Publications by authors named "Mohan Kumar S"

The present investigation evaluates three satellite precipitation products (SPPs), Multi-Source Weighted-Ensemble Precipitation (MSWEP), Global Precipitation Climatology Centre (GPCC), Climate Hazard Infrared Precipitation with Station Data (CHIRPS), and two reanalysis datasets, namely, the ERA5 atmosphere reanalysis dataset (ERA5) and Indian Monsoon Data Assimilation and Analysis (IMDAA), against the good quality gridded reference dataset (1991-2022) developed by the India Meteorological Department (IMD). The evaluation was carried out in terms of the rainfall detection ability and estimation accuracy of the products using metrics such as the false alarm ratio (FAR), probability of detection (POD), misses, root mean square error (RMSE), and percent bias (PBIAS). Among all the rainfall products, ERA5 had the best ability to capture rainfall events with a higher POD, followed by MSWEP.

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This study examines the sex-specific effects of gestational exposure (days 6-21) to endocrine-disrupting chemicals such as bisphenol A (BPA), diethylhexyl phthalate (DEHP), or their combination on brain monoamine levels that play an important role in regulating behavior. Pregnant Sprague-Dawley rats were orally administered saline, low doses (5 µg/kg BW/day) of BPA or DEHP, and their combination or a high dose (7.5 mg/kg BW/day) of DEHP alone or in combination with BPA during pregnancy.

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In this study, an extensive exploration survey of wild progeny was conducted which yielded 18 candidate plus trees (CPTs) of . Seeds of these CPTs were collected from diverse locations between 10°54' and 28°07' E longitude, and 76°27' and 95°32' N latitude, covering 18 different locations across 5 states of the Indian subcontinent. The objective of the progeny trial was to assess genetic associations and variability in growth and physio-chemical characteristics.

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  • The study investigates how prenatal exposure to endocrine disrupting chemicals (EDCs), specifically bisphenol A (BPA) and diethylhexyl phthalate (DEHP), affects the behavior of male and female rats.
  • Results show that female offspring exhibited reduced anxiety in certain behavioral tests, while males showed signs of feminization and maladaptive defensive behaviors, particularly with higher doses of DEHP.
  • The findings indicate that exposure to EDCs during pregnancy leads to sex-specific behavioral changes, altered corticosterone levels, and changes in adrenal gland weights, with varying effects based on dosage and chemical combinations.
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There is still a need for a better and affordable seasonal influenza vaccine and the use of an adjuvant could solve both issues. Therefore, immunogenicity of a combination of low dose of 1/5 (3 µg of HA) a licensed seasonal flu vaccine with the novel carbohydrate fatty acid monosulfate ester (CMS)-based adjuvant was investigated in ferrets and safety in rabbits. Without CMS, hemagglutination inhibition (HI) antibody titers ranged from ≤5 to 26 three weeks post immunization 1 (PV-1) and from 7 to 134 post-immunization 2 (PV-2) in ferrets.

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  • Aging significantly impacts the brain due to both external factors and changes in immune cells over time.
  • Immunosenescence and Inflammaging contribute to increased inflammation and oxidative stress in the brain, elevating cytokine levels.
  • This pro-inflammatory environment causes harmful alterations in brain structure and function, ultimately impairing central and neuroendocrine processes.
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Alzheimer's disease (AD) is an irreversible neurodegenerative disorder with a complex pathophysiology. Type 2 diabetes (T2D) is a strong risk factor for AD that shares similar abnormal features including metabolic dysregulation and brain pathology such as amyloid and/or Tau deposits. Emerging evidence suggests that circulating branched-chain amino acids (BCAAs) are associated with T2D.

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The yellow mosaic disease (YMD) of blackgram caused by Mungbean yellow mosaic virus has emerged as a serious threat to grain legume production, especially in Southeastern Asia. Seasonal incidence of YMD with its vector population was assessed in three different agroclimatic zones of Tamil Nadu in India for three consecutive cropping seasons namely, Rabi 2018 (October-December), Summer 2019 (March-May), and Kharif 2019 (June-August) at three different time intervals viz., 20, 40, and 60 days after sowing (DAS).

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  • Type 1 diabetes (T1D) leads to symptoms like increased hunger and high blood sugar levels, along with a stressed hormonal response.
  • Researchers tested whether injecting a gene therapy vector for leptin (a hormone that helps regulate hunger and energy) could improve these issues in diabetic rats.
  • Results showed that leptin gene therapy reduced blood sugar and some neuroendocrine dysfunctions in diabetic rats, but higher doses are needed for it to be a practical treatment for T1D.
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The objective of this study was to evaluate the effects of gestational exposure to low doses of bisphenol A (BPA), bisphenol S (BPS), and bisphenol F (BPF) on pregnancy outcomes and offspring development. Pregnant Sprague-Dawley rats were orally dosed with vehicle, 5 μg/kg body weight (BW)/day of BPA, BPS and BPF, or 1 μg/kg BW/day of BPF on gestational days 6-21. Pregnancy and gestational outcomes, including number of abortions and stillbirths, were monitored.

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Bisphenol A (BPA) and Diethylhexyl Phthalate (DEHP) are well-studied endocrine disrupting chemicals (EDCs), however, the effects of mixtures of these EDCs are not. To assess the consequences of prenatal exposure to a mixture of these EDCs, dams were orally administered either saline (control), BPA (5 μg/kg BW/day), high dose DEHP (HD-D; 7.5 mg/kg BW/day), or a combination of BPA with HD-D in experiment 1; saline, BPA (5 μg/kg BW/day), low-dose DEHP (LD-D; 5 μg/kg BW/day) or a combination of BPA with LD-D in experiment 2.

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  • The HPA axis is disrupted in obesity, leading to leptin resistance in the brain and issues with noradrenergic function in DIO rats.
  • Metformin treatment in these rats resulted in decreased weight gain, fat mass, and improved HPA axis activity by normalizing its functions and reducing corticotropin-releasing hormone levels.
  • The study highlights metformin's potential to address HPA axis dysfunction in obesity, suggesting a new therapeutic role for the drug in managing weight.
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  • Obesity is increasingly recognized as a global health issue, and high-fat intake may lead to increased levels of free fatty acids, impacting neuroendocrine functions related to obesity.
  • Researchers examined the effects of oleic acid on hypothalamic monoamines, proposing that it activates PPAR-α, a key factor in fatty acid metabolism, and that this effect would be diminished in rats with diet-induced obesity (DIO).
  • The study found that oleic acid significantly raised levels of norepinephrine, dopamine, and serotonin in a dose-dependent manner, but this response was reduced in DIO rats, indicating the importance of PPARα in the hypothalamus's response to fatty acids.
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  • Diet-induced obese rats have altered stress (HPA) axis activity compared to diet-resistant rats, likely due to impaired leptin signaling.
  • Leptin injection increased serum leptin levels and reduced norepinephrine levels in both rat groups, suggesting that noradrenergic neurons respond to leptin, but responses in DIO rats' CRH and corticosterone varied with high-fat diet exposure.
  • DIO rats showed reduced leptin signaling in brainstem neurons and higher levels of free fatty acids and IL-1β, indicating neuroendocrine impairments that become more pronounced with prolonged high-fat diet exposure.
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  • Type I Diabetes (T1D) leads to lower leptin levels and heightened stress response, as seen with increased norepinephrine (NE) in the hypothalamus.
  • In experiments with diabetic rats, leptin treatment reduced corticosterone levels significantly and showed a modest decrease in NE release.
  • The response of the hypothalamus to beta adrenergic agonists is altered in T1D, with only the alpha-2 adrenergic agonist clonidine effectively reversing leptin's impact on NE levels, while both agonists affected the corticosterone response.
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Women are chronically exposed to estrogens through oral contraceptives, hormone replacement therapy or environmental estrogens. We hypothesized that chronic exposure to low levels of estradiol-17β (E2) can induce inflammatory and degenerative changes in the tuberoinfundibular dopaminergic (TIDA) system leading to reduced dopamine synthesis and hyperprolactinemia. Young (Y; 3–4 months) and middle-aged (MA; 10–12 months) Sprague-Dawley rats that were intact or ovariectomized (OVX) were either sham-implanted or implanted with a slow-release E2 pellet (20 ng E2/day for 90 days).

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  • Estradiol (E2) is a key female hormone produced mainly by the ovaries, with various roles in both males and females, including bone health and protection against memory loss.
  • While E2 has many beneficial effects, the impact of its exposure on the neuroendocrine system is not fully understood due to variability in study methods.
  • Recent lab studies indicate that chronic low-level E2 exposure in young rats can lead to reproductive aging, hypertension, anxiety-like behavior, and neuronal degeneration.
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Purpose: The purpose of the study was to evaluate the feasibility and efficacy of an accelerated radiotherapy schedule using weekend boost in terms of tumor response, compliance, and acute toxicities for head and neck squamous cell carcinoma, and to report long-term clinical outcomes.

Materials And Methods: Twenty-six patients with stages III-IV head and neck squamous cell carcinoma receiving radical chemoradiotherapy were accrued prospectively into the study. External beam radiation therapy to a total dose of 66-70 Gy in 33-35 fractions, 1.

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Previously, we demonstrated that chronic exposure to low levels of estradiol-17β (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (SD) rats, however, the underlying mechanisms are unclear. Since endothelin-1 (ET-1) is implicated in blood pressure (BP) regulation, we hypothesized that E2's effects on MAP are mediated through central ET-1. To test this, young female SD rats were either sham implanted or implanted s.

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  • Prenatal exposure to Bisphenol-A (BPA) does not significantly change blood pressure or heart structure directly, but it affects heart gene expression and interacts with later overfeeding.
  • BPA-treated offspring show altered gene expression related to heart function, including increased atrial natriuretic peptide and reduced collagen in the right ventricle.
  • When overfed, these animals experience notable increases in body weight and some heart size parameters, but BPA exposure seems to counteract some of the negative cardiovascular impacts typically associated with obesity.
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  • Chronic exposure to estradiol-17β (E2) in female rats raises mean arterial pressure by promoting superoxide production in a specific brain region ( RVLM), although the exact mechanisms remain unclear.
  • E2 treatment leads to increased expression of inflammatory genes and NADPH oxidase components in the RVLM, with older rats showing greater upregulation of these inflammatory markers compared to younger ones.
  • While E2 exposure raises blood pressure and affects gene expression differently based on age, it does not significantly alter superoxide dismutase (SOD) activity, which was lower in middle-aged rats compared to younger ones.
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Stress during pregnancy is a known contributing factor for the development of obesity in the offspring. Since maternal obesity is on the rise, we wanted to identify the effects of prenatal stress in the offspring of diet-induced obese (DIO) rats and compare them with the offspring of dietary-resistant (DR) rats. We hypothesized that prenatal stress would make both DIO and DR offspring susceptible to obesity, but the effect would be more pronounced in DIO rats.

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Aging in female rats is characterized by a state called "constant estrous" in which rats are unable to ovulate, have polycystic ovaries and moderately elevated estrogen levels. We hypothesized that chronic exposure of young animals to low levels of E2 can produce reproductive changes similar to that seen in aging animals. Adult female rats were sham-implanted (control) or implanted with slow-release E2 (20 ng/day) pellets for 30, 60, or 90 days.

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  • Chronic exposure to estrogens like estradiol-17β (E2) can lead to significant reproductive issues in women, including cancer and anovulation, and research in female rats suggests this may occur through decreased norepinephrine (NE) release in the hypothalamus.
  • E2 exposure over time resulted in decreased LH secretion and failure of ovulation in rats, with specific mechanisms including increases in inflammatory markers like interleukin-1β and nitration of enzymes involved in NE synthesis.
  • Experimental findings showed that NE levels in the medial preoptic area were progressively reduced with longer E2 exposure, suggesting a link between chronic estrogen exposure and disruption of hormonal balance necessary for ovulation.
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  • IL-1β is a cytokine that impacts the body's stress and reproductive systems by altering norepinephrine (NE) levels in specific brain regions.
  • In a study with female rats, IL-1β injection led to decreased NE levels in areas responsible for reproduction and increased NE levels in stress-related areas.
  • The differential effects of IL-1β on these axes suggest a possible adaptive response to immune challenges by modulating NE concentrations in the brain.
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