High-Pitch Coronary CT Angiography at 70 kVp Adopting a Protocol of Low Injection Speed and Low Volume of Contrast Medium

Ruiqi Feng,Jiajie Tong,Xiaofei Liu,Yu Zhao,Liang Zhang 대한영상의학회 2017 Korean Journal of Radiology Vol.18 No.5

Objective: To evaluate the feasibility and image quality (IQ) of prospectively high-pitch coronary CT angiography (CCTA) with low contrast medium injection rate at 70 kVp. Materials and Methods: One hundred and four patients with suspected coronary artery disease (body mass index < 26 kg/m2, sinus rhythm and heart rate < 70 beats/min) were prospectively enrolled and randomly divided into two groups. In group A and group B, 28 mL and 40 mL of 370 mgI/mL iodinated contrast media was administrated at a flow rate of 3.5 and 5 mL/s, respectively. CT values, noise, signal-to-noise ratio, contrast-to-noise ratio (CNR) of the proximal segments of coronary arteries and subjective IQ were evaluated. Results: The CT values and noise in group A were significantly lower than those in group B (434–485 Hounsfield units [HU] vs. 772–851 HU, all p < 0.001; 17.8–22.3 vs. 23.3–26.4, all p < 0.005). The CNRs of the right coronary artery and left main artery showed no statistical difference between the two groups (42.1 ± 13.8 vs. 36.8 ± 16.0, p = 0.074; 38.7 ± 10.6 vs. 38.1 ± 17.0, p = 0.819). No statistical difference was observed between the two groups in IQ scores (3.04 ± 0.75 vs. 3.0 ± 0.79, p = 0.526) and diagnostic ratio (96.1% [50/52] vs. 94.2% [49/52], p = 0.647). Conclusion: Prospective high-pitch CCTA at 70 kVp with 28 mL of contrast media and injection rate of 3.5 mL/s could provide diagnostic IQ for normal-weight patients with heart rate of < 70 beats/min.

Characterization of Enterobacter cloacae under Phoxim Stress by Two-dimensional Gel Electrophoresis

Dijun Zhang,Jiajie Xu,Weina He,Qianqian Tong,Liping Chen,Jun Zhou,Xiurong Su 한국생물공학회 2015 Biotechnology and Bioprocess Engineering Vol.20 No.3

Phoxim, an organophosphorus pesticide, was widely used in agriculture but was banned because of its associated toxic runoff, which accumulated in surrounding water outlets. Here, Enterobacter cloacae was isolated from water outlets adjacent to industrial, agricultural and residential sewage having high organic phosphorus contents. To investigate the ability of E. cloacae to respond and survive under phoxim stress, both at the proteomic and transcriptional level, two-dimensional gel electrophoresis (2-DE), matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS/MS) and quantitative real-time PCR (qPCR) were used. A 2-DE analysis showed that 12 h post phoxim exposure, 46 proteins were differentially expressed and 21 protein spots were selected for MALDI-TOF-MS/MS identification. This resulted in the successful identification of 16 spots, nine up-regulated and seven down-regulated. Of these, stress response proteins, including the chaperone protein DnaK, GroEL, F0F1 ATP synthase subunit beta, phosphoenolpyruvate carboxykinase and outer membrane channel protein, were only expressed in the phoxim-treated experimental group. To validate these findings, seven genes were selected and positively confirmed using qPCR. The results suggest that the identified expression patterns relate to E. cloacae resistance and tolerance to high phoxim concentrations.

Guanine nucleotide-binding protein 2, GNBP2, accelerates the progression of clear cell renal cell carcinoma via regulation of STAT3 signaling transduction pathway

Cao Qingfei,Ma Jiaji,Li Weitao,Hong Peng,Shen Tong,Tong Ming 한국유전학회 2023 Genes & Genomics Vol.45 No.1

Background Guanine nucleotide-binding protein 2 (GNBP2) is a GTPase that has critical roles in host immunity and some types of cancer, but its function in clear cell renal cell carcinoma (ccRCC) is not fully understood. Objective This work explored the role of GNBP2 in ccRCC progression and the underlying molecular mechanism. Methods Two public human cancer databases TNMplot and TISIDB were employed to analyze the expression pattern of GNBP2 during ccRCC progression and the correlation between GNBP2 expression and clinical features of ccRCC patients. GNBP2 functions in ccRCC cells were determined by EdU staining, flow cytometry, scratch wound assay, transwell assay, and xenograft model. Gene expression was evaluated using qPCR, Western blot, immunofluorescence staining, and immunohistochemical staining. Results GNBP2 expression was significantly elevated in ccRCC tissues and increased gradually with the increasing tumor grades. Patients with higher GNBP2 expression had shorter overall survival times. Knockdown of GNBP2 suppressed tumor cell proliferation and cell cycle progression and reduced the capability of migration and invasion, while GNBP2 overexpression exhibited protumor effects. GNBP2 silencing by RNA interference significantly inhibited the tumor growth of tumor-bearing nude mice and decreased the proliferation marker Ki67. Mechanistically, GNBP2 downregulation suppressed the STAT3 signaling transduction, as it reduced the phosphorylation of STAT3 and modulated the expression of the target genes, including c-Myc, MMP2, N-cadherin, and E-cadherin. Conclusion These findings reveal that GNBP2 promotes ccRCC progression by regulating STAT3 signaling transduction, indicating that GNBP2 might be a promising molecular target for ccRCC therapy.

Phosphatidylcholine regulates NF-κB activation in attenuation of LPS-induced inflammation: evidence from in vitro study

Cheng, Meijuan,Pan, Hongying,Dai, Yining,Zhang, Jiajie,Tong, Yongxi,Huang, Yicheng,Wang, Mingshan,Huang, Haijun 한국통합생물학회 2018 Animal cells and systems Vol.22 No.1

Phosphatidylcholine (PC) has been demonstrated as anti-inflammatory and antioxidant/pro-oxidant molecules. In this study, we investigated the protective effects of PC on inflammatory bowel disease (IBD) caused by lipopolysaccharide (LPS)-induced injury in intestinal epithelia cells. The IEC-6 cells (intestinal epithelia cells) were stimulated with LPS ($1{\mu}g/mL$) for 24 h with or without PC pretreatment, in the next steps: (1) the level of the inflammatory cytokine tumor necrosis factor (TNF)-${\alpha}$ was measured with ELISA; (2) the nuclear translocation and phosphorylation of NF-${\kappa}B$ was investigated with Western blot, EMSA, immunofluorence assay; (3) the protein phosporylation levels in MAPK signaling pathway were detected with Western blot method. The results showed: (1) compared with the normal group, 10 and $20{\mu}g/mL$ of PC significantly inhibited the production and activation of TNF-${\alpha}$, (P < 0.01); (2) pretreatment with PC inhibited LPS-induced nuclear translocation and phosphorylation of p65 in IEC-6 cells; (3) pretreatment with PC inhibited the protein phosphorylation levels in MAPK signaling pathway. Our findings indicated that PC had the effect to protect IEC-6 cells from LPS-induced injury and this effect was exerted possibly through inhibiting the TNF-${\alpha}$ secretion, down-regulating nuclear translocation and phosphorylation of p65 and inhibiting MAPK signaling pathways.

Phosphatidylcholine regulates NF-κB activation in attenuation of LPS-induced inflammation: evidence from in vitro study

Meijuan Cheng,Hongying Pan,Yining Dai,Jiajie Zhang,Yongxi Tong,Yicheng Huang,Mingshan Wang,Haijun Huang 한국통합생물학회 2018 Animal cells and systems Vol.22 No.1

Phosphatidylcholine (PC) has been demonstrated as anti-inflammatory and antioxidant/pro-oxidant molecules. In this study, we investigated the protective effects of PC on inflammatory bowel disease (IBD) caused by lipopolysaccharide (LPS)-induced injury in intestinal epithelia cells. The IEC-6 cells (intestinal epithelia cells) were stimulated with LPS (1 μg/mL) for 24 h with or without PC pretreatment, in the next steps: (1) the level of the inflammatory cytokine tumor necrosis factor (TNF)-α was measured with ELISA; (2) the nuclear translocation and phosphorylation of NF-κB was investigated with Western blot, EMSA, immunofluorence assay; (3) the protein phosporylation levels in MAPK signaling pathway were detected with Western blot method. The results showed: (1) compared with the normal group, 10 and 20 μg/mL of PC significantly inhibited the production and activation of TNF-α, (P < 0.01); (2) pretreatment with PC inhibited LPS-induced nuclear translocation and phosphorylation of p65 in IEC-6 cells; (3) pretreatment with PC inhibited the protein phosphorylation levels in MAPK signaling pathway. Our findings indicated that PC had the effect to protect IEC-6 cells from LPS-induced injury and this effect was exerted possibly through inhibiting the TNF-ɑ secretion, down-regulating nuclear translocation and phosphorylation of p65 and inhibiting MAPK signaling pathways.