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Zheng Wang,Yanni Liang,Anqi Fan,Bao-Long Hou,Zhishu Tang,Ting Wang,Dongbo Zhang 한국식품영양과학회 2023 Journal of medicinal food Vol.26 No.12
Ulcerative colitis (UC), often known as UC, is an inflammatory disease of the intestines that has frequent andlong-lasting flare-ups. It is unknown precisely how the traditional Chinese drug Indigo Naturalis (IN) heals inflammatorybowel disease, despite its long-standing use in China and Japan. Finding new metabolite biomarkers linked to UC couldimprove our understanding of the disease, speed up the diagnostic process, and provide insight into how certain drugs work totreat the condition. Our work is designed to use a metabolomic method to analyze potential alterations in endogenoussubstances and their impact on metabolic pathways in a mouse model of UC. To determine which biomarkers and metabolismsare more frequently connected with IN’s effects on UC, liquid chromatography-tandem mass spectrometry analysis ofthe serum metabolomics of UC mice and normal mice was performed. The outcomes demonstrated that IN boosted the healthof UC mice and reduced the severity of their metabolic dysfunction. In the UC model, it was also found that IN changed theway 17 biomarkers and 3 metabolisms functioned.
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Shilabant Sen Sribastav,Jun Long,Peiheng He,Wei He,Fubiao Ye,Zemin Li,Jianru Wang,Hui Liu,Hua Wang,Zhaomin Zheng 대한척추외과학회 2018 Asian Spine Journal Vol.12 No.3
Study Design: A prospective cross-sectional study. Purpose: To evaluate the risk factors associated with the severity of pain intensity in patients with non-specific low back pain (NSLBP) in Southern China. Overview of Literature: Low back pain (LBP) is the leading cause of activity limitation and work absence throughout the world, so a firm understanding of the risk factor associated with NSLBP can provide early and prompt interventions that are aimed at attaining long-term results. Methods: Participants were recruited from January 2014 to January 2016 and were surveyed using a self-designed questionnaire. Anonymous assessments included Short Form 36-Item Health Survey (SF-36) and Visual Analogue Scale (VAS). The association between the severity of NSLBP and these potential risk factors were evaluated. Results: A total of 1,046 NSLBP patients were enrolled. The patients with primary school education, high body mass index (BMI), those exposed to sustained durations of driving and sitting, smoking, recurrent LBP had increased VAS and Oswestry Disability Index (ODI) scores with lower SF-36 scores (p <0.01). Workers and drivers compared with waiters and patients who lifted >10 kg objects in a quarter of their work time for >10 years had higher VAS and ODI scores with lower SF-36 scores (p <0.01). Multiple logistic regression showed lower levels of education, LBP for 1–7 days, long-lasting LBP in last year, smoking, long duration driving, and higher BMI were associated with more severe VAS score. Conclusions: The severity of NSLBP is associated with lower levels of education, poor standards of living, heavy physical labor, long duration driving, and sedentary lifestyle. Patients with recurrent NSLBP have more severe pain. Reducing rates of obesity, the duration of heavy physical work, driving or riding, and attenuating the prevalence of sedentary lifestyles and smoking may reduce the prevalence of NSLBP.
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文學龍,裵正烈,황인성,한천구 대한건축학회 2003 대한건축학회 학술발표대회 논문집 - 계획계/구조계 Vol.23 No.1(구조계)
This study is to investigate the influence of W/C and fineness modulus of aggregate on the bleeding of concrete. According to the result, the lower W/C is, the less bleeding occurs. As for the properties of bleeding with the variation of fineness modulus, the amount of bleeding is small with the continuous grading in the middle of the standard grading range in the case of coarse aggregate, and it grows smaller with a decrease of fineness modulus in the case of fine aggregate. Therefore, it proves that using coarse aggregate with the continuous grading in the middle of the standard grading range and fine aggregate with smaller fineness modulus in the standard grading range is the effective method for reducing bleeding at the same W/C.
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Zheng, Chun-Long,Qiu, Chen,Shen, Mei-Xiao,Qu, Xiao,Zhang, Tie-Hong,Zhang, Ji-Hong,Du, Jia-Jun Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5
Background: The vascular endothelial growth factor family has been implicated in tumorigenesis and metastasis. The prognostic value of each vascular endothelial growth factor family member, particular VEGF/VEGFR co-expression, in patients with non-small lung cancer remains controversial. Materials and Methods: Relevant literature was identified by searching PubMed, EMBASE and Web of Science. Studies evaluating expression of VEGFs and/or VEGFRs by immunohistochemistry or ELISA in lung cancer tissue were eligible for inclusion. Hazard ratios (HRs) and 95% confidence intervals (CIs) from individual study were pooled by using a fixed- or random-effect model, heterogeneity and publication bias analyses were also performed. Results: 74 studies covering 7,631 patients were included in the meta-analysis. Regarding pro-angiogenesis factors, the expression of VEGFA (HR=1.633, 95%CI: 1.490-1.791) and VEGFR1 (HR=1.924, 95%CI: 1.220-3.034) was associated separately with poor survival. Especially, VEGFA over-expression was an independent prognostic factor in adenocarcinoma (ADC) (HR=1.775, 95%CI: 1.384-2.275) and SCC (HR=2.919, 95%CI: 2.060-4.137). Co-expression of VEGFA/VEGFR2 (HR=2.011, 95%CI: 1.405-2.876) was also significantly associated with worse survival. For lymphangiogenesis factors, the expression of VEGFC (HR=1.611, 95%CI: 1.407-1.844) predicted a poor prognosis. Co-expression of VEGFC/VEGFR3 (HR=2.436, 95%CI: 1.468-4.043) emerged as a preferable prognostic marker. Conclusions: The expression of VEGFA (particularly in SCC and early stage NSCLC), VEGFC, VEGFR1 indicates separately an unfavorable prognosis in patients with NSCLC. Co-expression VEGFA/VEGFR2 is comparable with VEGFC/VEGFR3, both featuring sufficient discrimination value as preferable as prognostic biologic markers.
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Zheng, Long Tai,Hwang, Jaegyu,Ock, Jiyeon,Lee, Maan Gee,Lee, Won-Ha,Suk, Kyoungho Blackwell Publishing Ltd 2008 Journal of Neurochemistry Vol.107 No.5
<P>Abstract</P><P>Glial activation and neuroinflammatory processes play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and HIV dementia. Activated glia cells can secrete various proinflammatory cytokines and neurotoxic mediators, which may influence neuronal cell survival. Recent studies have demonstrated that glia cell-mediated neuroinflammation is also related to the pathophysiology of schizophrenia. In the present study, anti-inflammatory and neuroprotective effects of antipsychotics were investigated using cultured brain cells as a model. The results showed that spiperone significantly decreased the production of nitric oxide in lipopolysaccharide-stimulated BV-2 microglia cells, primary microglia and primary astrocyte cultures. Spiperone also significantly inhibited nitric oxide production in adenosine 5′-triphosphate (ATP)-stimulated primary microglia cultures. Spiperone markedly decreased the production of tumor necrosis factor-alpha in BV-2 microglia cells. Spiperone attenuated the expression of inducible nitric oxide synthase and proinflammatory cytokines such as interleukin-1&bgr; and tumor necrosis factor-alpha at mRNA levels in BV-2 microglia cells. Spiperone inhibited nuclear translocation and DNA binding of the p65 subunit of nuclear factor kappa B (NF-&kgr;B), inhibitor of kappa B (I&kgr;B) degradation, and phosphorylation of p38 mitogen-activated protein kinase in the lipopolysaccharide-stimulated BV-2 microglia cells. Moreover, spiperone was neuroprotective, as the drug reduced microglia-mediated neuroblastoma cell death in the microglia/neuron co-culture. These results imply that the antipsychotic spiperone has anti-inflammatory and neuroprotective effects in the central nervous system by modulating glial activation.</P>
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Down-regulation of lipocalin 2 contributes to chemoresistance in glioblastoma cells
Zheng, Long Tai,Lee, Shinrye,Yin, Guo Nan,Mori, Kiyoshi,Suk, Kyoungho Blackwell Publishing Ltd 2009 Journal of Neurochemistry Vol.111 No.5
<P>Abstract</P><P>Malignant gliomas are the most common primary brain tumor and have a poor clinical prognosis. 1, 3-Bis (2-chloroethyl)-1-nitrosourea (BCNU) is an alkylating agent that is commonly used in glioma therapy. However, BCNU chemotherapy often fails due to drug resistance. To gain better understanding of molecular mechanisms underlying the drug resistance of glioma, a BCNU-resistant variant (C6R) of C6 rat glioma cells was selected and characterized. The established C6R cells were resistant to BCNU-induced cell death and cell cycle arrest as confirmed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide reduction assay and flow cytometric analysis of DNA content. C6R cells showed an increased expression of common drug resistance-related genes such as O6-methylguanine-DNA methyltransferase and multiple drug resistance 1. In contrast, C6R cells showed a decreased expression of glial fibrillary acidic protein, therefore, displaying shorter cellular processes compared with parental C6 cells. More importantly, in conjunction with the morphological changes, the expression of lipocalin-2 (lcn2), a 25-kDa secreted proapoptotic protein, was markedly reduced in the BCNU-resistant C6R cells. However, there was no significant change in the expression of lcn2 receptors. Addition of recombinant LCN2 protein or introduction of lcn2 cDNA significantly increased the sensitivity of C6 cells and human glioma cells to BCNU or other anticancer drugs, while knockdown of lcn2 expression by antisense cDNA transfection decreased the sensitivity. When lcn2 was re-expressed in C6R cells, the BCNU sensitivity was restored. Lcn2 enhanced BCNU-induced Akt dephosphorylation providing a molecular basis of apoptosis sensitization. These results suggest that LCN2 protein may be involved in glioma drug resistance and may provide a new approach to sensitizing glioblastoma to chemotherapy.</P>
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( Long Zheng ),( Woo Yong Lee ),( Deuk Soo Hwang ),( Chan Kang ),( Chang Kyun Noh ) 대한고관절학회 2016 Hip and Pelvis Vol.28 No.2
Purpose: The purpose of this study was to compare preoperative clinical outcomes before occurrence of periprosthetic femoral fracture (status before trauma) with postoperative clinical outcomes (status after operation) in patients with periprosthetic femoral fracture after hip arthroplasty. Materials and Methods: A retrospective review was performed of all periprosthetic femoral fracture after hip arthroplasty treated surgically at our institution from January 2010 to January 2014. Among 29 patients who underwent surgical treatment for periprosthetic femoral fracture after hip arthroplasty, 3 patients excluded because of non-union of the fracture site. The clinical outcomes were determined by using visual analogue scale for pain (VAS), Harris hip score (HHS), and ambulatory ability using Koval classification. VAS, HHS and ambulatory ability was assessed for all the included patients at the last follow-up of status before trauma and after operation. Results: The mean VAS, HHS and ambulatory ability at the last follow-up of status before trauma was 2.2 (range, 0-4), 78.9 (range, 48-92) and 1.9 (range, 1-5), respectively. The mean VAS, HHS and ambulatory ability at the last follow-up of status after operation was 3.1 (range, 1-5), 68.4 (range, 46-81) and 2.9 (range, 2-6), respectively. The clinical outcome of VAS, HHS and ambulatory ability were significantly worsened after surgical treatment for periprosthetic femoral fracture (P=0.010, P=0.001, and P=0.002, respectively). Conclusion: Patients with periprosthetic femoral fracture after hip arthroplasty could not return to their status before trauma, although patients underwent appropriate surgical treatment and the fracture union achieved.
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Paw Edema was Reduced in Carrageenan Induced Acute Inflammation in Stat4 Deficient Mice
Zheng, Long-Tai,Baik, Haing-Woon,Lee, Seong-Kyu,Cho, Jeong-Je,Park, Cheung-Seog,Hong, Mee-Suk,Chung, Joo-Ho,Yim, Sung-Vin The Korean Society of Toxicogenomics and Toxicopro 2006 Molecular & cellular toxicology Vol.2 No.4
Signal transducer and activator of transcription 4 (STAT4) is one of the important mediators in generating inflammation and immune responses. To address the role of Stat4 in carrageenan induced acute inflammation, we performed paw edema measurement and 7.4 k mouse cDNA microarray analysis in carrageenan induced acute inflammation in Stat4 knockout (-/-) mice. Male BALB/c (n=8) and Stat4 -/- (n=5) were used and paw edema was induced with injection of $30\;{\mu}L$ of 1% carrageenan into plantar surface of right hind paw. Next, we isolated the mRNA in mouse whole brain and analyzed cDNA microarray profiles for the changes of the brain expression in Stat4 -/- mice. Interestingly, the increase in paw volume of Stat4 -/- mice was reduced by about 30% as compared to that of wild type. The cDNA microarray analysis revealed the altered expressions of several cytokines (Tnf, Il6, and Il4) and pain-associated proteins (Ptgs2, Gabra6, and Gabbr1) in Stat4 -/- mice. Our results suggest that Stat4 may be related to the inhibitory responses on carrageenan induced acute inflammation.
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