Search Results (2,266)

Understanding the chronic thermal acclimation capacity of chum salmon (Oncorhynchus keta) is essential for predicting species resilience and developing mitigation strategies under ocean warming. We investigated the upper limit of chronic thermal acclimation and its underlying molecular mechanisms in chum salmon smolts exposed to four constant temperatures (10, 14, 18, and 22 °C) for 6 weeks. Transcriptional responses of genes related to cellular stress protection, endocrine feedback regulation, antioxidant defense, metabolic regulation (AMPKα and mTOR), and protein degradation were quantified in the liver, skeletal muscle, and brain. Chronic exposure to elevated temperature elicited tissue-specific molecular responses, with the most pronounced effects observed at 22 °C. At this temperature, all tissues showed marked induction of heat shock proteins and ubiquitin, accompanied by suppression of antioxidant defenses, glucocorticoid receptor signaling, and AMPKα–mTOR-mediated metabolic regulation, particularly in the liver and muscle. These responses were consistent with previously reported impairments in growth performance, lipid reserves, and hematological indices from the same growth trial. In contrast, smolts maintained at 18 °C exhibited molecular signatures indicative of effective physiological compensation without severe cellular stress. Collectively, these results indicate that chum salmon smolts can acclimate to chronic warming up to 18 °C, whereas exposure to 22 °C exceeds their acclimation capacity and induces a tertiary stress response. Full article

Background: Type 1 diabetes (T1D) is associated with metabolic and neuromuscular impairments that may influence fatigue mechanisms and limit exercise tolerance. Although previous investigations have characterized muscle performance in T1D, the peripheral fatigue threshold, defined as the maximal sustainable level of peripheral fatigue, remains poorly understood in this population. This study aimed to compare the amplitude of the maximal peripheral fatigue threshold between individuals with T1D and healthy controls to elucidate the effects of T1D on neuromuscular function. Methods: Twenty-two participants (11 with T1D and 11 healthy controls) completed two randomized experimental sessions. In each session, 60 quadriceps maximal voluntary contractions (MVCs) were completed, performed for 3 s with 2 s of rest between contractions. One session was conducted under a non-fatigued control condition (CTRL), and the other followed a fatiguing neuromuscular electrical stimulation (FNMES) protocol. Central and peripheral fatigue were evaluated from the pre- to post-exercise changes in potentiated twitch force (ΔPtw) and voluntary activation (ΔVA), respectively. Critical torque (CT) was calculated as the average torque produced during the last 12 contractions, whereas the curvature constant of the torque–duration relationship (W′) was quantified as the area above CT. Results: Although both groups exhibited a decline in pre-exercise Ptw following the FNMES condition, no significant within-group differences in ΔPtw were observed between sessions (T1D: p = 0.34; controls: p = 0.23). Nevertheless, the extent of peripheral fatigue was significantly lower in participants with T1D than in controls (ΔPtw = −38 ± 11% vs. −52 ± 17%; p < 0.05). Additionally, W′ values were reduced by 24% in the T1D group relative to controls during the CTRL condition (p = 0.02), and CT was significantly lower in T1D participants (262 ± 49 N) compared to controls (353 ± 71 N; p < 0.01). A significant positive correlation was observed between ΔPtw and W′ across groups (r² = 0.62, p < 0.001), suggesting a mechanistic link between peripheral fatigue tolerance and work capacity. Conclusions: The present results indicate that, although individuals with T1D retain the capacity to develop peripheral fatigue, their fatigue threshold and critical torque are markedly attenuated relative to those of healthy individuals. This reduction reflects impaired neuromuscular efficiency and diminished tolerance to sustained contractile activity. The strong relationship between peripheral fatigue and work capacity underscores the contribution of peripheral mechanisms to exercise intolerance in T1D. These results enhance current understanding of fatigue physiology in diabetes and emphasize the need for tailored exercise and rehabilitation strategies to improve fatigue resistance and functional performance in this population. Full article

Peri-implantitis is an inflammatory disease caused by bacterial colonization that leads to progressive bone loss around dental implants. Implantoplasty is widely used for biofilm removal; however, it alters the titanium surface, generating particle release and impairing surface properties. This study evaluated whether a citric acid-based solution supplemented with collagen and magnesium cations could enhance hard and soft tissue regeneration following implantoplasty. Three surfaces were analyzed: physiological saline (Ctr), 25% citric acid (AC), and citric acid with collagen and magnesium nitrate hexahydrate (AC500/Mg). Surface roughness and wettability were assessed on titanium discs. Cytocompatibility, cell adhesion, and proliferation were evaluated using fibroblasts and osteoblasts up to 21 days, and mineralization was analyzed by alkaline phosphatase. In vivo studies were conducted in New Zealand rabbits with implants placed in the femur and muscle tissue. Surface roughness did not differ among treatments, while wettability significantly increased with citric acid-based solutions. All treatments showed good cytocompatibility. AC500/Mg significantly enhanced cell adhesion, proliferation, and osteoblast mineralization, showing threefold higher activity than controls at 21 days. In vivo, AC500/Mg exhibited greater bone contact (67%) and direct muscle integration, whereas AC and Ctr showed lower bone contact and fibrotic encapsulation. These results indicate that AC500/Mg improves soft and hard tissue responses without altering roughness, suggesting its potential as a regenerative strategy following implantoplasty. Full article

Background: Chronological age inadequately captures biological vulnerability among surgical patients. Frailty and muscle strength reflect physiological reserve, yet their combined contribution to postoperative length of stay (LOS) remains insufficiently explored. Methods: We conducted a prospective multicenter observational cohort study including 223 adults undergoing elective abdominal surgery. Frailty was assessed using the Fried phenotype, and admission handgrip strength (HGS) was measured with a calibrated dynamometer. Prolonged LOS was defined as >10 days (75th percentile) and also analyzed continuously using ln(LOS + 1). Multivariable logistic and linear regression models adjusted for age, sex, frailty status, and surgical indication. Patients were additionally stratified into four physiological reserve phenotypes combining frailty and HGS. Results: LOS ranged from 0 to 68 days; a total of 48 patients (21.6%) experienced prolonged hospitalization. In multivariable logistic regression, frailty (adjusted OR 3.12, 95% CI 1.72–5.67) and oncologic surgery (adjusted OR 7.63, 95% CI 3.12–18.65) were independently associated with prolonged LOS, whereas chronological age was not. Female sex was associated with lower odds of prolonged LOS (adjusted OR 0.39, 95% CI 0.18–0.87). Similar associations were observed when LOS was analyzed continuously. Physiological reserve phenotyping revealed graded LOS distributions: Fit–Strong patients had the shortest stays (mean 5.5 ± 4.3 days), while Frail–Weak patients experienced the longest and most variable hospitalization. Conclusions: Postoperative LOS clusters according to multidimensional physiological reserve rather than chronological age. Integrating frailty and muscle strength identifies clinically meaningful phenotypes that may improve perioperative risk stratification beyond age-based approaches and inform personalized perioperative planning, resource allocation, and patient-centered decision-making across heterogeneous surgical populations in worldwide settings. Full article

Background/Objectives: Mango is a tropical fruit rich in polyphenols and carotenoids that may support recovery-related physiological responses during athletic training. This study examined the effects of mango puree supplementation on inflammatory biomarkers, muscle damage, and selected T-cell subsets in Thai men’s national beach volleyball players during regular training. Methods: Fifteen male athletes completed a pilot randomized, single-blind, crossover trial. Participants consumed the mango puree or placebo (600 g/day) for 4 weeks, separated by a 2-week washout period. Blood samples and physiological measurements were collected at baseline and at the end of each intervention period. Outcomes were analyzed using linear mixed-effects models. Results: Mango puree supplementation was associated with lower concentrations of C-reactive protein (mean difference: −1.6 mg/L; 95% CI: −2.1 to −1.1; p < 0.001), interleukin-6 (−0.7 pg/mL; 95% CI: −1.2 to −0.3; p = 0.003), and creatine kinase (−290.1 U/L; 95% CI: −356.1 to −224.1; p < 0.001) compared with the placebo. The percentage of CD4+ T cells (9.82 percentage points; 95% CI: 5.0 to 14.6; p < 0.001) and the CD4/CD8 ratio (0.37; 95% CI: 0.11 to 0.63; p = 0.007) were higher during mango puree supplementation, while CD8+ T-cell percentage did not differ between conditions. No significant treatment effects were observed for body composition parameters or blood pressure (all p > 0.05). Total energy intake remained unchanged across intervention periods (p > 0.05). Conclusions: Mango puree supplementation during regular training was associated with lower inflammatory and muscle damage biomarkers and alterations in selected T-cell subsets compared with the placebo. Full article

Background/Objectives: Upper respiratory tract infections (URTIs) and exercise-induced immune perturbations are common in adults and may adversely affect quality of life, productivity, and physical performance. Immunoglobulin Y (IgY), a food-derived antibody with broad antimicrobial activity, has demonstrated immunomodulatory potential in preclinical and limited clinical studies. This study evaluated the effects of a multi-pathogen-specific IgY supplement (Muno-IgY) on respiratory health, immune and inflammatory markers, exercise-induced physiological stress, and gut microbiome composition in healthy adults. Methods: In this 12-week, double-blind, placebo-controlled trial, 28 healthy adults with a history of URTI were randomly allocated to receive Muno-IgY or placebo and URTI incidence, duration, and severity were recorded daily. Serum immune and inflammatory biomarkers were assessed longitudinally and in response to a standardized exercise challenge. Gut microbiome composition was analyzed using shotgun metagenomic sequencing at baseline and week 12. Safety and tolerability were assessed throughout the study. Results: URTI incidence was lower in the Muno-IgY group compared with placebo (14.3% vs. 35.7%), with shorter average duration and fewer missed workdays, though differences were not statistically significant (p > 0.05). Following an acute exercise challenge, Muno-IgY supplementation resulted in a significant increase in serum IgA at 24 h post-exercise (p = 0.022) and a significantly greater reduction in lactate dehydrogenase at 1 h post-exercise compared with placebo (p < 0.0001). Exploratory gut microbiome analyses suggested favorable directional shifts, though these changes were not statistically tested. Conclusions: In this exploratory pilot study, Muno-IgY supplementation was safe and associated with significant improvements in selected markers of exercise-induced immune response and muscle damage. Numerical trends in URTI incidence and gut microbiome composition were observed but were not statistically significant. These findings are hypothesis-generating and support further evaluation of Muno-IgY in larger, adequately powered clinical trials. Full article

Wearable sensing technologies are increasingly used to assess neuromuscular function during daily-life activities. This study presents and evaluates a multisensor wearable system integrating a textile-based surface Electromyography (sEMG) sleeve and a pressure-sensing insole for monitoring Tibialis Anterior (TA) and Gastrocnemius Lateralis (GL) activation during gait. Eleven healthy adults performed overground walking trials while synchronised sEMG and plantar pressure signals were collected and processed using a dedicated algorithm for detecting activation intervals across gait cycles. All participants completed the walking protocol without discomfort, and the system provided stable recordings suitable for further analysis. The detected activation patterns showed one to four bursts per gait cycle, with consistent TA activity in terminal swing and GL activity in mid- to terminal stance. Additional short bursts were observed in early stance, pre-swing, and mid-stance depending on the pattern. The area under the sEMG envelope and the temporal features of each burst exhibited both inter- and intra-subject variability, consistent with known physiological modulation of gait-related muscle activity. The results demonstrate the feasibility of the proposed multisensor system for characterising muscle activation during walking. Its comfort, signal quality, and ease of integration encourage further applications in clinical gait assessment and remote monitoring. Future work will focus on system optimisation, simplified donning procedures, and validation in larger cohorts and populations with gait impairments. Full article

Sex steroid hormones play a pivotal role in maintaining systemic homeostasis throughout life. Their age-related decline is closely associated with the onset of frailty, including sarcopenia and dementia. Here, this article provides a narrative review of the existing literature about the multifaceted roles of sex steroid hormones, particularly estrogens and androgens, in aging and age-related diseases. Sex steroid action is mediated by nuclear receptors such as estrogen receptor alpha (ERα) and androgen receptor (AR). Transcriptional activation through these receptors is orchestrated by epigenetic mechanisms, including histone modifications and chromatin remodeling. Beyond their reproductive functions, sex hormones also influence systemic physiology, metabolism, immune responses, and neuroplasticity. Clinical studies on hormone-deprivation therapies for prostate and breast cancers, as well as animal models, have revealed the key contributions of AR and ER activity to muscle integrity, bone density, and cognitive function. The sexual dimorphism in cognitive decline, especially in postmenopausal women, suggests the therapeutic potential of hormone supplementation and receptor-targeted strategies. Thus, AR- and ER-associated genes are considered promising targets for preventing frailty, sarcopenia, osteoporosis, and dementia. This review summarizes the current knowledge on sex hormone signaling in aging, with an emphasis on translational implications and future research directions. Full article

Background: Sleep quality (SQ) and physical activity (PA) are among the strongest behavioral determinants of healthy aging, while dietary behavior and psychological factors act as complementary modulators of these relationships. Although each domain has been studied extensively, their combined influence on subjective life expectancy (SLE)—an individual’s perceived likelihood of living to an advanced age—remains largely unexplored. Methods: This narrative review synthesizes evidence from sleep science, exercise physiology, behavioral medicine, and psychological aging. Literature published between January 2015 and 15 December 2025 was examined across PubMed, Scopus, and Web of Science using integrative keyword strategies. Studies addressing SQ, PA, circadian rhythms, psychological health, SLE, or aging-related outcomes were included. Results: The review identifies several converging pathways linking sleep and PA to aging trajectories. Sleep architecture, circadian stability, metabolic regulation, inflammatory balance, and autonomic function represent key biological mechanisms. PA contributes through improvements in mitochondrial efficiency, VO₂max, muscle metabolism, and anti-inflammatory signaling (IL-6 as a myokine). Across studies, both sleep and PA strongly influence psychological health, health perception, and future-oriented expectations, within a broader lifestyle context supported by nutritional status and dietary quality. SLE emerges as a central psychological mediator that shapes motivation, adherence to health behaviors, and long-term health outcomes. Contextual moderators—including age, gender, socioeconomic status, cultural norms, and wearable technology engagement—further influence these relationships. Conclusions: SQ and PA form the core behavioral components of a dynamic system that is further shaped by dietary behavior and psychological well-being and centered on SLE. Our proposed integrative model positions SLE as a key psychological link between lifestyle behaviors and longevity. This framework is hypothesis-generating and requires empirical validation through future longitudinal and interventional studies, underscoring the need for multidomain research integrating behavioral, biological, nutritional and psychological indicators of aging. Full article

Facial aging is not a singular phenomenon but a cascade of anatomical and biological transformations unfolding across the skeleton, fat, ligaments, muscles, dermis, and epidermis. Its clinical expression-volume loss, sagging, wrinkling, and surface irregularities-cannot be adequately explained by simplistic metaphors of “filling” or “lifting.” This article is a narrative review synthesizing current anatomical, physiological, and clinical evidence relevant to multimodal facial rejuvenation. Traditional monotherapies, while sometimes effective in isolation, are increasingly inadequate for contemporary patients who demand outcomes that are natural, harmonious, and durable. Modern esthetic practice has therefore shifted toward multimodal approaches that address aging across multiple planes. Hyaluronic acid (HA) fillers provide volumetric scaffolding and hydration; collagen stimulators such as poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA) induce neocollagenesis and long-term dermal remodeling; botulinum toxin restores balance to muscular vectors and improves expression dynamics; while energy-based devices (EBDs), including fractional lasers, radiofrequency microneedling, and high-intensity focused ultrasound (HIFU), enhance skin texture, tone, and elasticity. When applied in a sequenced and evidence-based manner, these modalities act synergistically to deliver results unattainable by any single intervention. In addition to established modalities, the field has recently witnessed aggressive promotion of “regenerative” therapies-growth factors, exosomes, platelet-rich plasma (PRP), and platelet-rich fibrin (PRF). While biologically plausible, their efficacy and safety remain uncertain due to the absence of robust, randomized clinical trials and the heterogeneity of current data. This raises a critical question: is aesthetic medicine advancing through science, or being driven by novelty and marketing? This review synthesizes current anatomical and physiological knowledge of aging, evaluates the mechanisms, clinical applications, and safety considerations of major treatment modalities, and proposes practical sequencing strategies. It also emphasizes the ethical imperative that aesthetic medicine, while innovative and fast-evolving, must remain anchored in scientific evidence and patient safety—because aesthetic medicine is, fundamentally, still medicine. Full article

Vitamin D, a fat-soluble secosteroid traditionally recognized for skeletal health, exerts pleiotropic effects on cardiovascular physiology and disease. Circulating 25-hydroxyvitamin D [25(OH)D], the principal biomarker of vitamin D status, is frequently suboptimal worldwide, particularly in older adults, individuals with darker skin pigmentation, and populations at higher latitudes. Observational studies consistently associate low 25(OH)D concentrations with increased risk of hypertension, atherosclerosis, myocardial infarction, heart failure, arrhythmias, stroke, and cardiovascular mortality. Mechanistic investigations have revealed that vitamin D modulates cardiomyocyte calcium handling, endothelial function, vascular smooth muscle proliferation, inflammation, oxidative stress, and renin–angiotensin–aldosterone system activity, establishing biologically plausible links to cardiovascular outcomes. Despite these associations, large randomized trials of vitamin D supplementation have failed to demonstrate reductions in major cardiovascular events, likely due to heterogeneity in baseline status, dosing regimens, intervention timing, genetic variability, and underlying comorbidities. Vitamin D may function more effectively as a biomarker of cardiovascular risk rather than a universal therapeutic agent, with deficiency reflecting systemic vulnerability rather than acting as a dominant causal factor. Emerging evidence supports precision approaches targeting individuals with severe deficiency, high renin activity, early endothelial dysfunction, or specific genetic profiles, potentially in combination with lifestyle or pharmacologic interventions. Future research should focus on defining optimal dosing strategies, intervention timing, and mechanistic biomarkers to identify subpopulations most likely to benefit, integrating vitamin D therapy into multifaceted cardiovascular prevention frameworks. This systematic review synthesizes molecular, observational, and clinical trial evidence, critically evaluating the current understanding of vitamin D in cardiovascular medicine and highlighting opportunities for targeted, personalized interventions. Vitamin D represents a complex, context-dependent modulator of cardiovascular health, offering both prognostic insight and potential therapeutic value when appropriately applied. Full article

Background and Objectives: Rapid physiological decline in terminal cancer is frequently accompanied by accelerated skeletal muscle loss. Although bedside ultrasonography (US) is practical and feasible in palliative care settings, the prognostic relevance of short-term muscle change remains unclear. This study aimed to evaluate whether the rate of muscle loss over a 10-day period, assessed by serial ultrasound, is associated with survival duration in terminally ill cancer patients. Materials and Methods: This single-center retrospective cohort study included 87 inpatients with end-stage cancer who underwent bedside ultrasound measurements of the biceps brachii (BB) and rectus femoris (RF). Baseline US was performed within the first three days of admission, followed by a repeat assessment 10 days after baseline (day-10 follow-up ultrasound). Muscle thickness (MT) measurements were normalized by height squared (m²), and 10-day changes were calculated as delta (Δ) indices, defined as baseline minus day-10 values. Because the exposure of interest (Δ) can only be determined after completion of the day-10 assessment, survival timing analyses were anchored to this prespecified landmark. Survival duration was defined as the number of days from the day-10 follow-up ultrasound to death among patients who died within one year. Associations between muscle changes and survival duration were evaluated using correlation analyses and multivariable linear regression adjusted for age, sex, body mass index, Eastern Cooperative Oncology Group (ECOG) performance status, and nutritional risk. The primary analyses focused on survival timing among decedents. Results: Significant muscle loss was observed over the 10-day interval between baseline and 10 days after baseline. Among the 58 patients who died within one year, greater short-term biceps muscle loss, reflected by higher Δ BB muscle thickness index (Δ BB MT-I), was moderately associated with shorter survival duration (r = −0.437, p = 0.0006). In multivariable linear regression analysis, Δ BB MT-I remained independently associated with survival duration (β = −701.19; 95% CI: −1102 to −301; p = 0.0006), whereas RF muscle changes and baseline clinical variables were not statistically significant. Conclusions: Short-term biceps muscle loss assessed by serial ultrasound, as reflected by Δ BB MT-I, is associated with shorter survival duration in terminally ill cancer patients. These findings suggest that dynamic muscle changes, rather than single-time-point measurements, may provide clinically meaningful insight into short-term survival timing. Serial bedside muscle ultrasound may serve as a low-burden adjunct for prognostic communication in palliative care, although prospective time-to-event studies are required for validation. Full article

Heavy metal contamination poses concerns for managing Twaite shad (Alosa fallax) populations, yet data remain sparse. Intermittent capture as bycatch, with negligible prospects for post-release survival and IUCN Red listing, provides a compelling case for investigation. Concentrations of six trace metals (As, Cd, Cr, Cu, Pb and Zn) in the dorsal muscle tissue of A. fallax from the Curonian Lagoon (Lithuania) and the Elbe Estuary (Germany) were analyzed to evaluate size-related patterns and compliance with international safety standards. Overall, metal levels were uniformly low, with Cd and Pb below EU limits. Cu exhibited a weak negative correlation with fish weight (ρ = −0.35; p < 0.05), while Zn tended to increase in larger individuals, reflecting its essential physiological role. Comparing both adult populations, Cr and Zn, which provide nutritional benefits, were higher in the Curonian Lagoon, whereas toxic As and Pb were higher in the Elbe Estuary. All concentrations complied with EU and FAO thresholds, indicating acceptable risk for human consumption. The findings provide baseline information for A. fallax as a potential bioindicator. Constraints on the number of A. fallax sampled, given its IUCN status, exclusion of Hg and lack of environmental parameters, limit conclusions, but would be mostly remediable by future research. Full article

Critical closing pressure (CCP) and the vascular waterfall have long been used to explain perfusion failure in shock, yet their physiological meaning has been inconsistently interpreted. CCP is frequently treated as a continuous downstream pressure and inserted into formulas such as mean arterial pressure (MAP) − CCP, implying that a collapse threshold behaves like an opposing pressure even when vessels remain open. Drawing on classical vascular mechanics, whole-bed flow studies, microvascular models, and contemporary clinical physiology, we show that this interpretation is incorrect. Tone-dependent arteriolar collapse does not behave as a Starling resistor: CCP is a threshold at which smooth-muscle tension exceeds intraluminal pressure and vessels close, not a pressure governing flow in patent vessels. Perfusion becomes heterogeneous because different vascular beds reach their collapse thresholds at different pressures (via excessive tone, extrinsic compression, or profound hypotension), disconnecting macro-haemodynamics from microcirculatory flow. This explains why systemic variables such as MAP and systemic vascular resistance (SVR) may appear adequate even while tissues are under-perfused, a phenomenon now termed haemodynamic incoherence. Reframing CCP as a binary collapse threshold resolves longstanding contradictions in the literature, clarifies why MAP-centred targets often fail, and unifies the behaviour of shock states within a four-interface model of circulatory coupling. Therapeutically, the aim is not to “restore a waterfall” but to reopen closed vascular territories by lowering excessive tone, relieving external pressure, or raising truly low arterial inflow. This mechanistic reinterpretation provides a more coherent, physiologically grounded approach to personalised perfusion management in critical illness. Full article

Sheep’s meat production and quality are influenced by genetic and physiological factors that affect muscle development, growth, and fat deposition metabolism. However, the breed-specific transcriptional landscapes driving these traits in Indian sheep breeds, especially in Nellore (meat-type) and Deccani (wool-meat type) breeds are remain unexplored. Therefore, this study aimed to investigate the differences in muscle growth and fat deposition between Nellore and Deccani breeds by integrating transcriptomic profiling, carcass characteristics, and histological analysis of longissimus dorsi muscle and liver tissues. Carcass assessment revealed higher Hot Carcass Weight (HCW), Cold Carcass Weight (CCW), Hot Carcass Yield (HCY) and Cold Carcass Yield (CCY), and larger myofibrillar cross-sectional area (p < 0.05), indicating enhanced musculature, which was observed in Nellore. Deccani showed elevated Intramuscular Fat (IMF) deposition (p < 0.05), indicating improved meat flavour/juiciness. Transcriptomic profiling revealed several Differentially Expressed Genes (DEGs) associated with meat quality and quantity traits. In Nellore, the genes WFIKKN2, FGFRL1, FKBP4, and IRF1 were upregulated, while the gene TAS1R2 was downregulated, leading to enhanced muscle development, superior carcass traits, thermotolerance, and immunity. While Deccani showed higher expression of lipid metabolism genes PLA2G4F, ACSL1, ACOX1, CPT1A, and PLIN1, which are linked to higher IMF content. Functional enrichment analysis revealed 46 significantly enriched GO terms for the DEGs (p < 0.05), including oxidoreductase activity, muscle development, etc. These outcomes demonstrate novel genetic markers and key biological insights into the regulation of muscle development, thermotolerance, immunity, and IMF for future validation in Indian sheep breeds. Full article