Subject(s)
Genetic Linkage , Hypertension/genetics , Lipoprotein Lipase/genetics , Microsatellite Repeats/genetics , Adult , Aged , Alleles , Blood Pressure/genetics , China , Chromosomes, Human, Pair 8/genetics , Female , Humans , Hypertension/physiopathology , Lod Score , Male , Middle Aged , Quantitative Trait LociABSTRACT
AIM: To study chemical characterization and immunological activities of an acidic polysaccharide, CHC-1, isolated and purified from the seeds of Cuscuta chinensis Lam. METHODS: Both chemical and spectral methods were used to investigate the chemical characterization of CHC-1. Effect of CHC-1 on the proliferation rates of T- and B-lymphocytes both in vivo and in vitro, and antibody production in vivo was measured at various concentrations of CHC-1. RESULTS: The molecular weight of CHC-1 was estimated to be more than 1.0 x 10(6). The analytical results of sugar components indicated that CHC-1 was composed of Rha, Ara, Gal, and GalA in a molar ratio of 0.8:1.0:1.5:0.3. Methylation analysis and 1H, 13C NMR further identified the linkages of the residues of CHC-1. CHC-1 0.1 g/L promoted remarkably the proliferation of T-cells and B-cells in vitro. CHC-1 25 mg/kg, 50 mg/kg caused an evident increase in spleen weight, lymphocyte proliferation, antibody production, etc. But its effect on IgG levels was not significant. CONCLUSION: CHC-1 is a highly branched heteropolysaccharide and possessed immune enhancement activities.
Subject(s)
B-Lymphocytes/cytology , Drugs, Chinese Herbal/chemistry , Plants, Medicinal/chemistry , Polysaccharides/pharmacology , T-Lymphocytes/cytology , Animals , Antibody Formation/drug effects , Cell Division/drug effects , Female , Magnoliopsida/chemistry , Mice , Mice, Inbred ICR , Molecular Weight , Polysaccharides/chemistry , Polysaccharides/isolation & purification , Random Allocation , Seeds/chemistryABSTRACT
Deoxygenation-induced cation fluxes in sickle cells were studied by measuring net cation movements in ouabain-treated cells. These deoxy cation fluxes were highly dependent on pH, showing inhibition at pH less than 7 and greater than 8 and a maximum at 7.4-7.5. Activation occurred at oxygen tensions around 40-50 torr and fluxes rose sharply as PO2 fell lower. Deoxy K efflux paralleled deoxy Na influx at pH values between 7 and 8, and at all oxygen tensions. Sickle cells were separated by density on Percol-Stractan gradients. Dense cells had lower deoxy cation fluxes of both Na and K than did lighter cell fractions, but in none of the fractionated populations did deoxy K efflux exceed deoxy Na influx. These data demonstrate that deoxy cation fluxes are activated at physiological pH and oxygen tensions and that there are no conditions of pH and PO2 and no cell populations in which cation fluxes induced by deoxygenation contribute directly to net cation loss in sickle cells. Chloride replacement (with nitrate) did not alter deoxy cation fluxes, and deoxy K efflux did not require the presence of external Na (tetramethylammonium replacement). Thus, deoxy cation fluxes do not have the characteristics of a cation-chloride cotransport or cation countertransport system.
