Raman studies of A2MWO6 tungstate double perovskites.

The Raman spectra of seven A(2)MWO(6) tungstate double perovskites are analysed. Ba(2)MgWO(6) is a cubic double perovskite with Fm3[combining macron]m symmetry and its Raman spectrum contain three modes that can be assigned in a straightforward manner. A fourth mode, the asymmetric stretch of the [WO(6)](6-) octahedron, is too weak to be observed. The symmetry of Ba(2)CaWO(6) is lowered to tetragonal I4/m due to octahedral tilting, but the distortion is sufficiently subtle that the extra bands predicted to appear in the Raman spectrum are not observed. The remaining five compounds have additional octahedral tilts that lower the symmetry to monoclinic P2(1)/n. The further reduction of symmetry leads to the appearance of additional lattice modes involving translations of the A-site cations and librations of the octahedra. Comparing the Raman spectra of fourteen different A(2)MWO(6) tungstate double perovskites shows that the frequency of the symmetric stretch (ν(1)) of the [WO(6)](6-) octahedron is relatively low for cubic perovskites with tolerance factors greater than one due to underbonding of the tungsten and/or M cation. The frequency of this mode increases rapidly as the tolerance factor drops below one, before decreasing gradually as the octahedral tilting gets larger. The frequency of the oxygen bending mode (ν(5)) is shown to be dependent on the mass of the A-site cation due to coupling of the internal bending mode with external A-site cation translation modes.

Human immunodeficiency virus-1 and hepatitis C virus RNA among South African blood donors: estimation of residual transfusion risk and yield of nucleic acid testing.

BACKGROUND AND OBJECTIVES: South Africa is an endemic area for human immunodeficiency virus 1 (HIV-1) infection, which has an impact on the safety of the blood supply. We studied the presence of HIV-1 and hepatitis C virus (HCV) RNA, and recent HIV seroconversion, in blood donors in order to estimate transfusion risk and to determine whether nucleic acid testing (NAT) could effectively improve blood safety. MATERIALS AND METHODS: Unlinked samples collected in 1999 from 9077 HIV-low prevalence (LP) and 10,632 HIV-high prevalence (HP) donors were studied. Donor demographic information and serology results were collected prior to breaking the linkage. All samples were individually tested using a multiplex NAT assay for HIV-1 and HCV RNA. HIV antibody-positive samples were further tested using a 'detuned' (less sensitive) enzyme immunoassay (EIA) procedure to determine whether a donor had recently acquired infection. Data were used to estimate the residual transfusion risk and to project NAT yield. RESULTS: HIV was 45 times more prevalent in the HP- than in the LP donor group; and among the HP group, female donors had a significantly higher prevalence of HIV than male donors. All seven HIV-1 p24 antigen-positive samples in the study were also HIV NAT positive. Two HIV NAT-positive samples were anti-HIV negative; both of these samples were from HP donors. Assuming that 10% of the 900,000 annual donations in South Africa are from the HP group, we projected an annual NAT yield of 8.5 cases over the current screening of antibody and p24 antigen. However, if p24 antigen testing were to be eliminated, this number would be increased to 17 cases per year. Based on 'detuned' EIA results, the incidence rate for HIV infection was estimated at 1.29 and 51.12 per 10,000 per year for the LP and HP donor groups, respectively. Assuming a 15-day earlier detection by HIV NAT compared with antibody tests, these incidence rates project that NAT may intercept an additional 23 (95% confidence interval: 15-33) HIV-positive donations per year. For HCV, two viral RNA and antibody-positive samples (one from the LP group and one from the HP group) and no NAT yield cases were found in the study. CONCLUSIONS: Implementation of routine NAT blood screening would allow elimination of HIV-1 p24 antigen testing and improve the safety of the blood supply in South Africa. However, the cost-benefit ratio of introducing such an expensive technology in a country with a limited health budget will have to be carefully considered.

Worldwide ethnic distribution of the G protein beta3 subunit 825T allele and its association with obesity in Caucasian, Chinese, and Black African individuals.

Recently, it was demonstrated that one allele (825T) of the gene encoding the G protein beta3 subunit (GNB3) is associated with hypertension in Germans. This study investigates a possible association with obesity in young male Germans, Chinese, and black South Africans with low, intermediate, and high 825T allele frequencies, respectively. In each of these three distinct cohorts, the 825T allele frequency was increased significantly in overweight (body mass index [BMI] > or =25 kg/m2) and obese individuals (BMI >27 kg/m2) compared to those with normal weight. The 825T allele frequencies in these three BMI groups were, respectively, 29.5, 39.3, and 47.7% in Germans, 46.8, 53.9, and 58.6% in Chinese, and 83.1, 87.7, and 90.9% in South Africans. In each of these three distinct groups, the 825T allele was significantly associated with obesity with odds ratios between 2 and 3. More urban than rural black Africans were overweight despite similar 825T allele frequencies in both populations, which underscores the role of both genetic and environmental factors. BP values in young male whites increased significantly with increasing BMI values but were independent of the C825T polymorphism, suggesting that hypertension associated with the 825T allele could be a consequence of obesity. Genotyping of 5254 individuals from 55 native population samples from Africa, the Americas, Europe, Asia, Australia, and New Guinea demonstrated highest 825T allele frequencies in black Africans (82%) and intermediate values in east Asians (47%). It is anticipated that high frequencies of the 825T allele in Africans and Asians may contribute to an obesity and hypertension epidemic if Westernization of lifestyles continues.

Kinetics of indium-111-labelled platelets in HIV-infected patients with and without associated thrombocytopaenia.

Seven to 12% of HIV-infected patients have thrombocytopaenia. The pathophysiology of the thrombocytopaenia is not clear. It has been variously suggested that it may be caused by an increased peripheral platelet destruction, a defect in platelet production, or by a combination of these. The aim of the study was to elucidate the pathogenesis of HIV-associated thrombocytopaenia. We determined the mean platelet life span (MPLS) and calculated the turnover of autologous indium-111-labelled platelets in 17 HIV-positive patients, seven with thrombocytopaenia. The sites of sequestration of labelled platelets were quantified. The thrombocytopaenic patients had a very short MPLS (3.0+/-3.8 h) and a marked increase in platelet production (18.2+/-12.6x10(9)/l/h). The majority of these patients (5 of 7) had excessive sequestration of platelets in the spleen. Five of the patients with a normal blood platelet count had a shortened MPLS (109+/-23 h) and increased platelet turnover (3.8+/-1.2x10(9)/l/h), i.e. the increased peripheral platelet destruction was compensated for by increased platelet production. The other five patients with a normal platelet count had normal MPLS (195+/-11 h) and slightly increased platelet production (2.5+/-0.6x10(9)/l/h). We conclude that patients with HIV-associated thrombocytopaenia have increased peripheral platelet destruction. Platelet production is elevated but is insufficient to maintain a normal peripheral platelet count. In these patients platelets are predominantly sequestrated in the spleen. Patients with HIV infection and a normal blood platelet count may also have increased platelet production. This may be an early subclinical phase in the development of full-blown HIV-associated thrombocytopaenia.

GB virus C prevalence in blood donors and high risk groups for parenterally transmitted agents from Gauteng, South Africa.

The prevalence of GBV-C infection in voluntary blood donors and in groups at high risk for parenteral exposure to infectious agents was studied. The high risk groups included chronic renal failure patients on haemodialysis, renal transplant patients and haemophiliacs from Gauteng. The presence of GBV-C RNA in these populations was determined using reverse transcription polymerase chain reaction (RT-PCR) in the 5' non-coding region (NCR) of the virus. Of the blood donors, 11.1% (95% CI 7.6, 15.8) were positive, whereas 23.8% (95% CI 12.6, 40.2) of haemodialysis patients and 23.5% (95% CI 15.9, 33.3) of the haemophiliacs were infected with GBV-C. The highest proportion of infection was in the renal transplant patients, where 41.2% (95% CI 35.1, 47.7) were found to have circulating GBV-C RNA. Serological markers for hepatitis B (HBV) and hepatitis C viruses (HCV) were also measured as indicators of other hepatitis viruses with important parenteral transmission routes. Of the GBV-C positive blood donors, 3.6% were also HBsAg positive and none were positive for HCV. The GBV-C positive patients on haemodialysis were not positive for either HBsAg or antibodies to HCV, but had evidence of past infection with HBV since 40% were anti-HBc positive. The greatest proportion of HCV positives was in the haemophiliac group, 91.3%, none of these were HBsAg positive but 39.1% had anti-HBc. In the GBV-C positive renal transplant patients, 4% had HBsAg, 13.3% had anti-HBc and 2.1% had antibodies to HCV. This is the first report describing the prevalence of GBV-C in South African populations.

Percentage cure of cement cured through various thicknesses of Cerec porcelain.

Highly filled luting resins are recommended for bonding porcelain restorations to tooth structure. This in vitro investigation was undertaken to determine the degree of cure of a 82 per cent filled dual-curing luting resin, after it was cured through various thicknesses of Cerec Vita Mark II porcelain. Infrared, as well as micro-Raman spectroscopy were used to determine the degree of cure of the cement at different time intervals after mixing and exposure to the curing light. The results indicated that Cerec porcelain thicknesses greater than 3 mm adversely affected the degree of cure of the luting resin, even at 24 hours after mixing the cement.

Blood transfusion in South Africa.

Sixty years of development have transformed previously small collection centres into major regional transfusion services. These organisations collect and process nearly 900,000 units of blood annually from a donor base of some 500,000 individuals with a male to female ratio of 5:3. Three quarters of the donations are from a regular pool of largely white people. The latter has both a cultural and socio-economic component that needs redress to meet expanding requests. The range of products and quality of newer technologies, including those that are centered on aphereses are commensurate with first world standards. Quality control is universally monitored and registration falls under prevailing legislation. The future of these vitally important services will need to accommodate changing priorities in South Africa. Specific challenges are a greater commitment to primary health care, the rapidly rising incidence of HIV-positivity and centralisation of some facilities including plasma fractionation.

Sensitivity and specificity of standard and rapid HIV-antibody tests evaluated by seroconversion and non-seroconversion low-titre panels.

BACKGROUND AND OBJECTIVES: The aim of this study is to compare the relative sensitivity and specificity of commercial HIV-antibody assays using seroconversion, non-seroconversion panels, and negative blood donor samples. MATERIALS AND METHODS: We evaluated the sensitivity of five standard ELISA HIV-antibody assays: Vironostika HIV Uni-Form II, Abbott recombinant HIV-1/HIV-2 third-generation EIA, Biotest Anti-HIV-1/-2 recombinant, Recombigen HIV-1/ HIV-2 EIA and Wellcozyme HIV 1 + 2 (VK54/55), and three rapid screening tests, Capillus HIV-1/HIV-2, Abott Test Pack HIV-1/HIV-2 third-generation EIA, and Sensy-Test HIV 1/2. All tests were assessed using four panels of plasma samples obtained from individuals who were seroconverting and a low-titre HIV-antibody panel of samples. Specificity of the standard screening tests was determined on 3.500 HIV-antibody-negative blood donor samples. RESULTS: There was no statistically significant difference in sensitivity between the five standard ELISA tests. One of these tests was significantly less specific than the others. The standard ELISA tests detected all the low-titre HIV-antibody-positive samples. Two of the rapid screening tests were significantly less sensitive on the seroconversion panels and all three tests failed to detect at least one of the positive samples in the low-titre panel. CONCLUSIONS: The additional risk of using one or other of the standard ELISA tests under review of not detecting all HIV-positive units of blood is not statistically significant. Using some of the rapid screening tests will, however, add a significant additional risk. A rapid screening test should therefore be adopted only after careful consideration of the effect of a possible lack of sensitivity on the safety of the blood supply.

Influence of platelet membrane sialic acid and platelet-associated IgG on ageing and sequestration of blood platelets in baboons.

Platelets were isolated from blood of baboons and treated with neuraminidase to remove platelet membrane sialic acid, a process which artificially ages the platelets. The platelets were then labelled with 111In and their mean life span, in vivo distribution and sites of sequestration were measured. The effect of removal of sialic acid on the attachment of immunoglobulin to platelets were investigated and related to the sequestration of the platelets by the spleen, liver, and bone marrow. Removal of sialic acid by neuraminidase did not affect the aggregation of platelets by agonists in vitro, nor their sites of sequestration. The removal of 0.51 (median, range 0.01 to 2.10) nmol sialic acid/10(8) platelets shortened their life span by 75 h (median, range 0 to 132) h (n = 19, p < 0.001), and there was an exponential correlation between the shortening of the mean platelet life span and the amount of sialic acid removed. The increase in platelet-associated IgG was 0.112 (median, range 0.007 to 0.309) fg/platelet (n = 25, p < 0.001) after 0.79 (median, range 0.00 to 6.70) nmol sialic acid/10(8) platelets was removed (p < 0.001). There was an exponential correlation between the shortening of mean platelet life span after the removal of sialic acid and the increase in platelet-associated IgG. The results suggest that platelet membrane sialic acid influences ageing of circulating platelets, and that the loss of sialic acid may have exposed a senescent cell antigen that binds IgG on the platelet membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

The in vivo effect in humans of pyridoxal-5'-phosphate on platelet function and blood coagulation.

Vitamin B6 has an antithrombotic effect. This, based on the results of in vitro studies, has been attributed to an antiplatelet effect. We assessed the in vivo effect of vitamin B6 by measuring the effect of long-term administration of vitamin B6 on platelet function and blood coagulation. Vitamin B6 (pyridoxine hydrochloride), 100mg twice daily p.o. for fifteen days, was administered to 10 healthy volunteers. The bleeding time was measured before the first dose and 15 days after. A baseline value, the acute effect, chronic effect, and the acute-on-chronic effect of vitamin B6 was estimated by measuring platelet function. The following tests were performed: platelet aggregation induced by collagen, ADP and epinephrine; thromboxane A2 (TxA2)-production and prostacyclin inhibition of ADP-induced aggregation. The effects on the coagulation system were monitored by measuring: the prothrombin time, activated partial thromboplastin time and levels of coagulation factor. Vitamin B6 significantly prolonged the bleeding time from 4.1 +/- 1.1 minutes to 6.8 +/- 1.0 minutes (p = 0.0063). Aggregation of platelets with collagen was slightly but not significantly inhibited. Platelet aggregation induced with the agonists ADP or epinephrine was significantly inhibited by vitamin B6, and the platelets tended to aggregate at a slightly decreased rate. The mean TxA2-production was slightly, but not significantly, decreased. Vitamin B6 had no effect on the sensitivity of platelets to prostacyclin, or on the coagulation system. Our results indicate that the antithrombotic effects of vitamin B6 is limited to inhibition of platelet function; there was no measurable influence on coagulation. The results of this in vivo study are however such that clinical trials are warranted to further assess the efficacy of vitamin B6 as an antiplatelet drug.

The influence of platelet-graft interaction on platelet survival in patients with aortobifemoral Dacron grafts.

In patients with arterial grafts, platelet consumption may be due either to platelet interaction with the graft, and/or concomitant platelet consumption in the rest of the arterial tree. This hypothesis was tested by quantifying the kinetics and platelet-graft interaction of indium-111-labelled platelets with double velour Dacron grafts in 13 patients with arterial insufficiency ascribed to atherosclerosis. Mean platelet lifespan (MPLS), 149 +/- 46 hours, was significantly shorter (P = 0.001) than normal. Labelled platelets were transiently deposited onto the graft surfaces. Peak 111In deposition on the grafts, 1.33 +/- 1.02% of injected labelled platelets, was reached at 70 +/- 33 hours. Thereafter the graft-platelet radioactivity decreased in parallel with platelet radioactivity in the circulation. There was no statistical correlation between MPLS and the factors known to be associated with graft platelet deposition: graft size; peak graft radioactivity; and the time to attain peak graft radioactivity. It is therefore concluded that in patients with arterial disease requiring graft implantation, the observed increased platelet consumption cannot only be ascribed to the interaction of platelets with the graft. Concomitant atherosclerosis is probably the important modifier of platelet consumption. The significant contribution of this factor to the shortening of the MPLS should be taken into account when assessing, by measuring platelet lifespan, the thrombogenicity of grafts.

Blood platelet kinetics in normal subjects modelled by compartmental analysis.

The purpose of this study was to describe the function of platelets throughout their life span by expressing their in vivo distribution and kinetic behaviour in mathematical terms by using multicompartmental analysis. The distribution of indium-111 labelled platelets in five normal subjects was imaged and quantified with a scintillation camera image processing system. Serial blood samples were also obtained. The data were modelled using the SAAM (Simulation Analysis and Modelling) compartmental computer program. Five models were entertained to evaluate the role of platelets that were either functional or injured during collection and their interaction with the liver, spleen and vascular endothelium. Models were evaluated by comparing F values calculated from the least squares estimate obtained from each model. The Dornhorst function was used to describe the sequestration of platelets in the compartmental model. Results indicated that the data could not be satisfactorily simulated when compartments were included that simulated only functional and sequestered platelets (model 1). It was necessary to include compartments that simulated the kinetics of collection-injured platelets in the liver (model 2) and spleen (model 3). The model that simulated the interaction with the vascular endothelium (model 5) showed a visual but not significant improvement in the fitting of the observed data compared to model 3. The mean organ uptake and range indicated in parentheses were calculated at equilibrium. There were 20% (15%-27%) of the injected platelets in the spleen, 10% (8%-11%) in the liver and 70% (64%-75%) in the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Reference values for red cell survival times.

The first purpose of this investigation was to investigate in 35 young normal male subjects the use of the Dornhorst function and the weighted-mean method to calculate reference values for mean red cell survival time with and without correction for elution of 51Cr. We compared survival times calculated with the Dornhorst and weighted-mean methods with survival time estimated with linear or exponential models. Two methods to correct for elution of 51Cr from red cells were investigated. For the first method, correction factors were generated using the Dornhorst function fitted to mean survival curves obtained from the normal subjects. In the second method, the new Dornhorst rate constant method, the survival time, corrected for elution of 51Cr, was directly calculated from the experimental survival curve without applying correction factors. Correction for elution using the Dornhorst rate constant method was not successful and resulted in nonphysiologic values. The 95% confidence range of red cell survival time for reference subjects without correction for 51Cr elution was 37-74 days for the weighted-mean method and 37 to 73 days for the Dornhorst method. The 95% confidence range for normal subjects when the survival curves were corrected for elution was 47-179 days for the Dornhorst method and 58-161 days for the weighted-mean method. The poor results obtained with the Dornhorst rate constant method and the large 95% confidence range were due to the rapid and large variation in elution rate of 51Cr from red cells.