Pituitary tumors are common intracranial neoplasms that can cause significant morbidity due to hormonal dysregulation and compression of surrounding structures. Despite advancements in surgical techniques, challenges persist in treating large, invasive, or recurrent tumors, where complete resection is often difficult. The molecular and genetic mechanisms underlying pituitary tumorigenesis are not yet fully understood, limiting the development of targeted therapies. This review provides a comprehensive overview of recent advancements in neuroendoscopic treatment of pituitary tumors, with a focus on pathogenesis, technological innovations, clinical outcomes, and future directions. We highlight the potential of neuroendoscopic surgery to improve patient outcomes while addressing persistent challenges, such as the steep learning curve and limitations in instrument maneuverability. Future research should prioritize enhancing instrument design, developing 3D and augmented reality visualization systems, and improving training programs to further advance neuroendoscopic techniques.

Prostate cancer (PCa) often manifests insidiously, with most patients being diagnosed at an advanced stage, leading to a poor prognosis. Early detection of PCa can significantly prolong overall survival by impeding the progression of metastasis. A commonly utilized screening method for detecting PCa is the prostate-specific antigen test. However, since the prostate-specific antigen lacks specificity and sensitivity for PCa identification, there is a paramount urgency to develop precise diagnostic biomarkers for early detection. Extracellular vesicles, known as exosomes, are released by cells into body fluids. Exosomes derived from cancer cells can carry genetic information about the tumor, including DNA, RNA, and proteins, which play crucial roles in tumor initiation, invasion, metastasis, and drug resistance. Studies have indicated that exosomes (including messenger RNAs, microRNAs, long noncoding RNAs and others) can enhance the sensitivity and specificity of PCa diagnosis, indicating their potential for early detection. This review highlights the biological characteristics and functions of exosomes, as well as recent advancements in their use for the diagnosis, prognosis, and treatment of prostate cancer.

Traditional Chinese medicine (TCM) is widely used in cancer care in China as an integral part of treatment. This study aimed to understand the motivations of cancer patients in China for adopting TCM in their treatment and to examine their communication with oncologists. Gaining insights into these factors can enhance culturally sensitive, patient-centered oncology care.

A consecutive sample of 287 outpatients with cancer was recruited. Sociodemographic and clinical data, TCM usage, primary reasons for adopting TCM, and communication about TCM with oncologists were collected. Descriptive statistics, binary logistic regression, and thematic analysis were used to analyze the data.

Patients’ primary reasons for choosing TCM fell into five main categories: (1) belief in the benefits of TCM itself, (2) recommendations from others (family, friends, or oncologists), (3) belief in the benefits of combining TCM with Western medicine (WM), (4) previous positive experiences with TCM, and (5) dissatisfaction with or intolerance to WM. Among the 103 patients who consulted external TCM providers, 65% disclosed this to their oncologists. A longer time since diagnosis was associated with a higher likelihood of disclosure, while employed patients were less likely to inform their oncologists. Oncologists’ responses varied, with 55% neither approving nor disapproving of external TCM prescriptions.

The primary reasons for TCM use were perceived benefits and recommendations from oncologists and family members. However, communication about TCM with oncologists remains inconsistent. Enhancing patient-provider communication through education and fostering the integration of TCM and WM can improve holistic cancer care.

Diagnosing and treating cytopenic myelofibrosis in children is challenging due to the wide spectrum of clinical and pathological features, underlying etiologies, and variable therapeutic responses. In this review, we summarize the related literature and present our diagnostic algorithm to differentiate pediatric myelofibrosis and guide therapy. In brief, primary myelofibrosis is extremely rare in children, while myelofibrosis secondary to non-neoplastic or neoplastic disorders should be thoroughly ruled out in ambiguous cases. Moreover, it is reasonable to closely follow up patients and repeat bone marrow biopsy before reaching a definitive diagnosis.

Balamuthia mandrillaris is a free-living amoeba that can cause granulomatous amoebic encephalitis, a lethal neurological condition in humans. This pathogen infects not only immunocompromised hosts but, more commonly, immunocompetent individuals. Balamuthia mandrillaris mainly infects the skin and nervous system. When it affects the nervous system, it can manifest as Balamuthia mandrillaris encephalitis (BAE). This article presents a case of BAE in central China, diagnosed through next-generation sequencing and histopathology. The patient is a 64-year-old male who was admitted to the Department of Neurosurgery with a one-week history of headache. Magnetic resonance imaging scans revealed a mass in the right temporal-occipital region, and postoperative pathological examination confirmed that the lesion was BAE. We will detail the clinical course of this disease in this patient, aiming to enhance clinicians’ understanding of Balamuthia mandrillaris infections.

Insulinoma is a neuroendocrine tumor originating in the pancreas that secretes excess amounts of insulin, leading to severe hypoglycemia. The clinical presentation of hypoglycemia is classically described by Whipple’s Triad. Due to the rarity of this diagnosis, it can often be mistaken for other etiologies with similar presentations. In this paper, we present the case of a woman in her 70s with metastatic insulinoma involving the liver, who was initially diagnosed with an insulin-like growth factor 2-secreting hepatocellular carcinoma. Biochemical and immunohistochemical analyses were instrumental in distinguishing between these two etiologies.

Lung Squamous cell carcinoma (LSCC) represents the second most common non-small cell lung cancer. Although studies identified adenocarcinoma-like driver mutations in LSCC using next-generation sequencing (NGS), the disease is challenging to treat due to the limited number of detectable mutations for targeted drug therapy. This study aimed to evaluate the mutation profiles of LSCC detected by NGS to assess the relationships between different driver mutations and clinicopathological parameters.

NGS with a panel of 72 cancer-related genes was used to evaluate the driver mutation profiles of 41 lung resection specimens from patients with LSCC at the Molecular Pathology Laboratory of Aydın Adnan Menderes University in Türkiye. Clinical and histopathological features were recorded for analysis.

Detection of 94 mutations in 23 genes in DNA extracted from the tissue samples of 36 patients revealed that the most prevalent mutations were TP53 (30.85%), NF1 (20.20%), PTEN (11.70%), PIK3CA (5.31%), FBXW7 (4.25%), KRAS (3.20%), respectively. We identified statistically significant relationships between PIK3CA and lower mean age (p = 0.007) and between PTEN and mild inflammatory reaction (p = 0.004). PTEN was associated with central localization (p = 0.13), NF1 with visceral pleural involvement (p = 0.09), and PIK3CA with severe inflammatory reaction (p = 0.053), as well as with advanced pathological T stage (p = 0.09) and pathological N stage (p = 0.057) according to the TNM staging system.

Our study highlights the importance of assessing mutation profiles in LSCC patients to identify driver mutations as potential therapeutic targets. Certain histopathological features are associated with these mutations, serving as indicators for treatment and follow-up decisions.

Chronic obstructive pulmonary disease (COPD) is an irreversible inflammatory lung disease. Studies have shown that macrophages and estrogen receptors play a pivotal regulatory role in the development of COPD. Ejiao (Colla Corii Asini, CCA, or donkey-hide gelatin), a traditional Chinese medicine, has anti-inflammatory and lung function-protective effects, but its specific mechanism in COPD remains unclear. This study aimed to explore the immunomodulatory effects of Ejiao on COPD, focusing on its impact on inflammatory pathways and macrophages.

This study is the first to apply a network pharmacology approach to explore the potential mechanisms underlying Ejiao’s therapeutic effects on COPD. We collected the peptides and chemical components of Ejiao and used the STRING database to screen for COPD-related targets of Ejiao components, constructing a drug-molecular network. Additionally, we established cigarette smoke extract (CSE) and lipopolysaccharide-induced cell injury models and treated them with Ejiao-containing serum. Western blot (WB) analysis was used to detect the expression of related proteins, enabling a preliminary exploration of Ejiao’s effects and regulatory mechanisms. In further experiments, a mouse COPD model was established, and eight weeks of Ejiao intervention were conducted. We assessed lung function, pathological changes in lung tissue, monitored cytokine levels in serum and bronchoalveolar lavage fluid, performed flow cytometry to evaluate abdominal macrophage levels, and conducted WB to analyze protein expression, providing an in-depth study of Ejiao’s regulatory effects on the mouse COPD model.

The findings from the network pharmacology analysis suggest a potential regulatory role of the estrogen receptor pathway in COPD. CSE stimulation of RAW264.7 cells resulted in elevated tumor necrosis factor-α levels, decreased interleukin-10 levels, reduced expression of estrogen receptors (ERs) α and β, decreased inhibitor of NF-κB levels, and increased p-AKT levels. Following Ejiao intervention, interleukin-10, ERα+β, and inhibitor of NF-κB levels increased, while p-AKT levels decreased. Ejiao significantly improved lung function in CSE/lipopolysaccharide-induced COPD mice, reduced the number of macrophages, lowered the levels of inflammatory factors in bronchoalveolar lavage fluid, and increased estradiol levels in serum. WB results indicated that Ejiao may ameliorate lung injury in COPD by modulating the ER/AKT/NF-κB pathway.

The results suggest that Ejiao may improve lung injury and inflammation in CSE/ lipopolysaccharide-induced COPD by regulating the ER/AKT/NF-κB pathway.

Metabolic dysfunction-associated steatotic liver disease (MASLD), is the most common form of chronic liver disease worldwide. This study aimed to explore the role of TM6SF2 in high-fat diet (HFD)-induced MASLD through the gut-liver axis.

The TM6SF2 gut-specific knockout (TM6SF2 GKO) mouse was constructed using CRISPR/Cas9 technology. TM6SF2 GKO and wild-type (CON) mice were fed either a HFD or a control diet for 16 weeks to induce MASLD. Blood, liver, and intestinal lipid content, as well as gut microbiota and serum metabolites, were then analyzed.

TM6SF2 GKO mice fed an HFD showed elevated liver and intestinal lipid deposition compared to CON mice. The gut microbiota of HFD-fed TM6SF2 GKO mice exhibited a decreased Firmicutes/Bacteroidetes ratio compared to HFD-fed CON mice. The HFD also reduced the diversity and abundance of the microbiota and altered its composition.Aspartate aminotransferase, alanineaminotransferase, and total cholesterol levels were higher in HFD-fed TM6SF2 GKO mice compared to CON mice, while triglyceride levels were lower. Serum metabolite analysis revealed that HFD-fed TM6SF2 GKO mice had an increase in the expression of 17 metabolites (e.g., LPC [18:0/0-0]) and a decrease in 22 metabolites (e.g., benzene sulfate). The differential metabolites of LPC (18:0/0-0) may serve as HFD-fed TM6SF2 serum biomarkers, leading to MASLD exacerbation in GKO mice.

TM6SF2 GKO aggravates liver lipid accumulation and liver injury in MASLD mice. TM6SF2 may play an important role in regulating intestinal flora and the progression of MASLD through the gut-liver axis.

We reported a case of recurrent liver dysfunction in an adult patient with a history of abnormal liver enzymes persisting for over ten years. The primary abnormalities included elevated levels of gamma-glutamyl transferase and alkaline phosphatase. Despite conducting a series of extensive etiological tests to identify common causes of liver disease, the diagnosis remained unclear. However, whole-exome next-generation sequencing revealed a homozygous intronic mutation in the ferrochelatase gene (c.315-48T>C), which may be associated with the patient’s cholestasis.