Publications by authors named "Ghose P"

Programmed cell death (PCD) is a crucial, genetically-encoded, and evolutionarily-conserved process required for development and homeostasis. We previously identified a genetically non-apoptotic, highly ordered, and stereotyped killing program called Compartmentalized Cell Elimination (CCE) in the C. elegans tail-spike epithelial cell (TSC).

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The prevalence of closed-system central nervous system (CNS) injuries underscores the need for an enhanced understanding of these traumas to improve protective and therapeutic interventions. Crucial to this research are animal models that replicate closed-system CNS injuries. In this context, a custom overpressure air system was engineered to reproduce a range of closed-system CNS injuries in murine models, including ocular, brain, and spinal cord trauma.

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Pharyngeal pumping and its reduction following mechanical insult are well-studied behaviors. Here, we assessed new applications of pharyngeal pumping assays in the study of neurodegenerative disease and psychiatric illness. We examined five genes implicated in two forms of neurodegeneration, Hereditary Spastic Paraplegia (HSPs) and Alzheimer's Disease (AD), for both baseline pharyngeal pumping and the depressive response after touch stimulus.

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Glaucoma, the second leading cause of irreversible blindness worldwide, is associated with age and sensitivity to intraocular pressure (IOP). We have shown that elevated IOP causes an early increase in levels of reactive oxygen species (ROS) in the microbead occlusion mouse model. We also detected an endogenous antioxidant response mediated by Nuclear factor erythroid 2-Related Factor 2 (NRF2), a transcription factor that binds to the antioxidant response element (ARE) and increases transcription of antioxidant genes.

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We propose SnBiTeto be a novel topological quantum material exhibiting temperature () mediated transitions between rich electronic phases. Our combined theoretical and experimental results suggest that SnBiTegoes from a low-semimetallic phase to a high-(room temperature) insulating phase via an intermediate metallic phase. Single crystals of SnBiTeare characterized by various experimental probes including synchrotron based x-ray diffraction, magnetoresistance, Hall effect, Seebeck coefficient and magnetization.

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Programmed cell death (PCD) is crucial for normal development and homeostasis. Our first insights into the genetic regulation of apoptotic cell death came from in vivo studies in the powerful genetic model system of C. elegans.

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COVID-19 has caused over 528 million infected cases and over 6.25 million deaths since its outbreak in 2019. The uncontrolled transmission of the SARS-CoV-2 virus has caused human suffering and the death of uncountable people.

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Here we highlight the increasingly divergent functions of the cell elimination genes in the nervous system, beyond their well-documented roles in cell dismantling and removal. We describe relevant background on the nervous system together with the apoptotic cell death and engulfment pathways, highlighting pioneering work in . We discuss in detail the unexpected, atypical roles of cell elimination genes in various aspects of neuronal development, response and function.

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Besides iron, ironically neodymium (Nd) is the most ubiquitously used metal for magnetic purposes, even among the lanthanides, when it comes to the field of molecular magnetism, yet it ranks among the least studied metals. However, strong apathy towards this magnetic lanthanide means that vital information will be missed, which is required for the advancement of the subject. Herein, we have successfully demonstrated the usefulness of a hexanuclear neodymium complex as a magnetic material, and also in electronic device fabrication.

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Programmed cell death (PCD) is a common cell fate in metazoan development. PCD effectors are extensively studied, but how they are temporally regulated is less understood. Here, we report a mechanism controlling tail-spike cell death onset during Caenorhabditis elegans development.

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Phagocytosis is an essential process by which cellular debris and pathogens are cleared from the environment. Cells extend their plasma membrane to engulf objects and contain them within a limiting membrane for isolation from the cytosol or for intracellular degradation in phagolysosomes. The basic mechanisms of phagocytosis and intracellular clearance are well conserved between animals.

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Cell death is an important facet of animal development. In some developing tissues, death is the ultimate fate of over 80% of generated cells. Although recent studies have delineated a bewildering number of cell death mechanisms, most have only been observed in pathological contexts, and only a small number drive normal development.

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We report transport properties of SbSnTe(⩽ 0.05) single crystals, where the tuning of the charge carrier densities via Sn doping significantly improves the magnetoresistance (MR) and the thermoelectric (TE) properties. The MR increases significantly at 2 K for= 0.

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Glaucoma is a group of optic neuropathies associated with aging and sensitivity to intraocular pressure (IOP). Early progression involves retinal ganglion cell (RGC) axon dysfunction that precedes frank degeneration. Previously we demonstrated that p38 MAPK inhibition abates axonal dysfunction and slows degeneration in the inducible microbead occlusion model of glaucoma in rat.

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Glaucoma is a group of optic neuropathies associated with aging and sensitivity to intraocular pressure (IOP). The disease causes vision loss through the degeneration of retinal ganglion cell neurons and their axons in the optic nerve. Using an inducible model of glaucoma, we elevated IOP in the squirrel monkey (Saimiri boliviensis) using intracameral injection of 35 μm polystyrene microbeads and measured common pathogenic outcomes in the optic projection.

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Phagocytosis of dying cells is critical in development and immunity. Although proteins for recognition and engulfment of cellular debris following cell death are known, proteins that directly mediate phagosome sealing are uncharacterized. Furthermore, whether all phagocytic targets are cleared using the same machinery is unclear.

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Many aerobic organisms encounter oxygen-deprived environments and thus must have adaptive mechanisms to survive such stress. It is important to understand how mitochondria respond to oxygen deprivation given the critical role they play in using oxygen to generate cellular energy. Here we examine mitochondrial stress response in C.

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A cell-culture-adapted reverse genetics strain of very virulent infectious bursal disease virus (IBDV) of chickens, designated as BD-3tcC, having four amino acid substitutions (Gln253His, Asp279Asn, Ala284Thr and Ser330Arg) in the capsid protein VP2 was tested for its genetic stability during serial passage in chickens and chicken embryo fibroblast (CEF) cell culture. Results of in vitro and in vivo experiments demonstrated that all four introduced mutations in BD-3tcC remained stable during serial passage in CEF cell culture, but during passage in chickens, amino acid residues at position 253 and 284 reverted from histidine to glutamine and threonine to alanine, respectively. In a parallel experiment, the same substitutions also occurred in a conventionally attenuated vaccine strain D-78 on serial passage in chickens.

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Ehrlichia chaffeensis is an obligate intracellular bacterium that infects primarily monocytes and macrophages and causes potentially fatal human monocytic ehrlichiosis (HME) that mimics toxic-shock-like syndrome in immunocompetent hosts. Early recruitment of neutrophils to the sites of infection is critical for the control of bacterial infection and inflammatory responses. We recently observed rapid and sustained neutrophil recruitment at a primary site of infection (peritoneum) following lethal murine ehrlichial infection compared to innocuous ehrlichial infection.

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Article Synopsis
  • C. elegans serves as a model organism to study the mechanisms behind healthy aging, focusing on changes in the nervous system.
  • The aging nervous system shows two key types of morphological changes: increased outgrowths from specific neurons and a decline in synaptic integrity.
  • Maintenance of certain neuron structures in older worms is linked to lowered insulin signaling and the protective roles of specific transcription factors, while the preservation of locomotion appears to correlate with better synaptic health.
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Background: Ehrlichia chaffeensis is a bacterial pathogen that causes fatal human monocytic ehrlichiosis (HME) that mimic toxic shock-like syndrome. Murine studies indicate that over activation of cellular immunity followed by immune suppression plays a central role in mediating tissue injury and organ failure during fatal HME. However, there are no human studies that examine the correlates of resistance or susceptibility to severe and fatal HME.

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Oxygen influences behaviour in many organisms, with low levels (hypoxia) having devastating consequences for neuron survival. How neurons respond physiologically to counter the effects of hypoxia is not fully understood. Here, we show that hypoxia regulates the trafficking of the glutamate receptor GLR-1 in C.

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The binding of IL-18 to IL-18Rα induces both proinflammatory and protective functions during infection, depending on the context in which it occurs. IL-18 is highly expressed in the liver of wild-type (WT) C57BL/6 mice following lethal infection with highly virulent Ixodes ovatus ehrlichia (IOE), an obligate intracellular bacterium that causes acute fatal toxic shock-like syndrome. In this study, we found that IOE infection of IL-18Rα(-/-) mice resulted in significantly less host cell apoptosis, decreased hepatic leukocyte recruitment, enhanced bacterial clearance, and prolonged survival compared with infected WT mice, suggesting a pathogenic role for IL-18/IL-18Rα in Ehrlichia-induced toxic shock.

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Fatty acid oxidation (FAO) defects cause abnormal lipid accumulation in various tissues, which provides an opportunity to uncover novel genes that are involved in lipid metabolism. During a gene expression study in the riboflavin deficient induced FAO disorder in the chicken, we discovered the dramatic increase in mRNA levels of an uncharacterized gene, ANKRD9. No functions have been ascribed to ANKRD9 and its orthologs, although their sequences are well conserved among vertebrates.

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The study of the Tally nulla wastewater system showed that the entire canal system is completely anoxic and unsuitable for sustaining aquatic life. Color and odor have exceeded the threshold limit. Tidal exchange is seemed to take place only up to six km.

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