Academic literature on the topic 'Ji bing'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Ji bing.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Ji bing"
1
WATANABE, Yukie. "Bing and Ji in the Mohe Zhiguan." Journal of Indian and Buddhist Studies (Indogaku Bukkyogaku Kenkyu) 61, no. 1 (2012): 499–94. http://dx.doi.org/10.4259/ibk.61.1_499.
Full text
2
Xu, Bing, Haoyu Lu, Donglei Zhao, Wei Wang, and Hong Ji. "Diversity of macrofungi in Yushan, Jiangsu, China." Mycotaxon 134, no. 3 (October 2, 2019): 581. http://dx.doi.org/10.5248/134.581.
Full textAbstract:
Mycotaxon is pleased to add a new annotated species distribution list to our 133 previously posted free-access fungae. The 9-page "Diversity of macrofungi in Yushan, Jiangsu, China" by Bing Xu, Haoyu Lu, Donglei Zhao, Wei Wang, and Hong Ji may be downloaded from our website via http://www.mycotaxon.com/mycobiota/index.html
3
Ji, Xiang, Huanping Li, Gang Wu, Qiguo Zhang, Xiaolin He, Yanpeng Wu, Bing Zong, et al. "Abstract 6050: Targeting KRAS G12D mutant tumors with the PROTAC degrader RP03707." Cancer Research 84, no. 6_Supplement (March 22, 2024): 6050. http://dx.doi.org/10.1158/1538-7445.am2024-6050.
Full textAbstract:
Abstract RAS oncogene mutations are prevalent in approximately 19% of cancer patients, with the most frequent alteration occurring in codon 12 of the KRAS gene, resulting in a variety of G12X oncoproteins. Recent advances in drug discovery have yielded several KRAS G12C inhibitors currently in clinical use, benefiting a subset of patients. However, addressing the high-prevalence G12D mutation remains a substantial unmet medical need. Targeted protein degradation using PROTAC molecules offers a promising approach for treating KRAS G12D-associated tumors, potentially providing superior efficacy and mitigating the development of resistance, a challenge frequently observed with KRAS G12C inhibitors in clinical settings. In the present study, we report a PROTAC compound RP03707 that efficiently induces the degradation of the KRAS G12D mutant protein and inhibits tumor growth. Treatment of AsPc-1 cells with RP03707 results in significant degradation of the KRAS G12D protein, with a DC50 value in the sub-nanomolar range. Within 24 hours, the compound eliminates over 90% of G12D proteins and effectively suppresses downstream cellular MAPK signaling. Additional in vitro experiments demonstrate that RP03707 inhibits cell proliferation in multiple KRAS G12D mutant cell lines, surpassing the anti-tumor efficacy of enzyme inhibitors. In a mouse GP2d xenograft tumor model, a single intravenous administration of RP03707 at 10 mpk results in excellent compound penetration and retention in tumor tissues, followed by 90% reduction of G12D protein levels for 7 days. Profound inhibition of tumor growth is observed not only in mouse GP2d xenograft but also in other mouse KRAS G12D tumor models, even when the compound is administered in low and infrequent doses. Moreover, RP03707 exhibits high selectivity for degrading the KRAS G12D protein and possesses favorable drug-like properties. RP03707, therefore, meets the criteria for advancing into drug development and represents a valuable therapeutic option for treating KRAS G12D-associated tumors. Citation Format: Xiang Ji, Huanping Li, Gang Wu, Qiguo Zhang, Xiaolin He, Yanpeng Wu, Bing Zong, Xiaojin Xu, Chao Liang, Beibei Wang, Yuwei Zhang, Qingyao Hu, Jiaxin Zhou, Weihui Guo, Bing Bai, Lin Wang, Jinchao Ai, Leduo Zhang, Honggui Zhou, Shihao Sun, Yijie Wang, Youhong Wang, Qiming Fan, Dawei Chen, Tianlun Zhou, Jiasheng Lu. Targeting KRAS G12D mutant tumors with the PROTAC degrader RP03707 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 6050.
4
Minehan, Bridie Andrews. "Zhang Daqing. Zhongguo jin dai ji bing she hui shi [A Social History of Diseases in Modern China (1912–1937)]. (Zhongguo jin xian dai ke xue ji shu shi yan jiu cong shu.) iv + 229 pp., illus., tables, bibl., index. Jinan: Shandong jiao yu chu ban she [Shandong Education Press], 2006. (Paper.)." Isis 100, no. 1 (March 2009): 192–93. http://dx.doi.org/10.1086/599688.
Full text
5
Bao, Wei, Ying-Ji Li, Jin-Fan Gu, Cong-Lin Yang, Yi-Da Wang, Tie-Jun Bing, and Wen-Jen Yu. "Abstract 107: Application of MSD on the lung cancer associated idiopathic pulmonary fibrosis." Cancer Research 84, no. 6_Supplement (March 22, 2024): 107. http://dx.doi.org/10.1158/1538-7445.am2024-107.
Full textAbstract:
Abstract Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible chronic disease that kill ten thousand of people in China every year. The risk of IPF is highly correlated with smoke, air pollution, dust, virus infection and aging. Average survival period of patients diagnosed as IPF is around 2.8 years which is less than several types of cancers, therefore, IPF is also thought to be a lung cancer-like disease. In the past few decades, many animal models were created to mimic human IPF, however, induction materials, animal species and strain differences, sex, physiology structure and progress of disease make the choice of IPF animal models selection more difficult. In addition, lack of strong evidence of cytokines biomarker detection hampered the discovery of anti-IPF drugs. Meso Scale Discovery (MSD) instrument is an efficient tool to high throughput analyze the lowest level of several cytokines and other biomarkers in the same time and was used to detect the bleomycin (BLM) induced mouse lung fibrosis. Meanwhile, animal sex and dose effects of BLM were also tested to define the proper mouse model for anti-IPF drugs development. Our results indicated that 0.6-0.8 mg/kg of intratracheal injection of single dose BLM is sufficient to create the IPF model without sex differences by examining the lung weight, lung ratio, soluble hydroxyproline, HE staining and mason staining. However, male mice were more resistant to the lethal effect of BLM due to the larger size or bodyweight. Using MSD detection, several mouse cytokines were measured simultaneously and showed that IFN-γ, IL-5, TNF-α, and IL-10 were increased in the IPF mouse model and were recovered after pirfenidone treatment at day 14 which mimics the cytokines profile in IPF patients. In summary, the MSD detection and pathological evaluation prove that male mouse treated with 0.8 mg/kg BLM through intratracheal injection is a suitable mouse model for the development of anti-IPF dugs. Citation Format: Wei Bao, Ying-Ji Li, Jin-Fan Gu, Cong-Lin Yang, Yi-Da Wang, Tie-Jun Bing, Wen-Jen Yu. Application of MSD on the lung cancer associated idiopathic pulmonary fibrosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 107.
6
Xu, Xin, Wilhelm G. Dirks, Hans G. Drexler, and Zhenbo Hu. "Small Molecular Modulators of Histone Demethylases Selectively Inhibits Growth of Hematopoietic Malignancies." Blood 132, Supplement 1 (November 29, 2018): 3941. http://dx.doi.org/10.1182/blood-2018-99-112376.
Full textAbstract:
Abstract Background: About 10% of acute leukemia (AL) patients harbor MLL-r(earrangements). MLLr acute myeloid leukemia (AML) mainly occurs in young-to-middle-aged adults whereas MLLr acute lymphoblastic leukemia (ALL) mainly occurs in patients younger than 1 year at diagnosis. AML with MLL fusion to MLLT3 via t(9;11)(p22;q23) predicts intermediate prognosis whereas MLL fusion to other partners predicts adverse prognosis. By contrast, in infants with ALL MLLr invariably confers poor prognosis. Much efforts have been made to identify and target proteins required for initiation and maintenance of MLLr AL, with an aim to improve the prognosis of this aggressive AL subtype. Multiple writers, erasers, and readers of histone post-translational modifications (PTMs) have been identified to be fundamental for the initiation and maintenance of MLLr AL. Small molecular inhibitors of some of these chromatin-associated proteins have been identified, such as EPZ004777 against DOT1L, JQ1 and I-BET151 against BRD4, and so on which are also under clinical trials for AL treatment. Among histone modification erasers essential for MLLr AL, JMJD1C and KDM4C that share Jumonji catalytic domain are fundamental for MLLr AL maintenance. Histone H3 lysine 9 (H3K9) demethylase JMJD1C is one of the most promising MLLr AL targets. Multiple independent studies identified JMJD1C as required for MLLr AML, RUNX1(AML1)/RUNX1T1(ETO) AML and even chronic myeloid leukemia and lymphoma cells but not normal hematopoiesis. KDM4C Is essential for Initiation and maintenance of MLLr AL transcriptional profiling of which is dependent on KDM4C. Moreover, pharmacological inhibition of KDM4C blocks leukemia development in syngeneic mouse model and human AML xenograft model. Although a large number of special inhibitors of histone demethylases have been developed, no special inhibitors against KDM3 family member like JMJD1C have been reported. Results: Here we focused on Jumonji domain that is responsible for enzymatic activities of histone demethylases for identifying potential small molecule modulators of histone demethylases. We selected Jumonji domain of histone H3 lysine (H3K9) demethylase JMJD1C with KDM4C as reference to screen for potential small molecular modulators from 149,519 natural products and 33,765 Chinese medicine components through virtual screening method. Although identified independently from each other, compound #4 and #12 both share a common structural backbone and surface plasmon resonance analysis showed that #4 and #12 bind to JMJD1C, KDM3 family member KDM3B, and KDM4 family member KDM4C with modest affinity. In vivo demethylation assay showed that #4 induces global increase of H3K9 methylation. In vitro demethylation assay showed that #4 is able to reverse H3K9 demethylation conferred by KDM3B and KDM4C. We thus named #4 and #12 as JI-4 and JI-12 (JI, Jumonji inhibitor). Cell proliferation and colony formation assays showed that JI-4 and JI-12 predominantly kill MLLr AL. To increase evidence, multiple similar compounds to JI-4 and JI-12 were tested for cell proliferation repression and JI-16 was found to show superior killing activities against hematopoietic malignant cells compared to JI-4 and JI-12. Mechanistically, JI-16 not only induces apoptosis but also differentiation of MLLr AL cells. Transcriptome analysis and quantitative PCR (QPCR) showed that JI-16 induced gene expression profiling is especially enriched in gene sets involved in metabolism. Conclusion: To sum up, we identified potential pan-inhibitors of the Jumonji domain of histone demethylases. Binding in-vivo is followed by selective killing of MLLr AL cells. Disclosures. No relevant conflicts of interest to declare. Disclosures No relevant conflicts of interest to declare.
7
Baykal, F., S. Erten, S. C. Güven, A. Kor, F. Eren, S. Neşelioğlu, B. Polat, et al. "AB1059 NETRIN-1 IN SPONDYLOARTHRITIS: A NOVEL MARKER TO PREDICT DISEASE ACTIVITY?" Annals of the Rheumatic Diseases 82, Suppl 1 (May 30, 2023): 1751.2–1751. http://dx.doi.org/10.1136/annrheumdis-2023-eular.6349.
Full textAbstract:
BackgroundNetrin-1 is a chemorepulsant and inhibits the migration of monocytes, neutrophils and lymphocytes by activation of its receptors. It has been revealed that netrin-1 can limit the inflammatory response, reduce tissue damage due to hypoxia and simultaneously suppress apoptosis. Due to this immune regulatory role, it has been hypothesized that netrin-1 can be used as a biomarker in rheumatic diseases.ObjectivesTo compare plasma netrin-1 levels in axial spondyloarthritis (SpA) patients with the healthy subjects and to evaluate its relationship with disease activity and other clinical and laboratory parameters.MethodsPatients with axial SpA between the ages of 18-65 who applied to Ankara City Hospital Rheumatology outpatient clinic between November 2021 and January 2022 were consecutively enrolled upon acceptance to participate. Pregnant patients, patients with systemic disease other than axial SpA and patients who were taking regular medication other than axial SpA treatment were excluded. A control group was formed from healthy volunteers with similar age and gender characteristics. In both groups, in addition to regular laboratory tests netrin-1 level was measured by an Enzyme Linked ImmunoSorbent Assay (ELISA) kit with an analytical unit of pg/mL (Elabscience, Texas, USA, Catalog No: E-EL-H2328; Lot No: GZWTKZ5SWK).ResultsA total of 60 axial SpA patients and 56 healthy controls were included in the study. There was no statistically significant difference between the groups in terms of age, gender andnetrin-1 levels between patients and controls (Table 1). Data regarding clinical characteristics, HLA-B27 positivity, acute phase reactants at the time of evaluation and disease activity scores of the axial SpA group was presented in Table 1. No significant differences were observed in netrin-1 levels in any comparison among all axial SpA patients, in ankylosing spondylitis (AS) and nonradiographic axial spondyloarthritis (nr-ax SpA) patient subgroups, and in healthy controls (all axial SpA vs control p=0,361, AS vs nr-axSpA p=0,790, AS vs control p=0,360, nr-axSpA vs control p=0,700). Netrin-1 levels had a significant positive correlation with BASDAI (r=0,301 p=0,032), ASDAS CRP (r=0,320 p=0,022), VAS pain (r=0,340 p=0,015).ConclusionOur results demonstrated a positive correlation between netrin-1 levels and disease activity in axial SpA patients, implying that netrin-1 may come to the forefront as a novel biomarker to predict disease activity in axial SpA.References[1]Tang Z, Xu C, Zhang G, Chen H. [Protect role of Netrin-1 in inflammatory response]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2016 Aug;28(8):756-60. Chinese. doi: 10.3760/cma.j.issn.2095- 4352.2016.08.020. PMID: 27434573.[2]Ranganathan PV, Jayakumar C, Mohamed R, Dong Z, Ramesh G. Netrin-1 regulates the inflammatory response of neutrophils and macrophages, and suppresses ischemic acute kidney injury by inhibiting COX-2-mediated PGE2 production. Kidney İnternational 2013;83(6):1087-1098.Table 1.Demographics of subject groups, clinical and laboratory characteristics of axial SpA patientsAxial SpA N=60Control N=56PAge, years, mean ± SD39,51 ± 10,8844,57 ± 13,870,057Gender, female, n (%)37 (53,6)32 (46,4)0,620Type of axial SpA, n (%) AS49 (81,66) Nr-ax SpA11 (18,33)HLA-B27 positivity, n (%)*22 (64,7)CRP, mg/L, mean ± SD8,09 ± 9,30ESR, mm/hour, years, mean ± SD13,4 ± 10,95Morning stiffness time, hours, mean ± SD1,6 ± 2,72VAS pain, mean ± SD4,11 ± 2,75BASDAI, mean ± SD3,00 ± 2,04ASDAS CRP, mean ± SD2,30 ± 1,04Serum Netrin-1, pg/mL, mean (min-max)74,436 (34,5-237,18)61,904 (35,85-175,33)0,361* Out of 34 patients with a HLA-B27 test result, SpA: spondyloarthritis, AS: ankylosing spondylitis, Nr-ax SpA: non-raidographic axial spondyloarthritis, HLA-b27: human leukocyte antigen B27, CRP: C-reactive protein, ESR: erythrocyte sedimentation rate, VAS: visual analogue scale, BASDAI: Bath Ankylosing Spondylitis Disease Activity Index, ASDAS CRP: Ankylosing Spondylitis Disease Activity Score CRPAcknowledgements:NIL.Disclosure of InterestsNone Declared.
8
Ghimire, Govinda, Archana Loganathan, Osama Awadallah, and Bilal El-Zahab. "Sulfurized Electrolyte Additives for Stable Lithium Metal Anodes." ECS Meeting Abstracts MA2022-02, no. 3 (October 9, 2022): 187. http://dx.doi.org/10.1149/ma2022-023187mtgabs.
Full textAbstract:
Researchers around the world are striving to develop new materials for energy-efficient and high energy density lithium-ion batteries [1]. Lithium metal with a theoretical specific capacity of 3860 mAh/g, low density (0.534 g/cm3), and the lowest potential (−3.040 V vs. standard hydrogen electrode) is consider the ultimate anode material for high specific energy batteries [2]. However, various issues remain to be address that hinder its use in commercial batteries, namely, cycling stability, Coulombic efficiency, and safety aspects associated with dendritic growth [3]. Inactive lithium, also known as “dead lithium,” originating from the dendrites that become separated from the surface over prolonged cycling contribute to anode capacity loss and require high negative to positive electrode capacity ratio (N/P). In addition, due to the extremely low standard redox potential of lithium, electrolytes readily react with the lithium metal surface even without any potential polarization. These reactions lead to the formation of mostly insoluble species in a layer often referred to as solid electrolyte interface, SEI. Ideally, the SEI layer is self-terminating; however, as fresh lithium gets exposed via dendritic growth, SEI formation continues. The steady and uncontrollable growth of SEI throughout the functional life of the battery leads to gradual resistant growth responsible for the capacity fade and eventual “death” of the battery. In previous art, alternative electrolytes, electrolyte additives, and artificial SEIs were studied [4] [5]. For example, the electrolyte additive lithium fluoride (LiF) was used in carbonate electrolytes and provided a strong protective layer that reduced side reactions and improved the life capacity of the battery [6]. Recently, 3-dimensional design of the anode’s current collector was shown to accommodate Li deposition resulting in suppressed SEI growth and volume expansion during cycling [7]. In the present work, we use sulfur-containing compounds as additives at a very low concentration (1 – 50 mM) in standard 1M LiPF6 EC:DMC (v:v = 1:1). Coin cells (2032) were assembled using lithium foil (100 mm thick), separator (Celgard), and NMC811 cathode (> 10 mg/cm2). Cells were first rested and activated at a slow rate then cycled at C/3 and 1C for charge and discharge respectively in prescribed voltage cutoff window. As shown in Figure 1, the sulfur-containing cell had more than 300 cycles before 90% capacity retention relative to the beginning of life (BOL) capacity. The sulfur-free control cell lasted less than 150 cycles above the 90% retention line. Electrochemical impedance spectroscopy (EIS) measurements for cycled cells showed lower interfacial resistance for cells with sulfur-containing additives compared to control cells. The reason for the improved cycle stability can be attributed to the stability afforded by the additives to the SEI layer. Figure 1: A comparison of cell performance between control (black) and sulfur-containing additive (green). The Red line indicates the 90% retention of the battery. References Yoshio, Masaki, Ralph J. Brodd, and Akiya Kozawa. Lithium-ion batteries. Vol. 1. New York: Springer, 2009. Liu, Bin, Ji-Guang Zhang, and Wu Xu. "Advancing lithium metal batteries." Joule2, no. 5 (2018): 833-845. Xiao, Jie, Qiuyan Li, Yujing Bi, Mei Cai, Bruce Dunn, Tobias Glossmann, Jun Liu et al. "Understanding and applying coulombic efficiency in lithium metal batteries." Nature Energy5, no. 8 (2020): 561-568. Tikekar, Mukul D., Snehashis Choudhury, Zhengyuan Tu, and Lynden A. Archer. "Design principles for electrolytes and interfaces for stable lithium-metal batteries." Nature Energy1, no. 9 (2016): 1-7. Wang, Qian, Chengkai Yang, Jijin Yang, Kai Wu, Cejun Hu, Jing Lu, Wen Liu, Xiaoming Sun, Jingyi Qiu, and Henghui Zhou. "Dendrite‐free lithium deposition via a superfilling mechanism for high‐performance Li‐metal batteries." Advanced Materials31, no. 41 (2019): 1903248. Choudhury, Snehashis. "Lithium fluoride additives for stable cycling of lithium batteries at high current densities." In Rational Design of Nanostructured Polymer Electrolytes and Solid–Liquid Interphases for Lithium Batteries, pp. 81-94. Springer, Cham, 2019. Yun, Qinbai, Yan‐Bing He, Wei Lv, Yan Zhao, Baohua Li, Feiyu Kang, and Quan‐Hong Yang. "Chemical dealloying derived 3D porous current collector for Li metal anodes." Advanced Materials28, no. 32 (2016): 6932-6939. Figure 1
9
Verdier, Maxime, Quentin Chesnais, Elodie Pirolles, Stéphane Blanc, and Martin Drucker. "The cauliflower mosaic virus transmission helper protein P2 modifies directly the probing behavior of the aphid vector Myzus persicae to facilitate transmission." PLOS Pathogens 19, no. 2 (February 6, 2023): e1011161. http://dx.doi.org/10.1371/journal.ppat.1011161.
Full textAbstract:
There is growing evidence that plant viruses manipulate their hosts and vectors in ways that increase transmission. However, to date only few viral components underlying these phenomena have been identified. Here we show that cauliflower mosaic virus (CaMV) protein P2 modifies the feeding behavior of its aphid vector. P2 is necessary for CaMV transmission because it mediates binding of virus particles to the aphid mouthparts. We compared aphid feeding behavior on plants infected with the wild-type CaMV strain B-JI or with a deletion mutant strain, B-JIΔP2, which does not produce P2. Only aphids probing B-JI infected plants doubled the number of test punctures during the first contact with the plant, indicating a role of P2. Membrane feeding assays with purified P2 and virus particles confirmed that these viral products alone are sufficient to cause the changes in aphid probing. The behavior modifications were not observed on plants infected with a CaMV mutant expressing P2Rev5, unable to bind to the mouthparts. These results are in favor of a virus manipulation, where attachment of P2 to a specific region in the aphid stylets–the acrostyle–exercises a direct effect on vector behavior at a crucial moment, the first vector contact with the infected plant, which is essential for virus acquisition.
10
Kim, Jeong-kook, A.-Ra Jeon, Jihyun Park, Ji Yea Choi, Ji Eun Park, Sun Kwang Song, Ji Hye Choi, et al. "Abstract 596: IOH-001, a novel CD47/PD-L1 bispecific antibody, enhances anti-tumor activity in solid tumors." Cancer Research 82, no. 12_Supplement (June 15, 2022): 596. http://dx.doi.org/10.1158/1538-7445.am2022-596.
Full textAbstract:
Abstract Background: The survived cancer cells after cytotoxic chemotherapy are known to promote immune evasion phenotype by increasing the expression of PD-L1 and CD47. Targeting of CD47 and PD-L1 is predicted to overcome immune evasion by coordinately restoring each innate and adaptive immunity. IOH-001, a CD47/PD-L1 dual-targeting bispecific antibody, has been shown to activate immune cells in tumor microenvironment by blocking PD-1/PD-L1 signals that inhibit cytotoxic T-cells, while also blocking interaction with CD47/SIRPa between cancer cells and macrophages. We have investigated whether IOH-001 inhibits tumor growth via co-targeting tumor cells or not. Methods: To assess the function of IOH-001, a series of in vitro functional assays including cell surface binding, antibody-dependent cellular cytotoxicity (ADCC), phagocytosis assays and mixed lymphocyte reaction (MLR) assay were performed compared with the parent antibody. In vivo efficacy of IOH-001 was tested in colon cancer mouse models with human genes KI. Results: IOH-001 has been shown to be bound strongly to various types of PD-L1/CD47-expressing cancer cells including the ones in solid and hematological cancers. In most cancer cells, IOH-001 was demonstrated to have a lower EC50 than the parental antibodies and to be bound in a dose-dependent manner as well. Interestingly, IOH-001 also has shown the selectivity to bind only to cancer cells even under the conditions of co-culturing RBC and cancer cells. IOH-001 has induced phagocytosis of cancer cells by human blood CD14+ monocyte-derived macrophages. Since IOH-001 is an IgG1 type antibody, ADCC and IFN-r expression have been increased compared with the parental antibodies. Consistent with the in vitro data, IOH-001 has more strongly suppressed tumor growth than the combination treatment of the parental antibodies in a dose-dependent manner in syngeneic animal models. Moreover, the tumor of the CR mouse has been identified not to be re-generated in the re-challenge model. Conclusion: IOH-001, dual-blockage of anti-CD47 and anti-PD-L1, has shown the benefits in treating some solid tumors. Bispecific antibody IOH-001 is more likely to work better in targeting tumor cells than the combination of anti-CD47 and anti-PD-L1. Preclinical efficacy results of IOH-001 provide a strong rationale for assessing therapeutic potential in clinical studies. Citation Format: Jeong-kook Kim, A-Ra Jeon, Jihyun Park, Ji Yea Choi, Ji Eun Park, Sun Kwang Song, Ji Hye Choi, Heewook Shin, Ji Hye Lee, Ji Hye Yun, Yoen Hee Ahn, Heung Tae Kim. IOH-001, a novel CD47/PD-L1 bispecific antibody, enhances anti-tumor activity in solid tumors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 596.
Dissertations / Theses on the topic "Ji bing"
1
Chen, Fangyang. "Xiao chuan bing yin bing ji tan tao ji huan jie qi zhi ben de duo yuan xing /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b19986300a.pdf.
Full text
2
Luo, Yusheng. ""Huangdi nei jing" dui shuai lao , lao nian bing de ren shi ji hou shi zhi fa zhan /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009598a.pdf.
Full text
3
Liang, Ruhai. "Pi wei gong neng yu pi fu bing guan xi de gu jin wen xian yan jiu /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009628a.pdf.
Full text
4
Wu, Min'er. "Mei ni ai bing ("er xuan yun") Zhong yi zhi liao de lin chuang wen xian yan jiu /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009306a.pdf.
Full text
5
Ye, Guohua. "Shen jing gen xing jing zhui bing sheng huo zhi su tiao cha ji qi shou fa zhi liao yan jiu /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009549a.pdf.
Full text
6
Chen, Yongshen. "Zhang zhe xi gu guan jie yan dui sheng huo zhi su de ying xiang ji xiang guan Zhong yi zhi liao yan jiu /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009355a.pdf.
Full text
7
Mei, Yunting. "Zhong yi yao zhou qi zhi liao zi gong nei mo yi wei zheng de yan jiu gai kuang /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b19987535a.pdf.
Full text
8
Pan, Xincheng. "Zhong yi yao zhi liao bao kuai xing zi gong nei mo yi wei zheng yan jiu gai kuang /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009318a.pdf.
Full text
9
Ping, Ping. "Cong "da er quan" de zu zhi dao zi chan zhuan yong xing de zu zhi Guangzhou yi jia ji qi zhi zao ye guo you qi ye de zu zhi bian qian /." online access from ProQuest databases, 2002. http://libweb.cityu.edu.hk/cgi-bin/er/db/pqdiss.pl?3052138.
Full text
10
Huang, Shaofen. "Zhen ci dui ying ji fan ying zhong xue ya he xin shuai de ying xiang ji qi ji li tan tao : wen xian zong shu /." click here to view the abstract and table of contents, 2006. http://net3.hkbu.edu.hk/~libres/cgi-bin/thesisab.pl?pdf=b20009537a.pdf.
Full textBooks on the topic "Ji bing"
2
Bo, Bing. Qi e ji bing: Bing bo tong hua ji. Beijing: Ren min jiao yu chu ban she, 2014.
Find full text
5
Yuyun, Wang, Wu Dunxu, Mao Xiao, and Li Qizhong, eds. Zhong yi bing yin bing ji xue. Shanghai: Shanghai Zhong yi xue yuan chu ban she, 1987.
Find full text
6
lai, Wei, and Han fang zheng. Gan zang ji bing. Bei jing: Zhong guo yi yao ke ji chu ban she, 2006.
Find full text
7
Zhong yang dian shi tai. CCTVjian kang zhi lu lan mu zu. Zi ji bing zi ji zhi. Shang hai: Shang hai ke xue ji zhu wen xian chu ban she, 2010.
Find full text
10
er, Ka li dai, and Fu yan guo. Shi ji bing mo. Hang zhou: Zhe jiang wen yi chu ban she, 1999.
Find full textBook chapters on the topic "Ji bing"
1
Liu, Huwy-min Lucia. "Introduction." In Governing Death, Making Persons, 1–16. Cornell University Press, 2023. http://dx.doi.org/10.7591/cornell/9781501767210.003.0001.
Full textAbstract:
This chapter introduces the concept of commemorating the dead in urban China. It explores the odd coexistence of religion and secular socialism that allowed Mao Zedong to be honored for being the inventor of memorial meetings. The popularity of memorial meetings was surprising not only because they were secular rituals but simultaneously being of socialist commemorative ceremonies. The chapter considers the rise of personalized funerals, individualism, and religious revivals. It elaborates on the concept of funeral governance in contemporary China, referring to the Chinese death rituals traditionally containing three interrelated sets of rituals: the bin (or sang), zang, and ji ceremonies.
2
Rasmussen, Søren G. F., and Ulrik Gether. "Structural mechanics of GPCR activation." In Understanding G protein-coupled receptors and their role in the CNS, 43–62. Oxford University PressOxford, 2002. http://dx.doi.org/10.1093/oso/9780198509165.003.0003.
Full textAbstract:
Abstract The majority of hormones, neurotransmitters, and other chemical signalling molecules in the human body exert their effects via G protein coupled receptors (GPCRs) (Strader et al. 1994; Ji et al. 1998; Gether 2000). Evidently, this extreme functional diversity raises some fundamental questions in relation to the function of GPCR at the molecular and cellular level. What are, for example, the molecular mechanisms underlying the ability of this broad variety of molecules to bind and activate receptors that presumably share a preserved overall tertiary structure? Or more specifically, what are the physical changes linking binding of an agonist to activation of intracellular signalling cascades? During the last few years our insight into these fundamental mechanisms have improved considerably. An important breakthrough has been the application of biophysical approaches that has allowed direct insight into the conformational changes that accompany activation of a GPCR (see Gether 2000; Hubbell et al. 2000).
Conference papers on the topic "Ji bing"
1
Xiaozhi Wang and Neil Pegg, ISSC 2022 Editors. "Proceedings of the 21st International Ship and Offshore Structures Congress VOLUME 2 Specialist Committee Reports." In 21st International Ship and Offshore Structures Congress, Volume 2. SNAME, 2022. http://dx.doi.org/10.5957/issc-2022-committee-vol-2.
Full textAbstract:
Table of Contents Preface ..............................................................................................................iii Committee V.1: Accidental Limit States .......................................................1 Bruce Quinton; Gaetano De Luca; Topan Firmandha; Mihkel Körgesaar; Hervé Le Sourne; Ken Nahshon; Gabriele Notaro; Kourosh Parsa; Smiljko Rudan; Katsuyuki Suzuki; Osiris Valdez Banda; CareyWalters; Deyu Wang; Zhaolong Yu Committee V.2: Experimental Methods ......................................................91 Soren Ehlers (Chair); Nagi Abdussamie; Kim Branner; ShiXiao Fu; Martijn Hoogeland; Kari Kolari; Paul Lara; Constantine Michailides; Hideaki Murayama; Cesare Rizzo; Jung Kwan Seo; Patrick Kaeding Committee V.3: Materials and Fabrication Technology ..........................163 Lennart Josefson (Chair); Konstantinos Anyfantis; Bianca de Carvalho Pinheiro; Bai-Qiao Chen; Pingsha Dong; Nicole Ferrari; Koji Gotoh; James Huang; Matthias Krause; Kun Liu; Stephane Paboeuf; Stephen van Duin; Fang Wang; Albert Zamarin Committee V.4: Offshore Renewable Energy ...........................................241 Atanasios Kolios (Chair); Kyong-Hwan Kim; Chen Hsing Cheng; Elif Oguz; Pablo Morato; Freeman Ralph; Chuang Fang; Chunyan Ji; Marc Le Boulluec; Thomas Choisnet; Luca Greco; Tomoaki Utsunomiya; Kourosh Rezanejad; Charles Rawson; Jose Miguel Rodrigues Committee V.5: Special Vessels ................................................................313 Darren Truelock (Chair); Jason Lavroff; Dustin Pearson; Zbigniew (Jan) Czaban; Hanbing Luo; Fuhua Wang; Ivan Catipovic; Ermina Begovic; Yukichi Takaoka; Claudia Loureiro; Chang Yong Song; Esther Garcia; Alexander Egorov; Jean-Baptiste Souppez; Pradeep Sensharma; Rachel Nicholls-Lee Committee V.6: Ocean Space Utilization ..................................................379 Sebastian Schreier (Chair); Felice Arena; Harry Bingham; Nuno Fonseca; Zhiqiang Hu; Debabrata Karmakar; Ekaterina Kim; Hui Li; Pengfei Liu; Motohiko Murai; Spiro J Pahos; Chao Tian; George Wang Committee V.7: Structural Longevity ........................................................445 Iraklis Lazakis (Chair); Bernt Leira; Nianzhong Chen; Geovana Drumond; Chi-Fang Lee; Paul Jurisic; Bin Liu; Alysson Mondoro; Pooria Pahlavan; Xinghua Shi; Ha Cheol Song; Tadashi Sugimura; Christian Jochum; Tommaso Coppola Committee V.8: Subsea Technology ..........................................................503 Agnes Marie Horn (Chair); Tauhid Rahman; Ilson Pasqualino; Menglan Duan; Zhuang Kang; Michael Rye Andersen; Yoshihiro Konno; Chunsik Shim; Angelo Teixeira; Selda Oterkus; Blair Thornton; Brajendra Mishra Subject Index .............................................................................................582 Author Index ...............................................................................................584
2
Xiaozhi Wang and Neil Pegg, ISSC 2022 Editors. "Proceedings of the 21st International Ship and Offshore Structures Congress VOLUME 3 Discussions." In 21st International Ship and Offshore Structures Congress Volume 3 Discussions. SNAME, 2022. http://dx.doi.org/10.5957/issc-2022-discussion-vol-3.
Full textAbstract:
Committee I.1: Environment Alexander Babanin (Chair); Mariana Bernardino; Franz von Bock und Polach; Ricardo Campos,; Jun Ding; Sanne van Essen; Tomaso Gaggero; Maryam Haroutunian; Vanessa Katsardi; Alexander Nilva; Arttu Polojarvi; Erik Vanem; Jungyong Wang; Huidong Zhang; Tingyao Zhu Floor Discussers: Florian Sprenger; Carlos Guedes Soares; Henk den Besten Committee I.2: Loads Ole Andreas Hermundstad (Chair); Shuhong Chai; Guillaume de Hauteclocque; Sheng Dong; Chih-Chung Fang; Thomas B. Johannessen; Celso Morooka; Masayoshi Oka; Jasna Prpić-Oršić; Alessandro Sacchet; Mahmud Sazidy; Bahadir Ugurlu; Roberto Vettor; Peter Wellens Official Discusser: Hayden Marcollo Committee II-1: Quasi-Static Response James Underwood (Chair); Erick Alley; Jerolim Andrić Dario Boote; Zhen Gao; Ad Van Hoeve; Jasmin Jelovica; Yasumi Kawamura; Yooil Kim; Jian Hu Liu; Sime Malenica; Heikki Remes; Asokendu Samanta; Krzysztof Woloszyk; Deqing Yang Official Discusser: Prof. T. Yoshikwa Committee II.2: Dynamic Response Gaute Storhaug (Chair); Daniele Dessi; Sharad Dhavalikar; Ingo Drummen; Michael Holtmann; Young-Cheol Huh; Lorenzo Moro; Andre Paiva; Svein Sævik; Rong-Juin Shyu; Shan Wang; Sue Wang; WenWei Wu; Yasuhira Yamada; Guiyong Zhang Floor Discussers: Ling Zhu; Tomoki Takami; Anriette (Annie) Bekker; Bruce Quinton; Robert Sielski Committee III.1: Ultimate Strength Paul E. Hess (Chair); Chen An; Lars Brubak; Xiao Chen; Jinn Tong Chiu; Jurek Czujko; Ionel Darie; Guoqing Feng; Marco Gaiotti; Beom Seon Jang; Adnan Kefal; Sukron Makmun; Jonas Ringsberg; Jani Romanoff; Saad Saad-Eldeen; Ingrid Schipperen; Kristjan Tabri; Yikun Wang; Daisuke Yanagihara Official Discusser: Jørgen Amdahl Committee III.2: Fatigue and Fracture Yordan Garbatov (Chair); Sigmund K Ås; Henk Den Besten; Philipp Haselbach; Adrian Kahl; Dale Karr; Myung Hyun Kim; Junjie Liu; Marcelo Igor Lourenço de Souza; Wengang Mao; Eeva Mikkola; Naoki Osawa; Fredhi Agung Prasetyo; Mauro Sicchiero; Suhas Vhanmane; Marta Vicente del Amo; Jingxia Yue Official Discusser Weicheng Cui Floor Discussers: Robert Sielski; Sören Ehlers; Stephane Paboeuf; Teresa Magoga Committee IV.1: Design Principles and Criteria Matthew Collette (Chair); Piero Caridis; Petar Georgiev; Torfinn Hørte; Han Koo Jeong; Rafet emek Kurt; Igor Ilnytskiy; Tetsuo Okada; Charles Randall; Zbigniew Sekulski; Matteo Sidari; Zhihu Zhan; Ling Zhu Official Discusser: Enrico Rizzuto Committee IV.2: Design Methods Andrea Ivaldi (Chair); Abbas Bayatfar; Jean-David Caprace; Gennadiy Egorov; Svein Erling Heggelund; Shinichi Hirakawa; Jung Min Kwon; Dan Mcgreer; Pero Prebeg; Robert Sielski; Mark Slagmolen; Adam Sobey; Wenyong Tang; Jiameng Wu Official Discusser: Mario Dogliani Committee V.1: Accidental Limit States Bruce Quinton; Gaetano De Luca; Topan Firmandha; Mihkel Körgesaar; Hervé Le Sourne; Ken Nahshon; Gabriele Notaro; Kourosh Parsa; Smiljko Rudan; Katsuyuki Suzuki; Osiris Valdez Banda; CareyWalters; Deyu Wang; Zhaolong Yu Official Discusser: Manolis Samuelides Committee V.2: Experimental Methods Sören Ehlers (Chair); Nagi Abdussamie; Kim Branner; ShiXiao Fu; Martijn Hoogeland; Kari Kolari; Paul Lara; Constantine Michailides; Hideaki Murayama; Cesare Rizzo; Jung Kwan Seo; Patrick Kaeding Official Discusser: Giles Thomas Committee V.3: Materials and Fabrication Technology Lennart Josefson (Chair); Konstantinos Anyfantis; Bianca de Carvalho Pinheiro; Bai-Qiao Chen; Pingsha Dong; Nicole Ferrari; Koji Gotoh; James Huang; Matthias Krause; Kun Liu; Stephane Paboeuf; Stephen van Duin; Fang Wang; Albert Zamarin Official Discusser: Frank Roland Floor Discussers Alessandro Caleo; Agnes Marie Horn; Krzysztof Woloszyk; Robert Sielski Committee V.4: Offshore Renewable Energy Atanasios Kolios (Chair); Kyong-Hwan Kim; Chen Hsing Cheng; Elif Oguz; Pablo Morato; Freeman Ralph; Chuang Fang; Chunyan Ji; Marc Le Boulluec; Thomas Choisnet; Luca Greco; Tomoaki Utsunomiya; Kourosh Rezanejad; Charles Rawson; Jose Miguel Rodrigues Official Discusser: Amy Robertson Committee V.5: Special Vessels Darren Truelock (Chair); Jason Lavroff; Dustin Pearson; Zbigniew (Jan) Czaban; Hanbing Luo; Fuhua Wang; Ivan Catipovic; Ermina Begovic; Yukichi Takaoka; Claudia Loureiro; Chang Yong Song; Esther Garcia; Alexander Egorov; Jean-Baptiste Souppez; Pradeep Sensharma; Rachel Nicholls-Lee Official Discusser: Jaye Falls Floor Discussers: Jasmin Jelovica; Stephane Paboeuf; Sören Ehlers Committee V.6: Ocean Space Utilization Sebastian Schreier (Chair); Felice Arena; Harry Bingham; Nuno Fonseca; Zhiqiang Hu; Debabrata Karmakar; Ekaterina Kim; Hui Li; Pengfei Liu; Motohiko Murai; Spiro J Pahos; Chao Tian; George Wang Official Discusser: Hideyuki Suzuki Floor Discussers: Robert Sielski; Sue Wang; Sarat Mohapatra; Gaute Storhaug; Henk den Besten Committee V.7: Structural Longevity Iraklis Lazakis (Chair); Bernt Leira; Nianzhong Chen; Geovana Drumond; Chi-Fang Lee; Paul Jurisic; Bin Liu; Alysson Mondoro; Pooria Pahlavan; Xinghua Shi; Ha Cheol Song; Tadashi Sugimura; Christian Jochum; Tommaso Coppola Official Discusser: Timo de Beer Floor Discusser: Krzysztof Woloszyk Committee V.8: Subsea Technology Agnes Marie Horn (Chair); Tauhid Rahman; Ilson Pasqualino; Menglan Duan; Zhuang Kang; Michael Rye Andersen; Yoshihiro Konno; Chunsik Shim; Angelo Teixeira; Selda Oterkus; Blair Thornton; Brajendra Mishra Official Discusser: Segen F. Estefen