Mitochondrial respiratory complexes (Complexes I–V) and their assembly into respiratory supercomplexes (SCs) are fundamental to liver bioenergetics, redox homeostasis, and metabolic adaptability. Disruption of these systems contributes to major liver diseases, including non-alcoholic fatty liver disease, alcoholic liver disease, drug-induced liver injury, viral hepatitis, and hepatocellular carcinoma, by impairing adenosine triphosphate synthesis, increasing oxidative stress, and altering metabolic pathways. Recent advances have clarified the structural-functional interdependence of individual complexes within SCs, revealing their dynamic remodeling in response to physiological stress and pathological injury. These insights open opportunities for clinical translation, such as targeting SC stability with pharmacological agents, nutritional strategies, or gene therapy, and employing mitochondrial transplantation in cases of severe mitochondrial failure. Precision medicine approaches, incorporating multi-omics profiling and patient-derived models, may enable individualized interventions and early detection using SC integrity as a biomarker. By linking molecular mechanisms to therapeutic strategies, this review underscores the potential of mitochondrial-targeted interventions to improve outcomes in patients with liver disease.

Ischemic stroke is a complex cerebrovascular disorder characterized by highly unpredictable outcomes influenced by patient-specific variables, including age, stroke severity, and preventable stroke-related complications such as infections. Analyses of clinical data have indicated a cumulative post-stroke infection rate of approximately 30%, with reported rates ranging from 5% to 65%. Post-stroke infections pose a significant challenge, as they not only increase the financial burden of stroke care but are also associated with adverse clinical outcomes, prolonged hospital stays, and a higher risk of stroke recurrence. The inflammatory response plays a pivotal role in the pathophysiology of ischemic stroke, encompassing the activation of inflammatory cells, the release of inflammatory mediators, and the engagement of inflammatory signaling pathways. Recent advances in molecular biology have facilitated the identification and investigation of numerous inflammation-related biomarkers. This article reviews the roles and mechanisms of key inflammatory biomarkers, including cytokines, chemokines, adhesion molecules, inflammation-related enzymes and mediators, receptors, signaling pathway molecules, and acute-phase proteins in the context of ischemic stroke, highlighting their significance in stroke pathophysiology and prognostic assessment. Additionally, in conjunction with the latest research advances, the article discusses novel biomarkers such as microRNAs and galectin-3, which are emerging as important tools in multiple domains, including diagnosis and treatment. Drawing on clinical diagnostic and therapeutic practices, this review analyzes the diagnostic and therapeutic roles of both novel and traditional biomarkers in the progression of ischemic stroke, following the temporal sequence from disease onset to prognosis. Finally, the article addresses the limitations of current research and offers perspectives on future directions, providing insights that may contribute to the advancement of precision medicine in the management of ischemic stroke.

Medulloblastoma (MB) is a malignant neoplasm that is relatively common in children but rare in young adults, accounting for less than 1% of all intracranial tumors. This study reports a rare case of MB metastasis to the right temporoparietal region in a 42-year-old woman, presenting with focal neurological symptoms such as weakness in the left arm and leg, speech disturbances, and impaired coordination. The patient had a history of cerebellar MB and underwent surgical resection, radiation therapy, and chemotherapy. Despite treatment, metastasis occurred, highlighting the diagnostic and therapeutic challenges in adult MB cases. The article also reviews the literature on MB in young adults, emphasizing the importance of dynamic neuroclinical monitoring and timely instrumental diagnosis for early detection and management of MB metastases.

Craniopharyngioma (CP), although histologically benign, is a surgically challenging sellar-region tumor for which stereotactic irradiation is increasingly used as an alternative or adjuvant strategy. This review summarizes the role of stereotactic radiosurgery (SRS) in managing CP, with a focus on treatment outcomes, technical advances, and emerging strategies to support evidence-based clinical practice. Literature reports indicate that Gamma Knife radiosurgery achieves variable tumor control rates (36–100%), with optimal outcomes (79.6–91.4%) when marginal doses ≥12 Gy are delivered and patients receive adequate follow-up. Smaller tumors (<5 cm3) and those with higher solid components show particularly favorable outcomes. SRS demonstrates a favorable safety profile, with visual impairment occurring in approximately 4% of cases and endocrine dysfunction in 6%. Compared to conventional radiotherapy, SRS significantly reduces the risk of hypothalamic obesity in pediatric patients. The identification of BRAF mutations in papillary CPs has created novel opportunities for combining targeted therapies with SRS. Collectively, these advances underscore the role of SRS as an essential component of multidisciplinary CP management, particularly in the treatment of residual or recurrent lesions. It offers a more favorable toxicity profile and may improve quality of life outcomes compared to conventional radiotherapy. Further studies are needed to optimize patient selection, dosing strategies, and integration with novel systemic therapies.

A long-term high-fat diet (HFD) exerts lipotoxic effects on multiple organs, particularly the liver, leading to metabolic diseases. This study aimed to delineate the dynamic effects of HFD on lipid metabolism, elucidate the mechanisms underlying hepatic lipotoxicity, and investigate the protective effects of Ganoderma lucidum against lipotoxicity both in vitro and in vivo.

C57BL/6 mice were fed either a 45% or 60% HFD, followed by measurements of body composition, serum lipid profile, and liver pathology at four, eight, twelve, and sixteen weeks. Inflammatory responses, the unfolded protein response (UPR), and endoplasmic reticulum (ER)-phagy were examined in the livers of mice at 16 weeks. Male C57BL/6 mice were randomly assigned to four groups (n = 12 per group): normal diet, 45% HFD, and two HFD + Ganoderma lucidum water extract (GLE) groups (1 g/kg/d and 2 g/kg/d of crude drug, orally administered by gavage for eight weeks following a four-week HFD induction).

Body weight, body fat, serum lipids, and hepatic steatosis increased progressively, accompanied by impaired glucose tolerance and liver injury, as indicated by elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. HFD also induced activation of the STING and NF-κB signaling pathways, as well as the PERK and IRE1 branches of the UPR. Similarly, ER-phagy selective receptors, particularly FAM134B, which is primarily expressed in hepatocytes as shown by single-cell sequencing, were upregulated after 16 weeks of HFD feeding. Furthermore, GLE mitigated palmitic acid-induced lipotoxicity in primary hepatocytes, as evidenced by improved cell viability, reduced ALT, AST, and lactate dehydrogenase levels in the culture supernatant, and decreased transferase dUTP nick-end labeling-positive cell counts. In 45% HFD-fed mice, GLE reduced serum total cholesterol, low-density lipoprotein, and hepatic triglyceride levels.

HFD-induced lipotoxicity causes hepatic tissue injury and inflammatory responses, which may be alleviated by coordinated regulation of compensatory UPR and ER-phagy. Ganoderma lucidum shows promise as a dietary supplement for managing metabolic disorders.

Lactate exerts regulatory effects on both cellular homeostasis and disease progression, far beyond being a mere metabolic waste product. As lactate accumulates, the level of lactylation increases significantly. Lactylation, a novel type of post-translational modification, bridges metabolic reprogramming and epigenetic regulation in malignant tumors, including gynecological malignancies. Both lactate and lactylation play critical roles in the tumor microenvironment, ultimately promoting tumor proliferation, metastasis, and drug resistance. Therapies targeting lactate production and transport show considerable anticancer potential, particularly through the inhibition of lactate dehydrogenase and monocarboxylate transporters. These inhibitors can also act as immunotherapy potentiators, producing a synergistic therapeutic effect when combined with immunotherapy. This review emphasizes how lactate and lactylation drive the malignant progression of gynecological cancers and explores promising perspectives on potential therapeutic targets.

Antralization is considered a critical, reversible stage preceding gastric cancer. However, available biomarkers for identifying antralization are lacking. This study aimed to explore antralization-specific biomarkers in peripheral blood and gastric mucosa.

In this prospective cohort study, adult patients presenting with upper gastrointestinal symptoms were enrolled and categorized into antralization and non-antralization groups based on pathological examination of gastric mucosa. Helicobacter pylori (H. pylori) infection was detected using the 13C-urea breath test, rapid urease test, and/or H. pylori serological test. Blood samples and gastric biopsies were collected for biomarker analysis.

Of the 92 patients studied, 42 (45.7%) were diagnosed with H. pylori infection and 61 (66.3%) with antralization. The rate of H. pylori infection and the incidence of acid reflux were higher in the antralization group than in the non-antralization group (both P < 0.05). Patients with antralization had higher plasma lymphocyte counts and lower serum levels of lipopolysaccharide (both P < 0.05). The positive rates and intensity of trefoil factor-2 and mucin (MUC) 6 expression were higher, whereas the positive rate and intensity of MUC5AC expression were lower in the incisura and body mucosa with antralization compared with those without antralization (all P < 0.05). Additionally, the intensity of MUC5B expression was higher in the gastric body mucosa with antralization than in those without antralization (P < 0.05).

Increased lymphocyte counts and decreased lipopolysaccharide levels in the blood, along with increased expression of trefoil factor-2, MUC6, and MUC5B and decreased MUC5AC expression in the proximal gastric mucosa, appear to be antralization-specific.

Preclinical studies of the serotonin 2A (5-HT2A) antagonist deramciclane suggested an anxiolytic profile, which has not been unequivocally established in the clinic. The same receptor profile also indicated that the compound may exhibit antidepressant potential. However, evidence for these effects remains inconclusive. The present study examined the effect of the drug in two preclinical tests with predictive validity for antidepressant activity.

The antidepressant-like activity of deramciclane was assessed in male Sprague-Dawley rats by measuring immobility time in the forced swim test (doses: 1, 5 mg/kg) and ambulation scores in the bilateral olfactory bulbectomized (doses: 5, 10 mg/kg) rat model. In both tests, the clinically effective antidepressant imipramine served as the control condition.

In the forced swim test, there was a statistically significant effect of treatment on immobility time (F2,34 = 5.77; p < 0.01; analysis of variance), which was attributable to the effect of the 5 mg/kg dose (p < 0.01; Bonferroni post-hoc test). Deramciclane at 1 mg/kg was not significantly different from vehicle-treated animals. By contrast, neither dose of deramciclane (5 mg/kg or 10 mg/kg) reversed the hyperactivity of olfactory bulbectomized rats, whereas imipramine was active in both tests.

Deramciclane demonstrates contradictory evidence for antidepressant-like activity in two validated pharmacological tools that identify such potential. The agent is clearly active in the forced swim test but not in the bulbectomized rat model. Further evaluation of the antidepressant-like potential of deramciclane in pharmacological models with predictive validity is warranted, and a more detailed examination of the dose-response relationship may be informative.

5-methylcytosine RNA modification is a key regulator of neuroblastoma oncogenesis and differentiation. NSUN6, a 5-methylcytosine-specific messenger RNA methyltransferase, modulates messenger RNA methyltransferase activity and translation termination. Yet, its potential link to neuroblastoma risk has not been previously reported. The present study aimed to reveal the relationship between NSUN6 gene polymorphisms and the risk of neuroblastoma in children from Jiangsu province.

In this case-control study, we investigated three NSUN6 gene polymorphisms (rs3740102 A>C, rs12780826 T>A, and rs61842187 G>C) in 402 neuroblastoma cases and 473 controls, all of whom were children from Nanjing City, Jiangsu Province, China. DNA from these subjects was assessed using the TaqMan method. Multivariate logistic regression analysis was employed to examine the association between NSUN6 gene polymorphisms and neuroblastoma risk. Additionally, the Genotype-Tissue Expression database was utilized to elucidate the impact of these polymorphisms on NSUN6 and nearby gene expression. Kaplan-Meier analysis and the non-parametric test were conducted on the R2 platform to assess the relationship between gene expression, prognosis, and neuroblastoma risk.

Carriage of two to three protective genotypes (rs3740102 AA/AC, rs12780826 TT/TA, rs61842187 CC) was significantly associated with a lower risk of neuroblastoma (adjusted odds ratio = 0.41, 95% confidence interval = 0.23–0.73, P = 0.002), with consistent results across all subgroups. Expression quantitative trait locus analysis showed these single-nucleotide polymorphisms may upregulate the expression of NSUN6 and CACNB2. Furthermore, higher NSUN6 and CACNB2 expression was correlated with a potentially lower risk of neuroblastoma, improved overall survival (NSUN6: P = 2.54e-03; CACNB2: P = 6.35e-06) and event-free survival (NSUN6: P = 7.90e-04; CACNB2: P = 4.64e-06), as well as a lower likelihood of MYCN amplification.

NSUN6 rs3740102 AA/AC, rs12780826 TT/TA, and rs61842187 CC genotypes may be associated with a better prognosis of neuroblastoma. This association may be related to the potential upregulation of NSUN6 gene expression and a lower likelihood of MYCN amplification.