Characterization of Zinc Nanoferrite Doped HPMC Polymers Using X-Ray Diffraction

HPMC Polymer composites were prepared by doping various concentrations of Zinc ferrite nanoparticles using solution casting method. These polymer composites were characterized using X-Ray Diffraction and conductivity measurements. The addition of nanoferrites in the polymer matrix do change the structural and the AC conductivity properties of the film, which is supported by the results obtained and they are discussed briefly in this paper

PREPARATION OF PLANT MUCILAGE CLARIFICANTS AND THEIR EFFECT ON JAGGERY PROCESSING OF SUGARCANE VARIETY Co 86032

Objective: The aim of the study was to prepare jaggery from sugarcane variety Co86032 using plants mucilage as clarificants and to determine the effect of plant mucilage on jaggery processing.Methods: Production of jaggery using five plant clarificants namely Aloe vera, Flax seeds, Fenugreek, Purslane and Malabar spinach at three different concentrations i.e., 0.1%, 0.2% and 0.4% of raw sugarcane juice and the jaggery prepared without any clarificants serves as control. During production, the processing parameters such as quantity of scum removed, total time taken for processing and jaggery yield was determined.Results: It was found that the jaggery prepared using plant mucilage at concentration of 0.4% found superior when compared to 0.2%, 0.1% and control respectively. Aloe vera at 0.4% removed maximum scum (4.07%), taken minimum processing time (72.33 min) and recorded maximum jaggery yield (10.92 kg). The efficacy of Aloe vera as mucilage clarificants in jaggery production was followed by fenugreek, flax seeds, purslane and Malabar spinach in the order respectively.Conclusion: The application of plants mucilage as clarificants in the jaggery production removed significant level of scum, reduced processing time and improved yield of jaggery. Therefore the selected plant mucilages can be used as clarificants in the jaggery production and can be considered as potential alternative to chemical clarificants.Â

Zfy genes are required for efficient meiotic sex chromosome inactivation (MSCI) in spermatocytes

During spermatogenesis, germ cells that fail to synapse their chromosomes or fail to undergo meiotic sex chromosome inactivation (MSCI) are eliminated via apoptosis during mid-pachytene. Previous work showed that Y-linked genes Zfy1 and Zfy2 act as "executioners" for this checkpoint, and that wrongful expression of either gene during pachytene triggers germ cell death. Here, we show that in mice, Zfy genes are also necessary for efficient MSCI and the sex chromosomes are not correctly silenced in Zfy-deficient spermatocytes. This unexpectedly reveals a triple role for Zfy at the mid-pachytene checkpoint in which Zfy genes first promote MSCI, then monitor its progress (since if MSCI is achieved, Zfy genes will be silenced), and finally execute cells with MSCI failure. This potentially constitutes a negative feedback loop governing this critical checkpoint mechanism

Extensive meiotic asynapsis in mice antagonises meiotic silencing of unsynapsed chromatin and consequently disrupts meiotic sex chromosome inactivation

Chromosome synapsis during zygotene is a prerequisite for the timely homologous recombinational repair of meiotic DNA double-strand breaks (DSBs). Unrepaired DSBs are thought to trigger apoptosis during midpachytene of male meiosis if synapsis fails. An early pachytene response to asynapsis is meiotic silencing of unsynapsed chromatin (MSUC), which, in normal males, silences the X and Y chromosomes (meiotic sex chromosome inactivation [MSCI]). In this study, we show that MSUC occurs in Spo11-null mouse spermatocytes with extensive asynapsis but lacking meiotic DSBs. In contrast, three mutants (Dnmt3l, Msh5, and Dmc1) with high levels of asynapsis and numerous persistent unrepaired DSBs have a severely impaired MSUC response. We suggest that MSUC-related proteins, including the MSUC initiator BRCA1, are sequestered at unrepaired DSBs. All four mutants fail to silence the X and Y chromosomes (MSCI failure), which is sufficient to explain the midpachytene apoptosis. Apoptosis does not occur in mice with a single additional asynapsed chromosome with unrepaired meiotic DSBs and no disturbance of MSCI

Multilevel HfO2-based RRAM devices for low-power neuromorphic networks

Training and recognition with neural networks generally require high throughput, high energy efficiency, and scalable circuits to enable artificial intelligence tasks to be operated at the edge, i.e., in battery-powered portable devices and other limited-energy environments. In this scenario, scalable resistive memories have been proposed as artificial synapses thanks to their scalability, reconfigurability, and high-energy efficiency, and thanks to the ability to perform analog computation by physical laws in hardware. In this work, we study the material, device, and architecture aspects of resistive switching memory (RRAM) devices for implementing a 2-layer neural network for pattern recognition. First, various RRAM processes are screened in view of the device window, analog storage, and reliability. Then, synaptic weights are stored with 5-level precision in a 4 kbit array of RRAM devices to classify the Modified National Institute of Standards and Technology (MNIST) dataset. Finally, classification performance of a 2-layer neural network is tested before and after an annealing experiment by using experimental values of conductance stored into the array, and a simulation-based analysis of inference accuracy for arrays of increasing size is presented. Our work supports material-based development of RRAM synapses for novel neural networks with high accuracy and low-power consumption. (C) 2019 Author(s)

IGF1-mediated human embryonic stem cell self-renewal recapitulates the embryonic niche.

Our understanding of the signalling pathways regulating early human development is limited, despite their fundamental biological importance. Here, we mine transcriptomics datasets to investigate signalling in the human embryo and identify expression for the insulin and insulin growth factor 1 (IGF1) receptors, along with IGF1 ligand. Consequently, we generate a minimal chemically-defined culture medium in which IGF1 together with Activin maintain self-renewal in the absence of fibroblast growth factor (FGF) signalling. Under these conditions, we derive several pluripotent stem cell lines that express pluripotency-associated genes, retain high viability and a normal karyotype, and can be genetically modified or differentiated into multiple cell lineages. We also identify active phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling in early human embryos, and in both primed and naïve pluripotent culture conditions. This demonstrates that signalling insights from human blastocysts can be used to define culture conditions that more closely recapitulate the embryonic niche

Studies on association of coefficient of coancestry with progeny performance in sugarcane

The utilization of superior parental lines and identification of superior families enhance the genetic gain in sugarcane. To identify the superior parental lines and superior progenies, 1889 progenies derived from twenty crosses involving genetically diverse historical parents were evaluated for juice quality and yield attributing traits.The historical parental lines were selected based on coefficient of coancestry from the tropical and subtropical parents maintained at National Hybridization Garden. Based on progeny performance, families of Co 99006 × CoSe 92423 and Co 86032 × 85R186 were found superior for number of millable canes, , Co 86032 × 85R186 and Co 8371 × CoT 8201 for cane thickness and CoSe 95422 × Co 775 and Co 8371 × CoV 92102 for sucrose content. Parental lines such as Co 86002, Co 99006 and CoLk 98184, Co 775, 85R186 and BO 130 were identified for HR Brix; Co 419 and Co 89010, CoS 510, CoV 92102 and CoSe 92423 for cane thickness; and CoLk 94184, BO 91 and BO 32 for number of millable canes. The estimates of coefficient of coancestry was negatively correlated with HR Brix and cane thickness suggesting that parental cross combination with lesser value of coefficient of coancestry or inbreeding coefficient resulted in produce the heterotic progenies. This study based on the historic parental lines selected based on the coefficient of coancestry and inference limited to only to this experimental material. The evaluation of families derived from the population parental cross combination and parental lines in replication family block design permits the estimation of BLUP based breeding values and helpful in selection of superior parental lines and superior progenies

Genetically enhanced asynapsis of autosomal chromatin promotes transcriptional dysregulation and meiotic failure

During meiosis, pairing of homologous chromosomes and their synapsis are essential prerequisites for normal male gametogenesis. Even limited autosomal asynapsis often leads to spermatogenic impairment, the mechanism of which is not fully understood. The present study was aimed at deliberately increasing the size of partial autosomal asynapsis and analysis of its impact on male meiosis. For this purpose, we studied the effect of t12 haplotype encompassing four inversions on chromosome 17 on mouse autosomal translocation T(16;17)43H (abbreviated T43H). The T43H/T43H homozygotes were fully fertile in both sexes, while +/T43H heterozygous males, but not females, were sterile with meiotic arrest at late pachynema. Inclusion of the t12 haplotype in trans to the T43H translocation resulted in enhanced asynapsis of the translocated autosome, ectopic phosphorylation of histone H2AX, persistence of RAD51 foci, and increased gene silencing around the translocation break. Increase was also on colocalization of unsynapsed chromatin with sex body. Remarkably, we found that transcriptional silencing of the unsynapsed autosomal chromatin precedes silencing of sex chromosomes. Based on the present knowledge, we conclude that interference of meiotic silencing of unsynapsed autosomes with meiotic sex chromosome inactivation is the most likely cause of asynapsis-related male sterility

Phosphorylation of Chromosome Core Components May Serve as Axis Marks for the Status of Chromosomal Events during Mammalian Meiosis

Meiotic recombination and chromosome synapsis between homologous chromosomes are essential for proper chromosome segregation at the first meiotic division. While recombination and synapsis, as well as checkpoints that monitor these two events, take place in the context of a prophase I-specific axial chromosome structure, it remains unclear how chromosome axis components contribute to these processes. We show here that many protein components of the meiotic chromosome axis, including SYCP2, SYCP3, HORMAD1, HORMAD2, SMC3, STAG3, and REC8, become post-translationally modified by phosphorylation during the prophase I stage. We found that HORMAD1 and SMC3 are phosphorylated at a consensus site for the ATM/ATR checkpoint kinase and that the phosphorylated forms of HORMAD1 and SMC3 localize preferentially to unsynapsed chromosomal regions where synapsis has not yet occurred, but not to synapsed or desynapsed regions. We investigated the genetic requirements for the phosphorylation events and revealed that the phosphorylation levels of HORMAD1, HORMAD2, and SMC3 are dramatically reduced in the absence of initiation of meiotic recombination, whereas BRCA1 and SYCP3 are required for normal levels of phosphorylation of HORMAD1 and HORMAD2, but not of SMC3. Interestingly, reduced HORMAD1 and HORMAD2 phosphorylation is associated with impaired targeting of the MSUC (meiotic silencing of unsynapsed chromatin) machinery to unsynapsed chromosomes, suggesting that these post-translational events contribute to the regulation of the synapsis surveillance system. We propose that modifications of chromosome axis components serve as signals that facilitate chromosomal events including recombination, checkpoint control, transcription, and synapsis regulation

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline