Optical and dielectric properties of isothermally crystallized nano-KNbO(3) in Er(3+)-doped K(2)O-Nb(2)O(5)-SiO(2) glasses

Precursor glass of composition 25K(2)O-25Nb(2)O(5)-50SiO(2) (mol%) doped with Er(2)O(3) (0.5wt% in excess) was isothermally crystallized at 800 degrees C for 0-100h to obtain transparent KNbO(3) nanostructured glass-ceramics. XRD, FESEM, TEM, FTIRRS, dielectric constant, refractive index, absorption and fluorescence measurements were carried out to analyze the morphology, dielectric, structure and optical properties of the glass-ceramics. The crystallite size of KNbO(3) estimated from XRD and TEM is found to vary in the range 7-23 nm. A steep rise in the dielectric constant of glass-ceramics with heat-treatment time reveals the formation of ferroelectric nanocrystalline KNbO(3) phase. The measured visible photoluminescence spectra have exhibited green emission transitions of (2)H(11/2). (4)S(3/2) -> (4)I(15/2) upon ;excitation at 377 nm ((4)[(15/2) -> (4)G(11/2)) absorption band of Er(3+) ions. The near infrared (NIR) emission transition (4)[(13/2) -> 4[(15/2) is detected around 1550 nm on excitation at 980 mn ((4)[(15/2) -> 4 [(11/2)) of absorption bands of Er(3+) ions. It is observed that photoluminescent intensity at 526 nm ((2)H(11/2) -> (4)I(15/2)), 550nm (4S(3/2) -> (4)I(15/2)) and 1550nm ((4)I(13/2) -> (4)I(15/2)) initially decrease and then gradually increase with increase in heat-treatment time.'rhe measured lifetime (tau(f)) of the (4)I(13/2) -> (4)I(15/2) transition also possesses a similar trend. The measured absorption and fluorescence spectra reveal that the Er(3+) ions gradually enter into the KNbO(3) nanocrystals. (C) 2009 Elsevier B.V. All rights reserved

Structure and dielectric properties of potassium niobate nano glass-ceramics

Glasses in the composition of 25K(2)O-25Nb(2)O(5)-50SiO(2) (mol %) have been prepared by melt quenching technique and isothermally heat-treated at 800 A degrees C for different duration (0-200 h). The formed nanocrystalline KNbO(3) phase, crystallite size and morphology are examined by X-ray diffraction, Fourier transform infrared reflection spectroscopy, field emission scanning and transmission electron microscopes. The frequency and temperature dependent dielectric constant and loss tangent are measured in the frequency and temperature ranges 0.1-1000 kHz and 200-500 A degrees C respectively. The dielectric constant and loss tangent are found to decrease with increasing frequency and increase with increasing temperature. The dielectric constant and loss tangent versus temperature curve at different frequency revealed the phase transition of KNbO(3) from paraelectric cubic to ferroelectric tetragonal around 425 and 397 A degrees C (Curie temperature) for nano glass-ceramics obtained after 1 and 200 h heat-treatment respectively

Structure, dielectric and optical properties of transparent Nd(3+):KNbO(3) nanocrystalline glass-ceramics

Here, glass in the composition of 25K2O–25Nb2O5–50SiO2 (mol%) doped with Nd2O3 (0.5 wt.% in excess)was isothermally crystallized at 800 C for 1–100 h. Their structures, dielectric and optical properties were analyzed with the progress of nanocrystallization of Nd3+: KNbO3 by XRD, FESEM, TEM, FTIRRS, DC, optical absorption and fluorescence measurements. Crystallization of KNbO3 is confirmed from XRD and the appearance of 749 cm-1 band in the FTIRRS spectra. The crystallite size estimated from XRD and TEM is found to vary in the range 7–11 nm. The formation of ferroelectric nano-crystalline KNbO3 phase is also attributed by a steep rise in the dielectric constant (e) of glass–ceramics with heat-treatment time. The measured photoluminescence spectra have exhibited emission transitions of 4F3/2?4IJ (J = 9/2, 11/2 and 13/2) from Nd3+ ions upon excitation at 817 nm. It is observed that the photoluminescent intensity and excited state lifetime of Nd3+ ions initially decrease and then gradually increase with increase in heat-treatment time. The absorption spectra and fluorescence measurements disclose that the Nd3+ ions gradually enter into the KNbO3 nanocrystals

Impact of land-use changes on soil properties and carbon pools in India: A meta-analysis

Not AvailableLand-use changes (LUC), primarily due to deforestation and soil disturbance, are one of the major causes of soil quality degradation and greenhouse gas emissions. Effects of LUC on soil physicochemical properties and changes in soil quality and land use management strategies that can effectively restore soil carbon and microbial biomass levels have been reported from all over the world, but the impact analysis of such practices in the Indian context is limited. In this study, over 1,786 paired datasets (for meta-analysis) on land uses (LUs) were collected from Indian literature (1990–2019) to determine the magnitude of the influence of LUC on soil carbon, microbial biomass, and other physical and chemical properties at three soil depths. Meta-analysis results showed that grasslands (36.1%) lost the most soil organic carbon (SOC) compared to native forest lands, followed by plantation lands (35.5%), cultivated lands (31.1%), barren lands (27.3%), and horticulture lands (11.5%). Our findings also revealed that, when compared to forest land, the microbial quotient was lower in other LUs. Due to the depletion of SOC stock, carbon dioxide equivalent (CO2 eq) emissions were significantly higher in all LUs than in forest land. Results also showed that due to the conversion of forest land to cultivated land, total carbon, labile carbon, non-labile carbon, microbial biomass carbon, and SOC stocks were lost by 21%, 25%, 32%, 26%, and 41.2%, respectively. Changes in soil carbon pools and properties were more pronounced in surface (0–15 cm) soils than in subsurface soils (15–30 cm and 30–45 cm). Restoration of the SOC stocks from different LUs ranged from a minimum of 2% (grasslands) to a maximum of 48% (plantation lands). Overall, this study showed that soil carbon pools decreased as LUC transitioned from native forestland to other LUs, and it is suggested that adopting crop-production systems that can reduce CO2 emissions from the intensive LUs such as the ones evaluated here could contribute to improvements in soil quality and mitigation of climate change impacts, particularly under Indian agro-climatic conditions.Not Availabl

Tubulin isoform composition tunes microtubule dynamics

Microtubules polymerize and depolymerize stochastically, a behavior essential for cell division, motility and differentiation. While many studies advanced our understanding of how microtubule-associated proteins tune microtubule dynamics in trans, we have yet to understand how tubulin genetic diversity regulates microtubule functions. The majority of in vitro dynamics studies are performed with tubulin purified from brain tissue. This preparation is not representative of tubulin found in many cell types. Here we report the 4.2Å cryo-EM structure and in vitro dynamics parameters of α1B/βI+βIVb microtubules assembled from tubulin purified from a human embryonic kidney cell line with isoform composition characteristic of fibroblasts and many immortalized cell lines. We find that these microtubules grow faster and transition to depolymerization less frequently compared to brain microtubules. Cryo-EM reveals that the dynamic ends of α1B/βI+βIVb microtubules are less tapered and that these tubulin heterodimers display lower curvatures. Interestingly, analysis of EB1 distributions at dynamic ends suggests no differences in GTP cap sizes. Lastly, we show that the addition of recombinant α1A/βIII tubulin, a neuronal isotype overexpressed in many tumors, proportionally tunes the dynamics of α1B/βI+βIVb microtubules. Our study is an important step towards understanding how tubulin isoform composition tunes microtubule dynamics

Innate immunity against HIV: a priority target for HIV prevention research

This review summarizes recent advances and current gaps in understanding of innate immunity to human immunodeficiency virus (HIV) infection, and identifies key scientific priorities to enable application of this knowledge to the development of novel prevention strategies (vaccines and microbicides). It builds on productive discussion and new data arising out of a workshop on innate immunity against HIV held at the European Commission in Brussels, together with recent observations from the literature

Antihyperlipidemic and antiperoxidative effect of Diasulin, a polyherbal formulation in alloxan induced hyperglycemic rats

BACKGROUND: This study was undertaken to investigation the effect of Diasulin, a poly herbal drug composed of ethanolic extract of ten medicinal plants on blood glucose, plasma insulin, tissue lipid profile, and lipidperoxidation in alloxan induced diabetes. METHODS: Ethanolic extract of Diasulin a, poly herbal drug was administered orally (200 mg/kg body weight) for 30 days. The different doses of Diasulin on blood glucose and plasma insulin in diabetic rats were studied and the levels of lipid peroxides [TBARS, and Hydroperoxide] and tissue lipids [cholesterol, triglyceride, phospholipides and free fatty acids] were also estimated in alloxan induced diabetic rats. The effects were compared with glibenclamide. RESULT: Treatment with Diasulin and glibenclamide resulted in a significant reduction of blood glucose and increase in plasma insulin. Diasulin also resulted in a significant decrease in tissue lipids and lipid peroxide formation. The effect produced by Diasulin was comparable with that of glibenclamide. CONCLUSION: The decreased lipid peroxides and tissue lipids clearly showed the antihyperlipidemic and antiperoxidative effect of Diasulin apart from its antidiabetic effect

A Novel Small Molecule Inhibitor of Hepatitis C Virus Entry

Small molecule inhibitors of hepatitis C virus (HCV) are being developed to complement or replace treatments with pegylated interferons and ribavirin, which have poor response rates and significant side effects. Resistance to these inhibitors emerges rapidly in the clinic, suggesting that successful therapy will involve combination therapy with multiple inhibitors of different targets. The entry process of HCV into hepatocytes represents another series of potential targets for therapeutic intervention, involving viral structural proteins that have not been extensively explored due to experimental limitations. To discover HCV entry inhibitors, we utilized HCV pseudoparticles (HCVpp) incorporating E1-E2 envelope proteins from a genotype 1b clinical isolate. Screening of a small molecule library identified a potent HCV-specific triazine inhibitor, EI-1. A series of HCVpp with E1-E2 sequences from various HCV isolates was used to show activity against all genotype 1a and 1b HCVpp tested, with median EC50 values of 0.134 and 0.027 µM, respectively. Time-of-addition experiments demonstrated a block in HCVpp entry, downstream of initial attachment to the cell surface, and prior to or concomitant with bafilomycin inhibition of endosomal acidification. EI-1 was equally active against cell-culture adapted HCV (HCVcc), blocking both cell-free entry and cell-to-cell transmission of virus. HCVcc with high-level resistance to EI-1 was selected by sequential passage in the presence of inhibitor, and resistance was shown to be conferred by changes to residue 719 in the carboxy-terminal transmembrane anchor region of E2, implicating this envelope protein in EI-1 susceptibility. Combinations of EI-1 with interferon, or inhibitors of NS3 or NS5A, resulted in additive to synergistic activity. These results suggest that inhibitors of HCV entry could be added to replication inhibitors and interferons already in development

De Novo Mutations in SLC1A2 and CACNA1A Are Important Causes of Epileptic Encephalopathies

Epileptic encephalopathies (EEs) are the most clinically important group of severe early-onset epilepsies. Next-generation sequencing has highlighted the crucial contribution of de novo mutations to the genetic architecture of EEs as well as to their underlying genetic heterogeneity. Our previous whole-exome sequencing study of 264 parent-child trios revealed more than 290 candidate genes in which only a single individual had a de novo variant. We sought to identify additional pathogenic variants in a subset (n = 27) of these genes via targeted sequencing in an unsolved cohort of 531 individuals with a diverse range of EEs. We report 17 individuals with pathogenic variants in seven of the 27 genes, defining a genetic etiology in 3.2% of this unsolved cohort. Our results provide definitive evidence that de novo mutations in SLC1A2 and CACNA1A cause specific EEs and expand the compendium of clinically relevant genotypes for GABRB3. We also identified EEs caused by genetic variants in ALG13, DNM1, and GNAO1 and report a mutation in IQSEC2. Notably, recurrent mutations accounted for 7/17 of the pathogenic variants identified. As a result of high-depth coverage, parental mosaicism was identified in two out of 14 cases tested with mutant allelic fractions of 5%–6% in the unaffected parents, carrying significant reproductive counseling implications. These results confirm that dysregulation in diverse cellular neuronal pathways causes EEs, and they will inform the diagnosis and management of individuals with these devastating disorders

Mutations in KEOPS-Complex Genes Cause Nephrotic Syndrome with Primary Microcephaly

Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms