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Abstract

This article discusses the thermoanalytical model developed in the current work to study the influence of the molecular interactions between binary condensed eutectic phases in terms of excess thermodynamic functions that exhort the ability of providing quantitative idea of the interactions. Non-ideality of binary eutectic systems over the entire range of mole fraction composition is ascertained by subjecting the experimentally determined solidus–liquidus equilibrium data to thermodynamic analysis and thereby, apprehending quantitative idea about the nature of molecular interactions. The estimation of molecular interactions model of binary naphthalene–o-nitrophenol, α-naphthol–naphthalene, diphenylamine–α-naphthol, benzil–diphenyl, acenaphthene–antimonytrichloride and cadmium–bismuth eutectic systems authenticates the reliability of the excess functions, since the mixing of the eutectic phases either side of solidus–liquidus equilibrium curves of the systems is found to follow the criteria of spontaneity and Planck formulation S = klnw; where S, k and w, respectively, are the configurational entropy, Boltzmann constant and complexion number of constituent phase molecules. Moreover, the Guggenheim lattice theory applied to solidus mixtures at their liquidus temperatures offers supporting evidence to the essence of the excess functions and hence the thermomolecular interactions model.

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The objective of this study was to develop an understanding about the genetics of terminal heat tolerance in wheat (Triticum aestivum L.). The minimum number of genes was assessed using Mendelian and quantitative genetic approach. Two crosses were made between heat tolerant and heat susceptible bread wheat cultivars: NW1014 × HUW468 and HUW234 × HUW468. Heat susceptible HUW468 was common in both the crosses. The F4, F5 and F6 generations were evaluated including F1 in two different dates of sowing (normal and very late) under field conditions in year 2006–07. The data was recorded for grain fill duration (GFD) and thousand-grain weight (TGW). Based on data of two dates, decline% and heat susceptibility index (HSI) of GFD and TGW were estimated. Heat tolerance in F1 showed absence of dominance. Estimation of genes using Mendelian approach in F4, F5 and F6 progenies (148–157) of the two crosses suggested that heat tolerance was governed by a minimum of three genes. Quantitative approach also indicated similar number of genes. The distribution of progeny lines in F4 and F6 supported the polygene nature of heat tolerance. These genes if mapped by molecular approach can play an important role through marker assisted selection (MAS) for developing improved thermo-tolerant lines of wheat.

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Interventional Medicine and Applied Science
Authors: Peethambaran Arun, Manojkumar Valiyaveettil, Lionel Biggemann, Yonas Alamneh, Yanling Wei, Samuel Oguntayo, Ying Wang, Joseph B. Long, and Madhusoodana P. Nambiar

Abstract

Emerging studies show that blast exposure causes traumatic brain injury (TBI) and auditory dysfunction without rupture of tympanic membrane, suggesting central auditory processing impairment after blast exposure. There is limited information on the mechanisms of blast-induced TBI and associated peripheral and central auditory processing impairments. We utilized a repetitive blast exposure mouse model to unravel the mechanisms of blast TBI and auditory impairment. C57BL/6J mice were exposed to three repeated blasts (20.6 psi) using a shock tube, and the cerebellum was subjected to proteomic analysis. The data showed that calretinin and parvalbumin, two major calcium buffering proteins, were significantly up-regulated after repeated blast exposures, and this was confirmed by Western blotting. Since these proteins are reportedly involved in auditory dysfunction, we examined the inner ear and found both calretinin and parvalbumin were up-regulated, suggesting that modulation of these proteins plays a role in blast-induced peripheral and central auditory processing impairments. Expression of cleaved caspase-3 was also up-regulated in both regions indicating ongoing cellular apoptosis, possibly due to altered calcium homeostasis. These results provide a molecular basis for changes in central and peripheral auditory processing involving abnormal calcium homeostasis resulting in hearing impairment after blast exposure.

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