Traumatic brain injury (TBI) induces neuroimmune activation and metabolic reprogramming in microglia, but the transcriptional regulators underlying these responses remain unclear. This study aimed to integrate single-cell and bulk transcriptomic datasets to identify microglia-associated regulatory genes and characterize their potential roles in post-TBI neuroinflammatory and immunometabolic dysregulation.

We integrated single-cell RNA sequencing data (GSE101901) with a bulk training dataset (GSE58485) and an independent bulk validation dataset (GSE242025) from murine TBI models. hdWGCNA, differential expression, pseudotime, CIBERSORT, and in silico transcription factor binding-site analyses were performed to identify and characterize candidate genes. Key-gene expression was additionally validated by RT-qPCR in male C57BL/6 mice assigned to Sham and TBI groups (n = 5 per group). The Drug Gene Interaction Database was used for exploratory drug-gene prediction.

Single-cell profiling suggested descriptive shifts in the proportions of microglia, astrocytes, and neurons after TBI. hdWGCNA identified 90 microglia-associated genes, 43 of which overlapped with nominally differentially expressed genes; 89 genes met the Benjamini–Hochberg-adjusted P < 0.05 threshold in the bulk analysis. Cross-dataset validation identified increased Ccl4 and Lgals3 expression and decreased Egr1 expression. Motif scanning identified four predicted EGR1 motif occurrences in the Ccl4 promoter and six occurrences at three unique locations in the Lgals3 promoter. RT-qPCR in TBI and Sham mice (n = 5 per group) supported the same directional expression changes in Ccl4, Lgals3, and Egr1.

A candidate Ccl4/Lgals3/Egr1 expression pattern characterized by Ccl4 and Lgals3 upregulation and Egr1 downregulation was associated with post-TBI neuroinflammatory and immunometabolic changes. Further mechanistic validation is required.

Hepatic sinusoidal obstruction syndrome (SOS) is characterized by hepatic sinusoidal endothelial cell injury and detachment, hepatic sinusoidal congestion, and hepatic cell necrosis. Currently, limited data exist concerning changes during the recovery period, especially histopathological changes. The purpose of this study was to investigate the evolution of pathology in patients with pyrrolizidine alkaloid (PA)-induced SOS and in a monocrotaline-induced SOS rat model.

Patients diagnosed with PA-induced SOS who underwent liver biopsy after achieving clinical remission were consecutively enrolled in this retrospective study. To compare the clinical and pathological differences between patients with acute and convalescent SOS, a 2:1 matched analysis was performed based on age, sex, treatment regimen, and baseline Drum Tower Severity Scoring (DTSS) during the acute phase. Additionally, an animal model of PA-induced SOS was established through the administration of monocrotaline.

Fourteen consecutive patients with SOS who had adequate liver biopsy specimens obtained during recovery were identified. During convalescence, most laboratory and imaging findings, such as the map-like enhancement observed on computed tomography, also disappeared. However, histopathological analysis revealed a distinct shift from hepatic sinusoidal endothelial cell injury in the acute phase to portal tract abnormalities, primarily characterized by portal vein stricture, in the recovery phase. These pathological changes were corroborated in our animal model.

Our study suggests that both patients with PA-induced SOS and rats in the convalescent stage may exhibit porto-sinusoidal vascular disease-like changes. Regular follow-up and dynamic pathological assessment are therefore recommended to facilitate the early detection of potential signs of portal hypertension.

EWSR1 fusions are recurrent genetic alterations in a wide spectrum of mesenchymal tumors and are often associated with specific clinicopathologic entities. However, the presence of an EWSR1 rearrangement does not always indicate a functional or disease-defining fusion.

We report a case of undifferentiated pleomorphic sarcoma with high-grade morphologic features harboring an EWSR1 rearrangement detected by fluorescence in situ hybridization. It was subsequently characterized by RNA sequencing as a likely nonfunctional fusion of EWSR1 exon 1 and NF2 intron 1. Histologically, the tumor was composed of pleomorphic spindle cells with brisk mitotic activity and lacked a specific line of differentiation. Immunohistochemically, the tumor showed diffuse cytoplasmic S100 positivity, with nuclear staining in a subset of tumor cells, while the overall immunophenotype did not support a specific line of differentiation. The EWSR1::NF2 fusion was inferred to have a tail-to-tail configuration, and additional KRAS and TP53 alterations were detected.

This case highlights that an EWSR1 rearrangement detected by fluorescence in situ hybridization should be interpreted cautiously and does not necessarily represent a functional or disease-defining fusion. Comprehensive molecular evaluation is important for the accurate interpretation and classification of sarcomas with atypical EWSR1 rearrangements.

Colorectal cancer is a major cause of cancer morbidity and mortality worldwide, including in China. Screening can facilitate earlier detection and reduce disease burden, while primary healthcare institutions are central to population outreach, risk assessment, referral, and follow-up. However, resource constraints, limited public awareness, low screening adherence, and fragmented coordination continue to hinder implementation in community and rural settings. This mini review summarizes the epidemiological and health-economic rationale for colorectal cancer screening in primary healthcare and discusses organizational models, risk-stratified screening and referral, workforce training, quality control, data management, and information sharing. Available evidence supports coordinated pathways that link noninvasive initial screening to timely colonoscopy and follow-up, supported by clear governance, trained personnel, and traceable data systems. The ongoing Yazhou District program is included briefly as a descriptive example of how these components may be organized in practice. Future research should evaluate uptake, positivity, colonoscopy completion, lesion detection, adverse events, costs, and longer-term outcomes in diverse primary-care settings.

Fuzheng Huayu, a patent herbal product, has shown promise in liver fibrosis and cirrhosis. The effect of Fuzheng Huayu on portal hypertension due to cirrhosis and the consequent complications needs further investigation. In this study, we aimed to evaluate the association of adjunctive Fuzheng Huayu plus entecavir with liver-related events and variceal regression in patients with compensated HBV-related cirrhosis.

A post hoc analysis was conducted using data from two randomized controlled trials implemented at eight clinical centers in China (ClinicalTrials.gov numbers: NCT02945982; NCT02945956). Patients with compensated hepatitis B virus-related cirrhosis were enrolled from October 2017 to March 2021. The primary endpoint was a composite of liver events and the individual components, including variceal bleeding, ascites, overt hepatic encephalopathy, and hepatocellular carcinoma.

A total of 218 participants (Fuzheng Huayu group: 110 and control group: 108; mean age, 51.5 years; 66.5% male; median observational follow-up time, 23.1 months) were included in the primary analysis. The occurrence of total liver events was less frequent in the Fuzheng Huayu group than in the control group (hazard ratio = 0.408 [0.187–0.892], P = 0.020). Among the individual components of liver events, the incidence of ascites was significantly lower in the Fuzheng Huayu group than in the control group (1.8% vs. 9.3%, P = 0.016). In addition, the rate of variceal regression was significantly higher in the Fuzheng Huayu group (27.3% vs. 10.2%, P < 0.001). Finally, there were no significant differences in the occurrence of adverse events between the two groups.

In this post hoc analysis of two randomized controlled trials, adjunctive Fuzheng Huayu plus entecavir was associated with fewer liver-related events, particularly ascites, and a higher rate of variceal regression than entecavir alone in patients with compensated hepatitis B virus-related cirrhosis. These findings warrant confirmation in adequately powered prospective studies.

Since their first inception, neuroendocrine neoplasms of the breast have undergone many iterations of classification and definition. Taken together with their extremely low incidence, the ever-evolving landscape has made diagnosis, treatment, and research exceedingly challenging.

Our patient is a 45-year-old female who had a breast mass with clinical workup favoring a breast primary. A diagnosis of small cell carcinoma was established after an extensive clinical and pathologic workup. The mass did not respond to traditional neoadjuvant platinum-based chemotherapy, and she underwent a total mastectomy. Shortly thereafter, imaging revealed widely metastatic disease involving the brain, chest, abdomen, and pelvis. She received whole-brain radiation and, given the previous lack of response to chemotherapy, was recommended to try off-label tarlatamab. To date, with a short-term follow-up of 5 months, after whole-brain radiotherapy administered concurrently with the first cycle of tarlatamab, subsequent imaging showed near-complete radiographic resolution of extracranial metastatic disease, while the brain lesions also showed radiographic resolution on follow-up MRI.

We report the novel and preliminary use of tarlatamab in a patient with small cell neuroendocrine carcinoma of the breast, with short-term follow-up. We also discuss the most critical challenges associated with this rare pathologic diagnosis and the important elements to consider to ensure that metastatic disease is excluded.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent worldwide and is frequently encountered in patients undergoing liver transplantation and hepatic surgery. Although hepatic steatosis was once considered a relatively benign condition, accumulating evidence indicates that MASLD is associated with reduced tolerance to ischemic stress and increased susceptibility to ischemia–reperfusion injury, which may contribute to graft dysfunction and postoperative liver injury. In this mini review, we used the concept of hepatic resilience, referring to the ability of the liver to maintain homeostasis during stress and recover after injury. We discussed how MASLD may reduce hepatic resilience through mechanisms involving lipotoxicity, mitochondrial dysfunction, oxidative stress, inflammatory activation, regulated cell death, and impaired regeneration. MASLD represents a heterogeneous disease spectrum, and susceptibility to ischemia–reperfusion injury may differ according to disease stage and phenotype, particularly in the presence of progressive inflammation and fibrosis. We further summarized strategies aimed at improving hepatic resilience, including metabolic optimization, mitochondrial protection, modulation of reperfusion-associated inflammation, and enhancement of tissue repair. However, current evidence remains limited by the paucity of human studies and validated approaches for assessing hepatic resilience. Further investigation of these mechanisms may help develop individualized strategies to protect the liver in patients with MASLD during hepatic surgery and transplantation.