Blood types of the native Americans of Oklahoma

Large numbers of Indians from Oklahoma were screened for a variety of red cell antigens. Sufficient numbers of Cherokees, Creeks, and Choctaws were studied to calculate gene frequencies. These tribes originated in the Southeastern United States and were forcibly moved to Oklahoma. The Creeks and Choctaws have not been studied previously. A small number of Cherokees remained in North Carolina, and their blood types have been reported. The blood types of the Oklahoma Cherokees are quite similar to those observed there but one important difference was discovered. The data previously reported concerning the Eastern Cherokees revealed the absence of the Dia antigen. The present study found that the Oklahoma Cherokees do have the Dia antigen, although in a lower percentage than the other southeastern tribes. The Creeks and Choctaws share a linguistic heritage as well as having similar red cell phenotypes.     

Estimations of the joint distribution of failure time and failure type with dependent truncation

In biomedical studies involving survival data, the observation of failure times is sometimes accompanied by a variable which describes the type of failure event (Kalbeisch and Prentice, 2002). This paper considers two specific challenges which are encountered in the joint analysis of failure time and failure type. First, because the observation of failure times is subject to left truncation, the sampling bias extends to the failure type which is associated with the failure time. An analytical challenge is to deal with such sampling bias. Second, in case that the joint distribution of failure time and failure type is allowed to have a temporal trend, it is of interest to estimate the joint distribution of failure time and failure type nonparametrically. This paper develops statistical approaches to address these two analytical challenges on the basis of prevalent survival data. The proposed approaches are examined through simulation studies and illustrated by using a real data set.     

Characterization of B and H blood-group active glycosphingolipids from human B erythrocyte membranes

Two blood group B active glycosphingolipids (B-I and B-II) previously isolated and highly purified from human B erythrocytes [21] were analysed first by degradation with α-D-galactosidase from coffee beans, α-L-fucosidase from bovine kidney and with 0,1 N trichloracetic acid; the native B-glycolipids as well as their degradation products were then investigated by methylation analysis with combined gas chromatography-mass spectrometry, by thin layer chromatography, twodimensional immunodiffusion and by the hemagglutination inhibition technique. Together with the results obtained by mass spectrometry of permethylated glycolipids [26] the following structures were elucidated: α-D-galactopyranosyl-(1 → 3)-[α-L-fucopyranosyl-(1 → 2)]-D-galactopyranosyl-(1 → 4)-N-acetyl-D-glucosaminosyl-(1 → 3)-D-galactopyranosyl-(1 → 4)-D-glucopyranosyl-(1 → 1)-ceramide for the B-I glycosphingolipid and α-D-galactopyranosyl-(1 → 3)-[α-L-fucopyranosyl-(1 → 2)]-D-galactopyranosyl-(1 → 4)-N-acetyl-D-glucosaminosyl-(1 → 3)-D-galactopyranosyl-(1 → 4)-N-acetyl-D-glucosaminosyl-(1 → 3)-D-galactopyranosyl-(1 → 4)-D-glucopyranosyl-(1 → 1)-ceramide for the B-II glycosphingolipid. A H active glycolipid fraction from B erythrocytes further purified by thin layer chromatography was also investigated by methylation analysis. The pattern of its partially methylated alditol acetates was essentially the same as that of the α-galactosidase treated and permethylated B-I glycolipid. It also exhibited strongly precipitating and hemagglutination inhibiting H properties as well as the two α-galactosidase treated B-I and B-II glycosphingolipids. Based upon these data the following tentative structure was proposed: α-L-fucopyranosyl-(1 → 2)-D-galactopyranosyl-(1 → 4)-N-acetyl-D-glucosaminosyl-(1 → 3)-D-galactopyranosyl-(1 → 4)-D-glucopyranosyl-(1 → 1)-ceramide. Gas chromatographic analysis revealed sphingosine and lignoceric, nervonic and behenic acids to be the main components of the ceramide residues of the three glycosphingolipids. From the data presented the H active substance very probably can be regarded as the immediate precursor of the B-I glycosphingolipid from human B erythrocyte membranes.     

Penetration of 2,4,6-trinitrobenzenesulfonate into human erythrocytes: Consequences for studies on phospholipid asymmetry

The glutathione content of human erythrocytes rapidly diminishes when cells are exposed to 2,4,6-trinitrobenzenesulfonate (20 μmol/l cells) at 37°C. Even at 0°C a slow decrease in glutathione content is observed. The uptake of trinitrobenzenesulfonate by the cells is retarded by inhibitors of the inorganic anion exchange system, indicating that trinitrobenzenesulfonate enters the cells by this pathway.The disappearance of glutathione most probably results from the reaction: 2 GSH + trinitrobenzenesulfonate → GSSG + aminodinitrobenzenesulfonate The reaction of trinitrobenzenesulfonate with glutathione occurs prior to its covalent binding to amino groups of hemoglobin which makes this reaction a more sensitive method of detection of penetration of trinitrobenzenesulfonate into erythrocytes. Results of studies on the asymmetric distribution of phospholipids using trinitrobenzenesulfonate as the only probe should be reconsidered in the light of these new data.     

CHROMOSOMAL REPATTERNING AND LINKAGE GROUP CONSERVATION IN MOSQUITO KARYOTYPIC EVOLUTION

Chromosome number and morphology in mosquitoes is remarkably uniform: virtually all mosquitoes have a diploid chromosome number of six (2N = 6), and their chromosomes are invariably metacentric or submetacentric. Numerical changes obviously have not been important in mosquito chromosomal evolution, and because of the morphological similarity of their chromosomes, it appears that structural changes have played little or no role in mosquito karyotypic evolution. The goal of the present study was to identify the types and relative numbers of chromosomal changes in mosquito evolution and to extend the comparison where possible to the higher diptera. To do this, we compared the enzyme linkage maps of six species of Aedes to each other and to enzyme maps of seven other mosquito species and to Drosophila melanogaster. Our results indicate that Aedes chromosomes have been modified by inversions, most which were paracentric, and by translocations, most which were Robertsonian. Intrageneric comparison of Aedes enzyme maps also revealed groups of linked enzyme loci whose integrity has been maintained throughout Aedes evolution (conserved linkages/syntenies). Intergeneric comparisons of Aedes enzyme maps with those of species in the genera Culex, Anopheles, and Toxorhynchites disclosed conserved associations of enzyme loci between mosquito genera. These findings lead us to postulate that the ancestral mosquito karyotype consisted of six chromosomal elements which, other than being combined in different ways in various mosquito groups, have remained essentially intact during mosquito evolution. Furthermore, the identification of groups of linked enzyme loci common to mosquitoes and to D. melanogaster indicates that linkage group conservation may characterize the karyotypic evolution of all dipteran insects.     

Sexual dimorphism in scales of marbled flounder Pseudopleuronectes yokohamae (Pleuronectiformes: Pleuronectidae), with comments on the relevance to their spawning behaviour

Variation of scales on the blind side of Pseudopleuronectes yokohamae in relation to sex, maturity and body size was examined. Immature males often have cycloid scales, while mature males have mostly ctenoid scales. Large females also often have ctenoid scales (but with fewer spines compared with males), and small females have mostly cycloid scales. The number of spines (ctenii) on the blind‐side scale increases with body size in both sexes, indicating an ontogenetic change in scale morphology. As P. yokohamae spawn demersal eggs with males positioning themselves above the females on the ocular side, it is hypothesized that ctenoid scales on the blind side in mature males function for maintaining contact with females during spawning.     

Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: Role of Ca2+/calmodulin-activated protein kinase II

Nitric oxide synthase (NOS) may be uncoupled to produce superoxide rather than nitric oxide (NO) under pathological conditions such as diabetes mellitus and insulin resistance, leading to cardiac contractile anomalies. Nonetheless, the role of NOS uncoupling in insulin resistance-induced cardiac dysfunction remains elusive. Given that folic acid may produce beneficial effects for cardiac insufficiency partially through its NOS recoupling capacity, this study was designed to evaluate the effect of folic acid on insulin resistance-induced cardiac contractile dysfunction in a sucrose-induced insulin resistance model. Mice were fed a sucrose or starch diet for 8 weeks before administration of folic acid in drinking water for an additional 4 weeks. Cardiomyocyte contractile and Ca²⁺ transient properties were evaluated and myocardial function was assessed using echocardiography. Our results revealed whole body insulin resistance after sucrose feeding associated with diminished NO production, elevated peroxynitrite (ONOO⁻) levels, and impaired echocardiographic and cardiomyocyte function along with a leaky ryanodine receptor (RYR) and intracellular Ca²⁺ handling derangement. Western blot analysis showed that insulin resistance significantly promoted Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) phosphorylation, which might be responsible for the leaky RYR and cardiac mechanical dysfunction. NOS recoupling using folic acid reversed insulin resistance-induced changes in NO and ONOO⁻, CaMKII phosphorylation, and cardiac mechanical abnormalities. Taken together, these data demonstrated that treatment with folic acid may reverse cardiac contractile and intracellular Ca²⁺ anomalies through ablation of CaMKII phosphorylation and RYR Ca²⁺ leak.