Khat (Catha edulis) is a plant native to East Africa and the Arabian Peninsula, chewed for its stimulant effects by millions worldwide. Its sympathomimetic properties, primarily due to cathinone and other pyrrolizidine alkaloids, resemble those of amphetamine. Emerging reports have linked khat use to the development of autoimmune hepatitis, supported by elevated autoimmune markers, characteristic liver biopsy findings, and clinical resolution following khat cessation or a prompt response to corticosteroid therapy without recurrence. In this review, we aimed to update knowledge on both acute and chronic forms of khat-associated AIH. We discuss cathinone metabolism, pharmacokinetics, and proposed mechanisms of khat hepatotoxicity. We also provide an updated synthesis of published cases of khat-associated autoimmune hepatitis, including our calculated Roussel-Uclaf Causality Assessment Method analysis and the simplified Hennes AIH score where data were available. Case presentations, diagnostic criteria, histopathological findings, and treatment approaches are summarized to help guide management.

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.

Harlequin ichthyosis, one of the rarest and most severe skin disorders, is mainly characterized by extreme hyperkeratosis, severely impairing the natural barrier function of the skin. This congenital disease results from a mutation in the ABCA12 gene responsible for lipid transport, whereby healthy skin development is assured. Harlequin ichthyosis is an autosomal recessive condition that requires parents to carry a defective gene copy for the disorder to manifest in their offspring. Babies born with Harlequin ichthyosis have thick skin plates that crack and flake off; they easily become dehydrated, infected, and may suffer from respiratory complications. With new improvements in neonatal care and systemic therapy, notably retinoid therapy, infants’ survival rates have improved. This review provides an inclusive overview of the pathophysiology, clinical features, diagnostic methods, management, and potential future therapies for Harlequin ichthyosis. In addition, a discussion on genetic counseling and its importance in managing family risk factors is also included, as well as a look into cutting-edge research focused on gene therapy and potential curative treatments.

circPVT1 has emerged as a key regulator in disease progression and clinical outcomes. However, its prognostic relevance and association with clinicopathological parameters in solid malignancies remain to be fully elucidated. To address this, we conducted a meta-analysis to elucidate the clinical significance of circPVT1 in solid tumors.

A comprehensive literature search was conducted across multiple databases, including PubMed, Web of Science, Embase, the Cochrane Library, and CNKI, with a cutoff date of December 31, 2024. Statistical analyses were conducted using STATA 12.0 to calculate pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs), assessing the impact of circPVT1 expression on overall survival (OS) and its association with clinicopathological characteristics.

This analysis included 27 clinical studies encompassing a total of 2,219 patients. Elevated circPVT1 expression was significantly associated with poorer OS in patients with solid tumors (HR = 1.68, 95% CI: 1.39–2.02, P < 0.001). This association was particularly notable in lung cancer (HR = 2.08, 95% CI: 1.51–2.88, P < 0.001) and osteosarcoma (HR = 1.65, 95% CI: 1.38–1.97, P < 0.001), with similar trends observed in hepatocellular carcinoma, colorectal cancer, and papillary thyroid carcinoma. Furthermore, the increased circPVT1 level was correlated with larger tumor size (OR = 1.36, 95% CI: 1.11–1.67, P = 0.004), lymph node metastasis (OR = 1.56, 95% CI: 1.22–2.00, P < 0.001), distant metastasis (OR = 1.80, 95% CI: 1.10–2.92, P = 0.017), and advanced tumor-node-metastasis stage (OR = 1.84, 95% CI: 1.50–2.25, P < 0.001).

Aberrant circPVT1 expression is associated with adverse OS and unfavorable clinicopathological features in solid tumors, underscoring its potential utility as a prognostic biomarker and indicator of tumor aggressiveness.

Emerging evidence implicates immune dysregulation and neuroinflammation in the pathogenesis of epilepsy, yet the causal mechanisms remain unclear. This study aimed to investigate the causal effects of immune cells and inflammatory proteins on epilepsy and evaluate the mediating role of inflammatory proteins.

This study utilized the largest available genome-wide association study data on immune cell phenotypes and inflammatory proteins as exposures, and epilepsy genome-wide association study data from the FinnGen dataset as outcomes. Five Mendelian randomization (MR) methods were applied within a two-sample MR framework to assess causal effects. Furthermore, a two-step MR analysis was conducted to quantify the proportion of epilepsy and its subtypes influenced by immune cells through inflammatory proteins.

The two-sample MR analysis identified 32 immune cell phenotypes associated with epilepsy risk (19 risk-increasing, e.g., CD19+ B cells; 13 protective, e.g., regulatory T cell subsets). Subtype analyses revealed 30 immune phenotypes associated with generalized epilepsy and 26 with focal epilepsy. Eight inflammatory proteins showed suggestive causal effects on epilepsy: C-C chemokine ligand 23, C-X-C motif chemokine ligand 6, C-X-C motif chemokine ligand 11, and vascular endothelial growth factor A increased epilepsy risk, while interleukin-13 (IL-13), leukemia inhibitory factor receptor, tumor necrosis factor, and osteoprotegerin conferred protection. Mediation analysis indicated that inflammatory proteins mediated 6.3–13.5% of the immune effects on epilepsy. Specifically, CD14+CD16+ monocytes increased epilepsy risk through elevated C-C chemokine ligand 23 levels (8.5% mediation), while effector memory double-negative (CD4−CD8−) T cells reduced epilepsy risk via upregulation of IL-13 (6.3%). Sensitivity analyses confirmed the robustness of these findings (P heterogeneity/pleiotropy > 0.05). Although no associations reached Bonferroni-corrected significance, the findings implicate B cells, monocytes, regulatory T cells, and cytokines (e.g., IL-13, leukemia inhibitory factor receptor) in the pathogenesis of epilepsy, with inflammatory proteins acting as partial mediators.

These results enhance our understanding of immune-inflammatory pathways in epilepsy and highlight potential therapeutic targets. Future studies should validate these findings across diverse populations and further elucidate the molecular mechanisms underlying the identified associations.

Myosteatosis is associated with poor outcomes in various liver diseases. However, standardized methods for assessing, defining, and diagnosing myosteatosis in the context of liver diseases remain unclear. Furthermore, the underlying mechanisms by which myosteatosis leads to pathophysiological progression and adverse health outcomes remain elusive. Therefore, in this review, we elaborate on the currently available measures, definitions, and diagnostic criteria of myosteatosis in the existing literature. We thoroughly clarify the recent evidence and data regarding the possible involvement of myosteatosis in the progression and deterioration of various liver diseases and resulting complications, including liver cirrhosis, chronic viral hepatitis, non-alcoholic/metabolic-associated fatty liver disease, primary sclerosing cholangitis, liver transplantation, and hepatocellular carcinoma. Additionally, it synthesizes insights from basic research on the pathogenesis of myosteatosis, which involves multifactorial mechanisms, including insulin resistance, mitochondrial dysfunction, and chronic inflammation. Finally, from an operational and pragmatic perspective, several regimens, including physical, nutritional, and pharmacological therapies, have been discussed as potential treatments for myosteatosis.

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.

Gastric cancer remains a significant global health burden, with limited therapeutic options and poor clinical outcomes. Although conventional treatments such as surgery and chemotherapy are widely used, their effectiveness is often hindered by adverse effects and high recurrence rates, highlighting the urgent need for safer and more effective alternatives. Scleromitrion diffusum (Willd.) (S. diffusum), a well-established anticancer herb in traditional Chinese medicine, has demonstrated promising clinical potential against gastric cancer. This review systematically examines the bioactive components of S. diffusum and their multi-target mechanisms of action against gastric cancer. Key active compounds, including flavonoids, anthraquinones, and terpenoids, have been identified as exerting synergistic anti-gastric cancer effects. These compounds collectively target critical pathways in gastric cancer pathogenesis, including apoptosis induction, suppression of proliferation and angiogenesis, and immune modulation. The mechanistic elucidation presented in this review not only validates the traditional use of S. diffusum in cancer management but also provides a molecular basis for its potential application in precision medicine strategies for gastric cancer. Beyond summarizing existing evidence, this work highlights critical gaps in current knowledge and proposes essential directions for future research, providing important references for integrating traditional medicine with modern oncology approaches.

The association between chronic inflammation and cancer has reshaped our understanding of tumorigenesis and cancer therapy. Inflammatory responses can both promote and suppress cancer, depending on the context and timing. Key molecular players, such as nuclear factor kappa-light-chain-enhancer of activated B cells, interleukin-6, signal transducer and activator of transcription 3, and a variety of immune cell types, including tumor-associated macrophages, myeloid-derived suppressor cells, and regulatory T cells, orchestrate an environment conducive to tumor survival, angiogenesis, metastasis, and immune evasion. In recent years, immunotherapy, particularly immune checkpoint inhibitors, has revolutionized cancer treatment. However, its success varies across tumor types and patients, underscoring the need to understand the tumor microenvironment and inflammatory context. This review examines the mechanistic underpinnings of inflammation-driven cancer, discusses translational research efforts targeting inflammatory pathways, and explores clinical applications, including the integration of immunotherapy with anti-inflammatory agents and biomarkers for personalized treatment. Future directions in the field include the application of artificial intelligence, microbiome research, single-cell technologies, and gene editing tools to further tailor therapies and overcome resistance mechanisms.

Giant invasive spinal schwannoma (GISS) is a rare benign tumor that extends over two or more vertebral levels with myofascial invasion. No previous case of GISS with vertebral body collapse has been reported. A 44-year-old man presented with a one-year history of progressive limb weakness and difficulty with defecation. He was initially misdiagnosed with a metastatic spinal tumor. Imaging revealed a large extradural mass with C4 vertebral body collapse. Histological examination of tumor tissue from both operations confirmed the diagnosis of schwannoma. The postoperative course was uneventful, and the patient’s limb weakness gradually improved. One year after surgery, the patient was able to walk and write independently. Muscle strength recovered to 4/5 in the upper extremities and 5/5 in the lower extremities, with a modified Japanese Orthopaedic Association score of 15/15. The patient’s neurological function improved significantly, and one-year follow-up showed no recurrence and stable spinal fixation. Currently, the patient’s bowel function has improved; however, the patient still requires defecation in bed. When magnetic resonance imaging reveals giant spinal tumors with imaging features suggestive of malignancy, GISS should be considered. Preoperative biopsy is essential for accurate diagnosis.