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The Effect of Different Fuels on Particle Size and Morphology of FTO Nano Powder Synth-sized by Gel Combustion Method

In this study, a gel combustion method was used to prepare fluorine-doped tin oxide (FTO) nano powders. Stannous chloride dehydrate, hydrofluoric acid, and different fuels of glycine, urea, and citric acid were used to synthesize FTO nano powder, followed by calcination at 600 °C. The results showed that using citric acid as a fuel gives homogenous FTO nano powder with average particle size of 40 nm and round morphology. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/3489

Preparation of chitosan beads and membranes for industrial applications [abstract]

Faculty Mentor: Dr. Tushar K. Gosh, Nuclear Science and Engineering Instite (NSEI)Abstract only availableIndustrial waste water contains a variety of toxic chemicals including toxic heavy metals that must be removed before discharging to the environment. A number of methods have been investigated to remove these heavy metals. The use of chitosan for removal of some of these toxic metals appears to be very promising. Chitosan is a natural product derived from chitin, a polysaccharide found in the exoskeleton of shellfish like shrimp or crabs. The term Chitosan does not refers to a uniquely defined compound; it merely refers to a family of copolymers with various fractions of acetylated units. Chitosan in its natural form is not suitable for industrial application. In this study, chitosan was modified and prepared as beads so that it can be easily used for various applications. Chitosan Beads were prepared under various conditions. Commercially available chitosan flakes were dissolved in either acetic acid or oxalic acid and a homogeneous mixture was prepared. The spherical beads were obtained by drop wise addition of the acidic mixture into a NaOH bath. The beads were washed with distilled water until the pH was neutral or 7. Beads were then dried either in a vacuum oven or by freeze drying. Theses beads can be used to remove metals and other contaminants from the ground and waste waters. Attempts were also made to prepare chitosan membrane that can have application in Fuel Cells. The beads were characterized by scanning electron microscope and were also evaluated for chromium (III) adsorption

Protein structure and phenotypic analysis of pathogenic and population missense variants in STXBP1

Background: Syntaxin-binding protein 1, encoded by STXBP1, is highly expressed in the brain and involved in fusing synaptic vesicles with the plasma membrane. Studies have shown that pathogenic loss-of-function variants in this gene result in various types of epilepsies, mostly beginning early in life. We were interested to model pathogenic missense variants on the protein structure to investigate the mechanism of pathogenicity and genotype–phenotype correlations. Methods: We report 11 patients with pathogenic de novo mutations in STXBP1 identified in the first 4293 trios of the Deciphering Developmental Disorder (DDD) study, including six missense variants. We analyzed the structural locations of the pathogenic missense variants from this study and the literature, as well as population missense variants extracted from Exome Aggregation Consortium (ExAC). Results: Pathogenic variants are significantly more likely to occur at highly conserved locations than population variants, and be buried inside the protein domain. Pathogenic mutations are also more likely to destabilize the domain structure compared with population variants, increasing the proportion of (partially) unfolded domains that are prone to aggregation or degradation. We were unable to detect any genotype–phenotype correlation, but unlike previously reported cases, most of the DDD patients with STXBP1 pathogenic variants did not present with very early-onset or severe epilepsy and encephalopathy, though all have developmental delay with intellectual disability and most display behavioral problems and suffered seizures in later childhood. Conclusion: Variants across STXBP1 that cause loss of function can result in severe intellectual disability with or without seizures, consistent with a haploinsufficiency mechanism. Pathogenic missense mutations act through destabilization of the protein domain, making it prone to aggregation or degradation. The presence or absence of early seizures may reflect ascertainment bias in the literature as well as the broad recruitment strategy of the DDD study

Purification, properties and alternate substrate specificities of arginase from two different sources: Vigna catjang cotyledon and buffalo liver

Arginase was purified from Vigna catjang cotyledons and buffalo liver by chromatographic separations using Bio-Gel P-150, DEAE-cellulose and arginine AH Sepharose 4B affinity columns. The native molecular weight of an enzyme estimated on Bio-Gel P-300 column for Vigna catjang was 210 kDa and 120 kDa of buffalo liver, while SDS-PAGE showed a single band of molecular weight 52 kDa for cotyledon and 43 kDa for buffalo liver arginase. The kinetic properties determined for the purified cotyledon and liver arginase showed an optimum pH of 10.0 and pH 9.2 respectively. Optimal cofactor Mn(++) ion concentration was found to be 0.6 mM for cotyledon and 2 mM for liver arginase. The Michaelis-Menten constant for cotyledon arginase and hepatic arginase were found to be 42 mM and 2 mM respectively. The activity of guanidino compounds as alternate substrates for Vigna catjang cotyledon and buffalo liver arginase is critically dependent on the length of the amino acid side chain and the number of carbon atoms. In addition to L-arginine cotyledon arginase showed substrate specificity towards agmatine and L-canavanine, whereas the liver arginase showed substrate specificity towards only L-canavanine

A Research Program on Very High Temperature Reactors

Track I: Power GenerationIncludes audio file (27 min.)Prismatic and pebble bed very high-temperature reactors (VHTRs) are very attractive both from a thermodynamic efficiency viewpoint and hydrogen-production capability. This project addresses numerous challenges associated with the fuel cycle, materials, and complex fluid dynamics and heat transfer. The objectives of the project are to: i. Conduct physical experiments for fission product transport phenomena in the overcoating and compact structural graphite and transport through TRISO coating layers; ii. Develop improved sorption measurement techniques to measure the accumulation of condensable radionuclides (“plateout”) in the VHTR primary coolant circuit and obtain representative data; iii. Develop advanced computations of charged, radioactive dust (aerosol) transport in the VHTR coolant circuit and confinement by exploring direct simulation Monte Carlo (DSMC) techniques for deposition and resuspension and conduct experiments to verify computational predictions; iv. Develop a program to measure emissivity for various VHTR component materials, both bare and oxidized, and obtain extensive data; v. Develop an experimental program to characterize gas, fission product, and particle flows in the complex geometries of pebble bed modular reactors (PBMRs) and help improve computational approaches and computer programs through experimental understandings. This project is leading to research training of about a dozen Ph D students at the participating universities. Upon graduation, these students will be able to contribute even more effectively to the future challenges in the global deployment of nuclear power generation and hydrogen technologies. We will discuss the VHTR technology and research challenges. We also describe progress on the project by the three Consortium participants

Role of twin Cys-Xaa\u3csub\u3e9\u3c/sub\u3e-Cys motif cysteines in mitochondrial import of the cytochrome c oxidase biogenesis factor Cmc1

The Mia40 import pathway facilitates the import and oxidative folding of cysteine-rich protein substrates into the mitochondrial intermembrane space. Here we describe the in vitro and in organello oxidative folding of Cmc1, a twin CX9C-containing substrate, which contains an unpaired cysteine. In vitro, Cmc1 can be oxidized by the import receptor Mia40 alone when in excess or at a lower rate by only the sulfhydryl oxidase Erv1. However, physiological and efficient Cmc1 oxidation requires Erv1 and Mia40. Cmc1 forms a stable intermediate with Mia40 and is released from this interaction in the presence of Erv1. The three proteins are shown to form a ternary complex in mitochondria. Our results suggest that this mechanism facilitates efficient formation of multiple disulfides and prevents the formation of non-native disulfide bonds

Clinical implications of augmenter of liver regeneration in cancer: A systematic review

Background/Aim: Hepatocellular carcinoma is a substantial healthcare burden with high prevalence and poor prognosiS. As such, efforts are continually made to uncover molecules relevant in cancer biology, that are exploitable as targets for therapy. The mitochondrion is the powerhouse of the cell and exhibits altered functionality in the malignant state, including aberrant regulation of apoptosis and cellular respiration. Augmenter of liver regeneration (ALR) is a multifunctional mitochondrial protein that demonstrates antioxidative and anti-apoptotic properties and plays a key role in liver regeneration. Materials and Methods: The present study systematically reviews the available literature on the role of ALR in cancer. Results: Systematic search of PubMed resulted in 12 studies discussing ALR in multiple types of cancer. More specifically, ALR appears to be up-regulated in malignant cells and tissueS. Furthermore, treatment of cells with exogenous ALR shows an anti-apoptotic effect while silencing or inhibiting ALR decreases cell and tumor survival. Conclusion: ALR clearly plays a role in cancer biology and demonstrates potential as a therapeutic target. Hepatocellular carcinoma (HCC) is a common oncologic condition with a poor prognosis that poses as a global burden on medical care (1). Between 2002 and 2012 the mortality rate of HCC rose by 34.8% in the United States and liver cancer, with HCC estimated as 70 to 90% of cases, was considered to be the second leading cause of cancer-related deaths among males on a global scale in 2012 (2, 3). Considering the metabolic aspect of several known risk factors for HCC, such as obesity, diabetes, and non-alcoholic fatty liver disease, a common underlying feature of mitochondrial dysfunction is of growing interest in molecular oncology. The regulation of specific mitochondrial proteins is of particular interest, as these proteins demonstrate potential as therapeutic targets for HCC (4). Augmenter of liver regeneration (ALR) is one particular protein of interest that localizes in the intermembrane space of the mitochondria of humans and has a prokaryotic homolog, Erv1, sharing 42% identical amino acid residueS. ALR/Erv1 has been known to contribute to mitochondrial biogenesis and function as a sulfhydryl oxidase in mitochondrial disulfide relay systems (5). It functions to oxidize the import receptor Mia40, both of which conjunctively import small translocase inner membrane (Tim) proteins through an oxidative-folding pathway (6). In turn, cytochrome c (cyt c), which constitutes an important member of the electron transport chain, oxidizes ALR through locomotion of electrons via FAD, thus connecting this redox regulated import pathway to electron transport (5, 7). During specific unfavorable conditions, cells must reprogram to undergo apoptosis during which cyt c activates a series of activated-caspase pathways that lead to cell suicide (8). It is a trademark of cancer cells to down-regulate apoptotic mechanisms and alter mitochondrial respiratory function, resulting in uncontrolled growth and eventual metastasis of cancerous cellS. ALR manifests anti-oxidative and anti-apoptotic properties and is known to support liver regeneration in cases of hepatic injury (9). Considering these properties, early investigations have suggested a role for ALR in cancer (particularly hepatocellular) pathogenesis, growth and progression. In this study, we systematically review the literature discussing ALR in cancer. Clinical implications including oncogenesis and targeted therapy are explored