THE RELATIONSHIP BETWEEN THE ASSETS LIQUIDITY AND THE TRADING LIQUIDITY: AN EMPIRICAL INVESTIGATION

Xu Shen Zhou,Yong H Kim People&Global Business Association 2007 Global Business and Finance Review Vol.12 No.1

In this paper. we examine the relationship between the liquidity of a firm's assets and trading liquidity of its stocks. The results show that the higher the firm's assets liquidity, the lower its stock's trading liquidity. This relationship does not hold for banks. Bank stocks have lower trading liquidity than other firms' stocks do. The results are consistent with market microstructure theory and support the paradox of assets liquidity suggested by recent theory. The results may suggest that firms with severe assets substitution and entrenching investment problems may have a different trading behavior of their stocks than those of others.

Distinctions Between Clinicopathological Factors and Prognosis of Alpha-fetoprotein Negative and Positive Hepatocelluar Carcinoma Patients

Xu, Jia,Liu, Chang,Zhou, Lei,Tian, Feng,Tai, Ming-Hui,Wei, Ji-Chao,Qu, Kai,Meng, Fan-Di,Zhang, Ling-Qiang,Wang, Zhi-Xin,Zhang, Jing-Yao,Chang, Hu-Lin,Liu, Si-Nan,Xu, Xin-Shen,Song, Yan-Zhou,Liu, Jun,Z Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.2

Serum alpha-fetoprotein (AFP) is a significant marker for clinical diagnosis and prognosis evaluation in hepatocellular carcinoma (HCC) patients. However, some proportion of liver cancer patients are AFP-negative (AFP ${\leq}$20ng/ml). In order to study the differences between clinicopathological factors and prognosis of alpha-fetoprotein negative and positive patients, a total of 114 cases (41 AFP-negative and 73 AFP-positive) were selected for our research. By systematically statistical analysis, the results demonstrated that compared with AFP-negative patients, AFP-positive examples were more likely to feature cirrhosis nodules, non-complete neoplasm capsules, and a poor Edmondson-steiner grade. Furthermore, AFP-negative patients demonstrated a favorable long-term prognosis. By univariate analysis and multivariate analysis with Cox's proportional hazards model, multiple tumors were found to be independent risk factors for worse survival of AFP negative patients; however, less tumor-free margins, multiple tumors and Edmondson-steiner grades III/IV, proved to be independent risk factors leading to a poor prognosis of AFP positive cases. Finally, we can infer that high levels of AFP signify a highly malignant tumor and unfavorable prognosis.

Disease burden of prostate cancer from 2014 to 2019 in the United States: estimation from the Global Burden of Disease Study 2019 and Medical Expenditure Panel Survey

Shen Lin,Dong Lin,Yiyuan Li,Lixian Zhong,Wei Zhou,Yajing Wu,Chen Xie,Shaohong Luo,Xiaoting Huang,Xiongwei Xu,Xiuhua Weng 한국역학회 2023 Epidemiology and Health Vol.45 No.-

OBJECTIVES: The aim of this study was to evaluate the disease burden of prostate cancer (PC) and assess key influencing factors associated with the disease expenditures of PC in the United States. METHODS: The total deaths, incidence, prevalence, and disability-adjusted life-years of PC were obtained from the Global Burden of Disease Study 2019. The Medical Expenditure Panel Survey was used to estimate healthcare expenditures and productivity loss and to investigate patterns of payment and use of healthcare resources in the United States. A multivariable logistic regression model was conducted to identify key factors influencing expenditures. RESULTS: For patients aged 50 and older, the burden for all age groups showed a modest increase over the 6-year period. Annual medical expenditures were estimated to range from US$24.8 billion to US$39.2 billion from 2014 to 2019. The annual loss in productivity for patients was approximately US$1,200. The top 3 major components of medical costs were hospital inpatient stays, prescription medicines, and office-based visits. Medicare was the largest source of payments for survivors. In terms of drug consumption, genitourinary tract agents (57.0%) and antineoplastics (18.6%) were the main therapeutic drugs. High medical expenditures were positively associated with age (p=0.005), having private health insurance (p=0.016), more comorbidities, not currently smoking (p=0.001), and patient self-perception of fair/poor health status (p<0.001). CONCLUSIONS: From 2014 to 2019, the national real-world data of PC revealed that the disease burden in the United States continued to increase, which was partly related to patient characteristics.

MED1 induces M2 polarization of tumor-associated macrophages to aggravate breast cancer

Shen Ye,Zhou Lianming,Xu Meiyu,Tan Zhanhai,Yao Kai,Wang Wenjie 한국유전학회 2023 Genes & Genomics Vol.45 No.12

Background Breast cancer is a common malignant tumor in female, and its 5-year survival rate remains low. The correlation between mediator subunit 1 (MED1) gene and macrophage phenotypic transformation may be a key factor affecting the therapeutic effect on cancer. Objective The present study intended to explore the role of MED1 in macrophage polarization and its further influence on the malignant behaviors of breast cancer. Methods Bioinformatics analysis was carried out to predict the expression pattern of MED1 in breast cancer. Flow cytometry was conducted to detect the effect of MED1 overexpression or silencing on macrophage polarization. ELISA was applied to analyze the effect of abnormal MED1 expression on cytokine secretion of macrophages. CCK-8, colony formation, Transwell and scratch healing assays were applied to investigate the effects of macrophage conditioned medium on the malignant behaviors of breast cancer cells. Results MED1 expression was prominently increased in M2 macrophages, and overexpression of MED1 significantly increased M2 polarization of tumor-associated macrophages (TAMs) and IL-10 cytokine level. Meanwhile, M2 macrophages with MED1 overexpression could significantly promote the malignant behaviors of breast cancer cells. Dasatinib rescue experiment further confirmed that MED1-induced M2 macrophage polarization could facilitate the malignant progression of breast cancer cells. Conclusion In summary, MED1 could induce M2 macrophage polarization and thus regulate the malignant behaviors of breast cancer cells.

Activating SIRT3 in peritoneal mesothelial cells alleviates postsurgical peritoneal adhesion formation by decreasing oxidative stress and inhibiting the NLRP3 inflammasome

Shen Tianli,Wu Yunhua,Wang Xingjie,Wang Zijun,Li Enmeng,Zhou Cancan,Yue Chenyang,Jiang Zhengdong,Wei Guangbing,Lian Jie,Xu Qinhong,Li Xuqi 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Peritoneal adhesions (PAs) are a serious complication of abdominal surgery and negatively affect the quality of life of millions of people worldwide. However, a clear molecular mechanism and a standard therapeutic strategy for PAs have not been established. Here, we developed a standardized method to mimic the pathological changes in PAs and found that sirtuin 3 (SIRT3) expression was severely decreased in adhesion tissues, which was consistent with our bioinformatics analysis and patient adhesion tissue analysis. Thus, we hypothesized that activating SIRT3 could alleviate postsurgical PAs. Sirt3-deficient (Sirt3−/−) mice exhibited many more PAs after standardized abdominal surgery. Furthermore, compared with wild-type (Sirt3+/+) mice, Sirt3-deficient (Sirt3−/−) mice showed more prominent reactive oxygen species (ROS) accumulation, increased levels of inflammatory factors, and exacerbated mitochondrial damage and fragmentation. In addition, we observed NLRP3 inflammasome activation in the adhesion tissues of Sirt3−/− but, not Sirt3+/+ mice. Furthermore, mesothelial cells sorted from Sirt3−/− mice exhibited impaired mitochondrial bioenergetics and redox homeostasis. Honokiol (HKL), a natural compound found in several species of the genus Magnolia, could activate SIRT3 in vitro. Then, we demonstrated that treatment with HKL could reduce oxidative stress and the levels of inflammatory factors and suppress NLRP3 activation in vivo, reducing the occurrence of postsurgical PAs. In vitro treatment with HKL also restored mitochondrial bioenergetics and promoted mesothelial cell viability under oxidative stress conditions. Taken together, our findings show that the rescue of SIRT3 by HKL may be a new therapeutic strategy to alleviate and block postsurgical PA formation.

miR-182-5p Inhibits NKAPL Expression and Promotes the Proliferation of Osteosarcoma

Shen Yang,Kaixi Chen,Kun Cao,Shenglin Xu,Chengxiao Ma,Yongping Cai,Yong Hu,Yejin Zhou 한국생물공학회 2021 Biotechnology and Bioprocess Engineering Vol.26 No.5

Purpose Osteosarcoma, a malignant bone tumor, has the lowest survival rate among all pediatric cancers. NF-κB-activating protein-like (NKAPL) is highly homologous with NKAP. The expression of NKAPL is downregulated in primary liver cancer and breast cancer, and plays a role of tumor suppressor gene. However, the role of NKAPL in osteosarcoma has not been reported. Materials and Methods We explored the effect of NKAPL on the proliferation of osteosarcoma cells by immunohistochemical, RT-PCR, Western blot, and double luciferase reporter gene analysis. Results The low expression of NKAPL mRNA was correlated with distant metastasis (P = 0.017), tumor size (P = 0.023), and clinical stage (P < 0.001). The NKAPL expression level in MG63 and U2OS cells was lower than that in Nhost cells. Downregulation of NKAPL expression in Nhost cells could promote cell proliferation and upregulation of NKAPL expression in MG63 and U2OS cells could inhibit cell proliferation. miR-182-5p expression was negatively correlated with NKAPL mRNA expression (R2 = 0.1169, P = 0.0099). After upregulating NKAPL expression, the Notch1, hes1, hey2, and cyclin D1 expression levels were significantly decreased, with G0/G1 phase arrest and G2/M phase reduction. Conclusions miR-182-5p targeted NKAPL and inhibit NKAPL expression in osteosarcoma. miR-182- 5p could regulate cell cycle and promote tumor proliferation through upregulating Notch signaling pathway.

Design Methodology of LLC Resonant Converters for Single-stage Power Factor Correction Application

Zhou Yufei,Liu Shuai,Ren Jiaqi,Wu Qibin,Hong Feng,Shen Ang,Xu Wei 대한전기학회 2021 Journal of Electrical Engineering & Technology Vol.16 No.5

This paper proposes a new design methodology for LLC resonant converter with single-stage power factor correction (PFC) function. By designing the achievable gain of resonant tank at a certain point of the AC voltage higher than the required gain, its gain will satisfy the requirement of the whole AC line voltage cycle and lead to a good single-stage PFC design. By adjusting switching frequency and changing voltage gain along with the AC voltage, the converter can realize PFC with high effi ciency. The proposed converter inherits the advantages of the traditional LLC resonant converter, including soft switching of power switches across the whole load range, buck-boost power conversion ability which benefi ts the optimization of the down-stream DC-DC converter. Gain characteristic and design consideration for PFC purpose are analyzed in detail. Experimental results are presented to show its validity and feasibility.

Circular RNA circ_0024037 suppresses high glucose-induced lens epithelial cell injury by targeting the miR-199a-5p/TP53INP1 axis

Zhou Liping,Zheng Yanhua,Xu Yue,Shen Pincheng 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2

Background Diabetic cataract is a common ocular complication of diabetes. Circular RNA (circRNA) can participate in a variety of regulatory processes of a variety of eye diseases, including diabetic cataract. Objective Nowadays, the biological mechanism underlying circ_0024037 during diabetic cataract is not completely understood. This study was designed to explore the biological role of circ_0024037 in high glucose (HG)-induced lens epithelial damage. Result Circ_0024037 and TP53INP1 were significantly up-regulated while miR-199a-5p was significantly down-regulated in the diabetic cataract tissues and HG-induced human lens epithelial cells (HLECs). Knockdown of circ_0024037 significantly promoted the HG-induced HLECs cell proliferation, inhibited apoptosis, decreased MDA level as well as increased GSH-PX level. The dual-luciferase reporter assay and RIP assay showed that circ_0024037 served as a sponge of miR-199a-5p and miR-199a-5p could directly target TP53INP1 in HLECs. Conclusion Circ_0024037 knockdown protected HLECs from the HG-induced dysfunction by regulating the miR-199a-5p/TP53INP1 pathway in diabetic cataract. Our findings provid novel insights into the pathogenesis of diabetic cataract. Background Diabetic cataract is a common ocular complication of diabetes. Circular RNA (circRNA) can participate in a variety of regulatory processes of a variety of eye diseases, including diabetic cataract. Objective Nowadays, the biological mechanism underlying circ_0024037 during diabetic cataract is not completely understood. This study was designed to explore the biological role of circ_0024037 in high glucose (HG)-induced lens epithelial damage. Result Circ_0024037 and TP53INP1 were significantly up-regulated while miR-199a-5p was significantly down-regulated in the diabetic cataract tissues and HG-induced human lens epithelial cells (HLECs). Knockdown of circ_0024037 significantly promoted the HG-induced HLECs cell proliferation, inhibited apoptosis, decreased MDA level as well as increased GSH-PX level. The dual-luciferase reporter assay and RIP assay showed that circ_0024037 served as a sponge of miR-199a-5p and miR-199a-5p could directly target TP53INP1 in HLECs. Conclusion Circ_0024037 knockdown protected HLECs from the HG-induced dysfunction by regulating the miR-199a-5p/TP53INP1 pathway in diabetic cataract. Our findings provid novel insights into the pathogenesis of diabetic cataract.

Disease burden of prostate cancer from 2014 to 2019: estimation from the Global Burden of Disease Study 2019 and Medical Expenditure Panel Survey

Lin Shen,Lin Dong,Li Yiyuan,Zhong Lixian,Zhou Wei,Wu Yajing,Xie Chen,Luo Shaohong,Huang Xiaoting,Xu Xiongwei,Weng Xiuhua 한국역학회 2023 Epidemiology and Health Vol.45 No.-

OBJECTIVES The aim of this study was to evaluate the disease burden of prostate cancer (PC) and assess key influencing factors associated with the disease expenditures of PC in the United States. METHODS The total deaths, incidence, prevalence, and disability-adjusted life-years of PC were obtained from the Global Burden of Disease Study 2019. The Medical Expenditure Panel Survey was used to estimate healthcare expenditures and productivity loss and to investigate patterns of payment and use of healthcare resources in the United States. A multivariable logistic regression model was conducted to identify key factors influencing expenditures. RESULTS For patients aged 50 and older, the burden for all age groups showed a modest increase over the 6-year period. Annual medical expenditures were estimated to range from US$24.8 billion to US$39.2 billion from 2014 to 2019. The annual loss in productivity for patients was approximately US$1,200. The top 3 major components of medical costs were hospital inpatient stays, prescription medicines, and office-based visits. Medicare was the largest source of payments for survivors. In terms of drug consumption, genitourinary tract agents (57.0%) and antineoplastics (18.6%) were the main therapeutic drugs. High medical expenditures were positively associated with age (p=0.005), having private health insurance (p=0.016), more comorbidities, not currently smoking (p=0.001), and patient self-perception of fair/poor health status (p<0.001). CONCLUSIONS From 2014 to 2019, the national real-world data of PC revealed that the disease burden in the United States continued to increase, which was partly related to patient characteristics.

Non-Gaussian wind features over complex terrain under atmospheric turbulent boundary layers: A case study

Hongtao Shen,Weicheng Hu,Qing-shan Yang,Fucheng Yang,Kunpeng Guo,Tong Zhou,Guowei Qian,Qinggen Xu,Ziting Yuan 한국풍공학회 2022 Wind and Structures, An International Journal (WAS Vol.35 No.6

In wind-resistant designs, wind velocity is assumed to be a Gaussian process; however, local complex topography may result in strong non-Gaussian wind features. This study investigates the non-Gaussian wind features over complex terrain under atmospheric turbulent boundary layers by the large eddy simulation (LES) model, and the turbulent inlet of LES is generated by the consistent discretizing random flow generation (CDRFG) method. The performance of LES is validated by two different complex terrains in Changsha and Mianyang, China, and the results are compared with wind tunnel tests and onsite measurements, respectively. Furthermore, the non-Gaussian parameters, such as skewness, kurtosis, probability curves, and gust factors, are analyzed in-depth. The results show that the LES method is in good agreement with both mean and turbulent wind fields from wind tunnel tests and onsite measurements. Wind fields in complex terrain mostly exhibit a left-skewed Gaussian process, and it changes from a softening Gaussian process to a hardening Gaussian process as the height increases. A reduction in the gust factors of about 2.0%-15.0% can be found by taking into account the non-Gaussian features, except for a 4.4% increase near the ground in steep terrain. This study can provide a reference for the assessment of extreme wind loads on structures in complex terrain.