2026年 · 第139卷第09期

Liver failure (LF) is characterized by a constellation of clinical syndromes, including ascites, coagulopathy, hepatic encephalopathy, and renal insufficiency, which arise from severe liver dysfunction resulting from multiple insults to the liver. The etiology of LF is complex, with viruses, drugs or toxins, autoimmune disorders, bacterial infections, and genetic defects being the major contributors to its development.^[1]LF is generally classified into four categories: (1) acute LF (ALF), (2) subacute LF, (3) acute-on-chronic LF (ACLF), and (4) chronic LF, based on the speed at which liver dysfunction progresses. LF-associated mortality remains high. For instance, approximately 40% of patients with ACLF die within 90 days of admission in a US cohort.^[2]Among patients with ALF lacking liver transplantation, the mortality rate is over 50%.^[3]Although liver transplantation has significantly improved survival rates among patients with LF, the ongoing shortage of available donors markedly limits clinical practice.

Significant disparities in the diagnosis and treatment of ovarian cancer persist across different regions in China. County-level hospitals, which serve a large portion of the rural population, often face challenges such as limited medical equipment, a shortage of specialized professionals, and restricted access to novel drugs, leading to nonstandardized care and suboptimal patient outcomes.

To the Editor: Atrial fibrillation (AF) is a prevalent arrhythmia, with aging recognized as a major risk factor. As the global population ages, the incidence of AF has been steadily increasing, particularly among individuals aged ≥65 years. AF increases the risk of stroke and heart failure and is strongly associated with cognitive impairment, frailty, and reduced quality of life. A comprehensive understanding of the mechanisms through which aging contributes to AF, particularly the role of telomere dysfunction, is crucial for identifying novel therapeutic targets.

To the Editor: Inflammatory bowel disease (IBD) is a chronic inflammatory condition with unclear causes, comprising ulcerative colitis (UC) and Crohn’s disease (CD). The disease alternates between active and remission phases, complicating monitoring and management. Current clinical biomarkers have limitations in specificity and predictability. Cellular free nucleic acids (cfNAs), as a non-invasive diagnostic tool, offer significant potential in diagnosis and precision medicine.

To the Editor: Since the introduction of Cologuard,^[1]which targets hemoglobin,KRASmutations, and the methylation of two genes in stool DNA, methods of colorectal cancer (CRC) screening based on stool DNA methylation have received increasing attention. In comparison to stool-based assays, tests based on blood cell-free DNA (cfDNA) methylation may be more readily accepted and better suited for clinical scenarios, although they are currently less widely available. Septin9 represents a promising initial approach; however, due to the limitations of insufficient early sensitivity, it is now not recommended by the American College of Gastroenterology (ACG) guidelines.^[2]The development of blood methylation tests is hindered by several significant challenges, including the low concentration of cfDNA, issues with tissue traceability, and leukocyte interference. One potential solution to these issues is the identification of more promising markers, which are likely to be entirely new targets, distinct from stool markers due to the different mechanisms by which cancer signals are present in these sample types. Furthermore, the advancement of sensitive detection techniques capable of identifying small amounts of cfDNA is crucial for the success of these tests.

To the Editor: Gastric cancer (GC) is one of the most common digestive system malignancies, and the incidences of proximal gastric cancer (PGC) and adenocarcinoma of esophagogastric junction (AEG) have recently increased.^[1]Compared to total gastrectomy (TG), proximal gastrectomy (PG) preserves more of the stomach’s volume and function and is increasingly used in clinical practice. However, PG disrupts the anatomical antireflux barrier, often leading to reflux esophagitis. To reduce complications and improve patients’ quality of life (QOL), various reconstruction methods have been proposed. However, an optimal reconstruction method has not been established.

To the Editor: Lung cancer is the leading cause of cancer death worldwide. The most prevalent pathological subtype of lung cancer is lung adenocarcinoma (LUAD).^[1]Genetic and epigenetic variants are crucial, as well as the gut and intratumor microbiota, in affecting lung cancer susceptibility and migration. Therefore, we retrospectively studied the molecular characteristics of patients with LUAD to determine whether the intratumor microbiota affects lymph node metastasis.

To the Editor: Uveal melanoma (UVM) is a rare yet highly aggressive cancer originating in the uvea, the vascular layer of the eye, encompassing the iris, ciliary body, and choroid.^[1,2]Although UVM has a lower incidence compared to other melanomas, it carries a high mortality rate due to its tendency to metastasize.^[3]The liver is the most common site of metastasis for UVM, and once the cancer has spread to the liver, the prognosis worsens significantly due to limited treatment options.^[4]Early detection and a thorough understanding of UVM and its metastatic patterns are crucial for improving patient outcomes.^[5]To address these challenges, we developed a comprehensive deep-learning network for diagnosing histological types and predicting liver metastasis in patients with UVM. Moreover, we created a deep-learning Cox model for risk classification, conducted bioinformatic analyses to explore the biological characteristics of subtypes, and constructed a prognostic gene signature validated across multiple cohorts. Furthermore, a nomogram model was developed by integrating clinical and molecular variables [Figure 1].

To the Editor: Keloid is a fibroproliferative disorder characterized by invasive growth beyond wound margins, causing significant physical and psychosocial morbidity. Persistent inflammation and aberrant extracellular matrix deposition by activated fibroblasts and myofibroblasts are central to keloid pathogenesis. Increasing evidence highlights the pivotal role of vascular endothelial cells (ECs) in disease progression.^[1]Features of pathological angiogenesis in keloids include disorganized microvasculature, luminal flattening, and functional impairments that paradoxically induce local hypoxia despite high blood flow. This dysfunctional vasculature increases vascular permeability, promoting perivascular accumulation of inflammatory cells and mediators, thereby amplifying inflammation and fibrotic signaling. Notably, clinical associations between endothelial dysfunction—such as that observed in hypertension—and increased keloid susceptibility underscore the central role of ECs in disease predisposition. These findings position vascular ECs not only as contributors to the profibrotic microenvironment but also as potential diagnostic and prognostic indicators. Thus, assessing endothelial function holds significant clinical promise for risk prediction, molecular classification, and the development of precision interventions in keloid management.