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The current investigation aimed to comprehend the inflammatory and related immune responses in intrauterine calves subjected to heat stress (HS) during late gestation. For this purpose, 48 Sahiwal cows in late gestation were chosen and categorized into four equal groups: naturally heat stressed (NHS), cooling-treated (CLT), spring, and winter, and likewise their neonate calves born in summer (IUHS - intrauterine heat stressed and IUCL – intrauterine cooled), spring, and winter seasons. Environmental parameters were recorded, and the temperature-humidity index (THI) was calculated daily throughout the study period. The average THI values ranged between 84.18 (summer-NHS), 73.88 (summer-CLT), 78.92 (spring), and 64.91 (winter). NHS and spring groups exhibited thermal stress based on THI (> 76.00). Various treatments significantly (P < 0.01) impacted parameters like rectal temperature (RT), respiratory rate (RR), pulse rate (PR), and skin temperature (ST) in Sahiwal cows and their calves during the study, except for heart rate (HR). Blood samples collected during different seasons and from cows housed in a climatic chamber were used to extract plasma. Plasma cortisol, interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and thiobarbituric acid reactive substances (TBARS) levels were notably higher (P < 0.05) in the NHS compared to the CLT group. Conversely, total antioxidant capacity (TAC) and immunoglobulin G (IgG) levels were higher (P < 0.05) in the CLT and winter groups. IUHS calves exhibited significantly (P < 0.05) lower overall mean plasma TAC and IgG levels but higher inflammatory and oxidative biomarkers, such as IL-6, TNF-α, and TBARS. Additionally, significant impacts on body weight were observed for factors such as interval (P < 0.01) and the interaction between treatment and interval (P < 0.05), exhibiting consistently lower body weight in IUHS calves throughout the study period. These findings suggest that late gestation heat stress may lead to physiological alterations in future calves. Strategies aimed at mitigating heat stress during late gestation should be considered not only for the productivity and well-being of the pregnant dam but also for the development and future performance of the calf.

The general objective of this study is to comparatively assess the climate-resilient potential of four different poultry genotypes-Giriraja (n = 8), Country chicken (n = 8), Naked neck (n = 8), and Kadaknath (n = 8)—reared in a hot-humid tropical environment. Birds from all genotypes had ad libitum access to feed and water and were exposed to identical environmental temperatures in the experimental shed. Diurnal meteorological data were recorded inside and outside the shed daily. Blood biochemical, hormonal, and endocrine variables were monitored monthly until the birds reached 12 weeks of age. Significant variations (P < 0.01) were observed at different intervals in variables, including total protein, albumin, globulin, triglycerides, and cholesterol. Genotype-specific differences were noted in triglycerides (P < 0.01), albumin (P < 0.01), total protein (P < 0.05), and cholesterol (P < 0.05). Inter-genotype variations (P < 0.05) were also observed in serum cortisol, T3, and T4 levels. Distinct variations (P < 0.05) were also observed during specific intervals, particularly in cortisol and T3 levels. The study of hepatic mRNA expression of HSPs and HSF-1 revealed a significant breed difference (P < 0.05) in the expression pattern of HSP60, HSP70, HSP90, and HSP110, while no difference was observed between genotypes for HSP40 and HSF-1. The study highlights the Naked Neck breed as an exemplar of resilience, showcasing its distinctive ability to maintain homeostasis under heat stress compared to other genotypes. The genetic and physiological insights gained from this investigation offer prospective pathways for aligning sustainable poultry farming with environmental exigencies.

This study evaluated the impact of combined stressors (heat and nutritional stresses) on the growth and adaptive capability of Sahiwal (SW) and Karan Fries (KF) calves during the summer season. Calves in each breed were randomly divided into four groups. In SW breed the groupings were as follows: SWC (n = 4; Sahiwal Control); SWHS (n = 4; Sahiwal Heat Stress); SWNS (n = 4; Sahiwal Nutritional Stress) and SWCS (n = 4; Sahiwal Combined Stresses). Likewise, in the KF breed, KFC (n = 4; Karan Fries Control); KFHS (n = 4; Karan Fries Heat Stress); KFNS (n = 4; Karan Fries Nutritional Stress), and KFCS (n = 4; Karan Fries Combined Stresses). Control (C) and Heat Stress (HS) calves were fed ad libitum while Nutritional Stress (NS) and Combined Stresses (CS) calves were fed restricted feed (50% of C calves of respective breed) to induce nutritional stress in both the breeds. SWHS, SWCS, KFHS, and KFCS were exposed to summer heat stress from 1000 to 1600 h. All growth and adaptation variables were recorded at fortnightly intervals. Respiration rate, pulse rate, and rectal temperature during the afternoon were significantly (P < 0.01) higher in the CS group in both breeds. Further, CS had significantly (P < 0.05) higher plasma growth hormone and cortisol levels. Insulin-like growth factor-1, Triiodothyronine, and Thyroxine levels significantly decreased (P < 0.05) in the CS group in both breeds. Interestingly, heat stress didn’t affect SWHS and KFHS bodyweight, however, a significant (P < 0.05) decrease in body weight of SWCS and KFCS was observed when compared with C. Hepatic mRNA expression of growth hormone, insulin-like growth factor-1, and growth hormone receptor significantly (P < 0.05) varied when compared between C and CS groups in both the breeds. The overall magnitude of stress was more pronounced in KF compared to the SW breed. This study concludes that when two stressors occur concurrently, they may have a greater influence on the adaptive capability of calves. Further, SW had better tolerance levels than KF, confirming the indigenous breed's superiority over cross-bred.

An investigation was conducted to assess the efficacy of a novel antioxidant supplementation, Transcare, in alleviating transportation-induced stress among Bannur sheep. Thirty female Bannur sheep of 10–12 months, were selected and randomly assigned to two groups: Bannur Non-supplemented (BNS) ( n  = 15) and Bannur Supplemented (BS) ( n  = 15). The BS was supplemented with antioxidant powder (Transcare) orally at a dose of 10 g/animal, dissolved in 10 mL drinking water, 45–60 min preload. The antioxidants supplementation significantly ( P  < 0.01) influenced the variables such as pulse rate (after transportation), mean corpuscular volume (after transportation), glucose (after transportation) and HSP70 (after transportation) , when juxtaposed between the BNS and BS cohorts. Marked reductions in transportation-induced stress were observed in Bannur sheep following antioxidant supplementation, as manifested by discernible alterations in stress-responsive metrics. These findings underscore the promising role of the novel oral antioxidant supplementation in alleviating transportation stress among Bannur sheep. Thus, advocating for the adoption of such supplementation strategies, particularly among economically constrained farmers, may present a viable approach to mitigate the economic ramifications associated with transportation-induced stress in sheep husbandry practices.

Uncarboxylated osteocalcin (UcOCN), a bone derived circulating protein, has been demonstrated to influence steroidogenesis in testicular Leydig cells of murine and human species. However, the role of UcOCN in testosterone biosynthesis remains unexplored in domestic animals. The present study aimed to investigate the impact of UcOCN on the expressions of steroidogenic genes (HSD3β1, HSD3β6, CYP17A1, CYP11A1), testosterone production and GPRC6A receptor localization in buffalo Leydig cells. Leydig cells from the testes of adult Murrah buffalo were isolated, with an average cell count and viability after digestion and Percoll enrichment of 1.43 × 106 cells/g of testes and 78.5%, respectively. Immunophenotyping of Percoll-enriched cell suspension by flow cytometry showed populations of Leydig cells ranging between 69 and 73.9%. Immunostaining confirmed the presence of GPRC6A receptors and CYP11A1 positive Leydig cells. When these cells were cultured and incubated with varying levels of UcOCN (6, 12, 24, and 48 ng/ml) and LH, there was a significant (P < 0.01) increase in testosterone production and up-regulation (P < 0.05) of CYP11A1, CYP17A1, HSD3β1 and HSD3β6 gene expression. In summary, the present study underscored the effects of UcOCN on testosterone biosynthesis, expression of crucial steroidogenic genes and interaction with GPRC6A receptors in buffalo Leydig cells, emphasizing its potential implications in andrology.

To better elucidate epigenetic mechanisms that correlate with the dynamic gene expression program observed upon T-cell differentiation, we investigated the genomic landscape of histone modifications in naive and memory CD8＋ T cells. Using a ChlP-Seq approach coupled with global gene expression profiling, we generated genome-wide histone H3 lysine 4 （H3K4me3） and H3 lysine 27 （H3K27me3） trimethylation maps in naive, T memory stem cells, central memory cells, and effector memory cells in order to gain insight into how histone architecture is remodeled during T cell differentiation. We show that H3K4me3 histone modifications are associated with activation of genes, while H3K27me3 is negatively correlated with gene expression at canonical loci and enhancers associated with T-cell metabolism, effector function, and memory. Our results also reveal histone modifications and gene expression signatures that distinguish the recently identified T memory stem cells from other CD8＋ T-cell subsets. Taken together, our results suggest that CD8＋ lymphocytes undergo chromatin remodeling in a progressive fashion. These findings have major implications for our understanding of peripheral T-cell ontogeny and the formation of immunological memory.

Glutamate delta-1 (GluD1) receptors are expressed throughout the forebrain during development with high levels in the hippocampus during adulthood. We have recently shown that deletion of GluD1 receptor results in aberrant emotional and social behaviors such as hyperaggression and depression-like behaviors and social interaction deficits. Additionally, abnormal expression of synaptic proteins was observed in amygdala and prefrontal cortex of GluD1 knockout mice (GluD1 KO). However the role of GluD1 in learning and memory paradigms remains unknown. In the present study we evaluated GluD1 KO in learning and memory tests. In the eight-arm radial maze GluD1 KO mice committed fewer working memory errors compared to wildtype mice but had normal reference memory. Enhanced working memory in GluD1 KO was also evident by greater percent alternation in the spontaneous Y-maze test. No difference was observed in object recognition memory in the GluD1 KO mice. In the Morris water maze test GluD1 KO mice showed no difference in acquisition but had longer latency to find the platform in the reversal learning task. GluD1 KO mice showed a deficit in contextual and cue fear conditioning but had normal latent inhibition. The deficit in contextual fear conditioning was reversed by D-Cycloserine (DCS) treatment. GluD1 KO mice were also found to be more sensitive to foot-shock compared to wildtype. We further studied molecular changes in the hippocampus, where we found lower levels of GluA1, GluA2 and GluK2 subunits while a contrasting higher level of GluN2B in GluD1 KO. Additionally, we found higher postsynaptic density protein 95 (PSD95) and lower glutamate decarboxylase 67 (GAD67) expression in GluD1 KO. We propose that GluD1 is crucial for normal functioning of synapses and absence of GluD1 leads to specific abnormalities in learning and memory. These findings provide novel insights into the role of GluD1 receptors in the central nervous system.

Ceramides draw wide attention as tumor suppressor lipids that act directly on mitochondria to trigger apoptotic cell death. However, molecular details of the underlying mechanism are largely unknown. Using a photoactivatable ceramide probe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide binding proteins. Coarse-grain molecular dynamics simulations reveal that both channels harbor a ceramide binding site on one side of the barrel wall. This site includes a membrane-buried glutamate that mediates direct contact with the ceramide head group. Substitution or chemical modification of this residue abolishes photolabeling of both channels with the ceramide probe. Unlike VDAC1 removal, loss of VDAC2 or replacing its membrane-facing glutamate with glutamine renders human colon cancer cells largely resistant to ceramide-induced apoptosis. Collectively, our data support a role of VDAC2 as direct effector of ceramide-mediated cell death, providing a molecular framework for how ceramides exert their anti-neoplastic activity. Ceramides are lipids that act directly on mitochondria to trigger apoptosis, but the underlying mechanism remains largely unclear. Here authors use a photoactivatable ceramide probe combined with a computation approach and functional studies to identify the voltage-dependent anion channel VDAC2 as a direct effector of ceramide-mediated cell death.

The delta family of ionotropic glutamate receptors consists of glutamate δ1 (GluD1) and glutamate δ2 (GluD2) receptors. While the role of GluD2 in the regulation of cerebellar physiology is well understood, the function of GluD1 in the central nervous system remains elusive. We demonstrate for the first time that deletion of GluD1 leads to abnormal emotional and social behaviors. We found that GluD1 knockout mice (GluD1 KO) were hyperactive, manifested lower anxiety-like behavior, depression-like behavior in a forced swim test and robust aggression in the resident-intruder test. Chronic lithium rescued the depression-like behavior in GluD1 KO. GluD1 KO mice also manifested deficits in social interaction. In the sociability test, GluD1 KO mice spent more time interacting with an inanimate object compared to a conspecific mouse. D-Cycloserine (DCS) administration was able to rescue social interaction deficits observed in GluD1 KO mice. At a molecular level synaptoneurosome preparations revealed lower GluA1 and GluA2 subunit expression in the prefrontal cortex and higher GluA1, GluK2 and PSD95 expression in the amygdala of GluD1 KO. Moreover, DCS normalized the lower GluA1 expression in prefrontal cortex of GluD1 KO. We propose that deletion of GluD1 leads to aberrant circuitry in prefrontal cortex and amygdala owing to its potential role in presynaptic differentiation and synapse formation. Furthermore, these findings are in agreement with the human genetic studies suggesting a strong association of GRID1 gene with several neuropsychiatric disorders including schizophrenia, bipolar disorder, autism spectrum disorders and major depressive disorder.