non-pregnant women were studied. Eight of the post-partum women underwent repeat studies 12-16 weeks after delivery. 3. NG-monomethyl-L-arginine (100 nmol/min) resulted in venoconstriction in non-constricted veins (baseline, 0%; 5 min, 26 +/- 9%; 10 min, 14 +/- 8%; 15 min, 8 +/- 7%; means +/- SEM) and noradrenaline-constricted veins (5 min, 30 +/- 7%; 10 min, 24 +/- 10%; 15 min, 14 +/- 11%). No constrictor response to NG-monomethyl-L-arginine was present in the same women 12 weeks post partum (5 min, 1 +/- 4%; 10 min, 0 +/- 3%; 15 min, 1 +/- 4%) or in the non-pregnant control subjects in non-constricted (5 min, 2 +/- 3%; 10 min, 4 +/- 3%; 15 min, 2 +/- 2%) or noradrenaline-constricted veins (5 min, -2 +/- 7%; 10 min, 1 +/- 9%; 15 min, -5 +/- 7%). 4. These findings indicate that nitric oxide activity is increased in the immediate post-partum period in venous vasculature, and support the hypothesis that increased nitric oxide activity may be responsible for the vasodilatation observed during normal pregnancy.

Adult↗
PubMed1996

Acute-phase response and the hypercoagulable state in pulmonary tuberculosis.

In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.

Acute-Phase Reaction↗
PubMed1996

Randomized trial of bolus phenylephrine or ephedrine for maintenance of arterial pressure during spinal anaesthesia for Caesarean section.

Thirty-eight healthy women undergoing elective Caesarean section under spinal anaesthesia at term were allocated randomly to receive boluses of either phenylephrine 100 micrograms or ephedrine 5 mg for maintenance of maternal arterial pressure. The indication for administration of vasopressor was a reduction in systolic pressure to < or = 90% of baseline values. Maternal arterial pressure (BP) and heart rate (HR) were measured every minute by automated oscillometry. Cardiac output (CO) was measured by cross-sectional and Doppler echocardiography before and after preloading with 1500 ml Ringer lactate solution and then every 2 min after administration of bupivacaine. Umbilical artery pulsatility index (PI) was measured using Doppler before and after spinal anaesthesia. The median (range) number of boluses of phenylephrine and ephedrine was similar; 6 (1-10) vs 4 (1-8) respectively. Maternal systolic BP and CO changes were similar in both groups, but the mean [95% CI] maximum percentage change in maternal HR was larger in the phenylephrine group (-28.5 [-24.2, -32.9]%) than in the ephedrine group (-14.4 [-10.6, -18.2]%). As a consequence atropine was required in 11/19 women in the phenylephrine group compared with 2/19 in the ephedrine group (P < 0.01). Mean umbilical artery pH [95% CI] was higher in the phenylephrine group (7.29 [7.28-7.30]) than in the ephedrine group (7.27 [7.25-7.28]). The results of the present study support the use of phenylephrine for maintenance of maternal arterial pressure during spinal anaesthesia for elective Caesarean section.

Adult↗
PubMed1996

Fibronectin fragments cause an underestimation of plasma fibronectin levels in severe pre-eclampsia.

Elevated fibronectin (Fn) concentrations in plasma from pregnant women have been suggested to be predictive for the development of pre-eclampsia. However, reported correlations between Fn concentration with gestational age or disease severity appear to be confounded by several variables. Our finding of degradation products of Fn in plasma from patients with severe pre-eclampsia led to a study of whether their presence could influence immunological and functional measurements of intact plasma Fn. Plasma samples (10 control pregnant and 10 severe pre-eclampsia patients) were studied for the presence of intact Fn and fragments by SDS-PAGE and Western blotting. Percentages of immunoreactive Fn fragmentation in control plasma (9.37 +/- 6.7%) and severe pre-eclampsia plasma (62.57 +/- 7.0%) were determined by densitometric scanning. Immunoassays by ELISA were performed on normal plasma samples and on purified Fn in the absence or presence of plasma digests of pure Fn. Artefactual underestimations of Fn concentration occurred in the presence of Fn fragments. The percentage underestimation increased with increasing digestion times (1 h, 46.52 +/- 3.69%; 3 h, 77.5 +/- 7.18%; 4 h, 100%) and with increasing concentrations of Fn digest products (1h) added to normal plasma samples (n = 10) (40 micrograms, 23 +/- 8.1%; 125 micrograms, 36.33 +/- 5.1%; 250 micrograms, 43.66 +/- 6.5%). The underestimation of Fn concentration in the presence of Fn fragments suggests that ELISAs for Fn may be unreliable and thus lose their predictive value in these patients. Opsonic activities of control pregnant and severe pre-eclamptic plasma were determined by gelatin-latex agglutination assay. The ratios of opsonic activity to Fn concentration in plasma from patients with pre-eclampsia were significantly lower than those of control pregnant plasma samples (p < 0.008). The impaired gelatin-latex agglutination of Fn in pre-eclamptic plasma suggests that Fn fragmentation could have biological sequelae in vivo.

Blotting, Western↗
PubMed1996

Genetic engineering of endothelial cells to ameliorate xenograft rejection.

The prospect of clinical xenotransplantation using pigs as donors (a discordant combination) holds out a potential solution to the shortage of human organs, as well as potentially widening the spectrum of patients who might benefit from a transplant procedure. While generalized clinical trials of pig to human organ transplantation (of immediately vascularized organs, such as the heart or kidney) will probably not occur in the very near future, there are reasons for optimism that this approach, deemed impossible a few decades ago, may find its way to the bedside. This optimism is based on two factors: First, a great increase in our understanding of the probable underlying causes of rejection and, second, the development of a number of important therapeutic approaches, including genetic manipulation of the donor animal, to tackle the manifold problems inherent in rejection of such a transplanted organ.

Animals↗
PubMed1996

Loss of rat glomerular ATP diphosphohydrolase activity during reperfusion injury is associated with oxidative stress reactions.

Endothelial cell ATP diphosphohydrolases or ATPDases degrade extracellular inflammatory mediators ATP and ADP, thus inhibiting the formation of platelet thrombi, but the modulation of these ecto-enzymes during vascular injury remains largely undetermined. Renal glomerular ATPDase levels were determined in the rat following ischemia-reperfusion or systemic complement activation, by direct biochemical methods and histochemistry. Ischemia followed by reperfusion times over 30 min were associated with loss of glomerular ATPDase activity. Cobra Venom Factor (CVF) inhibited ATPDase activity and potentiated the deleterious effects of reperfusion. Treatment with either soluble complement receptor type 1 (sCR1), an inhibitor of complement activation, or antioxidants prior to the ischemia-reperfusion was largely protective. Expression of rat glomerular ATPDase activity appears susceptible to the inflammatory injury associated with systemic complement activation and ischemia/reperfusion processes. Oxidative stress could, at least in part, result in the loss of ATPDase activity and thus thrombotic consequences of vascular injury.

Adenosine Diphosphate↗
PubMed1995

Treatment of acute myocardial infarction with streptokinase does not appear to modulate circulating neutrophil function.

The administration of thrombolytic therapy is the most common method of achieving patency of the occluded coronary artery in patients with acute myocardial infarction (AMI). However, thrombolytic agents and the byproducts of fibrinolysis have the potential to affect neutrophil activation and thus function, thereby augmenting myocardial damage further. This study assessed the effect of streptokinase administration on the function of circulating neutrophils in patients with AMI. For this neutrophil adherence to human umbilical vein endothelial cells, homotypic neutrophil aggregation, and CD11b and L-selectin expression on the neutrophil membrane prior to and 1 h and 6 h after thrombolytic therapy was monitored. The study population included patients with AMI who received aspirin and streptokinase, and healthy laboratory workers who received aspirin only; all subjects acted as their own controls. Circulating fibrin degradation products and white cells were markedly raised following administration of streptokinase. No significant differences in neutrophil adherence to endothelium, homotypic neutrophil interactions, and CD11b or L-selectin expression were demonstrated between neutrophils, either pre- or post-thrombolytic therapy in the infarct group, or between neutrophils from the infarct group and from the control group. It was concluded that streptokinase produces an abrupt neutrophil leukocytosis together with a marked increase in circulating levels of fibrin degradation products. The assay systems used were unable to show significant sequential changes in circulating neutrophil adhesion and L-selectin or CD11b expression in patients with AMI following thrombolytic therapy or when these patients were compared with controls.

CD18 Antigens↗