Right submammary thoracotomy and right vertical infra-axillary thoracotomy are performed for ventricular septal defect (VSD) to reduce the invasiveness of the conventional surgical repair through median sternotomy approach. No comparative studies have been conducted among these three procedures. From January 2016 to December 2016, 182 patients with isolated VSD who underwent surgical repair via one of these 3 approaches were reviewed to compare these three procedures. The procedure success rates were similar in these three groups. There was no statistically significant difference in operative time, aortic cross-clamping time, the duration of CPB, blood transfusion amount and medical cost. However, postoperative mechanical ventilation time, the duration of intensive care and postoperative length of hospital stay were longer in median sternotomy group than the other two groups. (P < 0.05) The median sternotomy group required the longest incision. No significant difference was noted in major adverse events. There were different advantages and disadvantages in the three kinds of operative procedures. Regarding conventional surgical repair VSD, right submammary thoracotomy and right vertical infra-axillary thoracotomy both delivered better cosmetic results for patients with isolated VSD, while all the three procedures could obtain satisfactory clinical effect.

NIMA-related kinase 7 (NEK7) is a serine/threonine kinase involved in cell cycle progression via mitotic spindle formation and cytokinesis. It has been related to multiple cancers, including breast cancer, hepatocellular cancer, lung cancer, and colorectal cancer. Moreover, NEK7 regulated the NLRP3 inflammasome to activate Caspase-1, resulting in cell pyroptosis. In the present study, we investigated whether NEK7 is involved in cell pyroptosis of hepatocellular carcinoma (HCC). Interestingly, we found that NEK7 was significantly related to expression of pyroptosis marker GSDMD in HCC. We found that NEK7 expression was significantly correlated with GSDMD expression in bioinformatics analysis, and NEK7 expression was significantly co-expressed with GSDMD in our HCC specimens. Cell viability, migration, and invasion capacity of HCC cell lines were inhibited, and the tumor growth in the xenograft mouse model was also suppressed following knockdown of NEK7 expression. Mechanistic studies revealed that knockdown of NEK7 in HCC cells significantly upregulated the expression of pyroptosis markers such as NLRP3, Caspase-1, and GSDMD. Coculture of HCC cells stimulated hepatic stellate cell activation by increasing p-ERK1/2 and α-SMA. Knockdown of NEK7 impaired the stimulation of HCC cells. Therefore, downregulation of NEK7 inhibited cancer–stromal interaction by triggering cancer cell pyroptosis. Taken together, this study highlights the functional role of NEK7-regulated pyroptosis in tumor progression and cancer–stromal interaction of HCC, suggesting NEK7 as a potential target for a new therapeutic strategy of HCC treatment.

Nonalcoholic fatty liver disease (NAFLD) is the most common metabolic liver disease globally, and the incidence of NAFLD has been increasing rapidly year by year. Currently, there is no effective pharmacotherapy for NAFLD. Therefore, studies are urgently needed to explore therapeutic drugs for NAFLD. In this study, we show that isoschaftoside (ISO) dramatically reduces lipid deposition in cells. Meanwhile, ISO treatment reverses the NAFLD and reduces hepatic steatosis in mice. Importantly, we reveal that ISO suppresses the expression of light-chain 3-II (LC3-II) and SQSTM1/p62 in palmitic acid (PA) induced autophagy inhibition in the cell model and the NAFLD mouse model, which suggests that ISO might reverse NAFLD through regulating autophagy flux. We propose that ISO might alleviate hepatic steatosis in NAFLD via regulating autophagy machinery. Consequently, our study suggests that ISO might be of potential clinical value in the field of NAFLD therapy. ISO might have the potential for future therapeutic application.

Clonorchis sinensis infections persist globally among humans. These pathogens mainly inhabit the intrahepatic biliary system. Most individuals with clonorchiasis exhibit mild symptoms. The absence of distinctive symptoms often results in delayed diagnosis and treatment, potentially leading to chronic infection. We herein report a case of a 29-year-old female presented with a year-long history of abdominal distention and dyspepsia. Imaging revealed intrahepatic bile duct dilatation, intrahepatic bile duct cyst, and associated deposits. One month post-cystectomy, the patient developed massive ascites and a significant increase in eosinophil count. After treatment, multiple worms were observed in the drainage tube. Morphological and DNA metagenomic analyses confirmed the presence of C. sinensis. Clinical manifestations of C. sinensis vary widely. Imaging serves as a valuable diagnostic tool in endemic areas, especially in detecting intrahepatic duct dilation where the flukes reside. In addition to intrahepatic bile duct dilation, abnormal echoes within the bile duct and the presence of floating objects in the gallbladder significantly aid in diagnosis. Clinicians may encounter these parasitic diseases unexpectedly, underscoring the importance of understating such cases in routine practice and contributing to our broader understanding of managing similar cases in clinical settings.

Background: Forkhead box protein 3 (FOXP3) plays a pivotal role in tumor progression and impacts the methylation status and levels of expression of an associated promoter region. However, the methylation status and how this parameter impacts the FOXP3 promoter in cases of human hepatocellular carcinoma (HCC) remains unclear. This study sought to investigate the relationship between methylation status of transcriptional FOXP3 gene promoter and the levels of expression of FOXP3 in human HCC afflicted cell lines and tissues. Methods: We used quantitative real-time PCR (Real-time qPCR) to detect the levels of expression of FOXP3 mRNA in human HCC afflicted cell lines and tissues. Immunohistochemistry and western blot were used to examine protein expression levels of FOXP3 in human HCC afflicted cell lines and tissues. Reverse transcription PCR was used to detect the levels of expression of the FOXP3 gene promoter in HCC afflicted cell lines. Finally, methylation sequencing was used to examine the influences of epigenetic regulation upon the FOXP3 promoter region in HCC afflicted cell lines. Results: Levels of FOXP3 expression were down-regulated in HCC afflicted tissues compared with adjacent non-tumorous tissues. Levels of expression of FOXP3 in portal vein tumor thrombus (PVTT) were much lower than were levels in HCC afflicted tissues. Further, FOXP3 was abnormally expressed in HCC afflicted cell lines. The FOXP3 promoter was also abnormally expressed among HCC afflicted cell lines. Lastly, the FOXP3 promoter was hypermethylated in HCC afflicted cell lines. Conclusions: Results suggest that levels of expression of the FOXP3 promoter were decreased for measures of both mRNA and protein expression levels in HCC afflicted tissues and cell lines. The FOXP3 gene promoter region when hypermethylated may help inhibit FOXP3 expression and the development and progression of HCC.

Purpose: Circulating tumor DNA (ctDNA) is a noninvasive biomarker for tumor burden. Blood-based assays utilizing ctDNA copy number aberrations and fragment size show promise in hepatocellular carcinoma (HCC), but their prognostic value is unclear. This study evaluated the clinical relevance of a ctDNA-based score in predicting HCC prognosis. Patients and Methods: Clinical and ctDNA data from 93 HCC patients were analyzed. Patients were stratified by a predefined ctDNA score cutoff. Group comparisons used chi-square tests. Kaplan-Meier and multivariate Cox regression analyses assessed prognostic relevance. Results: Elevated ctDNA scores were associated with aggressive features: higher AFP and PIVKA-II levels, larger tumor size, macrovascular invasion, and advanced TNM stage (all P < 0.001). Patients with ctDNA scores > 0.61199 had significantly worse overall survival (OS). Univariate analysis identified 19 OS-associated variables, including inflammatory markers, biochemical indices, and tumor burden parameters. Multivariate analysis confirmed ctDNA score > 0.61199 (HR = 6.99, 95% CI 2.34– 20.85, P < 0.001), AFP > 400 ng/mL (HR = 0.28, 95% CI 0.13– 0.61, P = 0.001), ALB < 35.6 g/L (HR = 3.29, 95% CI 1.34– 8.06, P = 0.009), and tumor number > 3 (HR = 3.85, 95% CI 1.58– 9.40, P = 0.003) as independent prognostic determinants. Conclusion: Elevated ctDNA scores are strongly associated with adverse outcomes in HCC, highlighting their potential as a noninvasive prognostic biomarker. Integrating ctDNA assessment could improve risk stratification and treatment decisions, warranting validation in prospective studies.