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To improve heat dissipation performance of panel-type radiator for transformer, this study investigated the flow and heat transfer characteristics of semi-detached inclined trapezoidal wing vortex generator (SDITW) in a closed channel on the air-side of the radiator. The SDITW was compared with the inclined delta wing (IDW) and inclined trapezoidal wing (ITW) channels. The effects of SDITW relative separation height (e 1/e 2), longitudinal pitch (p l), blockage ratio (e/(0.5H)), and inclination angle (α) were analyzed. First, compared with the IDW and ITW channels, the SDITW channel generates stable corner vortices and produces weaker transverse vortices and lower flow resistance due to the semi-detached structure of the wing. For Re = 5,125–15,375, the overall heat transfer performance (performance evaluation criteria; PEC) of the SDITW channel increases by 0.5–8.9 and 1.7–4.9% as compared with IDW and ITW channels, respectively. Furthermore, for the same e/(0.5H) and α, both the Nusselt number ratio and friction factor ratio of SDITW channel increase as e 1/e 2 and p l decrease. For p l = 70 mm, the SDITW channel exhibits a relatively better overall heat transfer performance. For the same e 1/e 2 and p l, the PEC of SDITW channel is maximum and the overall heat transfer performance is best when e/(0.5H) = 0.3 at Re = 10,250 and α = 30°–60°.

Background: Adenomatous polyposis coli (APC) gene, an oncogene, has been implicated in stomach adenocarcinoma (STAD), which is a common type of gastric cancer (GC). Although the relationship between APC gene mutations and gastric adenocarcinoma has been comprehensively studied, the potential role of these mutations in the prognosis and targeted therapy remains known. Methods: We utilized The Cancer Genome Atlas (TCGA) database to obtain gene expression matrices, clinical information, and mutation data from patients with STAD. The mutation status of the APC gene was analyzed, and its correlation with tumor mutational burden (TMB), microsatellite instability (MSI), and clinical prognosis in STAD was investigated. Gene set enrichment analysis (GSEA) was conducted to explore the pathological role of APC gene mutations in STAD metabolic pathways. Drug sensitivity analysis was conducted to identify potential targeted antitumor drugs for patients with APC gene mutations in gastric adenocarcinoma. Results: The results revealed that 88% (46/52) of STAD samples had nonsynonymous mutations. The mutation group exhibited a significantly higher TMB than the wild‐type group (p < 0.001), and the percentage of high MSI (MSI‐H) was significantly higher in the mutation group than in the wild‐type group (p < 0.001). Patients with APC mutations had a worse prognosis than those with APC wild‐type (p = 0.009). The APC gene mutation group displayed significant enrichment in amino acids, RNA, and several pathways (|NES| > 1 and nominal p value < 0.01). Compared to the wild‐type group, the mutation group exhibited a higher infiltration proportion of natural killer (NK) cells resting and eosinophils, whereas a lower infiltration proportion of monocytes and resting mast cells (p value < 0.05). AZD5991 exhibited significant sensitivity in patients with STAD carrying APC mutations (p = 0.028). Conclusion:APC gene mutations play a crucial role in the prognosis, molecular characteristics, and potential therapeutic strategies for gastric adenocarcinoma. [ABSTRACT FROM AUTHOR]

Background: Abnormal lipid deposition is an important driver of the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). MicroRNA-411-5p (miR-411-5p) and eukaryotic translation initiation factor 4γ2 (EIF4G2) are related to abnormal lipid deposition, but the specific mechanism is unknown. Methods: A high-fat, high-cholesterol diet (HFHCD) and a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) and a high-fructose diet (HFrD) were used to establish MASLD rat and mouse models, respectively. MiR-411-5p agomir and mimic were used to upregulate the miR-411-5p in vivo and in vitro, respectively. Adeno-associated virus type 8 (AAV8) carrying EIF4G2 short hairpin RNA (shRNA) and small interfering RNA (siRNA) were used to downregulate the EIF4G2 expression in vivo and in vitro, respectively. Liver histopathological analysis, Biochemical analysis and other experiments were used to explore the functions of miR-411-5p and EIF4G2. Results: MiR-411-5p was decreased in both MASLD rats and mice, and was negatively correlated with liver triglycerides and serum alanine transaminase (ALT) and aspartate transaminase (AST) levels. Upregulation of miR-411-5p alleviated liver lipid deposition and hepatocellular steatosis. Moreover, miR-411-5p targeted and downregulated EIF4G2. Downregulation of EIF4G2 not only reduced liver triglycerides and serum ALT and AST levels in MASLD model, but also alleviated lipid deposition. Notably, upregulation of miR-411-5p and downregulation of EIF4G2 led to the reduction of forkhead box class O3 (FOXO3) and inhibited the expression of sterol regulatory-element binding protein 1 (SREBP1), acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase (FASN), thereby reducing fatty acid synthesis. Conclusions: Upregulation of miR-411-5p inhibits EIF4G2 to reduce the FOXO3 expression, thereby reducing fatty acid synthesis and alleviating abnormal lipid deposition in MASLD. [ABSTRACT FROM AUTHOR]

Background and Aim: Hepatitis B virus (HBV) load and antigens are related to the innate and adaptive immunity of chronic hepatitis B (CHB) patients. As a new HBV biomarker, the role of pregenomic RNA (pgRNA) in host immunity is not known. This study aimed to identify the relationship between serum HBV pgRNA and host immunity in CHB patients. Methods: Two hundred twenty‐five treatment‐naïve CHB patients were enrolled. Serum cytokines were measured by cytokine antibody array (Luminex multiplex platform). Th1 (T‐helper cell, Th) and Th2 cells were tested by flow cytometry. Serum HBV pgRNA was detected by a reverse transcription‐polymerase chain reaction. Results: Serum HBV pgRNA was significantly different among patients in different disease phases and significantly associated with both HBV antigens and antibodies. Serum HBV pgRNA was positively correlated with the HBsAg level (P <.001) and the presence of HBeAg (P <.001). Patients with higher HBcAb levels showed lower serum HBV pgRNA levels (P =.003). Notably, HBsAb positivity was associated with higher levels of serum HBV pgRNA in HBeAg(−) patients (P =.049). Serum HBV pgRNA was positively associated with ALT level, Th2 cell frequency, and related cytokine sCD30 (P <.001, P <.001, and P =.003, respectively), but negatively associated with Th1‐related cytokine interleukin (IL)‐12P70 and cytotoxic lymphocytes (CTLs) (P =.017 and P <.001, respectively). Conclusion: Our study confirmed the relationship between serum HBV pgRNA and host immunity. The results demonstrated that serum HBV pgRNA is positively correlated with Th2 immunity but negatively correlated with Th1 immunity, indicating that it might have a relationship with HBV antigen conversion and CTL immunodeficiency in CHB patients. Highlights: Serum HBV pgRNA had a relationship with host immunity.Serum HBV pgRNA was positively correlated with Th2 cells and cytokines.Serum HBV pgRNA was negatively correlated with CTLs and Th1 cytokine. [ABSTRACT FROM AUTHOR]