Effect of Co-Solvents on Bulk And Interfacial Characteristics of Room Temperature Ionic Liquids

Ionic liquids (ILs) are special class of molten salts constituted by large and asymmetric organic cations and inorganic or organic anions, with melting temperatures below 100oC. Due to the large size and the conformational flexibility of constituent ions, ILs present low lattice enthalpies and large entropy changes upon melting which favour the liquid state. ILs with melting point below ambient temperatures are regarded as Room Temperature Ionic Liquids (RTILs). RTILs have attracted increasing attention in recent years from both academia and industry due to their interesting properties and potential applications. RTILs as a hybrid of neutral and ionic entities, exhibit many unique physicochemical properties, such as negligible volatility, nonflammability under ambient conditions, large liquidus range, high thermal and chemical stability, wide electrochemical window, wide range of densities and viscosities, high potential for recycling, high ionic conductivity, and miscibility with a wide range of organic and inorganic compounds which confer them their reputation as “green solvents” and make them a good alternative to traditional organic solvents. In addition, the high polarity of the ILs makes them to form very strong effective adsorption films and redy tribochemical reactions, which contributes to their prominent antiwear capability. On account of above mentioned specialities, RTILs have found wide applications in chemical synthesis, catalysis, lubrication, thermal separation processes and electrochemistry

Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder

Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are both highly heritable neurodevelopmental disorders. Evidence indicates both disorders co-occur with a high frequency, in 20–50% of children with ADHD meeting criteria for ASD and in 30-80% of ASD children meeting criteria for ADHD. This review will provide an overview on all available studies [family based, twin, candidate gene, linkage, and genome wide association (GWA) studies] shedding light on the role of shared genetic underpinnings of ADHD and ASD. It is concluded that family and twin studies do provide support for the hypothesis that ADHD and ASD originate from partly similar familial/genetic factors. Only a few candidate gene studies, linkage studies and GWA studies have specifically addressed this co-occurrence, pinpointing to some promising pleiotropic genes, loci and single nucleotide polymorphisms (SNPs), but the research field is in urgent need for better designed and powered studies to tackle this complex issue. We propose that future studies examining shared familial etiological factors for ADHD and ASD use a family-based design in which the same phenotypic (ADHD and ASD), candidate endophenotypic, and environmental measurements are obtained from all family members. Multivariate multi-level models are probably best suited for the statistical analysis

ANK2 loss-of-function variants are associated with epilepsy, and lead to impaired axon initial segment plasticity and hyperactive network activity in hiPSC-derived neuronal networks

PURPOSE: To characterize a novel neurodevelopmental syndrome due to loss-of-function (LoF) variants in Ankyrin 2 (ANK2), and to explore the effects on neuronal network dynamics and homeostatic plasticity in human-induced pluripotent stem cell-derived neurons. METHODS: We collected clinical and molecular data of 12 individuals with heterozygous de novo LoF variants in ANK2. We generated a heterozygous LoF allele of ANK2 using CRISPR/Cas9 in human-induced pluripotent stem cells (hiPSCs). HiPSCs were differentiated into excitatory neurons, and we measured their spontaneous electrophysiological responses using micro-electrode arrays (MEAs). We also characterized their somatodendritic morphology and axon initial segment (AIS) structure and plasticity. RESULTS: We found a broad neurodevelopmental disorder (NDD), comprising intellectual disability, autism spectrum disorders and early onset epilepsy. Using MEAs, we found that hiPSC-derived neurons with heterozygous LoF of ANK2 show a hyperactive and desynchronized neuronal network. ANK2-deficient neurons also showed increased somatodendritic structures and altered AIS structure of which its plasticity is impaired upon activity-dependent modulation. CONCLUSIONS: Phenotypic characterization of patients with de novo ANK2 LoF variants defines a novel NDD with early onset epilepsy. Our functional in vitro data of ANK2-deficient human neurons show a specific neuronal phenotype in which reduced ANKB expression leads to hyperactive and desynchronized neuronal network activity, increased somatodendritic complexity and AIS structure and impaired activity-dependent plasticity of the AIS

Effect of Land use Change on Total Phosphorus and Its Fractions in North-Western Himalayas

Aims: Conversion of land from forest to cropping has a serious effect on soil phosphorus and its fractions Results: Land use is now widely understood to be a primary factor in environmental change across all time and space scales. The purpose of this research was to ascertain how different land uses affected the concentration of phosphorus in soil. Soil phosphorus (P) reserves are depleted when land is converted from natural vegetation to permanent agricultural cropping. The transformation of North-Western Himalayas from a forest-dominated to a grassland-dominated ecosystem is just one example of the diversity of land significantly less soil aggregation occurred when agricultural land was cleared of its native vegetation. Total organic carbon in soils was reduced when grassland was converted to cropland.  Reduced total organic carbon (TOC) concentrations by 62-79% and organic phosphorus (Po) concentrations by 47-53%. Even though, the total silt+clay fraction's contribution was negligible, it contained a significant amount of C and Po reserves and the C/Po ratio has been holding fairly steady, they have proven to be more robust. This impact of cropping on soil P reserves has been demonstrated in research, but changing land use practices can alleviate these problems significantly

Utility of procalcitonin in predicting mortality among cases of hospital-acquired pneumonia: a North Indian study

Bckground Data regarding the role of biomarkers like procalcitonin (PCT) in predicting treatment outcomes in hospital-acquired pneumonia (HAP) are limited in an Indian setting. We set out to determine the usefulness of PCT in predicting mortality among the cases of nosocomial pneumonia, at an 800-bed, apex tertiary care centre, in Kashmir (North India). Patients and methods Of the 318 confirmed cases of HAP, 60 consenting cases were selected randomly. Quantitative determination of PCT was done using immunofluorescence assays. Levels greater than 0.5 ng/ml were taken as positive. Data were collected on clinical parameters, and Acute Physiology and Chronic Health Evaluation II (APACHE-II) scores pneumonia severity index were calculated. Appropriate blood and respiratory cultures were performed. Results Of the 60 cases included in the study, 19 (32%) died during the hospital stay, of which 14 (74%) deaths occurred in PCT-positive cases (P=0.001). The median PCT level was higher in the in-hospital mortality group (1.07 vs. 0.25), with a mean value of 1.2±2.8 vs. 1.2±2.5 in the group with no mortality (P=0.000). Using multivariate analysis, positive PCT level was strongly associated with in-hospital mortality (odds ratio: 6.767, 95%CI: 1.992–22.984, P=0.002) and APACHE-II score greater than 20 (n=14, odds ratio=4.5, 95%CI=1.448–13.984, P=0.009). Using receiver operating characteristic analysis, PCT had apropos discrimination power for in-hospital mortality (0.713 of area under the curve) and higher APACHE-II scores (0.753 of area under the curve). Using Cox regression model for mortality in PCT-positive group, the calculated hazard ratio was 3.273 (95%CI: 1.076–9.951, P=0.037). Conclusion PCT might have a vital role in the management of HAP, as a predictor of the poor treatment outcome

Distribution, Etiology, Molecular Genetics and Management Perspectives of Northern Corn Leaf Blight of Maize (Zea mays L.)

Not AvailableMaize is cultivated extensively throughout the world and has the highest production among cereals. However, Northern corn leaf blight (NCLB) disease caused by Exherohilum turcicum, is the most devastating limiting factor of maize production. The disease causes immense losses to corn yield if it develops prior or during the tasseling and silking stages of crop development. It has a worldwide distribution and its development is favoured by cool to moderate temperatures with high relative humidity. The prevalence of the disease has increased in recent years and new races of the pathogen have been reported worldwide. The fungus E. turcicum is highly variable in nature. Though different management strategies have proved effective to reduce economic losses from NCLB, the development of varieties with resistance to E. turcicum is the most efficient and inexpensive way for disease management. Qualitative resistance for NCLB governed by Ht genes is a race-specific resistance which leads to a higher level of resistance. However, some Ht genes can easily become ineffective under the high pressure of virulent strains of the pathogen. Hence, it is imperative to understand and examine the consistency of the genomic locations of quantitative trait loci for resistance to NCLB in diverse maize populations. The breeding approaches for pyramiding resistant genes against E. turcicum in maize can impart NCLB resistance under high disease pressure environments. Furthermore, the genome editing approaches like CRISPR-cas9 and RNAi can also prove vital for developing NCLB resistant maize cultivars. As such this review delivers emphasis on the importance and current status of the disease, racial spectrum of the pathogen, genetic nature and breeding approaches for resistance and management strategies of the disease in a sustainable manner.Not Availabl

ANK2 loss-of-function variants are associated with epilepsy, and lead to impaired axon initial segment plasticity and hyperactive network activity in hiPSC-derived neuronal networks

PURPOSE: To characterize a novel neurodevelopmental syndrome due to loss-of-function (LoF) variants in Ankyrin 2 (ANK2), and to explore the effects on neuronal network dynamics and homeostatic plasticity in human-induced pluripotent stem cell-derived neurons.METHODS: We collected clinical and molecular data of 12 individuals with heterozygous de novo LoF variants in ANK2. We generated a heterozygous LoF allele of ANK2 using CRISPR/Cas9 in human-induced pluripotent stem cells (hiPSCs). HiPSCs were differentiated into excitatory neurons, and we measured their spontaneous electrophysiological responses using micro-electrode arrays (MEAs). We also characterized their somatodendritic morphology and axon initial segment (AIS) structure and plasticity.RESULTS: We found a broad neurodevelopmental disorder (NDD), comprising intellectual disability, autism spectrum disorders and early onset epilepsy. Using MEAs, we found that hiPSC-derived neurons with heterozygous LoF of ANK2 show a hyperactive and desynchronized neuronal network. ANK2-deficient neurons also showed increased somatodendritic structures and altered AIS structure of which its plasticity is impaired upon activity-dependent modulation.CONCLUSIONS: Phenotypic characterization of patients with de novo ANK2 LoF variants defines a novel NDD with early onset epilepsy. Our functional in vitro data of ANK2-deficient human neurons show a specific neuronal phenotype in which reduced ANKB expression leads to hyperactive and desynchronized neuronal network activity, increased somatodendritic complexity and AIS structure and impaired activity-dependent plasticity of the AIS.</p