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.

Systemic light chain (AL) amyloidosis is a rare and potentially fatal disease characterized by the abnormal deposition of homogeneous, amorphous amyloid proteins in tissues and organs. This deposition leads to varying degrees of structural and functional abnormalities, ultimately causing organ dysfunction and failure. The disease often involves multiple systems and organs, including the heart, kidneys, gastrointestinal tract, liver, and nervous system, with cardiac and renal involvement being the most common. Due to its rarity, multisystem involvement, and rapid progression, a comprehensive summary of the diagnosis and treatment of AL amyloidosis is crucial for guiding clinical practice and advancing research in this field. This article reviews the progress in diagnosis and discusses future treatment of AL amyloidosis, aiming to provide expanded options for clinical practice.

Sedation monitoring is crucial in neurosurgical intensive care units to ensure optimal patient comfort and safety. However, sedation practices vary significantly. This study aimed to evaluate and summarize the evidence related to sedation monitoring in neurocritical care patients, with a focus on identifying best practices for improving monitoring accuracy and patient outcomes.

This study was conducted as an evidence summary, following the evidence summary reporting standards of the Fudan University Evidence-based Nursing Center. The evidence on sedation monitoring management in neurocritical care patients was systematically retrieved using the 6S evidence model, including clinical decisions, best practices, guidelines, expert consensus, evidence summaries, systematic reviews, and more. Searches of domestic and international databases covered all records from the databases’ inception to June 2024. Two researchers independently selected literature that met the inclusion criteria and conducted quality assessment, evidence-level evaluation, and evidence synthesis.

Ten high-quality studies were ultimately included. From these, twenty pieces of best evidence were extracted, covering four categories: monitoring personnel, monitoring targets, monitoring tools, and monitoring timing and content. Among these, fifteen pieces of evidence were classified as strong recommendations, while five were classified as weak recommendations.

This study summarized the best evidence on sedation monitoring for neurocritical care patients, providing guidance for clinical staff to improve sedation monitoring accuracy and patient outcomes in neurosurgical intensive care units.

Chronic subdural hematoma (CSDH) is a common disease in neurosurgery, with epidemiological characteristics showing an overall annual incidence of 1.7–20.6 per 100,000 people and a higher prevalence in the elderly. However, despite the increased disease burden, there have been limited breakthroughs in treatment options over the past 20 years. A significant gap exists in our understanding of the exact pathophysiological mechanism of CSDH, leading to a lack of specific clinical treatment options based on a clear pathological mechanism. Current research suggests that the development of CSDH involves dual mechanisms of trauma and inflammation, and that these pathologic processes together promote pathological changes such as angiogenesis, inflammatory response, and neovascularization. Therapies for CSDH encompass both surgical (e.g., twist-drill drainage, burr-hole drainage, craniotomy) and non-surgical approaches (e.g., clinical observation, medication, intracranial pressure monitoring, anticoagulation). Meanwhile, middle meningeal artery embolization, as an emerging minimally invasive interventional technique, has shown good prospects for clinical application. This review aims to bridge the gap between current treatment options and the need for effective strategies by providing a comprehensive summary of the epidemiological trends, pathophysiological advances, and optimization of therapeutic strategies for CSDH.

Cell cycle checkpoint-related genes (CCCRGs) are implicated in the development and progression of hepatocellular carcinoma (HCC). However, their precise roles and underlying mechanisms remain insufficiently characterized and require further investigation. This study aimed to explore the prognostic significance of CCCRGs in HCC, and to investigate the mechanism by which they promote the progression of HCC.

HCC datasets from The Cancer Genome Atlas and International Cancer Genome Consortium were analyzed to identify hub genes. A prognostic model was constructed and validated using Kaplan–Meier analysis, nomogram, calibration curves, decision curve analysis, and receiver operating characteristic analysis. Immune infiltration patterns were assessed using single sample gene set enrichment analysis, while pathway activities were evaluated via gene set variation analysis. Single-cell RNA sequencing data from GSE149614 were analyzed with Seurat and CellChat to investigate cell–cell communication. Patient-derived HCC specimens were examined through immunohistological evaluation, HCC cell lines were used for in vitro functional assays, and in vivo tumor growth was assessed through animal experiments.

CCCRGs showed significant associations with prognosis, malignant biological behavior, and immune responses in HCC. Centromere protein (CENP) I was identified as a critical hub gene that markedly promoted HCC proliferation, metastasis, and epithelial–mesenchymal transition, while inhibiting apoptosis. Mechanistically, CENPI suppressed YAP phosphorylation, enhancing its nuclear translocation and thereby driving malignant progression. Additionally, CENPI impaired immune effector cell infiltration, likely by disrupting tumor antigen presentation and chemokine-mediated CD8+ T cell chemotaxis, thereby promoting immune escape.

This study underscores the prognostic significance of CCCRGs in HCC and identifies CENPI as a key driver of tumor progression through the Hippo pathway. Furthermore, it reveals CENPI’s role in promoting immune escape, suggesting novel therapeutic targets for HCC treatment.