Effect of organic and inorganic nutrients on rice (Oryza sativa var. CO 51) productivity and soil fertility in the Western zone of Tamil Nadu, India

In sustainable agriculture, to ensure high-quality food production, a combination of organic and inorganic nutrient sources are required. During the winter season of 2020, a field experiment was undertaken in the western zone of Tamil Nadu to assess the effects of organics and inorganics on the growth, yield, and soil properties of rice, Oryza sativa var. CO 51. The experiment was framed in Random Block Design (RBD) comprising of 8 treatments viz., Recommended dose of fertilizer Soil Test Crop Response (STCR) approach (T1), RDF 75 % + Farm yard manure @ 12.5 t ha-1 (T2), T2 + Seed treatment with Azospirillum and Phosphobacteria + Soil application of AM fungi (T3), RDF 75 % + Vermicompost @ 5 t ha-1 (T4), T4 + Seed treatment with Azospirillum and Phosphobacteria + Soil application of AM fungi (T5), FYM @ 12.5 t ha-1 + Seed treatment with Azospirillum and Phosphobacteria + Soil application of AM fungi (T6), Vermicompost @ 5 t ha-1+ Seed treatment with Azospirillum and Phosphobacteria + Soil application of AM fungi (T7) and absolute control (T8) , replicated thrice. Among the integrated nutrient management practices, T5 proved its superiority over other treatments with respect to growth and physiological parameters followed by T3. This would have been because of the solubilization of phosphorus in the soil by AM organisms which is made accessible for crop growth. Utilization of biofertilizer enhanced the N availability and solubilized the inaccessible phosphorus, which thus recorded higher N accessibility and better phosphorus uptake when applied along with a recommended dose of fertilizer for rice.

Analysis of nitrofurantoin sensitivity in multi drug resistant gram negative bacilli causing UTI in a teaching hospital – A cost effective option

Background Antimicrobial resistance is a growing concern globally, leading to more difficult-to-treat infections and higher mortality rates. Urinary tract infections (UTI) are one of the major indications for prescribing antibiotics, with multidrug resistant Gram-negative bacilli being responsible for a growing proportion of community-acquired uncomplicated UTIs. Our goal is to determine nitrofurantoin, a less costly effective substitute in treating uncomplicated UTI caused by multidrug resistant gram negative bacilli

Functional analysis of structural variants in single cells using Strand-seq

Somatic structural variants (SVs) are widespread in cancer, but their impact on disease evolution is understudied due to a lack of methods to directly characterize their functional consequences. We present a computational method, scNOVA, which uses Strand-seq to perform haplotype-aware integration of SV discovery and molecular phenotyping in single cells by using nucleosome occupancy to infer gene expression as a readout. Application to leukemias and cell lines identifies local effects of copy-balanced rearrangements on gene deregulation, and consequences of SVs on aberrant signaling pathways in subclones. We discovered distinct SV subclones with dysregulated Wnt signaling in a chronic lymphocytic leukemia patient. We further uncovered the consequences of subclonal chromothripsis in T cell acute lymphoblastic leukemia, which revealed c-Myb activation, enrichment of a primitive cell state and informed successful targeting of the subclone in cell culture, using a Notch inhibitor. By directly linking SVs to their functional effects, scNOVA enables systematic single-cell multiomic studies of structural variation in heterogeneous cell populations

Validating the concept of mutational signatures with isogenic cell models.

The diversity of somatic mutations in human cancers can be decomposed into individual mutational signatures, patterns of mutagenesis that arise because of DNA damage and DNA repair processes that have occurred in cells as they evolved towards malignancy. Correlations between mutational signatures and environmental exposures, enzymatic activities and genetic defects have been described, but human cancers are not ideal experimental systems-the exposures to different mutational processes in a patient's lifetime are uncontrolled and any relationships observed can only be described as an association. Here, we demonstrate the proof-of-principle that it is possible to recreate cancer mutational signatures in vitro using CRISPR-Cas9-based gene-editing experiments in an isogenic human-cell system. We provide experimental and algorithmic methods to discover mutational signatures generated under highly experimentally-controlled conditions. Our in vitro findings strikingly recapitulate in vivo observations of cancer data, fundamentally validating the concept of (particularly) endogenously-arising mutational signatures

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe