Blood folate and vitamin B12: United States, 1988-94.
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OBJECTIVES: This report presents national estimates of serum and red blood cell (RBC) folate and serum vitamin B12 distributions for persons 4 years and over, by sociodemographic variables. METHODS: The third National Health and Nutrition Examination Survey (NHANES III) (1988-94), provides information on the health and nutritional status of the civilian noninstitutionalized U.S. population. The analytic sample included 23,378 participants with serum folate data, 23,082 with RBC folate data, and 11,851 with serum vitamin B12 data. RESULTS: The mean serum and RBC folate concentrations are 7.2 and 196 nanograms per milliliter (ng/mL), respectively, and the mean serum vitamin B12 concentration is 518 picograms per milliliter (pg/mL). Non-Hispanic white people have higher mean serum and RBC folate concentrations than non-Hispanic black or Mexican American people. Serum vitamin B12 concentrations are lowest for older adults, and non-Hispanic black people have higher serum B12 concentrations than non-Hispanic white individuals. Only approximately 3 percent of the population has a serum B12 concentration less than 200 pg/mL. CONCLUSIONS: Inadequate folate status may be more prevalent among non-Hispanic black and Mexican American people. Data also suggest a modest prevalence of low serum B12 concentrations. Future assessments of folate and vitamin B12 status will be important to evaluate the impact of a recently enacted fortification policy. (+info)
Identification of the Plasmodium chabaudi homologue of merozoite surface proteins 4 and 5 of Plasmodium falciparum.
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Previous studies of Plasmodium falciparum have identified a region of chromosome 2 in which are clustered three genes for glycosylphosphatidylinositol (GPI)-anchored merozoite surface proteins, MSP2, MSP5, and MSP4, arranged in tandem. MSP4 and MSP5 both encode proteins 272 residues long that contain hydrophobic signal sequences, GPI attachment signals, and a single epidermal growth factor (EGF)-like domain at their carboxyl termini. Nevertheless, the remainder of their protein coding regions are quite dissimilar. The locations and similar structural features of these genes suggest that they have arisen from a gene duplication event. Here we describe the identification of the syntenic region of the genome in the murine malaria parasite, Plasmodium chabaudi adami DS. Only one open reading frame is present in this region, and it encodes a protein with structural features reminiscent of both MSP4 and MSP5, including a single EGF-like domain. Accordingly, the gene has been designated PcMSP4/5. The homologue of the P. falciparum MSP2 gene could not be found in P. chabaudi; however, the amino terminus of the PcMSP4/5 protein shows similarity to that of MSP2. The PcMSP4/5 gene encodes a protein with an apparent molecular mass of 36 kDa, and this protein is detected in mature stages of the parasite. The protein partitions in the detergent-enriched phase after Triton X-114 fractionation and is localized to the surfaces of trophozoites and developing and free merozoites. The PcMSP4/5 gene is transcribed in both ring and trophozoite stages but appears to be spliced in a stage-specific manner such that the central intron is spliced from the mRNA in the parasitic stage in which the protein is expressed. (+info)
Green fluorescent protein as a marker in Plasmodium berghei transformation.
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We present a new marker that confers both resistance to pyrimethamine and green fluorescent protein-based fluorescence on the malarial parasite Plasmodium berghei. A single copy of the cassette integrated into the genome is sufficient to direct fluorescence in parasites throughout the life cycle, in both its mosquito and vertebrate hosts. Erythrocyte stages of the parasite that express the marker can be sorted from control parasites by flow cytometry. Pyrimethamine pressure is not necessary for maintaining the cassette in transformed parasites during their sporogonic cycle in mosquitoes, including when it is borne by a plasmid. This tool should thus prove useful in molecular studies of P. berghei, both for generating parasite variants and monitoring their behavior. (+info)
Effect of breed (Angus vs Simmental) on immune function and response to a disease challenge in stressed steers and preweaned calves.
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Two experiments were conducted with feeder steer calves and preweaned calves to determine the effects of breed on immune response. In Exp. 1, newly weaned Angus (n = 24) and Simmental (n = 24) steer calves were blocked by weight within breed and randomly assigned to 12 pens with four calves per pen. The basal diet consisted of 87% corn silage (DM basis) and 13% of a soybean meal-mineral-vitamin supplement. Steers were allowed ad libitum access to feed throughout the study. On d 2 following weaning, calves received an intranasal inoculation of infectious bovine rhinotraecheitis virus (IBRV; 2.7 x 10(8) CCID50). Rectal temperatures in response to the IBRV were higher (P < .05) in Angus calves. On d 9, calves were injected i.m. with 10 mL of a 25% pig red blood cell (PRBC) suspension. Total immunoglobulin (Ig) and IgM titers against PRBC were higher (P < .05) for the Angus calves. Breed did affect cell-mediated immune response to phytohemagglutinin (PHA). In Exp. 2, preweaned (16 Angus and 16 Simmental) calves were selected based on breed, body weight, and sex. On 0 d, all selected calves were injected i.m. with 10 mL of a 25% PRBC suspension. Total Ig and IgG titers against PRBC were higher (P < .05) for Angus calves. On d 28, lymphocytes were isolated from peripheral blood obtained from eight calves per breed. Peripheral lymphocytes from the Angus calves had a greater (P < .07) blastogenic response to 6.25 microg/mL of PHA than lymphocytes from Simmental calves. Results indicate that the immune response of Angus and Simmental calves may differ. (+info)
Increased erythrocyte 3-DG and AGEs in diabetic hemodialysis patients: role of the polyol pathway.
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BACKGROUND: 3-Deoxyglucosone (3-DG) accumulating in uremic serum plays an important role in the formation of advanced glycation end products (AGEs). To determine if 3-DG is involved in the formation of intracellular AGEs, we measured the erythrocyte levels of 3-DG and AGEs such as imidazolone and N epsilon-carboxymethyllysine (CML) in hemodialysis (HD) patients with diabetes. Further, to determine if the polyol pathway is involved in the formation of erythrocyte 3-DG and AGEs, an aldose reductase inhibitor (ARI) was administered to these patients. METHODS: The erythrocyte levels of sorbitol, 3-DG, imidazolone, and CML were measured in ten diabetic HD patients before and after treatment with ARI (epalrestat) for eight weeks, and were compared with those in eleven healthy subjects. 3-DG was incubated in vitro with hemoglobin for two weeks to determine if imidazolone and CML are formed by reacting 3-DG with hemoglobin. RESULTS: The erythrocyte levels of sorbitol, 3-DG, imidazolone, and CML were significantly elevated in diabetic HD patients as compared with healthy subjects. The erythrocyte levels of 3-DG significantly decreased after HD, but sorbitol, imidazolone or CML did not. The administration of ARI significantly decreased the erythrocyte levels of sorbitol, 3-DG and imidazolone, and tended to decrease the CML level. Imidazolone was rapidly produced in vitro by incubating 3-DG with hemoglobin, and CML was also produced, but less markedly as compared with imidazolone. CONCLUSION: The erythrocyte levels of 3-DG and AGEs are elevated in diabetic HD patients. The administration of ARI reduces the erythrocyte levels of 3-DG and AGEs, especially imidazolone, as well as sorbitol. Thus, 3-DG and AGEs, especially imidazolone, in the erythrocytes are produced mainly via the polyol pathway. ARI may prevent diabetic and uremic complications associated with AGEs. (+info)
Red cell distribution and the recruitment of pulmonary diffusing capacity.
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The distribution of red blood cells in alveolar capillaries is typically nonuniform, as shown by intravital microscopy and in alveolar tissue fixed in situ. To determine the effects of red cell distribution on pulmonary diffusive gas transport, we computed the uptake of CO across a two-dimensional geometric capillary model containing a variable number of red blood cells. Red blood cells are spaced uniformly, randomly, or clustered without overlap within the capillary. Total CO diffusing capacity (DLCO) and membrane diffusing capacity (DmCO) are calculated by a finite-element method. Results show that distribution of red blood cells at a fixed hematocrit greatly affects capillary CO uptake. At any given average capillary red cell density, the uniform distribution of red blood cells yields the highest DmCO and DLCO, whereas the clustered distribution yields the lowest values. Random nonuniform distribution of red blood cells within a single capillary segment reduces diffusive CO uptake by up to 30%. Nonuniform distribution of red blood cells among separate capillary segments can reduce diffusive CO uptake by >50%. This analysis demonstrates that pulmonary microvascular recruitment for gas exchange does not depend solely on the number of patent capillaries or the hematocrit; simple redistribution of red blood cells within capillaries can potentially account for 50% of the observed physiological recruitment of DLCO from rest to exercise. (+info)
cGMP and cAMP cause pulmonary vasoconstriction in the presence of hemolysate.
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We recently reported that addition of a small amount of hemolysate to the salt solution that perfused isolated rat lungs hypersensitized the vasculature to subsequent additions of ANG II or exposure to hypoxia, and addition of NO gas (. NO) to the perfusate that contained hemolysate caused a strong vasoconstrictor rather than a vasodilator response. In the present study, we demonstrate that CO and the secondary messengers cGMP and cAMP (usually associated with vasodilation) exert similar effects in hemolysate-perfused lungs. Analogs of the cyclic nucleotides cGMP or cAMP (8-bromo-cGMP and dibutyryl-cAMP, respectively) caused profound vasoconstriction in the isolated rat lung perfused with a salt solution that contained hemolysate. The cGMP- or cAMP-analog-induced vasoconstriction was inhibited by chemically dissimilar Ca2+ antagonists, by the protein phosphatase inhibitor okadaic acid, and, to a lesser degree, by protein kinase inhibitor H-7. Antiphosphothreonine immunoblotting demonstrated that lungs perfused with hemolysate exhibit increased phosphorylation of several proteins. These data indicate that, in the presence of hemolysate, pulmonary vasculature responds to nominally vasodilatory stimuli, including analogs of cGMP and cAMP, with vasoconstriction rather than vasodilation. The importance of our finding is the paradoxical nature of the response to (analogs of) cyclic nucleotides because, to our knowledge, cyclic nucleotide-induced vasoconstriction has not been previously reported. (+info)
Elevated levels of circulating procoagulant microparticles in patients with paroxysmal nocturnal hemoglobinuria and aplastic anemia.
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Paroxysmal nocturnal hemoglobinuria (PNH), frequently occurring during suppressed hematopoiesis including aplastic anemia (AA), is a clonal disorder associated with an increased incidence of thrombotic events. Complement-mediated hemolysis, impairment of the fibrinolytic system, or platelet activation are thought to be responsible for the associated thrombotic risk. We investigated here the elevation of membrane-derived procoagulant microparticles in the blood flow of such patients. Elevated levels of circulating microparticles were in fact detected in both de novo PNH patients and AA subjects with a PNH clone, but not in those with AA without a PNH clone. The cellular origin of the microparticles was determined in PNH samples; most stemmed from platelets. Glycophorin A+ particles were rarely detected. Therefore, platelet activation, resulting in the dissemination of procoagulant phospholipids in the blood flow, could be one of the main causes for the elevated thrombotic risk associated with PNH. These observations suggest that shed membrane particles can be considered a valuable biological parameter for the assessment of possible thrombotic complications in patients with PNH. (+info)