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Gadekar, V. P.

Publications and source records attributed to Gadekar, V. P..

2 recordsLinked to original sources

Microbial communities on station and train surfaces in Chennai Metro: Insights into urban transit microbiome

BackgroundUrban public transport systems, particularly metro networks, serve as key hubs for microbial transmission, yet the urban microbiome in densely populated regions like India remains poorly characterized. These environments harbour diverse microbial communities, including beneficial and pathogenic species, which can influence public health. The COVID-19 pandemic has further underscored the need to monitor microbial ecosystems, particularly with respect to antimicrobial resistance (AMR) genes, which may have escalated due to the increased use of antibiotics during health crises. In a first-of-its-kind study in India, we comprehensively characterized microbial communities and the prevalence of AMR genes in the Chennai Metro system. We collected 96 surface swab samples from 12 stations across two metro lines, targeting four surfaces: bannisters, kiosks, rods, and ticket counters. Forty-seven samples passed quality control and were analyzed using whole-genome metagenomic sequencing. We employed taxonomic classification and conducted comparative and diversity analyses, as well as differential taxa profile analyses, across the sample collection objects. We studied the prevalence and abundance of AMR genes using AMR annotations from the CARD database. We performed pangenome analysis by constructing Metagenome Assembled Genomes (MAGs) from the collected samples and comparing them with the NCBI reference genome. ResultsComparative analysis with global urban microbiome datasets revealed distinct microbial profiles, including nine species that are differentially prevalent in Chennai samples. Surface type significantly influenced microbial diversity, with kiosks exhibiting the highest diversity. We successfully reconstructed several high-quality MAGs, providing insights into the genomic potential and adaptability of dominant taxa in this environment. While the overall prevalence of AMR genes was minimal, genes associated with Sulfonamide and Rifamycin resistance were detected. ConclusionThese findings highlight unique microbial signatures and emphasize the need for ongoing surveillance and targeted interventions to mitigate microbial transmission risks in densely populated urban areas.

ecology↗

Golgi Fragmentation - One of the Earliest Organelle Phenotypes in Alzheimer's Disease Neurons

Alzheimers disease (AD) is the most common cause of dementia, with no current cure. Consequently, alternative approaches focusing on early pathological events in specific neuronal populations, besides targeting the well-studied Amyloid beta (A{beta}) accumulations and Tau tangles, are needed. In this study, we have investigated disease phenotypes specific to glutamatergic forebrain neurons and mapped the timeline of their occurrence, by implementing familial and sporadic human induced pluripotent stem cell models as well as the 5xFAD mouse model. We recapitulated characteristic late AD disease phenotypes, such as increased A{beta} secretion and Tau hyperphosphorylation, as well as previously well documented mitochondrial and synaptic deficits. Intriguingly, we identified Golgi fragmentation as one of the earliest AD phenotypes, indicating potential impairments in protein processing and post-translational modifications. Computational analysis of RNA sequencing data revealed differentially expressed genes involved in glycosylation and glycan patterns, whilst total glycan profiling revealed minor glycosylation differences. This indicates general robustness of glycosylation besides the observed fragmented morphology. Importantly, we identified that genetic variants in Sortilin-related receptor 1 (SORL1) associated with AD could aggravate the Golgi fragmentation and subsequent glycosylation changes. In summary, we identified Golgi fragmentation as one of the earliest disease phenotypes in AD neurons in various in vivo and in vitro complementary disease models, which can be exacerbated via additional risk variants in SORL1. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=140 SRC="FIGDIR/small/519571v1_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@98a8eeorg.highwire.dtl.DTLVardef@7aa7b7org.highwire.dtl.DTLVardef@991e33org.highwire.dtl.DTLVardef@8dabb4_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗