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101. Sterile neutrino search at NEOS Experiment

Author: Ko, Y. J., Kim, B. R., Kim, J. Y., Han, B. Y., Jang, C. H., Jeon, E. J., Joo, K. K., Kim, H. J., Kim, H. S., Kim, Y. D., Lee, Jaison, Lee, J. Y., Lee, M. H., Oh, Y. M., Park, H. K., Park, H. S., Park, K. S., Seo, K. M., Siyeon, Kim, and Sun, G. M.
Subjects: High Energy Physics - Experiment, Physics - Instrumentation and Detectors
Abstract: An experiment to search for light sterile neutrinos was conducted at a reactor with a thermal power of 2.8 GW located at the Hanbit nuclear power complex. The search was done with a detector consisting of a ton of Gd-loaded liquid scintillator in a tendon gallery approximately 24 m from the reactor core. The measured antineutrino event rate is 1976 per day with a signal to background ratio of about 22. The shape of the antineutrino energy spectrum obtained from eight-month data-taking period is compared with a hypothesis of oscillations due to active-sterile antineutrino mixing. It is found to be consistent with no oscillation. An excess around 5 MeV prompt energy range is observed as seen in existing longer baseline experiments. The parameter space of $\sin^{2}2\theta_{14}$ down below 0.1 for $\Delta m^{2}_{41}$ ranging from 0.2 eV$^{2}$ to 2.3 eV$^{2}$ and the optimum point for the previously reported reactor antineutrino anomaly are excluded with a confidence level higher than 90%., Comment: 6 pages, 4 figures. 1 supplemental material (Fig. S1). Version published in Physical Review Letters
Published: 2016
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102. Comparing nanoparticle polymeric micellar paclitaxel and solvent-based paclitaxel as first-line treatment of advanced non-small-cell lung cancer: an open-label, randomized, multicenter, phase III trial

Author: Shi, M., Gu, A., Tu, H., Huang, C., Wang, H., Yu, Z., Wang, X., Cao, L., Shu, Y., Yang, R., Li, X., Chang, J., Hu, Y., Shen, P., Guo, Z., Tao, M., Zhang, Y., Liu, X., Sun, Q., Zhang, X., Jiang, Z., Zhao, J., Chen, F., Yu, H., Zhang, W., Sun, J., Li, D., Zhou, J., Han, B., and Wu, Y.L.
Published: 2021
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103. Regularly Truncated M-Estimators for Learning With Noisy Labels.

Author: Xia, X, Lu, P, Gong, C, Han, B, Yu, J, Liu, T, Xia, X, Lu, P, Gong, C, Han, B, Yu, J, and Liu, T
Abstract: The sample selection approach is very popular in learning with noisy labels. As deep networks "learn pattern first", prior methods built on sample selection share a similar training procedure: the small-loss examples can be regarded as clean examples and used for helping generalization, while the large-loss examples are treated as mislabeled ones and excluded from network parameter updates. However, such a procedure is arguably debatable from two folds: (a) it does not consider the bad influence of noisy labels in selected small-loss examples; (b) it does not make good use of the discarded large-loss examples, which may be clean or have meaningful information for generalization. In this paper, we propose regularly truncated M-estimators (RTME) to address the above two issues simultaneously. Specifically, RTME can alternately switch modes between truncated M-estimators and original M-estimators. The former can adaptively select small-losses examples without knowing the noise rate and reduce the side-effects of noisy labels in them. The latter makes the possibly clean examples but with large losses involved to help generalization. Theoretically, we demonstrate that our strategies are label-noise-tolerant. Empirically, comprehensive experimental results show that our method can outperform multiple baselines and is robust to broad noise types and levels.
Published: 2024

104. Partition Speeds Up Learning Implicit Neural Representations Based on Exponential-Increase Hypothesis

Author: Liu, K, Liu, F, Wang, H, Ma, N, Bu, J, Han, B, Liu, K, Liu, F, Wang, H, Ma, N, Bu, J, and Han, B
Abstract: Implicit neural representations INRs aim to learn a continuous function i e a neural network to represent an image where the input and output of the function are pixel coordinates and RGB Gray values respectively However images tend to consist of many objects whose colors are not perfectly consistent resulting in the challenge that image is actually a discontinuous piecewise function and cannot be well estimated by a continuous function In this paper we empirically investigate that if a neural network is enforced to fit a discontinuous piecewise function to reach a fixed small error the time costs will increase exponentially with respect to the boundaries in the spatial domain of the target signal We name this phenomenon the exponential increase hypothesis Under the exponential increase hypothesis learning INRs for images with many objects will converge very slowly To address this issue we first prove that partitioning a complex signal into several sub regions and utilizing piecewise INRs to fit that signal can significantly speed up the convergence Based on this fact we introduce a simple partition mechanism to boost the performance of two INR methods for image reconstruction one for learning INRs and the other for learning to learn INRs In both cases we partition an image into different sub regions and dedicate smaller networks for each part In addition we further propose two partition rules based on regular grids and semantic segmentation maps respectively Extensive experiments validate the effectiveness of the proposed partitioning methods in terms of learning INR for a single image ordinary learning framework and the learning to learn framework Code is released here
Published: 2024

105. Effect Modification by Sex of the Hemoglobin Concentration on Frailty Risk in Hospitalized Older Patients

Author: Li Q, Chen X, and Han B
Subjects: hemoglobin concentration, frailty phenotype, older inpatient, interaction effect, Geriatrics, RC952-954.6
Abstract: Qiuping Li, Xi Chen, Binru Han Department of Nursing, Xuanwu Hospital, Capital Medical University, Beijing, People’s Republic of ChinaCorrespondence: Binru HanXuanwu Hospital, Capital Medical University, Chang Chun St.45, Xicheng District, Beijing, 100053, People’s Republic of ChinaTel +86 10-83198219Fax +86 10-83198258Email kinv246@126.comBackground: Hemoglobin concentration differs by sex, possibly affecting any association between hemoglobin and frailty. This study aimed to evaluate the potential interaction effect of hemoglobin and sex on frailty in Chinese older inpatients.Methods: A cross-sectional study was conducted between February 2015 and November 2017 in a tertiary hospital. Frailty was defined by the Fried phenotype. Hemoglobin concentration was measured with a standard procedure. Covariates included demographics, clinical characteristics, and serum biomarkers. Logistic regression was applied to examine the association between hemoglobin concentration and frailty. The relative excess risk due to interaction (RERI), attributable proportion due to interaction (AP), and synergy index (SI) were used to evaluate the additive interaction.Results: A total of 619 older inpatients [mean age 69.26± 7.44 years; 334 men, 285 women] were included. The mean hemoglobin concentration was significantly lower in the elderly who were frail (11.9 g/L in frail versus 13.1g/L in non-frail; p< 0.001). In the multivariable regression models, lower hemoglobin in patients was significantly associated with frailty (adjusted odds ratio (OR) = 2.51, 95% CI:1.37, 4.60). The stratified analyses indicated that lower hemoglobin was associated with frailty among older inpatients with different characteristics. Female inpatients with lower hemoglobin had the highest risk of frailty (adjusted OR=6.43, 95%: 2.38, 17.3); there were interactions between hemoglobin and sex on the development of frailty (RERI=4.30, 95% CI=− 1.41, 10.01; AP=0.67, 95% CI=0.37, 0.97;SI=4.80, 95% CI=1.22, 18.84).Conclusions and Implications: Our study provided evidence that sex and lower hemoglobin have an interaction effect on frailty; it is suggested that clinicians may consider sex-specific strategies for the elderly to conform the concept of precision medicine.Keywords: hemoglobin concentration, frailty phenotype, older inpatient, interaction effect
Published: 2021

106. Identification of Metabolic-Associated Genes for the Prediction of Colon and Rectal Adenocarcinoma

Author: Cui Y, Han B, Zhang H, Liu H, Zhang F, and Niu R
Subjects: metabolism-related gene, colon adenocarcinoma, rectum adenocarcinoma, prognosis, enpp2, gsr, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Yanfen Cui, Baoai Han, He Zhang, Hui Liu, Fei Zhang, Ruifang Niu Public Laboratory, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Tianjin, 300060, People’s Republic of ChinaCorrespondence: Ruifang Niu; Fei Zhang Tel +86 13752668992; +86 18622221365Email rniu@tmu.edu.cn; feizhang03@tmu.edu.cnBackground and Aim: Uncontrolled proliferation is the most prominent biological feature of tumors. In order to rapidly proliferate, tumor cells regulate their metabolic behavior by controlling the expression of metabolism-related genes (MRGs) to maximize the utilization of available nutrients. In this study, we aimed to construct prognosis models for colorectal adenocarcinoma (COAD) and rectum adenocarcinoma (READ) using MRGs to predict the prognoses of patients.Methods: We first acquired the gene expression profiles of COAD and READ from the TCGA database, and then utilized univariate Cox analysis, Lasso regression, and multivariable Cox analysis to identify the MRGs for risk models.Results: Eight genes (CPT1C, PLCB2, PLA2G2D, GAMT, ENPP2, PIP4K2B, GPX3, and GSR) in the colon cancer risk model and six genes (TDO2, PKLR, GAMT, EARS2, ACO1, and WAS) in the rectal cancer risk model were identified successfully. Multivariate Cox analysis indicated that these two models could accurately and independently predict overall survival (OS) for patients with COAD or READ. Furthermore, functional enrichment analysis was used to identify the metabolism pathway of MRGs in the risk models and analyzed these genes comprehensively. Then, we verified the prognosis model in independent COAD cohorts (GSE17538) and detected the correlations of the protein expression levels of GSR and ENPP2 with prognosis for COAD or READ.Conclusion: In this study, 14 MRGs were identified as potential prognostic biomarkers and therapeutic targets for colorectal cancer.Keywords: metabolism-related gene, colon adenocarcinoma, rectum adenocarcinoma, prognosis, ENPP2, GSR
Published: 2021

107. Extragastrointestinal Stromal Tumor Presenting as a Recurrent Vaginal Mass: Case Report

Author: Liu S, Pan P, Han B, Wang J, Sun M, and Sun Y
Subjects: extragastrointestinal stromal tumors, vagina, c-kit, mutation, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Shuai Liu,1 Pan Pan,2 Bing Han,3 Jingnan Wang,1 Meili Sun,1 Yuping Sun1 1Department of Oncology, Jinan Central Hospital Affiliated to Shandong University; Jinan Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013, Shandong, People’s Republic of China; 2Department of Pathology, Jinan Central Hospital Affiliated to Shandong University; Jinan Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013, Shandong, People’s Republic of China; 3Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People’s Republic of ChinaCorrespondence: Yuping Sun Tel +86-13370582181Email 13370582181@163.comAbstract: Gastrointestinal stromal tumors (GISTs) are the dominant mesenchymal tumors of the digestive tract. Extragastrointestinal stromal tumors (EGISTs) usually originate outside the gastrointestinal tract without connection to the gastric or intestinal wall. However, EGISTs arising from the vaginal wall are very rare. Here, we report a case of EGIST that occurred in the vagina of a 60-year-old woman. The tumor was present in the posterior vaginal wall. It was surgically excised, and histological examination revealed spindle cell morphology with up to 14 mitoses per 50 high power field (HPF) and necrosis with the tumor-negative margins. Immunohistochemical analyses showed strongly positive CD34, CD117, and DOG-1 expression, but negative SMA, S-100, CD10, desmin, and actin expression. The patient underwent surgery and is currently being followed up. A literature review of EGSTs and treatments is also discussed in this report.Keywords: extragastrointestinal stromal tumors, vagina, c-kit, mutation
Published: 2021

108. Overexpression of Nucleolin is a Potential Prognostic Marker in Endometrial Carcinoma

Author: Lin Q, Ma X, Hu S, Li R, Wei X, Han B, Ma Y, Liu P, and Pang Y
Subjects: nucleolin, endometrial carcinoma, prognostic marker, tcga, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Qianhan Lin,1,2,* Xiaoxue Ma,1,2,* Shunxue Hu,3 Rui Li,1,2 Xuan Wei,1,2 Bing Han,1 Yanhui Ma,1 Peishu Liu,1,2,4 Yingxin Pang1,2,4 1Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People’s Republic of China; 2Key Laboratory of Gynecologic Oncology of Shandong Province, Jinan, 250012, Shandong, People’s Republic of China; 3Department of Pathology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People’s Republic of China; 4Shandong Engineering Laboratory for Urogynecology, Jinan, 250012, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Peishu LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People’s Republic of ChinaTel +8618560081988Email peishuliu@126.comYingxin PangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People’s Republic of ChinaTel +8618560081127Email yingxinpang@126.comPurpose: Nucleolin (NCL) is a multifunctional protein with oncogenic properties. NCL expression levels have been linked to the outcomes of various malignancies, but the clinical value of NCL in patients with endometrial carcinoma (EC) remains unclear. Here, the expression of NCL in EC tissues and its associations with patient outcomes were assessed.Patients and Methods: Data on NCL mRNA expression in EC and adjacent nonneoplastic tissues from The Cancer Genome Atlas (TCGA) were analyzed. In addition, NCL protein expression in 82 endometroid endometrial adenocarcinoma tissues and 15 non-malignant tissues was detected by immunohistochemistry.Results: Elevated NCL expression was markedly correlated with serous endometrial carcinoma (P< 0.001), advanced stage (P=0.029), and grade 3 (P< 0.001). High NCL levels were associated with poorer overall survival (OS) and disease-free survival (DFS) compared with intermediate or low NCL levels (OS: P=0.001, DFS: P=0.006). The multivariate Cox proportional hazards model showed that NCL expression was an independent poor prognostic factor for DFS (HR=1.282, CI=1.027– 1.601, P=0.028). A similar correlation between high expression levels of NCL and unfavorable DFS was found in endometrioid endometrial adenocarcinoma (HR=1.411, CI=1.083– 1.840, P=0.011). Positive extra-nuclear NCL expression (HR=3.377, 95% CI=1.029– 11.186, P=0.046) and low nuclear NCL expression (HR=0.233, 95% CI=0.068– 0.796, P=0.020) were independent prognostic factors for DFS in endometrioid endometrial adenocarcinoma.Conclusion: Heterotopic NCL is a potential prognostic biomarker for EC. Inhibiting the distribution of NCL from the nucleus to the cytoplasm and membrane may be a promising therapeutic strategy to improve outcomes in patients with EC with high NCL expression.Keywords: nucleolin, endometrial carcinoma, prognostic marker, TCGA
Published: 2021

109. Ouabain Exhibited Strong Anticancer Effects in Melanoma Cells via Induction of Apoptosis, G2/M Phase Arrest, and Migration Inhibition

Author: Wang L, Cai W, Han B, Zhang J, Yu B, and Chen M
Subjects: melanoma, ouabain, apoptosis, cell cycle, migration., Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Lei Wang,1 Wei Cai,2 Bing Han,1 Jue Zhang,1 Bing Yu,1 Ming Chen1 1Burn and Plastic Surgery, Zhongda Hospital Affiliated Southeast University, Nanjing, 210009, People’s Republic of China; 2Burn and Plastic Surgery, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, People’s Republic of ChinaCorrespondence: Wei CaiBurn and Plastic Surgery, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210009, People’s Republic of ChinaEmail caiwei8656@163.comBackground: Malignant melanoma was characterized by insensitive chemotherapy, drug resistance, and high metastatic ability, which resulted in the main reason for the mortality among skin-related cancers. The current agents were not sufficient to improve the treatment status of melanoma patients, and it was still needed to develop new chemotherapeutic drugs for melanoma. Our study aimed to study the anticancer effects and potential mechanisms of ouabain on melanoma cells.Methods: The inhibitory effects of ouabain were determined by CCK8 and colony formation assays, and the morphological changes of melanoma cells were observed by inverted microscope. The apoptosis induction and cell cycle distribution were detected by annexin V/PI double staining and PI staining, respectively. The expression of the biomarker proteins in apoptosis and G2/M phase were determined by Western blotting analysis. The effects of ouabain on the migration of melanoma cells were measured by transwell migration assay and wound closure analysis. The potential mechanisms of ouabain in melanoma cells were analyzed by transcriptome sequencing.Results: Our present study demonstrated that ouabain exhibited strong inhibitory effects on cell proliferation and triggered dramatical morphological changes of melanoma cells. Moreover, ouabain induced significant apoptosis in A375 rather than SK-Mel-28 cells via upregulation of bax expression and downregulation of bcl-2 expression. Consistently, ouabain treatment induced cell cycle arrest at G2/M phase in both A375 and SK-Mel-28 cells via upregulation of cyclin B1 and downregulation of cdc2 and cdc25c. Importantly, ouabain suppressed the migration of A375 and SK-Mel-28 cells. Furthermore, the transcriptome sequencing demonstrated that p53 and MAPK signaling pathway might play important roles in the inhibitory effects of ouabain.Conclusion: Our study revealed that ouabain exhibited dramatical anticancer effects, which provided a novel application for cardiac glycoside drugs in the clinical treatment of melanoma.Keywords: melanoma, ouabain, apoptosis, cell cycle, migration
Published: 2021

110. Application of Zintl–Klemm rules to silicon-based LIB anodes

Author: Vaughey, J., primary, Li, X., additional, Han, B., additional, Zhang, Y., additional, Uppulari, R., additional, Key, B., additional, Dogan, F., additional, Cora, Saida S., additional, and Sa, Niya, additional
Published: 2021
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111. Engineering of biomaterials for tumor modeling

Author: Choi, S.R., Yang, Y., Huang, K.Y., Kong, H.J., Flick, M.J., and Han, B.
Published: 2020
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112. Early drain removal does not increase the rate of surgical site infections following an open transversus abdominis release

Author: Kushner, B., Smith, E., Han, B., Otegbeye, E., Holden, S., and Blatnik, J.
Published: 2021
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113. Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell

Author: Li, X., Zhao, C., Han, B., Qu, L., Liu, C., Yang, N., and Lian, L.
Published: 2021
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114. Immune cell infiltration features and related marker genes in lung cancer based on single-cell RNA-seq

Author: Zhong, R., Chen, D., Cao, S., Li, J., Han, B., and Zhong, H.
Published: 2021
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115. The Use of Cardiovascular CT in Repaired CHD

Author: Han, B. Kelly, Crean, Andrew, Lesser, John R., and Schoepf, U. Joseph, Series Editor
Published: 2019
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116. miR-613 Suppresses Chemoresistance and Stemness in Triple-Negative Breast Cancer by Targeting FAM83A

Author: Liu C, Jiang Y, and Han B
Subjects: triple negative breast cancer, mir-613, fam83a, chemoresistance, stemness, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Cuiping Liu,1 Yizhou Jiang,2 Baosan Han3 1Department of Breast Surgery, Affiliated Hospital of Chifeng University, Chifeng, Inner Mongolia 024005, People’s Republic of China; 2Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, People’s Republic of China; 3Department of Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, People’s Republic of ChinaCorrespondence: Baosan HanXin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 1665 Kongjiang Road, Yangpu District, Shanghai 200092, People’s Republic of ChinaTel +86-2165792951Email shhanbs311@126.comIntroduction: Triple-negative breast cancer (TNBC) is the most aggressive malignancy of breast cancer, which represents about 20% of all cases. The prognosis of TNBC remains unfavorable due to the lack of targeted therapy and chemoresistance. The aim of this study is to investigate the role of miR-613 in TNBC.Material and Methods: Quantitative RT-PCT was used to explore the expression of miR-613 in breast cancer clinical samples and cell lines. MTT, colony formation assay, spheroid formation assay and xenograft tumor growth assay were used to investigate the role of miR-613 in vitro and in vivo. Cell apoptosis and surface marker expression were measured by flow cytometry. Dual-luciferase reporter assay was used to explore the function of miR-613 in regulating FAM83A 3ʹUTR. Immunohistochemical staining was used to investigate the expression of FAM83A in TNBC tissues.Results: We found that miR-613 expression was significantly downregulated in breast cancer tissues and was even lower in TNBC compared with that in other types of breast cancer. A similar result was found in breast cancer cell lines. Further analysis indicated that miR-613 could suppress TNBC cell growth, chemoresistance and stem-cell-like phenotype. Moreover, we also demonstrated that miR-613 suppressed tumorigenesis in vivo. Mechanically, we explored the downstream target of miR-613 and identified that miR-613 could directly bind to the 3ʹUTR of FAM83A, which contributed to the miR-613 mediated tumor suppression. The expression of miR-613 and FAM83A was negatively correlated. Restoring the expression of FAM83A attributed to the chemoresistance and stemness of TNBC cells.Conclusion: We demonstrated that loss of miR-613 was critical for TNBC malignancy and restoring its expression could be served as a potential approach for TNBC treatment.Keywords: triple-negative breast cancer, miR-613, FAM83A, chemoresistance, stemness
Published: 2020

117. Sinapultide-Loaded Microbubbles Combined with Ultrasound to Attenuate Lipopolysaccharide-Induced Acute Lung Injury in Mice

Author: Liu D, Chen Y, Li F, Chen C, Wei P, Xiao D, and Han B
Subjects: sinapultide, microbubbles, lipopolysaccharide, lung injury, safety, Therapeutics. Pharmacology, RM1-950
Abstract: Dong Liu,1– 3 Yanjun Chen,1,2 Fang Li,1,2 Cunwu Chen,1,2 Peipei Wei,1,2 Deli Xiao,4,5 Bangxin Han1,2 1School of Biological and Pharmaceutical Engineering, West Anhui University, Lu’an 237012, People’s Republic of China; 2Anhui Engineering Laboratory for Conservation and Sustainable Utilization of Traditional Chinese Medicine Resources, Lu’an 237012, People’s Republic of China; 3School of Biomedical Sciences and Medical Engineering, Southeast University, Nanjing 210009, People’s Republic of China; 4Department of Analytical Chemistry, China Pharmaceutical University, Nanjing 210009, People’s Republic of China; 5Key Laboratory of Biomedical Functional Materials, China Pharmaceutical University, Nanjing 210009, People’s Republic of ChinaCorrespondence: Deli XiaoDepartment of Analytical Chemistry, China Pharmaceutical University, Nanjing 210009, People’s Republic of ChinaTel +86 25 86185160Email xiao49562001@163.comBangxin HanSchool of Biological and Pharmaceutical Engineering, West Anhui University, Lu’an 237012, People’s Republic of ChinaTel +86 564 3305073Email hanbx1978@sina.comPurpose: Pulmonary surfactants (eg, sinapultide) are widely used for the treatment of lung injury diseases; however, they generally induce poor therapeutic efficacy in clinics. In this study, sinapultide-loaded microbubbles (MBs) were prepared and combined with ultrasound (US) treatment as a new strategy for improved treatment of lung injury diseases.Methods: The combination treatment strategy of MBs combined with ultrasound was tested in a lipopolysaccharide (LPS)-induced mouse model of alveolar epithelial cells (AT II) and acute lung injury. Firstly, cytotoxicity, cytokines, and protein levels in LPS-mediated AT II cells were assessed. Secondly, the pathological morphology of lung tissue, the wet/dry (W/D) weight ratio, cytokines, and protein levels in LPS-mediated acute lung injury mice after treatment with the MBs were evaluated. Moreover, histology examination of the heart, liver, spleen, lung and kidney of mice treated with the MBs was performed to initially evaluate the safety of the sinapultide-loaded MBs.Results: Sinapultide-loaded MBs in combination with ultrasound treatment significantly reduced the secretion of inflammatory cytokines and increased the expression of surfactant protein A (SP-A) in AT II cells. Furthermore, the pathological morphology of lung tissue, the wet/dry (W/D) weight ratio, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and SP-A expression level of mice treated with MBs and ultrasound were significantly improved compared to those of non-treated mice. In addition, the histology of the examined organs showed that the MBs had a good safety profile.Conclusion: Sinapultide-loaded MBs combined with ultrasonic treatment may be a new therapeutic option for lung injury diseases in the clinic.Keywords: sinapultide, microbubbles, lipopolysaccharide, lung injury, safety
Published: 2020

118. Effective Tacrolimus Treatment for Patients with Non-Severe Aplastic Anemia That is Refractory/Intolerant to Cyclosporine A: A Retrospective Study

Author: Du Y, Huang Y, Zhou W, Liu X, Chen F, Yang C, Chen M, Ruan J, and Han B
Subjects: non-severe aplastic anemia, tacrolimus, cyclosporine a., Therapeutics. Pharmacology, RM1-950
Abstract: Yali Du,1 Yuzhou Huang,1 Wenzhe Zhou,1 Xinjian Liu,2 Fangfei Chen,1 Chen Yang,1 Miao Chen,1 Jing Ruan,1 Bing Han1 1Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, People’s Republic of China; 2Department of Hematology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Institute of Hematology of Henan Province, Zhengzhou, People’s Republic of ChinaCorrespondence: Bing HanDepartment of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, People’s Republic of ChinaEmail hanbing_li@sina.com.cnBackground: For symptomatic non-severe aplastic anemia (NSAA) patients who cannot afford anti-thymocyte globulin (ATG) or allogeneic hematopoietic stem cell transplantation (HSCT), tacrolimus (FK) may be an option if these patients do not respond or become tolerant to cyclosporine A (CsA).Methods: We enrolled 101 NSAA patients who were refractory or intolerant to CsA with no chance of HSCT or ATG treatment and treated these patients with tacrolimus for at least 6 months, with follow-up for at least one year.Results: The overall response rate (ORR) was 38.6% (complete response: 9.9%; partial response: 28.7%), and the median time to optimal response was 6 (3～10) months. Thirty-two (31.7%) cases had elevated creatinine levels. Eight (7.9%) cases had elevations in AST/ALT. A total of 25.6% (10/39) of patients relapsed at the end of follow-up. Age (P=0.0005), FK concentration (4.0∼ 12 ng/mL, P=0.0005) and intolerance to CsA (P=0.012) were the independent risk factors for ORR. Treg cell levels pre-FK treatment were much lower than those of healthy controls (3.7± 0.6% vs 6.8± 0.7%, P=0.0004) but increased significantly after FK treatment (3.7± 0.6% vs 7.1± 0.8%, P=0.0039).Conclusion: Our data suggest that tacrolimus is a salvage treatment for patients with NSAA that is refractory or intolerant to CsA.Keywords: non-severe aplastic anemia, tacrolimus, cyclosporine A
Published: 2020

119. The Association Between RAPSN Methylation in Peripheral Blood and Early Stage Lung Cancer Detected in Case–Control Cohort

Author: Qiao R, Di F, Wang J, Wei Y, Zhang Y, Xu T, Wang Y, Gu W, Han B, and Yang R
Subjects: lc, early detection, dna methylation, rapsn, peripheral blood, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Rong Qiao,1,* Feifei Di,2,* Jun Wang,2 Yujie Wei,2 Yanman Zhang,2 Tian Xu,3 Yue Wang,1 Wanjian Gu,3 Baohui Han,1 Rongxi Yang2,4 1Department of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, People’s Republic of China; 2Department of Research and Academic, Nanjing TANTICA Biotechnology Co. Ltd, Nanjing 210000, People’s Republic of China; 3Department of Clinical Laboratory, Jiangsu Province Hospital of Chinese Medicine, Nanjing 210000, People’s Republic of China; 4Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing 210000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Rongxi Yang; Baohui Han Email rongxiyang@njmu.edu.cn; 18930858216@163.comBackground: Early detection is essential to improve the survival and life quality of lung cancer (LC) patients. Changes of peripheral blood DNA methylation could be associated with malignancy but were mostly studied in Caucasians.Methods: Here, in a Chinese population, we performed mass spectrometry assays to investigate the association between very early stage LC and methylation levels of RAPSN in the peripheral blood by a case–control cohort using of 221 LC patients (93.2% LC at stage I) and 285 unrelated cancer free control individuals.Results: The odds ratios (ORs) of all CpG sites were evaluated for their risk to LC using inter-quartile analyses by logistic regression. In general, we observed an association between very early LC and decreased methylation of RAPSN_CpG_1.15 and RAPSN_CpG_3.4 (referring to Q4, OR range from 1.64 to 1.81, p< 0.05). Stratified by gender, while hypomethylation of RAPSN_CpG_1.15, RAPSN_CpG_3.4 and RAPSN_CpG_7.14 were associated with LC in males (referring to Q4, ORs range from 1.94 to 2.31, p< 0.05), RAPSN_CpG_2 and RAPSN_CpG_5 showed significantly lower methylation in female LC patients comparing to controls (referring to Q4, ORs range from 2.49 to 3.60, p< 0.05). The risk of RAPSN hypomethylation to LC was enhanced by aging, and typically for people older than 55 years (referring to Q4, ORs range from 2.17 to 3.61 in six out of all 10 analyzed CpG groups, p< 0.05).Conclusion: Our study reveals an association between RAPSN hypomethylation in peripheral blood and LC and suggests the occurrence of altered blood-based methylation at the early stage of cancer.Keywords: LC, early detection, DNA methylation, RAPSN, peripheral blood
Published: 2020

120. Systematic identification of genes encoding cell surface and secreted proteins that are essential for in vitro growth and infection in Leishmania donovani.

Author: Adam J Roberts, Han B Ong, Simon Clare, Cordelia Brandt, Katherine Harcourt, Susanne U Franssen, James A Cotton, Nicole Müller-Sienerth, and Gavin J Wright
Subjects: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract: Leishmaniasis is an infectious disease caused by protozoan parasites belonging to the genus Leishmania for which there are no approved human vaccines. Infections localise to different tissues in a species-specific manner with the visceral form of the disease caused by Leishmania donovani and L. infantum being the most deadly in humans. Although Leishmania spp. parasites are predominantly intracellular, the visceral disease can be prevented in dogs by vaccinating with a complex mixture of secreted products from cultures of L. infantum promastigotes. With the logic that extracellular parasite proteins make good subunit vaccine candidates because they are directly accessible to vaccine-elicited host antibodies, here we attempt to discover proteins that are essential for in vitro growth and host infection with the goal of identifying subunit vaccine candidates. Using an in silico analysis of the Leishmania donovani genome, we identified 92 genes encoding proteins that are predicted to be secreted or externally anchored to the parasite membrane by a single transmembrane region or a GPI anchor. By selecting a transgenic L. donovani parasite that expresses both luciferase and the Cas9 nuclease, we systematically attempted to target all 92 genes by CRISPR genome editing and identified four that were required for in vitro growth. For fifty-five genes, we infected cohorts of mice with each mutant parasite and by longitudinally quantifying parasitaemia with bioluminescent imaging, showed that nine genes had evidence of an attenuated infection although all ultimately established an infection. Finally, we expressed two genes as full-length soluble recombinant proteins and tested them as subunit vaccine candidates in a murine preclinical infection model. Both proteins elicited significant levels of protection against the uncontrolled development of a splenic infection warranting further investigation as subunit vaccine candidates against this deadly infectious tropical disease.
Published: 2022
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121. Recommendations for risk stratified use of cardiac computed tomography for congenital heart disease during the COVID-19 pandemic

Author: Farooqi, Kanwal M., Ghoshhajra, Brian B., Shah, Amee M., Chelliah, Anjali, Einstein, Andrew J., Hlavacek, Anthony, and Han, B. Kelly
Published: 2020
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122. Superior high-temperature properties and deformation-induced planar faults in a novel L12-strengthened high-entropy alloy

Author: Zhao, Y.L., Yang, T., Li, Y.R., Fan, L., Han, B., Jiao, Z.B., Chen, D., Liu, C.T., and Kai, J.J.
Published: 2020
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123. Plastic modeling of porous rocks in drained and undrained conditions

Author: Han, B., Shen, W.Q., Xie, S.Y., and Shao, J.F.
Published: 2020
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124. P1194 Single-cell analysis reveals clonal expansions of pro-inflammatory tissue-resident memory Th17 cells in Crohn's disease

Author: Lee, Y, primary, Baek, J, additional, Park, S, additional, Kim, Y, additional, Lee, J L, additional, Hwang, S W, additional, Park, S H, additional, Yang, S K, additional, Han, B, additional, Kweon, M N, additional, Song, K, additional, Yoon, Y S, additional, Ye, B D, additional, and Lee, H S, additional
Published: 2024
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125. Microstructure and wear property of WMoTaNb refractory high entropy alloy coating by laser cladding

Author: Chen, Z.B., primary, Zhang, G.G., additional, Chen, J.J., additional, Guo, C.H., additional, Sun, W.Y., additional, Yang, Z.L., additional, Li, H.X., additional, Jiang, F.C., additional, and Han, B., additional
Published: 2023
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126. Seasonal and Interannual Variations in the Schumann Resonance Observed in the ELF Electromagnetic Networks in China

Author: Han, B., primary, Tang, J., additional, Zhao, G. Z., additional, Wang, L. F., additional, Dong, Z. Y., additional, and Xu, Y. C., additional
Published: 2023
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127. EP02.01-12 PEG2000-PLA-Based Nanoscale Polymeric Micellar Reduces Paclitaxel-Related Toxicity in Beagles

Author: Lu, J., primary, Han, B., additional, Zhang, B., additional, Zou, B., additional, Zhou, J., additional, and Zhong, H., additional
Published: 2023
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128. EP06.03-01 Genetic Characterization of Driving Metastasis in TP53-Mutant Non-small Cell Lung Cancer Patients

Author: Lu, J., primary, Lou, Y., additional, Zhong, R., additional, Zhang, Y., additional, Zhang, L., additional, Wu, J., additional, Zhang, W., additional, Zhong, H., additional, and Han, B., additional
Published: 2023
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129. P2.09-40 Efficacy of Anlotinib in T790M-positive NSCLC Patients with Osimertinib Resistance: A Retrospective and Exploratory Study

Author: Chen, Y., primary, Liu, H., additional, Zhang, J., additional, and Han, B., additional
Published: 2023
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130. 53 Intracranial hypertension following alitretinoin treatment for chronic hand eczema: a case report

Author: Han, B., primary, Choi, Y.J., additional, Lee, J.M., additional, Lee, Y.J., additional, Lee, Y.S., additional, and Lee, J.H., additional
Published: 2023
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131. P1.02-02 Co-inhibition of MEK/RTKs Pathways via Trametinib Plus Anlotinib forKRAS-Mutant NSCLC

Author: Lu, J., primary, Hu, M., additional, Zhao, Y., additional, Zhang, Y., additional, Lou, Y., additional, Tao, S., additional, Zhu, L., additional, Wu, Y., additional, Ji, H., additional, Zhong, H., additional, and Han, B., additional
Published: 2023
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132. EP11.02-06 Atezolizumab vs Single-Agent Chemo in NSCLC Patients Ineligible for a 1L Platinum Regimen: Asian Subgroup Analysis of IPSOS

Author: Lee, S.M., primary, Han, B., additional, Peters, S., additional, Le, A.T., additional, Huang, D., additional, Wu, G., additional, Cao, L., additional, Pham, C.P., additional, Zhao, J., additional, Wang, K., additional, Yang, N., additional, Zhong, H., additional, Hu, Y., additional, Morris, S., additional, Lam, V., additional, Graupner, V., additional, Gitlitz, B., additional, Hoglander, E., additional, and Schulz, C., additional
Published: 2023
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133. EP11.02-03 First Line Sintilimab plus Anlotinib vs Platinum-based Chemotherapy in Metastatic NSCLC (SUNRISE): Updated Efficacy and Safety Analysis

Author: Chu, T., primary, Han, B., additional, Yu, Z., additional, Wang, J., additional, Zhao, Y., additional, Mu, X., additional, Yu, X., additional, Shi, X., additional, Shi, Q., additional, Guan, M., additional, Ding, C., additional, and Geng, N., additional
Published: 2023
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134. P1.27-09 Efficacy and Safety of Aumolertinib as Adjuvant Therapy in Resectable Stage I NSCLC with High-grade Patterns and EGFR Mutations (APPOINT)

Author: Han, B., primary, Fang, W., additional, Chen, C., additional, Zhang, W., additional, Zhang, B., additional, Yao, F., additional, Shi, J., additional, Yue, D., additional, Qi, Y., additional, Zhu, Z., additional, and Xie, J., additional
Published: 2023
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135. The Physics of the B Factories

Author: Bevan, A. J., Golob, B., Mannel, Th., Prell, S., Yabsley, B. D., Abe, K., Aihara, H., Anulli, F., Arnaud, N., Aushev, T., Beneke, M., Beringer, J., Bianchi, F., Bigi, I. I., Bona, M., Brambilla, N., rodzicka, J. B, Chang, P., Charles, M. J., Cheng, C. H., Cheng, H. -Y., Chistov, R., Colangelo, P., Coleman, J. P., Drutskoy, A., Druzhinin, V. P., Eidelman, S., Eigen, G., Eisner, A. M., Faccini, R., Flood, K. T ., Gambino, P., Gaz, A., Gradl, W., Hayashii, H., Higuchi, T., Hulsbergen, W. D., Hurth, T., Iijima, T., Itoh, R., Jackson, P. D., Kass, R., Kolomensky, Yu. G., Kou, E., Križan, P., Kronfeld, A., Kumano, S., Kwon, Y. J., Latham, T. E., Leith, D. W. G. S., Lüth, V., Martinez-Vidal, F., Meadows, B. T., Mussa, R., Nakao, M., Nishida, S., Ocariz, J., Olsen, S. L., Pakhlov, P., Pakhlova, G., Palano, A., Pich, A., Playfer, S., Poluektov, A., Porter, F. C., Robertson, S. H., Roney, J. M., Roodman, A., Sakai, Y., Schwanda, C., Schwartz, A. J., Seidl, R., Sekula, S. J., Steinhauser, M., Sumisawa, K., Swanson, E. S., Tackmann, F., Trabelsi, K., Uehara, S., Uno, S., van der Water, R., Vasseur, G., Verkerke, W., Waldi, R., Wang, M. Z., Wilson, F. F., Zupan, J., Zupanc, A., Adachi, I., Albert, J., Banerjee, Sw., Bellis, M., Ben-Haim, E., Biassoni, P., Cahn, R. N., Cartaro, C., Chauveau, J., Chen, C., Chiang, C. C., Cowan, R., Dalseno, J., Davier, M., Davies, C., Dingfelder, J. C., nard, B. Eche, Epifanov, D., Fulsom, B. G., Gabareen, A. M., Gary, J. W., Godang, R., Graham, M. T., Hafner, A., Hamilton, B., Hartmann, T., Hayasaka, K., Hearty, C., Iwasaki, Y., Khodjamirian, A., Kusaka, A., Kuzmin, A., Lafferty, G. D., Lazzaro, A., Li, J., Lindemann, D., Long, O., Lusiani, A., Marchiori, G., Martinelli, M., Miyabayashi, K., Mizuk, R., Mohanty, G. B., Muller, D. R., Nakazawa, H., Ongmongkolkul, P., Pacetti, S., Palombo, F., Pedlar, T. K., Piilonen, L. E., Pilloni, A., Poireau, V., Prothmann, K., Pulliam, T., Rama, M., Ratcliff, B. N., Roudeau, P., Schrenk, S., Schroeder, T., Schubert, K. R., Shen, C. P., Shwartz, B., Soffer, A., Solodov, E. P., Somov, A., Starič, M., Stracka, S., Telnov, A. V., Todyshev, K. Yu., Tsuboyama, T., Uglov, T., Vinokurova, A., Walsh, J. J., Watanabe, Y., Won, E., Wormser, G., Wright, D. H., Ye, S., Zhang, C. C., Abachi, S., Abashian, A., Abe, N., Abe, R., Abe, T., Abrams, G. S., Adam, I., Adamczyk, K., Adametz, A., Adye, T., Agarwal, A., Ahmed, H., Ahmed, M., Ahmed, S., Ahn, B. S., Ahn, H. S., Aitchison, I. J. R., Akai, K., Akar, S., Akatsu, M., Akemoto, M., Akhmetshin, R., Akre, R., Alam, M. S., Albert, J. N., Aleksan, R., Alexander, J. P., Alimonti, G., Allen, M. T., Allison, J., Allmendinger, T., Alsmiller, J. R. G., Altenburg, D., Alwyn, K. E., An, Q., Anderson, J., Andreassen, R., Andreotti, D., Andreotti, M., Andress, J. C., Angelini, C., Anipko, D., Anjomshoaa, A., Anthony, P. L., Antillon, E. A., Antonioli, E., Aoki, K., Arguin, J. F., Arinstein, K., Arisaka, K., Asai, K., Asai, M., Asano, Y., Asgeirsson, D. J., Asner, D. M., Aso, T., Aspinwall, M. L., Aston, D., Atmacan, H., Aubert, B., Aulchenko, V., Ayad, R., Azemoon, T., Aziz, T., Azzolini, V., Azzopardi, D. E., Baak, M. A., Back, J. J., Bagnasco, S., Bahinipati, S., Bailey, D. S., Bailey, S., Bailly, P., van Bakel, N., Bakich, A. M., Bala, A., Balagura, V., Baldini-Ferroli, R., Ban, Y., Banas, E., Band, H. R., Banerjee, S., Baracchini, E., Barate, R., Barberio, E., Barbero, M., Bard, D. J., Barillari, T., Barlow, N. R., Barlow, R. J., Barrett, M., Bartel, W., Bartelt, J., Bartoldus, R., Batignani, G., Battaglia, M., Bauer, J. M., Bay, A., Beaulieu, M., Bechtle, P., Beck, T. W., Becker, J., Becla, J., Bedny, I., Behari, S., Behera, P. K., Behn, E., Behr, L., Beigbeder, C., Beiline, D., Bell, R., Bellini, F., Bellodi, G., Belous, K., Benayoun, M., Benelli, G., Benitez, J. F., Benkebil, M., Berger, N., Bernabeu, J., Bernard, D., Bernet, R., Bernlochner, F. U., Berryhill, J. W., Bertsche, K., Besson, P., Best, D. S., Bettarini, S., Bettoni, D., Bhardwaj, V., Bhimji, W., Bhuyan, B., Biagini, M. E., Biasini, M., van Bibber, K., Biesiada, J., Bingham, I., Bionta, R. M., Bischofberger, M., Bitenc, U., Bizjak, I., Blanc, F., Blaylock, G., Blinov, V. E., Bloom, E., Bloom, P. C., Blount, N. L., Blouw, J., Bly, M., Blyth, S., Boeheim, C. T., Bomben, M., Bondar, A., Bondioli, M., Bonneaud, G. R., Bonvicini, G., Booke, M., Booth, J., Borean, C., Borgland, A. W., Borsato, E., Bosi, F., Bosisio, L., Botov, A. A., Bougher, J., Bouldin, K., Bourgeois, P., Boutigny, D., Bowerman, D. A., Boyarski, A. M., Boyce, R. F., Boyd, J. T., Bozek, A., Bozzi, C., Bračko, M., Brandenburg, G., Brandt, T., Brau, B., Brau, J., Breon, A. B., Breton, D., Brew, C., Briand, H., Bright-Thomas, P. G., Brigljević, V., Britton, D. I., Brochard, F., Broomer, B., Brose, J., Browder, T. E., Brown, C. L., Brown, C. M., Brown, D. N., Browne, M., Bruinsma, M., Brunet, S., Bucci, F., Buchanan, C., Buchmueller, O. L., Bünger, C., Bugg, W., Bukin, A. D., Bula, R., Bulten, H., Burchat, P. R., Burgess, W., Burke, J. P., Button-Shafer, J., Buzykaev, A. R., Buzzo, A., Cai, Y., Calabrese, R., Calcaterra, A., Calderini, G., Camanzi, B., Campagna, E., Campagnari, C., Capra, R., Carassiti, V., Carpinelli, M., Carroll, M., Casarosa, G., Casey, B. C. K., Cason, N. M., Castelli, G., Cavallo, N., Cavoto, G., Cecchi, A., Cenci, R., Cerizza, G., Cervelli, A., Ceseracciu, A., Chai, X., Chaisanguanthum, K. S., Chang, M. C., Chang, Y. H., Chang, Y. W., Chao, D. S., Chao, M., Chao, Y., Charles, E., Chavez, C. A., Cheaib, R., Chekelian, V., Chen, A., Chen, E., Chen, G. P., Chen, H. F., Chen, J. -H., Chen, J. C., Chen, K. F., Chen, P., Chen, S., Chen, W. T., Chen, X., Chen, X. R., Chen, Y. Q., Cheng, B., Cheon, B. G., Chevalier, N., Chia, Y. M., Chidzik, S., Chilikin, K., Chistiakova, M. V., Cizeron, R., Cho, I. S., Cho, K., Chobanova, V., Choi, H. H. F., Choi, K. S., Choi, S. K., Choi, Y., Choi, Y. K., Christ, S., Chu, P. H., Chun, S., Chuvikov, A., Cibinetto, G., Cinabro, D., Clark, A. R., Clark, P. J., Clarke, C. K., Claus, R., Claxton, B., Clifton, Z. C., Cochran, J., Cohen-Tanugi, J., Cohn, H., Colberg, T., Cole, S., Colecchia, F., Condurache, C., Contri, R., Convert, P., Convery, M. R., Cooke, P., Copty, N., Cormack, C. M., Corso, F. Dal, Corwin, L. A., Cossutti, F., Cote, D., Ramusino, A. Cotta, Cottingham, W. N., Couderc, F., Coupal, D. P., Covarelli, R., Cowan, G., Craddock, W. W., Crane, G., Crawley, H. B., Cremaldi, L., Crescente, A., Cristinziani, M., Crnkovic, J., Crosetti, G., Cuhadar-Donszelmann, T., Cunha, A., Curry, S., D'Orazio, A., Dû, S., Dahlinger, G., Dahmes, B., Dallapiccola, C., Danielson, N., Danilov, M., Das, A., Dash, M., Dasu, S., Datta, M., Daudo, F., Dauncey, P. D., David, P., Davis, C. L., Day, C. T., De Mori, F., De Domenico, G., De Groot, N., De la Vaissière, C., de la Vaissière, Ch., de Lesquen, A., De Nardo, G., de Sangro, R., De Silva, A., DeBarger, S., Decker, F. J., Sanchez, P. del Amo, Del Buono, L., Del Gamba, V., del Re, D., Della Ricca, G., Denig, A. G., Derkach, D., Derrington, I. M., DeStaebler, H., Destree, J., Devmal, S., Dey, B., Di Girolamo, B., Di Marco, E., Dickopp, M., Dima, M. O., Dittrich, S., Dittongo, S., Dixon, P., Dneprovsky, L., Dohou, F., Doi, Y., Doležal, Z., Doll, D. A., Donald, M., Dong, L., Dong, L. Y., Dorfan, J., Dorigo, A., Dorsten, M. P., Dowd, R., Dowdell, J., Drásal, Z., Dragic, J., Drummond, B. W., Dubitzky, R. S., Dubois-Felsmann, G. P., Dubrovin, M. S., Duh, Y. C., Duh, Y. T., Dujmic, D., Dungel, W., Dunwoodie, W., Dutta, D., Dvoretskii, A., Dyce, N., Ebert, M., Eckhart, E. A., Ecklund, S., Eckmann, R., Eckstein, P., Edgar, C. L., Edwards, A. J., Egede, U., Eichenbaum, A. M., Elmer, P., Emery, S., Enari, Y., Enomoto, R., Erdos, E., Erickson, R., Ernst, J. A., Erwin, R. J., Escalier, M., Eschenburg, V., Eschrich, I., Esen, S., Esteve, L., Evangelisti, F., Everton, C. W., Eyges, V., Fabby, C., Fabozzi, F., Fahey, S., Falbo, M., Fan, S., Fang, F., Fanin, C., Farbin, A., Farhat, H., Fast, J. E., Feindt, M., Fella, A., Feltresi, E., Ferber, T., Fernholz, R. E., Ferrag, S., Ferrarotto, F., Ferroni, F., Field, R. C., Filippi, A., Finocchiaro, G., Fioravanti, E., da Costa, J. Firmino, Fischer, P. -A., Fisher, A., Fisher, P. H., Flacco, C. J., Flack, R. L., Flaecher, H. U., Flanagan, J., Flanigan, J. M., Ford, K. E., Ford, W. T., Forster, I. J., Forti, A. C., Forti, F., Fortin, D., Foster, B., Foulkes, S. D., Fouque, G., Fox, J., Franchini, P., Sevilla, M. Franco, Franek, B., Frank, E. D., Fransham, K. B., Fratina, S., Fratini, K., Frey, A., Frey, R., Friedl, M., Fritsch, M., Fry, J. R., Fujii, H., Fujikawa, M., Fujita, Y., Fujiyama, Y., Fukunaga, C., Fukushima, M., Fullwood, J., Funahashi, Y., Funakoshi, Y., Furano, F., Furman, M., Furukawa, K., Futterschneider, H., Gabathuler, E., Gabriel, T. A., Gabyshev, N., Gaede, F., Gagliardi, N., Gaidot, A., Gaillard, J. -M., Gaillard, J. R., Galagedera, S., Galeazzi, F., Gallo, F., Gamba, D., Gamet, R., Gan, K. K., Gandini, P., Ganguly, S., Ganzhur, S. F., Gao, Y. Y., Gaponenko, I., Garmash, A., Tico, J. Garra, Garzia, I., Gaspero, M., Gastaldi, F., Gatto, C., Gaur, V., Geddes, N. I., Geld, T. L., Genat, J. -F., George, K. A., George, M., George, S., Georgette, Z., Gershon, T. J., Gill, M. S., Gillard, R., Gilman, J. D., Giordano, F., Giorgi, M. A., Giraud, P. -F., Gladney, L., Glanzman, T., Glattauer, R., Go, A., Goetzen, K., Goh, Y. M., Gokhroo, G., Goldenzweig, P., Golubev, V. B., Gopal, G. P., Gordon, A., Gorišek, A., Goriletsky, V. I., Gorodeisky, R., Gosset, L., Gotow, K., Gowdy, S. J., Graffin, P., Grancagnolo, S., Grauges, E., Graziani, G., Green, M. G., Greene, M. G., Grenier, G. J., Grenier, P., Griessinger, K., Grillo, A. A., Grinyov, B. V., Gritsan, A. V., Grosdidier, G., Perdekamp, M. Grosse, Grosso, P., Grothe, M., Groysman, Y., Grünberg, O., Guido, E., Guler, H., Gunawardane, N. J. W., Guo, Q. H., Guo, R. S., Guo, Z. J., Guttman, N., Ha, H., Ha, H. C., Haas, T., Haba, J., Hachtel, J., Hadavand, H. K., Hadig, T., Hagner, C., Haire, M., Haitani, F., Haji, T., Haller, G., Halyo, V., Hamano, K., Hamasaki, H., de Monchenault, G. Hamel, Hamilton, J., Hamilton, R., Hamon, O., Han, B. Y., Han, Y. L., Hanada, H., Hanagaki, K., Handa, F., Hanson, J. E., Hanushevsky, A., Hara, K., Hara, T., Harada, Y., Harrison, P. F., Harrison, T. J., Harrop, B., Hart, A. J., Hart, P. A., Hartfiel, B. L., Harton, J. L., Haruyama, T., Hasan, A., Hasegawa, Y., Hast, C., Hastings, N. C., Hasuko, K., Hauke, A., Hawkes, C. M., Hayashi, K., Hazumi, M., Hee, C., Heenan, E. M., Heffernan, D., Held, T., Henderson, R., Henderson, S. W., Hertzbach, S. S., Hervé, S., Heß, M., Heusch, C. A., Hicheur, A., Higashi, Y., Higasino, Y., Higuchi, I., Hikita, S., Hill, E. J., Himel, T., Hinz, L., Hirai, T., Hirano, H., Hirschauer, J. F., Hitlin, D. G., Hitomi, N., Hodgkinson, M. C., Höcker, A., Hoi, C. T., Hojo, T., Hokuue, T., Hollar, J. J., Hong, T. M., Honscheid, K., Hooberman, B., Hopkins, D. A., Horii, Y., Hoshi, Y., Hoshina, K., Hou, S., Hou, W. S., Hryn'ova, T., Hsiung, Y. B., Hsu, C. L., Hsu, S. C., Hu, H., Hu, T., Huang, H. C., Huang, T. J., Huang, Y. C., Huard, Z., Huffer, M. E., Hufnagel, D., Hung, T., Hutchcroft, D. E., Hyun, H. J., Ichizawa, S., Igaki, T., Igarashi, A., Igarashi, S., Igarashi, Y., Igonkina, O., Ikado, K., Ikeda, H., Ikeda, K., Ilic, J., Inami, K., Innes, W. R., Inoue, Y., Ishikawa, A., Ishino, H., Itagaki, K., Itami, S., Itoh, K., Ivanchenko, V. 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R., Kharakh, D., Kibayashi, A., Kichimi, H., Kiesling, C., Kikuchi, M., Kikutani, E., Kim, B. H., Kim, C. H., Kim, D. W., Kim, H., Kim, H. J., Kim, H. O., Kim, H. W., Kim, J. B., Kim, J. H., Kim, K. T., Kim, M. J., Kim, P., Kim, S. K., Kim, S. M., Kim, T. H., Kim, Y. I., Kim, Y. J., King, G. J., Kinoshita, K., Kirk, A., Kirkby, D., Kitayama, I., Klemetti, M., Klose, V., Klucar, J., Knecht, N. S., Knoepfel, K. J., Knowles, D. J., Ko, B. R., Kobayashi, N., Kobayashi, S., Kobayashi, T., Kobel, M. J., Koblitz, S., Koch, H., Kocian, M. L., Kodyš, P., Koeneke, K., Kofler, R., Koike, S., Koishi, S., Koiso, H., Kolb, J. A., Kolya, S. D., Kondo, Y., Konishi, H., Koppenburg, P., Koptchev, V. B., Kordich, T. M. B., Korol, A. A., Korotushenko, K., Korpar, S., Kouzes, R. T., Kovalskyi, D., Kowalewski, R., Kozakai, Y., Kozanecki, W., Kral, J. F., Krasnykh, A., Krause, R., Kravchenko, E. 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M., Zhulanov, V., Ziegler, T., Ziegler, V., Zioulas, G., Zisman, M., Zito, M., Zürcher, D., Zwahlen, N., Zyukova, O., Živko, T., and Žontar, D.
Subjects: High Energy Physics - Experiment, High Energy Physics - Phenomenology
Abstract: This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C. Please note that version 3 on the archive is the auxiliary version of the Physics of the B Factories book. This uses the notation alpha, beta, gamma for the angles of the Unitarity Triangle. The nominal version uses the notation phi_1, phi_2 and phi_3. Please cite this work as Eur. Phys. J. C74 (2014) 3026., Comment: 928 pages, version 3 (arXiv:1406.6311v3) corresponds to the alpha, beta, gamma version of the book, the other versions use the phi1, phi2, phi3 notation
Published: 2014
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136. TiO2 Nanoparticles Caused DNA Damage in Lung and Extra-Pulmonary Organs Through ROS-Activated FOXO3a Signaling Pathway After Intratracheal Administration in Rats

Author: Han B, Pei Z, Shi L, Wang Q, Li C, Zhang B, Su X, Zhang N, Zhou L, Zhao B, Niu Y, and Zhang R
Subjects: nano-tio2, dna damage, pi3k/akt/foxo3a signaling pathway, dna repair，gadd45α/chk2/ xrcc1 signaling pathway, Medicine (General), R5-920
Abstract: Bin Han1 ,* Zijie Pei2 ,* Lei Shi,3 Qian Wang,4 Chen Li,1 Boyuan Zhang,1 Xuan Su,1 Ning Zhang,1 Lixiao Zhou,1 Bo Zhao,5 Yujie Niu,3,6 Rong Zhang1,6 1Department of Toxicology, Hebei Medical University, Shijiazhuang 050017, Hebei, People’s Republic of China; 2Department of Pathology, Medical School, China Three Gorge University, Yichang 443002, People’s Republic of China; 3Occupational Health and Environmental Health, Hebei Medical University, Shijiazhuang 050017, Hebei, People’s Republic of China; 4Experimental Center, Hebei Medical University, Shijiazhuang 050017, Hebei, People’s Republic of China; 5Department of Laboratory Diagnosis, Hebei Medical University, Shijiazhuang 050017, Hebei, People’s Republic of China; 6Hebei Key Laboratory of Environment and Human Health, Hebei Medical University, Shijiazhuang 050017, Hebei, People’s Republic of China*These authors contributed equally to this workCorrespondence: Rong ZhangDepartment of Toxicology, Hebei Medical University, 361 Zhongshan East Road, Shijiazhuang, Hebei 050017, People’s Republic of ChinaFax +86-311-86265605Email rongzhang@hebmu.edu.cnIntroduction: Because of the increased production and application of manufactured Nano-TiO2 in the past several years, it is important to investigate its potential hazards. TiO2 is classified by IARC as a possible human carcinogen; however, the potential mechanism of carcinogenesis has not been studied clearly. The present study aimed to investigate the mechanism of DNA damage in rat lung and extra-pulmonary organs caused by TiO2nanoparticles.Methods: In the present study, SD rats were exposed to Nano-TiO2 by intratracheal injection at a dose of 0, 0.2, or 1 g/kg body weight. The titanium levels in tissues were detected by ICP-MS. Western blot was used to detect the protein expression levels. The DNA damage and oxidative stress were detected by comet assay and ROS, MDA, SOD, and GSH-Px levels, respectively.Results: The titanium levels of the 1 g/kg group on day-3 and day-7 were significantly increased in liver and kidney as well as significantly decreased in lung compared to day-1. ROS and MDA levels were statistically increased, whereas SOD and GSH-Px levels were statistically decreased in tissues of rats in dose-dependent manners after Nano-TiO2 treatment. PI3K, p-AKT/AKT, and p-FOXO3a/FOXO3a in lung, liver, and kidney activated in dose-dependent manners. The levels of DNA damage in liver, kidney, and lung in each Nano-TiO2 treatment group were significantly increased and could not recover within 7 days. GADD45α, ChK2, and XRCC1 in liver, kidney, and lung of rats exposed to Nano-TiO2 statistically increased, which triggered DNA repair.Conclusion: This work demonstrated that Ti could deposit in lung and enter extra-pulmonary organs of rats and cause oxidative stress, then trigger DNA damage through activating the PI3K-AKT-FOXO3a pathway and then promoting GADD45α, ChK2, and XRCC1 to process the DNA repair.Keywords: Nano-TiO2, DNA damage, PI3K/AKT/FOXO3a signaling pathway, DNA repair, GADD45α/ChK2/XRCC1 signaling pathway
Published: 2020

137. CircHIPK3 Promotes Clear Cell Renal Cell Carcinoma (ccRCC) Cells Proliferation and Metastasis via Altering of miR-508-3p/CXCL13 Signal

Author: Han B, Shaolong E, Luan L, Li N, and Liu X
Subjects: circhipk3, mir-508-3p, cxcl13, proliferation, metastasis, ccrcc, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Bin Han,1 E Shaolong,1 Lan Luan,2 Nanyang Li,2 Xuefeng Liu1 1Department of Urology, Shengjing Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Pathology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, People’s Republic of ChinaCorrespondence: Xuefeng LiuDepartment of Urology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, People’s Republic of ChinaEmail xuefengliu78@163.comIntroduction: Accumulating evidence has demonstrated that circular RNAs (circRNAs) play a key role in the tumorigenesis of various types of cancers, including clear cell renal cell carcinoma (ccRCC).Materials and Methods: Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of circRNA homeodomain interacting protein kinase 3 (circHIPK3) and microRNAs (miRNAs), including miR-508-3p. The clinical measurement of circHIPK3 was evaluated by Kaplan–Meier survival analysis and receiver operating characteristic analysis. Cell Counting Kit-8 and Transwell chamber assays were performed to determine the changes in the proliferative and metastatic ability of A498 and 786-O cells. C-X-C motif chemokine ligand 13 (CXCL13) protein expression was detected by Western blot analysis. The targeted binding effect between miR-508-3p and circHIPK3 or CXCL13 was confirmed by constructed luciferase and RNA immunoprecipitation (RIP) assays, respectively. Fluorescence in situ hybridization (FISH) assay was used to measure the subcellular localization of circHIPK3 and miR-508-3p.Results: It was found that circHIPK3 was markedly upregulated in ccRCC tissue and cell lines, and circHIPK3-upregulation was closely correlated with poor clinicopathological features in patients with ccRCC. It was found that both miR-508-3p and circHIPK3 were localized in the cytoplasm of ccRCC cells. The up- and downregulation of circHIPK3 positively regulated ccRCC cell proliferation and metastasis, and this regulatory effect was reversed by miR-508-3p. Through luciferase and RIP assays, it was confirmed that circHIPK3 could interacted with miR-508-3p. Furthermore, it was revealed that CXCL13, which was negatively correlated with miR-508-3p, was upregulated in ccRCC. It was also shown that CXCL13 was a downstream target of miR-508-3p. miR-508-3p suppressed ccRCC cell proliferation and metastasis by targeting CXCL13. Lastly, it was demonstrated that circHIPK3 promoted CXCL13 to facilitate ccRCC cell proliferation and metastasis by decoying miR-508-3p.Conclusion: In brief, the results of the present study showed that circHIPK3 promoted ccRCC cell proliferation and metastasis by altering miR-5083p/CXCL13 signaling. The present findings might provide a novel target for the molecular treatment of ccRCC.Keywords: circHIPK3, miR-508-3p, CXCL13, proliferation, metastasis, ccRCC
Published: 2020

138. Expression Level of Wnt5a Was Related to the Therapeutic Effects of First-Generation EGFR-TKIs

Author: Zhang H, Yang X, Hu F, Li C, Xu J, Nie W, Shen Y, Lou Y, Han B, Zhong H, and Zhang X
Subjects: tyrosine-kinase inhibitors, wnt5a, epidermal growth factor receptor mutation, therapeutic effect, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Hai Zhang,1,* Xiaohua Yang,2,* Fang Hu,1,* Changhui Li,1 Jianlin Xu,1 Wei Nie,1 Yinchen Shen,1 Yuqing Lou,1 Baohui Han,1 Hua Zhong,1 Xueyan Zhang1 1Department of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, People’s Republic of China; 2Central Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xueyan Zhang; Hua ZhongDepartment of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, People’s Republic of ChinaTel +86 18017321319; +86 13818200560Fax +86-021-62821990Email zxychest@163.com; eddiedong8@hotmail.comBackground and Objective: The first-generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have shown significant therapeutic effects on patients harboring sensitive EGFR mutations, while the mechanisms related to drug resistance have still remained elusive. This study aimed to indicate the relationship between the expression level of Wnt5a with therapeutic effects of first-generation EGFR-TKIs on lung adenocarcinoma patients harboring sensitive EGFR mutations.Methods: The medical records of 75 lung adenocarcinoma patients harboring sensitive EGFR mutations, who were admitted to our hospital and received first-generation EGFR-TKIs from June 1, 2010 to December 31, 2016, were analyzed. According to the efficacy of first-generation EGFR-TKIs, patients were divided into ineffective groups (progression-free survival (PFS) < 5 months) and effective groups (PFS > 26 months). Immunofluorescence staining, immunohistochemical staining and reverse transcription polymerase chain reaction (RT-PCR) methods were utilized to detect the expression level of Wnt5a in the two groups.Results: Among 75 patients, 36 patients were sensitive to first-generation EGFR-TKIs (effective group) and 39 patients were resistant to first-generation EGFR-TKIs (ineffective group). The location of Wnt5a was detected by immunofluorescence staining. Immunohistochemical staining demonstrated that the expression level of Wnt5a in the ineffective group was significantly higher than that in the effective group (P=0.0216). Besides, results of RT-PCR showed that the relative expression level of Wnt5a was remarkably higher in the ineffective group than that in the effective group (P=0.0135).Conclusion: The expression level of Wnt5a was found to be associated with therapeutic effects of first-generation EGFR-TKIs in lung adenocarcinoma patients harboring sensitive EGFR mutations.Keywords: tyrosine-kinase inhibitors, Wnt5a, epidermal growth factor receptor mutation, therapeutic effect
Published: 2020

139. Tyrosine Kinase Inhibitor-Related Hepatotoxicity in Patients with Advanced Lung Adenocarcinoma: A Real-World Retrospective Study

Author: Qian J, Zhang X, Zhang B, Yan B, Wang L, Gu P, Wang W, Wang H, and Han B
Subjects: lung adenocarcinoma, hepatotoxicity, tyrosine kinase inhibitor, gefitinib, erlotinib, icotinib, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Jie Qian,1,2,* Xueyan Zhang,2,* Bo Zhang,2 Bo Yan,2 Lin Wang,3 Ping Gu,2 Weimin Wang,2 Huimin Wang,2 Baohui Han2 1Department of Emergency Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, People’s Republic of China; 2Department of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, People’s Republic of China; 3Department of Laboratory Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, People’s Republic of China*These authors contributed equally to this workCorrespondence: Baohui HanDepartment of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 # West Huaihai Road, Shanghai 230030, People’s Republic of ChinaTel +86 21 62821990 ext.1421Fax +86 21 32260806Email 18930858216@163.comPurpose: Hepatic injury is a common side effect following tyrosine kinase inhibitor (TKI) therapy and our understanding usually comes from clinical trials. In this retrospective study, we aimed to investigate the characteristics, risk factors and regimen-related differences of epidermal growth factor receptor (EGFR)-TKI-related hepatic toxicity in patients with advanced lung adenocarcinoma (LAD).Patients and Methods: Liver function tests were documented in 424 patients admitted into the Shanghai Chest Hospital between January 2014 and December 2016 with advanced (IIIB/IV) LAD who received first-line gefitinib, erlotinib or icotinib. Hepatotoxicity was graded according to the Common Terminology Criteria for Adverse Events (CTCAE), version 4.0. The clinical spectrum and onset time of hepatic injury were evaluated. The risk factors of hepatic dysfunction were determined using a logistic regression analysis.Results: A total of 87 (20.5%) patients experienced hepatotoxicity and 5.7% were of grade 3/4 liver dysfunction. The median onset time of hepatotoxicity was 7 weeks. Presence of hepatitis virus (HR: 2.593, 95% CI: 1.090– 6.170, P=0.031) and pretreatment liver impairment (HR: 3.460, 95% CI: 1.746– 6.855, P< 0.001) were risk factors associated with increased risk of hepatotoxicity. Gefitinib (HR: 1.872, 95% CI: 1.028– 3.412, P=0.040) and erlotinib (HR: 3.578, 95% CI: 1.683– 7.609, P=0.001) had increased risk of hepatotoxicity compared to icotinib.Conclusion: The different toxic profile of EGFR-TKIs should be taken into account in the choice of treatment based on the patients’ comorbidity.Keywords: lung adenocarcinoma, hepatotoxicity, tyrosine kinase inhibitor, gefitinib, erlotinib, icotinib
Published: 2020

140. Effect and Mechanism of miR-26a-5p on Proliferation and Apoptosis of Hepatocellular Carcinoma Cells

Author: Zhu WJ, Yan Y, Zhang JW, Tang YD, and Han B
Subjects: mir-26a-5p, hepatocellular carcinoma cells, proliferation, apoptosis, mechanism research, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Wen-Jing Zhu,1 Ying Yan,2 Jiu-Wei Zhang,1 Yan-Dong Tang,3 Bo Han4 1Abdominal Ultrasonic Department, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, People’s Republic of China; 2Oncology Department, The First Hospital of Harbin, Harbin, Heilongjiang Province, People’s Republic of China; 3Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang Province, People’s Republic of China; 4Oncology Department, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, People’s Republic of ChinaCorrespondence: Bo HanOncology Department, The First Affiliated Hospital of Harbin Medical University, 23 Post Street, Harbin 150001, Heilongjiang Province, People’s Republic of ChinaEmail hanbo1964@163.comAim: This study aimed to investigate the effect and mechanism of miR-26a-5p on proliferation and apoptosis of hepatocellular carcinoma (HCC) cells.Methods: RT-PCR was used to analyze the expression of miR-26a-5p in HCC cells and its targeted gene HMGA2 mRNA determined by biological information prediction. The rate of proliferation, invasion, apoptosis, and expression levels of related proteins of HCC cells overexpressing miR-26a-5p or those after knocking down HMGA2 expression were detected by MTT, invasion and apoptosis rate tests. Moreover, the apoptosis-promoting protein bax was upregulated and the anti-apoptosis-related protein Bcl-2 was downregulated.Results: RT-qPCR results showed that the level of miR-26a-5p was downregulated in HCC tissues and cells, and the expression of HMGA2 was upregulated; besides, the expression of miR-26a-5p and HMGA2 was negatively correlated; miR-26a-5p was correlated with tumor diameter, differentiation degree, TNM staging and lymph node metastasis. Cell tests confirmed that miR-26a-5p functioned in tumor suppression, including inhibiting cell proliferation and invasion in two hepatocellular carcinoma cell lines and promoting apoptosis. Bioinformatics prediction and subsequent experiments proved that HMGA2 was the direct target of miR-26a-5p; moreover, after knocking down HMGA2 expression in HCC cells, cell proliferation and invasion ability were significantly inhibited, and apoptosis rate increased significantly.Conclusion: miR-26a-5p can inhibit the proliferation and invasion of HCC cells and promote their apoptosis by directly targeting HMGA2. Abnormal decrease of miR-26a-5p and increase of its target HMGA2 are important factors that may participate in the occurrence and development of HCC. miR-26a-5p may be a new potential target for its treatment.Keywords: miR-26a-5p, hepatocellular carcinoma cells, proliferation, apoptosis, mechanism research
Published: 2020

141. Preparation, Characterization, and Pharmacokinetic Study of a Novel Long-Acting Targeted Paclitaxel Liposome with Antitumor Activity

Author: Han B, Yang Y, Chen J, Tang H, Sun Y, Zhang Z, Wang Z, Li Y, Luan X, Li Q, Ren Z, Zhou X, Cong D, Liu Z, Meng Q, Sun F, and Pei J
Subjects: breast cancer, estrogen receptors, paclitaxel, long-acting liposomes, targeted drug delivery, Medicine (General), R5-920
Abstract: Bing Han,1,* Yue Yang,1,2,* Jinglin Chen,1 Huan Tang,1 Yuxin Sun,1 Zheng Zhang,1 Zeng Wang,1 Yan Li,1 Yao Li,1 Xue Luan,1 Qianwen Li,1 Zhihui Ren,1 Xiaowei Zhou,1 Dengli Cong,1 Zhiyi Liu,1 Qin Meng,1 Fei Sun,1 Jin Pei1 1Department of Biopharmacy, School of Pharmaceutical Sciences, Jilin University, ChangChun, People’s Republic of China; 2Department of Pharmacy, Ministry of Health Service, Chinese PLA General Hospital, Beijing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jin Pei Tel +86 431 85619725Email peijin@jlu.edu.cnBackground: Breast cancer is the leading cause of cancer death in women. Chemotherapy to inhibit the proliferation of cancer cells is considered to be the most important therapeutic strategy. The development of long-circulating PEG and targeting liposomes is a major advance in drug delivery. However, the techniques used in liposome preparation mainly involve conventional liposomes, which have a short half-life, high concentrations in the liver and spleen reticuloendothelial system, and no active targeting.Methods: Four kinds of paclitaxel liposomes were prepared and characterized by various analytical techniques. The long-term targeting effect of liposomes was verified by fluorescence detection methods in vivo and in vitro. Pharmacokinetic and acute toxicity tests were conducted in ICR mice to evaluate the safety of different paclitaxel preparations. The antitumor activity of ES-SSL-PTX was investigated in detail using in vitro and in vivo human breast cancer MCF-7 cell models.Results: ER-targeting liposomes had a particle size of 137.93± 1.22 nm and an acceptable encapsulation efficiency of 88.07± 1.25%. The liposome preparation is best stored at 4°C, and is stable for up to 48 hrs. Cytotoxicity test on MCF-7 cells demonstrated the stronger cytotoxic activity of liposomes in comparison to free paclitaxel. We used the near-infrared fluorescence imaging technique to confirm that ES-SSL-PTX was effectively targeted and could quickly and specifically identify the tumor site. Pharmacokinetics and acute toxicity in vivo experiments were carried out. The results showed that ES-SSL-PTX could significantly prolong the half-life of the drug, increase its circulation time in vivo, improve its bioavailability and reduce its toxicity and side effects. ES-SSL-PTX can significantly improve the pharmacokinetic properties of paclitaxel, avoid allergic reaction of the original solvent, increase antitumor efficacy and reduce drug toxicity and side effects.Conclusion: ES-SSL-PTX has great potential for improving the treatment of breast cancer, thereby improving patient prognosis and quality of life.Keywords: breast cancer, estrogen receptors, paclitaxel, long-acting liposomes, targeted drug delivery
Published: 2020

142. Experimental and Numerical Study of the Drying Process of a Consolidated Clay Soil

Author: Wen-Qing Cheng, Han-B ing Bian, Qian-Feng Gao, and Mahdia Hattab
Subjects: Engineering (General). Civil engineering (General), TA1-2040
Abstract: The clay soil is composed of solid skeleton and porous and can be studied in the framework of porous media. During the drying process, the initial saturated clay soil deforms mainly due to the changes of water content and capillary pressure. With the further increase in capillary pressure, the soil cracks. In fact, the deformation and the stress in clay soil are tightly related with the water content and capillary pressure. Therefore, it is of great interest to understand the changes in capillary pressure and water content within the clay soil during the drying process. However, it is difficult to obtain these field variables by experiments alone. Therefore, the numerical simulation could be good choice for deeper understanding of the dry process in clay soil. In current research, the combined numerical simulation and laboratory experiments research are conducted; the numerical results are compared with the laboratory observation. This research is the basis for the further study of the cracking process of clay soil due to drying.
Published: 2022
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143. Tunable exciton-polaritons emerging from WS2 monolayer excitons in a photonic lattice at room temperature

Author: Lackner, L., Dusel, M., Egorov, O. A., Han, B., Knopf, H., Eilenberger, F., Schröder, S., Watanabe, K., Taniguchi, T., Tongay, S., Anton-Solanas, C., Höfling, S., and Schneider, C.
Published: 2021
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144. Mapping the benefits of nature in cities with the InVEST software

Author: Hamel, P., Guerry, A. D., Polasky, S., Han, B., Douglass, J. A., Hamann, M., Janke, B., Kuiper, J. J., Levrel, H., Liu, H., Lonsdorf, E., McDonald, R. I., Nootenboom, C., Ouyang, Z., Remme, R. P., Sharp, R. P., Tardieu, L., Viguié, V., Xu, D., Zheng, H., and Daily, G. C.
Published: 2021
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145. Decoding accelerometry for classification and prediction of critically ill patients with severe brain injury

Author: Bhattacharyay, Shubhayu, Rattray, John, Wang, Matthew, Dziedzic, Peter H., Calvillo, Eusebia, Kim, Han B., Joshi, Eshan, Kudela, Pawel, Etienne-Cummings, Ralph, and Stevens, Robert D.
Published: 2021
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146. Long Non-Coding RNA TTN-AS1 Promotes the Proliferation and Invasion of Colorectal Cancer Cells by Activating miR-497-Mediated PI3K/Akt/mTOR Signaling

Author: Cui Z, Han B, Wang X, Li Z, Wang J, and Lv Y
Subjects: colorectal cancer, long non-coding rna ttn-as1, epithelial-mesenchymal transition, microrna-497, pi3k/akt/mtor signaling, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Zhenhua Cui,1 Bingbing Han,2 Xianren Wang,1 Zhiwen Li,1 Jianxin Wang,1 Yanfeng Lv1 1Department of Colorectal & Anal Surgery, The Second Hospital of Shandong University, Jinan 250033, People’s Republic of China; 2Microcirculation Laboratory, Shandong University of Traditional Chinese Medicine, Jinan, 250014, People’s Republic of ChinaCorrespondence: Yanfeng LvDepartment of Colorectal & Anal Surgery, The Second Hospital of Shandong University, No. 247 BeiYuan Street, Jinan 250033, People’s Republic of ChinaEmail ttdpilsxpsle11@163.comIntroduction: Long non-coding RNAs (lncRNAs) have obtained increasing attention due to their regulatory functions in many cancers. This work aimed to investigate the functional roles of lncRNA TTN-AS1 in colorectal cancer (CRC) and to explore the underlying mechanisms.Methods: The expression profiles of TTN-AS1 and miR-497 in CRC tissues and cell lines were determined by RT-qPCR analysis. MTT assay, transwell assay, western blot analysis, and xenograft tumors in nude mice were employed to analyze the effects of TTN-AS1 on the proliferation, migration, invasion, EMT, and in vivo tumorigenesis of CRC cells. Bioinformatics analysis and dual-luciferase reporter assay determined the direct binding relation between TTN-AS1 and miR-497 in CRC.Results: We observed a significant increase of TTN-AS1 expression level in CRC tissues and cell lines compared with normal counterparts. High expression of TTN-AS1 predicted a poor prognosis and was correlated with aggressive clinicopathological characteristics in CRC patients. Functionally, gain- and loss-of-function studies indicated that TTN-AS1 knockdown suppressed the proliferation, migration, invasion and epithelial–mesenchymal transition of CRC cells in vitro, whereas TTN-AS1 overexpression showed the complete opposite effects. Mechanistically, we found that TTN-AS1 could directly interact with miR-497, and co-transfection with miR-497 mimics blocked the activation of PI3K/Akt/mTOR signaling, and reversed the effects of TTN-AS1 overexpression in CRC cells.Conclusion: To conclude, our findings provide novel insight into CRC tumorigenesis and indicate that TTN-AS1 may serve as a potential therapeutic target for CRC treatment.Keywords: colorectal cancer, long non-coding RNA TTN-AS1, epithelial-mesenchymal transition, microRNA-497, PI3K/Akt/mTOR signaling
Published: 2019

147. miR-449a Is Related to Short-Term Recurrence of Hepatocellular Carcinoma and Inhibits Migration and Invasion by Targeting Notch1

Author: Han B, Huang J, Yang Z, Zhang J, Wang X, Xu N, Meng H, Wu J, Huang Q, Yang X, Shen R, and Sun C
Subjects: signal pathway, microrna, epithelial-mesenchymal transition, bioinformatics, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Bing Han,1,2,* Jiawei Huang,3,* Zhenjie Yang,1 Jiaqi Zhang,3 Xiaomin Wang,3 Ning Xu,3 Haining Meng,3 Junyu Wu,3 Qiao Huang,3 Xi Yang,3 Ruowu Shen,3 Chuandong Sun1 1Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, Qingdao City 266003, Shandong Province, People’s Republic of China; 2Asian Liver Center, Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA; 3Department of Special Medicine, School of Basic Medical College, Qingdao University, Qingdao City 266021, Shandong Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chuandong SunDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao City 266003, Shandong Province, People’s Republic of ChinaTel +86 18661802672Email sunchuandong@hotmail.comRuowu ShenDepartment of Special Medicine, School of Basic Medical College, Qingdao University, Qingdao City 266021, Shandong Province, People’s Republic of ChinaTel +86 18661785993Email shenruowu@aliyun.comPurpose: To explore the effect of miR-449a inhibits migration and invasion by targeting Notch1 and regulating epithelial–mesenchymal transition (EMT) in hepatocellular carcinoma (HCC), and further study on the molecular mechanism.Patients and methods: The expression of miR-449a and Notch1 in HCC cells and tissues was detected by qRT-PCR. The HCC cell line HCCLM3 and SMMC-7721 were transfected with miR-449a. The invasion and migration of HCC cell lines were detected by transwell assay and wound healing assay. The Notch pathway and EMT related protein were detected with Western Blotting. The specific binding site of mir-449a on notch1 gene was detected by luciferase assay.Results: We found the expression of miR-449a was related to short-term recurrence of hepatocellular carcinoma after hepatectomy and acted as independent risk factors of DFS and OS. The expression of miR-449a decreased in tumor tissues and HCC cell lines, but the expression of Notch1 increased. The overexpressed miR-449a promoted the invasiveness in vitro by regulating EMT via Notch pathway. Mechanically, miR-449a inhibited the translation of Notch1 protein by binding to 3ʹ UTR of its mRNA directly.Conclusion: miR-449a is short-term recurrence-related miRNA and inhibits the invasion and metastasis ability of HCC cells by regulating EMT via Notch pathway. miR-449a may be a new effective therapeutic target for HCC.Keywords: signal pathway, microRNA, epithelial-mesenchymal transition, bioinformatics
Published: 2019

148. High Inflammatory Factor Grading Predicts Poor Disease-Free Survival in AJCC Stage I-II Hepatocellular Carcinoma Patients After R0 Resection

Author: Zhang M, Chua MS, Hu J, Li H, Zhang S, Wu L, and Han B
Subjects: hepatocellular carcinoma, recurrence, prognosis, inflammation, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Mao Zhang,1 Mei-Sze Chua,2 Jie Hu,3 Haoran Li,1 Shun Zhang,1 Liqun Wu,1 Bing Han1 1Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People’s Republic of China; 2Asian Liver Center, Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA; 3Department of General Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan, People’s Republic of ChinaCorrespondence: Bing Han; Liqun WuDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao, Shandong 266003, People’s Republic of ChinaTel +86-186 6180 8308Fax +86-532-8291 1323Email wfkevinhan@163.com; wulq581031@163.comPurpose: In this study, we established the inflammatory factor grade system (IFGs) based on the hepatocellular carcinoma (HCC) microenvironment to investigate the role of inflammatory factor grade (IFG) in predicting the prognosis of patients with American Joint Committee on Cancer (AJCC) stage I-II.Patients and methods: We enrolled 87 HCC patients with AJCC stage I-II who underwent R0 resection between 2000 and 2012 and had paraffin-embedded specimens. Immunohistochemistry (IHC) was performed to investigate the expression of 12 inflammatory factors and then to establish the IFGs (grade A or B) based on the IHC data. Subsequently, Kaplan-Meier and Cox univariate/multivariate survival analyses were performed to examine the potential prognostic significance.Results: Higher IFG (IFG-B) is significantly associated with greater tumor size (P=0.037), and IFG-B predicts a worse disease-free survival (DFS, P
Published: 2019

149. Investigation of cyclic pile-sand interface weakening mechanism based on large-scale CNS cyclic direct shear tests

Author: Liu, J.W., Cui, L., Zhu, N., Han, B., and Liu, J.
Published: 2019
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150. Sleep and hypertension

Author: Han, B., Chen, W. Z., Li, Y. C., Chen, J., and Zeng, Z. Q.
Published: 2020
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