Anti-cardiolipin, anti-cardiolipin plus bovine, or human beta(2)glycoprotein-I and anti-human beta(2)glycoprotein-I antibodies in a healthy infant population

BACKGROUND: Pathogenic antiphospholipid antibodies studies are usually conducted on populations of adults. Studies involving normal children are scant. METHODS: Antibody reactivity against CL alone (true aCL), CL-complexed to bovine beta(2)GP-I (aCL-bovine beta(2)GP-I), or human (aCL-human beta(2)GP-I) beta(2)GP-I, or to phospholipid-free human beta(2)GP-I (anti-human beta(2)GP-I) was determined by ELISA in serum samples from 360 Mexican children ranging from 1 month through 8 years of age. RESULTS: Statistical analysis of variance and rankings of Kruskal-Wallis demonstrated no significant difference in all tested antibody activities between ages and genders of the study population. Values are presented as a percentile distribution included between 5 and 99, corresponding to the percentages of the studied population. Normal arbitrary units (AU) for IgG, IgA, and IgM true aCL that correspond to the 95 and 99 percentiles are as follows: 2.15 and 3.5; 2.35 and 5.0, and 3.15 and 4.5, respectively. IgG, IgA, and IgM aCL-bovine beta(2)GP-I activities are 2.6 and 5.0, 3.0 and 5.0, and 2.7 and 6.0 AU, respectively, while IgG activities of aCL-bovine and human beta(2)GP-I are 1.45 and 1.80, respectively. Normal values for IgG anti-human beta(2)GP-I are 1.85 AU. CONCLUSIONS: While elevated serum levels of antibodies to CL and/or beta(2)GP-I have been associated with thrombotic and hematologic manifestations, the majority of reports deal with adult populations. We report the cut-off values (in AU, international PL units, and international units for beta(2)GP-I) of the specific serologic response of true aCL, aCL-bovine beta(2)GP-I, aCL-human beta(2)GP-I, and anti-human beta(2)GP-I in healthy Mexican children.     

Molecular characterization of the vanE gene cluster in vancomycin-resistant Enterococcus faecalis N00-410 isolated in Canada

The vanE operon was characterized from Enterococcus faecalis N00-410 (MIC of vancomycin = 24 microg/ml). The organization of the vanE operon was identical to that of the vanC1 operon from Enterococcus gallinarum, with protein identities ranging from 46 to 63%. An open reading frame located downstream of the vanE operon showed significant homology to a number of integrase genes, all of which are located downstream of the chromosomal GMP synthase gene guaA.     

Differential sensitivity of four Lobaria lichens to copper in vitro

Treatment of Lobaria amplissima, Lobaria pulmonaria, Lobaria scrobiculata, and Lobaria virens with 0 to 500 microM CuSO4 for 0 to 120 min at 25.0 degrees C resulted in a time- and copper-concentration-dependent decrease in the thallus total potassium content and a release of K- from the thallus, indicating that copper damaged the cytoplasmic membrane of the fungal hyphae. Lobaria pulmonaria was the most sensitive species, L virens the most resistant to copper treatment. Lobaria amplissima and L. scrobiculata displayed intermediate sensitivity. Treatment with copper also resulted in a time-dependent increase in the thallus copper content. For all four Lobaria species, the thallus potassium content decreased linearly with increasing thallus copper content, suggesting that, as cupric ions bound to the thallus, they reach target sites in the membrane. Acetone extracts contained low concentrations of chlorophyll a, amino acids, polyols, and sugars, but detectable or considerable amounts of lichen substances, i.e.. constictic, norstictic, stictic, and usnic acids and scrobiculin. Titration of the extracts with copper and assay of free Cu2+ revealed the presence of copper-binding ligands, most probably corresponding to the lichen substances detected in the extracts. Acetone extracts of L. amplissima and L. virens bound small or very small amounts of Cu2+; binding was monophasic and probably involved scrobiculin. Acetone extracts of L. pulmonaria and L. scrobiculata bound high or intermediate amounts of copper; binding was polyphasic and probably involved the lichen acids detected in the extracts. It was concluded that, in the studied Lobaria species, acetone extracts containing lichen substances could bind, in vitro, considerable amounts of Cu2+, but this binding did not prevent membrane damage in the thallus. Several hypotheses are presented to explain these results.     

A critical role for a tyrosine residue in the cannabinoid receptors for ligand recognition

Previous mutation and modeling studies have identified an aromatic cluster in the transmembrane helix (TMH) 3-4-5 region as important for ligand binding at the CB(1) and CB(2) cannabinoid receptors. Through novel mixed mode Monte Carlo/Stochastic Dynamics (MC/SD) calculations, we tested the importance of aromaticity at position 5.39(275) in CB(1). MC/SD calculations were performed on wild-type (WT) CB(1) and two mutants, Y5.39(275)F and Y5.39(275)I. Results indicated that while the CB(1) Y5.39(275)F mutant is very similar to WT, the Y5.39(275)I mutant shows pronounced topology changes in the TMH 3-4-5 region. Site-directed mutagenesis studies of tyrosine 5.39 to phenylalanine (Y-->F) or isoleucine (Y-->I) in both CB(1) and CB(2) were performed to determine the functional role of this amino acid in each receptor subtype. HEK 293 cells transfected with mutant receptor cDNAs were evaluated in radioligand binding and cyclic AMP assays. The CB(1) mutant and WT receptors were also co-expressed with G-protein-coupled inwardly rectifying channels (GIRK1 and GIRK4) in Xenopus oocytes to assess functional coupling. The Y-->F mutation resulted in cannnabinoid receptors with subtle differences in WT binding and signal transduction. In contrast, the Y-->I mutations produced receptors that could not produce signal transduction or bind to multiple cannabinoid compounds. However, immunofluorescence data indicate that the Y-->I mutation was compartmentalized and expressed at a level similar to that of the WT cannabinoid receptor. These results underscore the importance of aromaticity at position CB(1) 5.39(275) and CB(2) 5.39(191) for ligand recognition in the cannabinoid receptors.     

The influence of cellular apoptotic capacity on N-nitrosodimethylamine- induced loss of heterozygosity mutations in human cells

The induction of loss of heterozygosity (LOH) by the environmental carcinogen N-nitrosodimethylamine (NDMA), and the factors that influence the recovery of LOH mutations were studied in two directly related human lymphoblastoid cell lines, AHH-1 (h2E1.v2) and MCL-5. Initially, the NDMA-induced mutation frequency at the heterozygous tk locus in AHH-1 cells was observed to be 5-fold higher in AHH-1 compared with MCL-5. Molecular analysis of NDMA-induced TK- mutants indicated that the induced mutant fraction attributable to small intragenic mutations was similar in both cell lines. However, the induced mutant fraction, because of LOH, was 18-fold greater in AHH-1. In addition, LOH mutations were more extensive among TK- mutants derived from AHH-1 cells. We hypothesized that the increased recovery of large LOH mutations in AHH-1 cells could be attributable to reduced apoptotic capacity, as it has been reported that AHH-1 cells carry a heterozygous mutation in the p53 locus, whereas MCL-5 cells are homozygous wild- type. Analysis of the kinetics of apoptosis showed that the apoptotic response of the AHH-1 cell line was diminished and delayed compared with MCL-5. Based on the analyses presented here, and several recent reports, it is suggested that the recovery of LOH mutations in p53 deficient cell lines is affected not only by abnormalities in cellular apoptotic response, but also involves a number of p53-mediated responses to DNA damage.      

Stent placement in coeliac and superior mesenteric arteries to restore vascular perfusion following aortic dissection

The main trunks of both coeliac and superior mesenteric arteries were sheared off the abdominal aorta by an anterior dissection that spared the renal arteries. Both vessels were cannulated and a Walstent inserted across the false lumen to restore normal coeliac and superior mesenteric perfusion. This produced a successful haemodynamic and angiographic result with improvement in the patient's clinical condition.     

Perinatal Mortality in Bahrain

A review of 583 perinatal deaths at the Ministry of Health hospitals in Bahrain, during the years 1985-1987 revealed a perinatal mortality rate of 19.6 per 1,000 total births. Lethal congenital malformations accounted for 145 (24.9%) deaths. Of the 438 normally formed infants there were 42.2% antepartum, 115 (26.3%) intrapartum and 138 (31.5%) early neonatal deaths; in 82.7% of cases the death was considered to be unavoidable. The population of Bahrain for 1986 according to the Central Statistics Organization (1) was 435,065, the majority of which was served by the Ministry of Health Maternity Service with approximately 10,000 deliveries per annum. The Ministry of Health provides maternity services through one main maternity hospital and 2 peripheral hospitals with consultant obstetric care. In addition to these, there are 3 maternity units run by midwives. High risk cases are usually delivered in the main hospital as there is a neonatal intensive care unit attached to it. The latter also acts as a referral centre for all sick babies in Bahrain. An analysis of the causes of perinatal deaths is an effective way of assessing the efficiency of maternity services. The objective of this study was to identify and improve the various factors influencing perinatal mortality in Bahrain.     

Subcutaneous fat necrosis or adipo necrosis in the newborn. Report of a case

A case of subcutaneous fat necrosis that occurred at Hospital e Maternidade S?o Luiz is described. A brief review of the literature is made and the authors verify that the risk group for fat necrosis is constituted by full-term newborns who experienced fetal distress. It is shown that hypercalcemia is frequently present in this condition and its symptomatology,etiology, and treatment are also discussed. Finally, the authors suggest the close follow up of these patients until 16 weeks of life to try to identify the laboratorial and clinical signs of hypercalcemia promptly.