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233 results on '"Saha P"'

4. Periodic heat waves-induced neuronal etiology in the elderly is mediated by gut-liver-brain axis: a transcriptome profiling approach.

Author

Roy, Subhajit, Bose, Dipro, Trivedi, Ayushi, More, Madhura, Lin, Christina, Wu, Jie, Oakes, Melanie, Chatterjee, Saurabh, and Saha, Punnag

Subjects
Climate change, Gut-liver-brain axis, Human health, Hyperthermia, ORM2, RANTES, Animals, Mice, Liver, Brain, Gene Expression Profiling, Male, Transcriptome, Brain-Gut Axis, Heat-Shock Response, Mice, Inbred C57BL, Signal Transduction, Aging
Abstract

Heat stress exposure in intermittent heat waves and subsequent exposure during war theaters pose a clinical challenge that can lead to multi-organ dysfunction and long-term complications in the elderly. Using an aged mouse model and high-throughput sequencing, this study investigated the molecular dynamics of the liver-brain connection during heat stress exposure. Distinctive gene expression patterns induced by periodic heat stress emerged in both brain and liver tissues. An altered transcriptome profile showed heat stress-induced altered acute phase response pathways, causing neural, hepatic, and systemic inflammation and impaired synaptic plasticity. Results also demonstrated that proinflammatory molecules such as S100B, IL-17, IL-33, and neurological disease signaling pathways were upregulated, while protective pathways like aryl hydrocarbon receptor signaling were downregulated. In parallel, Rantes, IRF7, NOD1/2, TREM1, and hepatic injury signaling pathways were upregulated. Furthermore, current research identified Orosomucoid 2 (ORM2) in the liver as one of the mediators of the liver-brain axis due to heat exposure. In conclusion, the transcriptome profiling in elderly heat-stressed mice revealed a coordinated network of liver-brain axis pathways with increased hepatic ORM2 secretion, possibly due to gut inflammation and dysbiosis. The above secretion of ORM2 may impact the brain through a leaky blood-brain barrier, thus emphasizing intricate multi-organ crosstalk.

Published
2024

11. Antimicrobial stewardship implementation in primary and secondary tier hospitals in India: interim findings from a need assessment study using mixed method design

Author

Debnath, Falguni, De, Rajyasree Ghosh, Chakraborty, Debjit, Majumdar, Agniva, Mukhopadhyay, Sandip, Sarkar, Munmun Das, Singh, Taru, Patra, Sanjit Kumar, Saha, Surangana, Rehman, Julius, Roy, Dhiraj, Chakrabarti, Atreyi, Basu, Sulagna, Mukhopadhyay, Asish Kumar, Mondal, Amitabha, Soren, Shyamal, Datta, Kalpana, Pain, Shantasil, Mondal, Supreeti Biswas, Mondal, Palash, Walia, Kamini, Maji, Dipankar, Deb, Alok Kumar, and Dutta, Shanta

Published
2024
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41. Utilizing photonic band gap in triangular silicon carbide structures for efficient quantum nanophotonic hardware

Author

Saha, Pranta, Majety, Sridhar, and Radulaski, Marina

Subjects
Quantum Physics, Engineering, Electronics, Sensors and Digital Hardware, Physical Sciences
Abstract

Silicon carbide is among the leading quantum information material platforms due to the long spin coherence and single-photon emitting properties of its color center defects. Applications of silicon carbide in quantum networking, computing, and sensing rely on the efficient collection of color center emission into a single optical mode. Recent hardware development in this platform has focused on angle-etching processes that preserve emitter properties and produce triangularly shaped devices. However, little is known about the light propagation in this geometry. We explore the formation of photonic band gap in structures with a triangular cross-section, which can be used as a guiding principle in developing efficient quantum nanophotonic hardware in silicon carbide. Furthermore, we propose applications in three areas: the TE-pass filter, the TM-pass filter, and the highly reflective photonic crystal mirror, which can be utilized for efficient collection and propagating mode selection of light emission.

Published
2023

47. Prior exposure to microcystin alters host gut resistome and is associated with dysregulated immune homeostasis in translatable mouse models

Author

Saha, Punnag, Bose, Dipro, Stebliankin, Vitalii, Cickovski, Trevor, Seth, Ratanesh K, Porter, Dwayne E, Brooks, Bryan W, Mathee, Kalai, Narasimhan, Giri, Colwell, Rita, Scott, Geoff I, and Chatterjee, Saurabh

Subjects
Microbiology, Biological Sciences, Biomedical and Clinical Sciences, Genetics, Antimicrobial Resistance, Aetiology, 2.1 Biological and endogenous factors, Infection, Inflammatory and immune system, Animals, Anti-Bacterial Agents, Drug Resistance, Bacterial, Gastrointestinal Microbiome, Homeostasis, Immunosenescence, Interleukin-6, Mice, Microcystins, Toll-Like Receptor 2
Abstract

A strong association between exposure to the common harmful algal bloom toxin microcystin and the altered host gut microbiome has been shown. We tested the hypothesis that prior exposure to the cyanotoxin microcystin-LR may alter the host resistome. We show that the mice exposed to microcystin-LR had an altered microbiome signature that harbored antibiotic resistance genes. Host resistome genotypes such as mefA, msrD, mel, ant6, and tet40 increased in diversity and relative abundance following microcystin-LR exposure. Interestingly, the increased abundance of these genes was traced to resistance to common antibiotics such as tetracycline, macrolides, glycopeptide, and aminoglycosides, crucial for modern-day treatment of several diseases. Increased abundance of these genes was positively associated with increased expression of PD1, a T-cell homeostasis marker, and pleiotropic inflammatory cytokine IL-6 with a concomitant negative association with immunosurveillance markers IL-7 and TLR2. Microcystin-LR exposure also caused decreased TLR2, TLR4, and REG3G expressions, increased immunosenescence, and higher systemic levels of IL-6 in both wild-type and humanized mice. In conclusion, the results show a first-ever characterization of the host resistome following microcystin-LR exposure and its connection to host immune status and antimicrobial resistance that can be crucial to understand treatment options with antibiotics in microcystin-exposed subjects in clinical settings.

Published
2022

48. Glyoxylate protects against cyanide toxicity through metabolic modulation

Author

Nielson, Jason R, Nath, Anjali K, Doane, Kim P, Shi, Xu, Lee, Jangwoen, Tippetts, Emily G, Saha, Kusumika, Morningstar, Jordan, Hicks, Kevin G, Chan, Adriano, Zhao, Yanbin, Kelly, Amy, Hendry-Hofer, Tara B, Witeof, Alyssa, Sips, Patrick Y, Mahon, Sari, Bebarta, Vikhyat S, Davisson, Vincent Jo, Boss, Gerry R, Rutter, Jared, MacRae, Calum A, Brenner, Matthew, Gerszten, Robert E, and Peterson, Randall T

Subjects
Vaccine Related, Prevention, Biodefense, Animals, Cyanides, Glyoxylates, Mammals, Pyruvic Acid, Zebrafish
Abstract

Although cyanide's biological effects are pleiotropic, its most obvious effects are as a metabolic poison. Cyanide potently inhibits cytochrome c oxidase and potentially other metabolic enzymes, thereby unleashing a cascade of metabolic perturbations that are believed to cause lethality. From systematic screens of human metabolites using a zebrafish model of cyanide toxicity, we have identified the TCA-derived small molecule glyoxylate as a potential cyanide countermeasure. Following cyanide exposure, treatment with glyoxylate in both mammalian and non-mammalian animal models confers resistance to cyanide toxicity with greater efficacy and faster kinetics than known cyanide scavengers. Glyoxylate-mediated cyanide resistance is accompanied by rapid pyruvate consumption without an accompanying increase in lactate concentration. Lactate dehydrogenase is required for this effect which distinguishes the mechanism of glyoxylate rescue as distinct from countermeasures based solely on chemical cyanide scavenging. Our metabolic data together support the hypothesis that glyoxylate confers survival at least in part by reversing the cyanide-induced redox imbalances in the cytosol and mitochondria. The data presented herein represent the identification of a potential cyanide countermeasure operating through a novel mechanism of metabolic modulation.

Published
2022

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