Cirrhosis remains a significant global health burden, responsible for nearly 4% of annual deaths worldwide. Despite progress in antiviral therapies and public health measures, its prevalence has plateaued, particularly in regions affected by viral hepatitis, alcohol misuse, and metabolic syndrome. This review presents a comprehensive synthesis of the multifactorial drivers of cirrhosis, including hepatocyte injury, liver stellate cell activation, and immune-mediated inflammation. The emphasis is on the central role of metabolic dysfunction, characterized by mitochondrial impairment, altered lipid and glucose metabolism, hormonal imbalance, and systemic inflammation, in exacerbating disease progression. While current therapies may slow the progression of early-stage disease, they are very often ineffective in reversing established fibrosis. Emerging molecular strategies offer promising alternatives by targeting key pathogenic pathways. These include AMPK activators (e.g., metformin, AICAR), FGF21 analogs, and mitochondria-targeted agents (e.g., MitoQ, urolithin A, NAD+ precursors) to restore bioenergetic balance and reduce oxidative stress. Other approaches, such as mesenchymal stem cell therapy, inflammasome inhibition, and hormonal modulation, aim to suppress fibrogenesis and restore liver homeostasis. The integration of systems biology and multi-omics profiling supports patient stratification and precision medicine. This review highlights a shift toward mechanism-based interventions that have the potential to alter cirrhosis outcomes and improve patient survival.

Nanotechnology offers innovative methodologies for enhancing the diagnosis and treatment of ovarian cancer by utilizing specialized nanoparticles. The utilization of nanoparticles offers distinct advantages, specifically that these entities enhance the bioavailability of therapeutic agents and facilitate the targeted delivery of pharmacological agents to neoplastic cells. A diverse array of nanoparticles, including but not limited to liposomes, dendrimers, and gold nanoparticles, function as proficient carriers for drug delivery. Nevertheless, notwithstanding the auspicious potential of these applications, challenges pertaining to toxicity, biocompatibility, and the necessity for comprehensive clinical evaluations pose considerable barriers to the widespread implementation of these technologies. The incorporation of nanotechnology into clinical practice holds the promise of significantly transforming the management of ovarian cancer, offering novel diagnostic tools and therapeutic strategies that enhance patient outcomes and prognoses. In summary, the deployment of nanotechnology in the context of ovarian cancer epitomizes a revolutionary paradigm in medical science, amalgamating sophisticated materials and methodologies to enhance both diagnostic and therapeutic outcomes. Continued research and development endeavors are essential to fully realize the extensive potential of these innovative solutions and address the existing challenges associated with their application in clinical settings.

Steroid hormones exert diverse and tissue-specific biological effects despite sharing a conserved tetracyclic scaffold. Among these, anabolic–androgenic steroids (AAS) present a longstanding paradox: structurally related compounds can elicit markedly different anabolic, androgenic, and cardiovascular outcomes. This narrative review integrates advances in steroid structural chemistry, androgen receptor (AR) biology, and intracellular signaling to elucidate the molecular mechanisms underlying anabolic–androgenic dissociation. We summarize classical genomic and emerging non-genomic modes of steroid action, emphasizing how receptor conformation, ligand-binding domain architecture, co-regulator recruitment, and signaling bias shape downstream biological responses. Particular focus is placed on the structure–activity relationships of endogenous and synthetic androgens, with C17-substitution chemistry highlighted as a central determinant of receptor affinity, metabolic stability, pharmacokinetics, and tissue selectivity. By linking molecular structure to receptor-level mechanisms, we contextualize the physiological and pathophysiological effects of major AAS classes used clinically and non-medically, including testosterone esters, 19-nor derivatives, 17α-alkylated steroids, heterocyclic compounds, and halogenated compounds. While much of the mechanistic evidence derives from preclinical models, the integrated framework presented here provides a coherent basis for interpreting divergent anabolic, androgenic, and cardiovascular effects observed in humans. Collectively, this review bridges fundamental steroid biology with applied physiology and sports medicine, offering mechanistic insight relevant to therapeutic development, anti-doping science, and risk assessment of supraphysiological androgen exposure.

Background/Objectives: The objective of this study was to expose the ability of neurophysiotherapeutic management to reduce spasticity through a modified Ashworth Scale. Methods: The sample, consisting of 102 subjects divided into control and study groups, was selected from an initial pool of N = 1007 patients diagnosed with stroke by a neurosurgeon that was later confirmed with imaging (MRI, CT). The study scheme included statistical differentiation between the study and control groups before and after applying specific rehabilitation programs and statistical differentiation within these groups before and after their rehabilitation procedures. Results: The results of this study revealed statistically significant improvements in reducing spasticity, as assessed by the Ashworth scale, within the group that participated in the neurorehabilitation program. It also confirmed that using neurophysiological methods is a highly effective approach to managing spasticity in post-stroke patients. Conclusions: Using neurophysiological methods in the standard physiotherapy treatment of spasticity is very effective for managing post-stroke spasticity.

Background: Vitamins are micronutrients involved in multiple physiological processes critical for athletic performance. Because athletes are often exposed to increased oxidative stress, higher metabolic turnover, and greater nutritional demands, which can potentially lead to deficiencies in vitamins, understanding vitamin supplementation as a function of sport discipline is of fundamental importance. Methods: This narrative review synthesizes research findings from the past decade, supplemented with earlier studies where necessary, focusing on vitamins A, C, D, E, and the B-complex vitamins. Peer-reviewed literature was evaluated for evidence on the prevalence of deficiencies in athletes, physiological mechanisms, supplementation strategies, and their effects on performance, injury prevention, and recovery. Results: Vitamin D deficiency is highly prevalent among athletes, particularly in indoor sports and during the winter months. Supplementation has been shown to improve musculoskeletal health and potentially reduce injury risk. The antioxidant vitamins C and E can attenuate exercise-induced oxidative stress and muscle damage; however, excessive intake may impair adaptive responses such as mitochondrial biogenesis and protein synthesis. Vitamin A contributes to immune modulation, metabolic regulation, and mitochondrial function, while B-complex vitamins support energy metabolism and red blood cell synthesis. Conclusions: Vitamin supplementation in athletes should be individualized, targeting confirmed deficiencies and tailored to sport-specific demands, age, sex, and training intensity. Dietary optimization should remain the primary strategy, with supplementation serving as an adjunct when intake is insufficient. Further high-quality, sport-specific, and long-term studies are needed to establish clear dosing guidelines and to assess the balance between performance benefits and potential risks associated with over-supplementation.

Objective: To examine acute BEFORE–AFTER changes in maximum, mean, and median surface-EMG RMS amplitudes recorded from four shoulder-girdle muscles around scheduled collegiate volleyball training sessions. Methods: Sixteen male collegiate volleyball players representing one university team participated in this exploratory prospective repeated-measures study. Surface EMG was recorded from the upper trapezius, lower trapezius, infraspinatus, and serratus anterior during muscle-specific maximal voluntary isometric effort tasks. A standardized dynamic warm-up was completed before the BEFORE assessment. Surface EMG was then recorded immediately after warm-up and before the volleyball-specific training components of the session (BEFORE), and again within 5–10 min after completion of the scheduled team-training session (AFTER), on three weekly measurement days. For each EMG outcome, the main inferential estimand was the marginal AFTER–BEFORE contrast averaged across muscles and measurement days. Linear mixed-effects models included assessment condition, muscle, measurement day, and the assessment condition × muscle term; interaction analyses were treated as exploratory because the participant-level sample comprised 16 independent experimental units. Marginal AFTER–BEFORE contrasts were adjusted across the three RMS-amplitude outcomes using the Bonferroni method. Results: Mean RMS amplitude was lower AFTER than BEFORE the training sessions by 4.16 µV (95% CI: −6.32 to −2.01; Bonferroni-adjusted p < 0.001). Maximum RMS amplitude was also lower by 5.77 µV (95% CI: −11.19 to −0.35), but this contrast was not supported after multiplicity adjustment (adjusted p = 0.115). Median RMS amplitude showed an estimated increase of 3.88 µV (95% CI: −0.19 to 7.94; adjusted p = 0.181). Exploratory assessment condition × muscle interactions were not statistically significant for any of the three RMS-amplitude outcomes. Conclusions: Only the decrease in mean RMS amplitude remained statistically supported after adjustment across the three EMG outcomes. Because both assessments were performed after the standardized warm-up, warm-up status was held constant with respect to completion of the warm-up. The AFTER assessment additionally followed the subsequent volleyball-specific training components and a 5–10-min post-session interval. Accordingly, the contrast represents a within-session AFTER–BEFORE difference associated with the intervening training exposure and temporal/order effects rather than an isolated causal effect of training. Exploratory condition × muscle interactions were not statistically significant, but the small sample does not establish equivalent responses among muscles. The findings do not establish altered mechanical force or localized neuromuscular fatigue.