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Yttrium-modified bismuth-layered ferroelectric SrBi2Ta2O9 (SBT) with general formula SrBi2-xY3x/4Ta2O9 (where x = 0.00, 0.025, 0.05, 0.075 and 0.10) are prepared by mixed oxide route. The structural, dielectric, ferroelectric and conductivity behavior of the above compounds for each composition of Y is discussed. The formation of monophase materials is noted from the X-ray diffraction pattern. The structure of the grains is studied using Scanning electron microscopy. The variation of the dielectric permittivity with temperature at some particular frequencies manifests a diffuse order phase transition with reduced Tc (ferroelectric transition temperature) and ϵr (relative permittivity) with respect to higher concentration of Y. The ferroelectric properties in the materials are confirmed using hysteresis (P-E) loops. The remnant polarization of the materials is found to increase with the addition of Y while the coercive field follows the reverse trend. [ABSTRACT FROM AUTHOR]

A new, simple, specific, rapid, precise, highly accurate, reproducible and cost effective Ultraviolet-Visible spectrophotometric method was developed and validated, according to the International Harmonization Guidelines, for the determination of naringenin from solid lipid nanoparticles. Absorption maximum of Naringenin was found to be at 287.49nm in methanol. The linearity range was found to be 5-25μg/mL with high correlation coefficient value of 0.999. The detection and quantification limits were found to be 0.1879μg/mL and 0.5694μg/mL, respectively. This method was shown to be specific, selective, precise at the intra-day (relative standard deviation less than 0.7046%) and inter-day (relative standard deviation less than 1.5424%) level and accurate with recoveries between 98.77-100.43% (relative standard deviation less than 0.3924%). Method robustness observation indicates that method was robust. The suitability of the method for naringenin quantifications was assessed by the determination of entrapment parameters and by studying the naringenin release profile from SLNs. High entrapment efficiency (91.922 ± 0.717%) and drug loading (3.506 ± 0.027%) were observed. Kinetic models (zero order, first order, Higuchi, Hixson-Crowell, Korsmeyer-Peppas and Baker-Lonsdale) were used to fit the obtained release profile and to predict the in vivo performance of naringenin-loaded SLNs. An anomalous non-Fickian transport was found, which indicate a controlled drug release system. [ABSTRACT FROM AUTHOR]

Uranyl nitrate inhibited root growth of Allium cepa at > or = 25 microM concentration. Fluorimetric analysis of metal uptake indicated the entry and accumulation of uranium into the root cell. Uranyl nitrate was neither clastogenic nor aneugenic as it failed to induce micronuclei significantly, but between 25 and 100 microM concentration, it increased significantly the frequency of sister chromatid exchange over that of control, implying its genotoxicity that possibly interfered with DNA replication and/or repair process.

The functional significance of naturally occurring variants of human hepatitis B virus (HBV) remains largely unknown. Previously, we reported an immature secretion phenotype caused by a highly frequent mutation at amino acid 97 of the HBV core (capsid) protein (HBcAg). This phenotype is characterized by a nonselective and excessive secretion of virions containing an immature genome of single-stranded viral DNA. To extend our study of virion secretion to other naturally occurring variants, we have characterized mutations at HBcAg codons 5, 38, and 60 via site-directed mutagenesis. Although the phenotype of the mutation at codon 38 is nearly identical to that for the wild-type virus, our study reveals that a single mutation at codon 5 or 60 exhibits a new extracellular phenotype with significantly reduced virion secretion yet maintains normal intracellular viral DNA replication. A complementation study indicates that the mutant core protein alone is sufficient for the "low-secretion" phenotype. Furthermore, the low-secretion phenotype of the codon 5 mutant appears to be induced by the loss of a parental proline residue, rather than by the gain of a new amino acid. Our study underscores the core protein as another crucial determinant in virion secretion, in addition to the known envelope proteins. Our present results suggest that a very precise structure of both alpha-helical and nonhelical loop regions of the entire HBcAg molecule is important for virion secretion. The low-secretion variants may contribute to the phenomenon of gradually decreasing viremia in chronic carriers during the late phase of persistent infection.

A very frequent missense mutation at codon 97 of human hepatitis B virus (HBV) core antigen (HBcAg) has been found in chronic carriers worldwide. Functional characterization of this mutant revealed one intracellular and two extracellular phenotypes in contrast to wild-type HBV: (i) a 6- to 12-fold decrease in the level of the full-length relaxed circular DNA, a 4- to 5-fold decrease in the plus-strand DNA, and an approximately 1.8-fold decrease in the minus-strand and overall DNA levels in the intracellular viral core particles; (ii) a 5.7-fold increase in the immature secretion of Dane particles, containing minus-strand, single-stranded virion DNA; and (iii) a significant reduction of nonenveloped core particles in the medium. The steady-state levels of mutant and wild-type core proteins expressed from the same vector appeared to be similar. Using a complementation assay and gradient centrifugation analysis, we demonstrated that this mutant core protein alone is necessary and sufficient for immature secretion. The decreased level of intracellular HBV DNA is caused by both the cis defect of the mutant genome and the trans defect of the mutant core protein. We have dissected further the relationship between the intracellular and extracellular phenotypes of mutant F97L. The pleiotropic effects of the HBcAg codon 97 mutation were observed consistently in several different experimental settings. The mechanism and biological significance of these findings are discussed.

The Vibrio cholerae rpoH gene coding for the heat-shock sigma factor, sigma 32, has been cloned and shown to functionally complement Escherichia coli rpoH mutants. The nt sequence of the gene has been determined and the deduced aa sequence is more than 80% homologous to the E. coli rpoH gene product. Downstream of the V. cholerae rpoH gene, an unidentified dehydrogenase gene (udhA) is present on the opposite strand facing rpoH. The predicted secondary structure of the 5'-proximal region of V. cholerae rpoH mRNA is apparently different from the conserved secondary structures of the rpoH mRNA reported for several bacterial species. The 'RpoH box', a stretch of 9 aa (QRKLFFNLR) unique to sigma 32 factors, and the 'downstream box' sequence complementary to a part of the 16S rRNA, have been detected.