Search

Objective To explore the role of G protein pathway suppressor 2(GPS2)in regulating proliferation, migration and invasion in hepatocellular carcinoma cell line MHCC-97H.Methods The expression of GPS2 in hepatocellular carcinoma (HCC) cells were detected using quantitative PCR or Western blot; GPS2 was either over-expressed or knocked down in HCC cells using over-expression vectors or short hairpin RNAs (shRNAs) for GPS2, respectively. Clone formation assay, scratch assay and Transwell assay were used to detect the effects of GPS2 on proliferation, migration and invasion of HCC cells. Results In HCC cells, over-expression of GPS2 was found to inhibit the proliferation, migration and invasion of HCC cells MHCC-97H, while knockdown of GPS2 up-regulated proliferation, migration and invasion of MHCC-97H(P＜0.05). The over-expression of GPS2 in MHCC-97H cells was found to inhibit the expression of cell proliferation, migration and invasion-related factors such as EGFR, MMP1, MMP3 and MMP9, while knockdown of GPS2 upregulated the expression of these factors(P＜0.05). Conclusions GPS2 is a novel HCC regulatory factor that inhibits proliferation, migration and invasion of HCC cells.

Abstract UFMylation is a ubiquitination-like modification that is related to endoplasmic reticulum stress and unfolded protein response. A recent study reported that Ufl1, a key enzyme of UFMylation, protects against heart failure, indicating that UFMylation may be associated with heart function regulation. In the present study, we initially constructed a Flag-6×His-tagged Ufm1ΔSC transgenic (Tg-Ufm1) mouse model that enables UFMylation studies in vivo. Tg-Ufm1 mice showed significant activation of UFMylation in hearts. By using this model, we identified 38 potential Ufm1-binding proteins in heart tissues through LC‒MS/MS methods. We found that these proteins were associated with mitochondria, metabolism and chaperone binding. By using transcriptomic screening, we identified Tnfaip2 as a novel UFMylation-associated gene. Overexpression of Ufm1 significantly upregulated the protein expression of Tnfaip2, whereas isoproterenol treatment decreased Tnfaip2 expression in Tg-Ufm1 mice. These data may provide novel clues for UFMylation in cardiac hypertrophy.

To solve the problem that it is difficult to extract the weak fault features of rolling bearing effectively under the interference of strong background noise，a method of extracting the weak fault features based on the combination of maximum second-order cyclostationary blind deconvolution （CYCBD） and envelope spectrum is proposed.Firstly，a reasonable cycle frequency set is set by the fault characteristic frequency，and CYCBD is used to reduce the noise of weak fault impulse signal with strong noise，so as to enhance the periodic impulse component in the signal.Then，the noise reduction signal is analyzed by Hilbert envelope spectrum to identify the fault characteristic frequency.The simulation and experimental results show that the method can effectively extract the weak fault features submerged by strong noise.

A compressible cavitation model is developed in this paper, in which the bubble wall velocity is obtained by solving the compressible Rayleigh–Plesset (R–P) equation. Additionally, vapor compressibility is also included during evaporation/condensation to correct the phase change rate. The predicted results around a National Advisory Committee for Aeronautics (NACA) 66 (mod) hydrofoil are compared with the available experimental data, and a satisfied agreement is obtained. By (mod), we mean the NACA 66 hydrofoil modified by Brockett ["Minimum pressure envelopes for modified NACA-66 sections with NACA a = 0.8 camber and BuShips type I and type II sections," Technical Report No. 1780 (David Taylor Model Basin Washington DC Hydromechanics Lab, 1966)] and Valentine ["The effect of nose radius on the cavitation-inception characteristics of two-dimensional hydrofoils," Technical Report No. 3813 (Naval Ship Research and Development Center, 1974)]. Several crucial flow properties, e.g., fluid compressibility, cavitation evolution features, and pressure statistical characteristics, are studied in detail. The results suggest that the developed compressible cavitation model is better suited for predicting the collapse behavior of cavitation. Moreover, our work captures the liquid re-entrant jet and bubbly shock waves well and reveals that these two mechanisms jointly dominate the cavity shedding dynamics. Shock-induced pressure pulses play a more important role in flow features, with a maximum amplitude exceeding 200 kPa, significantly larger than the pressure pulse caused by liquid re-entrant jets. Finally, the statistical analysis indicates that the pulsating pressure presents non-Gaussian nature with positive skewness, and shock waves exhibit high-frequency and high-energy characteristics. [ABSTRACT FROM AUTHOR]

Background: Mutations in the F10-coding gene can cause factor X (FX) deficiency, leading to abnormal coagulation activity and severe tendency for hemorrhage. Therefore, identifying mutations in F10 is important for diagnosing congenital FX deficiency. Methods: We studied a 63-year-old male patient with FX deficiency and 10 of his family members. Clotting and immunological methods were used to determine activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin time (TT), fibrinogen levels, FX activity, and FX antigen levels. The platelet count was determined. A mixing study was performed to eliminate the presence of coagulation factor inhibitors and lupus anticoagulant. Mutations were searched using whole-exome sequencing and certified by Sanger sequencing. Results: Genetic analysis of the proband identified two single-base substitutions: c.1085G>A (p.Ser362Asn) and c.1152C>A (p.Tyr384Ter, termination codon, caused by the DNA sequence TAA). His FX activity and antigen levels were 1.7% and 408.53 pg/mL, respectively; aPTT and PT were 52.3 and 48.0 s, respectively. One brother had the same compound heterozygous mutations, and his FX activity and antigen levels were 1.3% and 465.47 pg/mL, respectively; his aPTT and PT were 65.2 and 54.5 s, respectively. His mother, another brother, and one sister were heterozygous for c.1085G>A (p.Ser362Asn), and his daughter and grandson (6 years old) were heterozygous for c.1152C>A (p.Tyr384Ter). Conclusion: The heterozygous variants p.Ser362Asn or p.Tyr384Ter indicate mild FX deficiency, but the compound heterozygous mutation of the two causes severe congenital FX deficiency and bleeding. Genetic analysis of these two mutations may help characterize the bleeding tendency and confirm congenital FX deficiency. [ABSTRACT FROM AUTHOR]

Background: Loss of immune homeostasis to enteric pathogens is considered to be involved in the pathogenesis of ulcerative colitis (UC), and regulatory T cells (Tregs) are key for this immune homeostasis. Helios exhibits an important effect on regulating the suppressive function of Tregs. Epstein–Barr virus (EBV) is more commonly detected in UC. However, whether there is an association between EBV infection and Helios+Tregs and its impact on disease activity of UC remain unclear. We aimed to explore the clinical significance of Helios+Tregs and their potential association with EBV infection in UC. Methods: Seventy-six UC patients and 38 controls were consecutively enrolled. Helios+FoxP3+Tregs were analyzed using flow cytometry and compared among groups. Eight active UC patients treated with 5-aminosalicylic acid were followed up. Correlation analyses were conducted between Helios+FoxP3+Tregs and disease activity indicators. In addition, EBV viral loads in the mucosal lesion were quantified in active UC by quantitative polymerase chain reaction and were comprehensively analyzed in subgroups of different disease severity, and their associations with Helios+FoxP3+Tregs were also analyzed. Results: Helios+FoxP3+Tregs were significantly decreased in active UC and were inversely correlated with serum C-reactive protein and Mayo score. Moreover, we observed the recovery of Helios+FoxP3+Tregs in followed-up active UC achieving remission after treatment. EBV loads were higher in active UC, and levels of Helios+FoxP3+Tregs in the EBV-positive subgroup were lower than the EBV-negative subgroup in moderate and severe active patients. Most importantly, we found that Helios+FoxP3+Tregs were significantly negatively correlated with EBV viral loads. Conclusion: Helios+FoxP3+Tregs are likely to play a pivotal role in disease activity of UC and may be influenced by EBV infection. [ABSTRACT FROM AUTHOR]