Pan-cancer analysis of the immune aspects and prognostic value of NCAPG2.

NCAPG2 has been reported to be associated with tumorigenesis in various types of cancer. However, data on the pathological mechanisms of NCAPG2 in pan-cancers remain lacking. Therefore, the study aimed to comprehensively elucidate the immune characteristics and prognostic of NCAPG2 in tumor microenvironments (TMEs). NCAPG2 was overexpressed in many tumor types, and this overexpression is related to poor clinical stages and prognosis. Furthermore, elevated NCAPG2 expression was strongly associated with TMEs. Moreover, gene set enrichment analysis was performed to investigate the pathways associated with NCAPG2, revealing its involvement in several immune-related pathways. Finally, we predicted the immunotherapeutic value and sensitivity to drugs based on NCAPG2 expression. Our study revealed that NCAPG2 could be utilized as an immune-related biomarker for both diagnosing and predicting the prognosis of multiple cancer types. Therefore, our findings suggest that targeting NCAPG2 in TMEs could be a promising therapeutic strategy.

Hybrid LAE-CMOS Force-Sensing System Employing TFT-Based Compressed Sensing for Scalability of Tactile Sensing Skins.

Tactile sensing requires form-fitting and dense sensor arrays over large-areas. Hybrid systems, combining Large-Area Electronics (LAE) and silicon-CMOS ICs to respectively provide diverse sensing and high-performance computation/control, enable a platform for such sensing. A key challenge is that hybrid systems require a large number of interfaces between the LAE and CMOS domains, particularly as the number of sensors scales. This paper presents an architecture that exploits the attribute of signal sparsity, commonly exhibited in large-scale tactile-sensing applications, to reduce the interfacing complexity to a level set by the sparsity rather than the number of sensors. This enhances scalability compared to sequential-scanning and active-matrix approaches. The architecture implements compressed sensing via thin-film-transistor (TFT) switches, and is demonstrated in a force-sensing system with 20 force sensors, a TFT die (with 161 ZnO TFTs) per sensor, and a custom CMOS IC for system readout and control. Acquisition error of 0.7 k[Formula: see text] is achieved over a 100 k Ω-20 k Ω sensing range, at energy and rate of 2.46  µ J/frame and 31 fps.

Sophocarpine attenuates liver fibrosis by inhibiting the TLR4 signaling pathway in rats.

AIM: To explore the effect of sophocarpine on experimental liver fibrosis and the potential mechanism involved. METHODS: Sophocarpine was injected intraperitoneally in two distinct rat hepatic fibrosis models induced either by dimethylnitrosamine or bile duct ligation. Masson's trichrome staining, Sirius red staining and hepatic hydroxyproline level were used for collagen determination. Primary hepatic stellate cells (HSCs) were isolated and treated with different concentrations of sophocarpine. Real-time reverse transcription-polymerase chain reaction was used to detect the mRNA levels of fibrotic markers and cytokines. The expression of pathway proteins was measured by Western blot. The Cell Counting Kit-8 test was used to detect the proliferation rate of activated HSCs treated with a gradient concentration of sophocarpine. RESULTS: Sophocarpine decreased serum levels of aminotransferases and total bilirubin in rats under chronic insult. Moreover, administration of sophocarpine suppressed extracellular matrix deposition and prevented the development of hepatic fibrosis. Furthermore, sophocarpine inhibited the expression of α-smooth muscle actin (SMA), interleukin (IL)-6, transforming growth factor-ß1 (TGF-ß1), Toll-like receptor 4 (TLR4), and extracellular-related kinase (ERK) in rats. Sophocarpine also down-regulated the mRNA expression of α-SMA, collagen I, collagen III, TGF-ß1, IL-6, tumor necrosis factor-α and monocyte chemoattractant protein-1, and decreased protein levels of TLR4, p-ERK, p-JNK, p-P38 and p-IKK in vitro after Lipopolysaccharide induction. In addition, sophocarpine inhibited the proliferation of HSCs accompanied by a decrease in the expression of Cyclin D1. The protein level of proliferating cell nuclear antigen was decreased in activated HSCs following a gradient concentration of sophocarpine. CONCLUSION: Sophocarpine can alleviate liver fibrosis mainly by inhibiting the TLR4 pathway. Sophocarpine may be a potential chemotherapeutic agent for chronic liver diseases.

[Andrographolide inhibits extracellular signal-regulated kinase 1/2 signaling pathway in activated macrophages].

OBJECTIVE: To investigate the effects of andrographolide on extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and tumor necrosis factor-α (TNF-α) expression in lipopolysaccharide (LPS)-activated macrophages. METHODS: LPS-activated mouse peritoneal macrophages were cultured in media with different concentrations of andrographolide. Cytotoxicity of andrographolide was detected by cell counting kit-8. The macrophages were lysed, and then expressions of phosphorylated ERK1/2, JNK and p38 and nuclear factor-κB inhibitor (IκBα) protein were detected by Western blotting and TNF-α mRNA expression was detected by reverse transcription-polymerase chain reaction. Supernatants of the macrophages were used to detect content of TNF-α protein by enzyme-linked immunosorbent assay. RESULTS: Andrographolide at 1-100 µg/mL showed no cytotoxicity on LPS-activated mouse peritoneal macrophages. Andrographolide inhibited ERK1/2 phosphorylation in LPS-activated murine peritoneal macrophages, which was concentration-dependent (P<0.01). Andrographolide at 1-25 µg/mL had no effects on phosphorylation levels of JNK and p38 and IκBα degradation in LPS-stimulated mouse peritoneal macrophages. In activated macrophages, TNF-α expression was inhibited by 12 µg/mL andrographolide and 20 µmol/L PD98059 (inhibitor of ERK1/2 signaling pathway) at both mRNA expression and protein secretion levels. CONCLUSION: In LPS-activated macrophages, andrographolide may inhibit the expression of TNF-α by inhibiting ERK1/2 signaling pathway.

Sophocarpine alleviates non-alcoholic steatohepatitis in rats.

BACKGROUND AND AIM: Non-alcoholic steatohepatitis (NASH) is one entity in the spectrum of non-alcoholic fatty liver disease (NAFLD). The aim of this study was to explore the prevention and therapeutic effect of sophocarpine on experimental rat NASH. METHODS: Sophocarpine with the dosage of 20 mg/kg/day was injected into NASH rats. At the end of 12 weeks, all rats were killed to detect the degree of fatty degeneration, inflammation and fibrosis. RESULTS: Sophocarpine intervention (in the pro-treated and treated groups) resulted in a significant decrease of liver weight, liver index, serum transaminase and serum lipids. Messenger RNA expressions of leptin, interleukin (IL)-6, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-ß1, procollagen-I and α-smooth muscle actin (SMA) and deposition of IL-6, TNF-α and TGF-ß1 in liver decreased, whereas the messenger RNA expression of adiponectin increased significantly compared with that in the model group. Moreover, histological improvement was also observed in the sophocarpine intervention group. In addition, there was no significant difference in any detected indicator between the pro-treated and treated group. CONCLUSIONS: Sophocarpine could decrease the level of serum transaminase, improve lipid metabolism, reduce synthesis of inflammatory cytokines TNF-α, TGF-ß1 and IL-6, activate protective adipocytokine adiponectin, and might be selected as a promising agent for the clinical prevention and therapy of NASH.