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.

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.

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.

Uterine fibroids (UFs) are common hormone-dependent tumors with a complex etiology involving both genetic and environmental factors. This study aimed to investigate, for the first time, the associations between loci from genome-wide association studies (GWAS) and environmental risk factors in UF development, with a particular focus on gene–environment interactions.

DNA samples from 737 women with UF and 451 healthy controls were genotyped for ten UF-associated GWAS single nucleotide polymorphisms (SNPs) using probe-based polymerase chain reaction in this case-control study.

SNP rs66998222 (LOC102723323, G/A) was associated with decreased UF risk in the total sample (odds ratio (OR) = 0.81, p = 0.038) and in patients with a history of induced abortion (OR = 0.70, p = 0.009). SNP rs11031731 (THEM7P, WT1, G/A) increased UF risk overall (OR = 1.39, p = 0.01), and in women with abortion history (OR = 1.60, p = 0.008) or without pelvic inflammatory disease (OR = 1.43, p = 0.02). SNPs rs641760 (PITPNM2, C/T) and rs2553772 (LOC105376626, G/T) showed protective effects depending on abortion history. SNP rs1986649 (FOXO1, C/T) was associated with later UF onset (p = 0.049) and slower growth (p = 0.017). GWAS loci influence UF-related genes involved in proliferation, inflammation, and hormone metabolism, underscoring their pathogenic role.

Induced abortions and inflammation modify the effects of GWAS-identified UF risk loci, with allele-specific impacts on hormonal, inflammatory, and repair pathways. Replication in diverse cohorts is needed to validate these population-specific effects.

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.

Breast cancer remains one of the most common cancers affecting women globally, with late detection frequently contributing to its high mortality rate. Multiple factors drive these delays, including a lack of awareness, financial constraints in low-income countries, and limited access to non-invasive and accurate biomarkers. This review aims to introduce biomarkers, particularly hematological and biochemical serum markers, as essential, non-invasive, and accurate tools for improving the diagnosis, prognosis, and therapeutic management of breast cancer. Hematological markers are measurable blood parameters that reflect physiological and pathological processes such as inflammation, infection, cardiovascular stress, autoimmune conditions, and cancer. Routinely measured hematological markers, such as the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and red blood cell indices, are typically obtained from standard tests like the complete blood count. Regular monitoring through complete blood count is essential during cancer treatment to evaluate changes in blood cell counts and detect potential adverse effects. Because of their affordability, minimal infrastructure requirements, and broad accessibility, hematological parameters have been increasingly studied for their association with high-risk factors in breast cancer, particularly in resource-limited settings. Their utility underscores their critical role in improving patient outcomes across diverse healthcare environments. This review summarizes the clinical value of various hematological and serum-based biochemical markers in the screening and diagnosis of breast cancer. Prediction methods that incorporate hematological and serum-based biochemical parameters can support screening, diagnosis, and staging. Overall, individual or combined blood indicators hold significant potential to enhance diagnostic accuracy and effectiveness.

Hepatic metastasis (HM) and lymph node metastasis in pancreatic ductal adenocarcinoma (PDAC) are associated with worse overall survival, largely due to the immunosuppressive microenvironment. However, the key immunosuppressive cells within this microenvironment remain inadequately defined. This study aimed to identify the cells contributing to HM and lymph node metastasis in PDAC and to investigate their regulatory mechanisms.

Single-cell RNA sequencing was used to profile the tumor microenvironment in HM, lymph node-negative, and lymph node-positive (LNP) PDAC tissues. Bioinformatic analyses revealed subtypes of immunosuppressive myeloid-derived suppressor cells (MDSCs). Immunofluorescence and flow cytometry were performed to detect the distribution and proportion of interleukin-1 receptor antagonist (IL1RA+) MDSCs. The immunosuppressive and pro-tumorigenic functions of IL1RA+ MDSCs were analyzed using enzyme-linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, Western blotting, and Transwell assays. Patient-derived xenograft mouse models were employed to validate the role of IL1RA+ MDSCs in vivo.

Polymorphonuclear-MDSCs were found to be recruited to metastatic PDAC tissues. Among these, IL1RA+ MDSCs were enriched in HM/LNP tissues and correlated with poorer prognosis. IL1RA+ MDSCs promoted M2 macrophage polarization and suppressed the activity of natural killer cells and cytotoxic T cells. Furthermore, IL1RA+ MDSCs accelerated PDAC migration and progression by upregulating epithelial–mesenchymal transition-related proteins in both in vitro and in vivo models.

IL1RA+ MDSCs represent a key immunosuppressive and pro-tumorigenic subtype in HM/LNP PDAC, providing a solid theoretical basis for prognostic prediction and the development of immunotherapeutic strategies targeting these cells in HM/LNP PDAC.