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学者姓名：李可
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Abstract ：
© 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim Long blood circulation in vivo remains a challenge to dual-drug-loaded nanocarriers for synergistic chemotherapy. Herein, a novel strategy to prepare lollipop-like dual-drug-loaded nanoparticles (DOX–PDA–gossypol NPs) is developed based on the self-assembly of gossypol, doxorubicin (DOX), and polydopamine (PDA) via π–π stacking. Dopamine polymerizes to PDA and fills the gaps between the gossypol and DOX molecules to form the super compact long-circulating nanoparticles. The DOX–PDA–gossypol NPs show a suitable particle size of 59.6 ± 9.6 nm, high drug loading of 91%, superb stability, high maximum-tolerated dose (MTD) of over 60 mg kg-1, and negligible toxicity. These NPs also exhibit pH-dependent drug release and low combination index (0.23). Notably, they show dramatically ultralong blood circulation (>192 h) with elimination half times 458-fold and 258-fold longer than that of free DOX and free gossypol, respectively. These values are markedly higher than most of the reported results. Therefore, the DOX–PDA–gossypol NPs have a high tumor accumulation of 12% remaining on the 8th day postinjection. This characteristic contributes to the excellent tumor comprehensive synergistic therapeutic efficacy (TIR > 90%) with low administration dosage and is benefitted for widening the drug therapeutic window. Thus, the proposed strategy has remarkable potential for tumor synergistic therapy.
Keyword ：
self-assembly synergistic therapy tumor ultralong circulating nanoparticles π–π stacking
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| GB/T 7714 | Wang, Ya , Wu, Youshen , Li, Ke et al. Ultralong Circulating Lollipop-Like Nanoparticles Assembled with Gossypol, Doxorubicin, and Polydopamine via π–π Stacking for Synergistic Tumor Therapy [J]. | Advanced Functional Materials , 2019 , 29 (1) . |
| MLA | Wang, Ya et al. "Ultralong Circulating Lollipop-Like Nanoparticles Assembled with Gossypol, Doxorubicin, and Polydopamine via π–π Stacking for Synergistic Tumor Therapy" . | Advanced Functional Materials 29 . 1 (2019) . |
| APA | Wang, Ya , Wu, Youshen , Li, Ke , Shen, Shihong , Liu, Zeying , Wu, Daocheng . Ultralong Circulating Lollipop-Like Nanoparticles Assembled with Gossypol, Doxorubicin, and Polydopamine via π–π Stacking for Synergistic Tumor Therapy . | Advanced Functional Materials , 2019 , 29 (1) . |
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Keyword ：
Urinary tract infections (UTI) Phagocytosis activity Inflammatory responses C3a/C3aR axis
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| GB/T 7714 | Wu, Kun-Yi , Zhang, Ting , Zhao, Guoxiu et al. C3a/C3aR axis confers the protection against urinary tract infection [C] . 2018 : 235-235 . |
| MLA | Wu, Kun-Yi et al. "C3a/C3aR axis confers the protection against urinary tract infection" . (2018) : 235-235 . |
| APA | Wu, Kun-Yi , Zhang, Ting , Zhao, Guoxiu , Zhou, Wuding , Li, Ke . C3a/C3aR axis confers the protection against urinary tract infection . (2018) : 235-235 . |
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Keyword ：
Cystitis Inflammation C5a/C5aR1 axis
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| GB/T 7714 | Zhao, Guoxiu , Wu, Kunyi , Zhang, Ting et al. C5aR1 promotes acute cystitis induced by uropathogenic Escherichia coli in mice [C] . 2018 : 233-233 . |
| MLA | Zhao, Guoxiu et al. "C5aR1 promotes acute cystitis induced by uropathogenic Escherichia coli in mice" . (2018) : 233-233 . |
| APA | Zhao, Guoxiu , Wu, Kunyi , Zhang, Ting , Zhou, Wuding , Li, Ke . C5aR1 promotes acute cystitis induced by uropathogenic Escherichia coli in mice . (2018) : 233-233 . |
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C3aR/ApoE double knockout mice C3a receptor Mono/macrophage Atherosclerosis Proinflammatory cytokines
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| GB/T 7714 | Ma, Ning , Wei, Linlin , Wang, Jiaxing et al. C3a receptor mediates protection of apolipoprotein E-deficient (ApoE(-/-)) mice from the development of atherosclerosis [C] . 2018 : 186-186 . |
| MLA | Ma, Ning et al. "C3a receptor mediates protection of apolipoprotein E-deficient (ApoE(-/-)) mice from the development of atherosclerosis" . (2018) : 186-186 . |
| APA | Ma, Ning , Wei, Linlin , Wang, Jiaxing , Chen, Daxin , Li, Ke . C3a receptor mediates protection of apolipoprotein E-deficient (ApoE(-/-)) mice from the development of atherosclerosis . (2018) : 186-186 . |
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Cytokine secretion Dendritic cells Phenotypic maturation/activation Collectin-11
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| GB/T 7714 | Qiang, Cui , Wu, Weiju , Li, Ke et al. Novel role for collectin-11 in modulation of dendritic cell maturation and function [C] . 2018 : 202-202 . |
| MLA | Qiang, Cui et al. "Novel role for collectin-11 in modulation of dendritic cell maturation and function" . (2018) : 202-202 . |
| APA | Qiang, Cui , Wu, Weiju , Li, Ke , Zhou, Wuding . Novel role for collectin-11 in modulation of dendritic cell maturation and function . (2018) : 202-202 . |
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| GB/T 7714 | Wei, Linlin , Ma, Ning , Gao, YaFeng et al. THE RECEPTOR FOR COMPLEMENT COMPONENT C3A MEDIATES PROTECTION FROM THE DEVELOPMENT OF ATHEROSCLEROSIS IN APOLIPOPROTEIN E DEFICIENT (APOE-/-) MICE [C] . 2018 : 173-173 . |
| MLA | Wei, Linlin et al. "THE RECEPTOR FOR COMPLEMENT COMPONENT C3A MEDIATES PROTECTION FROM THE DEVELOPMENT OF ATHEROSCLEROSIS IN APOLIPOPROTEIN E DEFICIENT (APOE-/-) MICE" . (2018) : 173-173 . |
| APA | Wei, Linlin , Ma, Ning , Gao, YaFeng , Wang, JiaXing , Bai, Liang , Chen, Daxin et al. THE RECEPTOR FOR COMPLEMENT COMPONENT C3A MEDIATES PROTECTION FROM THE DEVELOPMENT OF ATHEROSCLEROSIS IN APOLIPOPROTEIN E DEFICIENT (APOE-/-) MICE . (2018) : 173-173 . |
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Abstract ：
Fibrocytes are myeloid lineage cells implicated in wound healing, repair, and fibrosis. We previously showed that fibrocytes are mobilized into the circulation after vascular injury, including the immune-mediated injury that occurs after allogeneic transplantation. A common response to inflammatory vascular injury is intimal hyperplasia (IH), which, alongside vascular remodeling, results in progressive loss of blood flow, downstream ischemia, and end-organ fibrosis. This forms the pathological basis of transplant arteriosclerosis and other diseases including post-angioplasty re-stenosis. In investigating whether fibrocytes contribute to IH, we previously showed that subpopulations expressing smooth muscle actin and CD31 are recruited to the site of injury and accumulate in the neointima. Expression of tissue factor (TF) by these "CD31+ myofibrocytes" is needed for progressive neointimal expansion, such that TF inhibition limits the neointima to a single layer of cells by day 28 post-injury. The aim of this study was to determine pathophysiological mediators downstream of TF that contribute to myofibrocyte-orchestrated IH. We first show that myofibrocytes make up a significant component of the neointima 28 days following injury. Using a previously defined adoptive transfer model, we then show that CD31+ myofibrocytes get recruited early to the site of injury; this model allows manipulations of the adoptively transferred cells to study how IH develops. Having confirmed that inhibition of TF on adoptively transferred cells prevents IH, we then show that TF, primarily through the generation of thrombin, induces secretion of angiopoietin-2 by myofibrocytes and this directly stimulates proliferation, inhibits apoptosis, and induces CXCL-12 production by neointimal cells, including non-fibrocytes, all of which promote progressive IH <i>in vivo</i>. Prior incubation to inhibit angiopoietin-2 secretion by or block TIE-2 signaling on adoptively transferred fibrocytes inhibits IH. These novel data indicate that angiopoietin-2 production by early recruited myofibrocytes critically influences the development of IH after vascular injury and suggest new therapeutic avenues for exploration.
Keyword ：
tissue factor angiopoietin-2 vascular diseases thrombin fibrocyte CXCL12 intimal hyperplasia
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| GB/T 7714 | Chen Daxin , Li Ke , Tham El-Li et al. Inhibition of Angiopoietin-2 Production by Myofibrocytes Inhibits Neointimal Hyperplasia After Endoluminal Injury in Mice. [J]. | Frontiers in immunology , 2018 , 9 : 1517 . |
| MLA | Chen Daxin et al. "Inhibition of Angiopoietin-2 Production by Myofibrocytes Inhibits Neointimal Hyperplasia After Endoluminal Injury in Mice." . | Frontiers in immunology 9 (2018) : 1517 . |
| APA | Chen Daxin , Li Ke , Tham El-Li , Wei Lin-Lin , Ma Ning , Dodd Philippa C et al. Inhibition of Angiopoietin-2 Production by Myofibrocytes Inhibits Neointimal Hyperplasia After Endoluminal Injury in Mice. . | Frontiers in immunology , 2018 , 9 , 1517 . |
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Abstract ：
© 1983-2012 IEEE. In this paper, we theoretically analyze the wavelength temperature stability of multifunctional integrated optical chips (MIOCs) applied on fiber optic gyroscopes (FOGs). This study is critical for improving the temperature stability of the FOG scale factor, which is a significant parameter used to evaluate the dynamic characteristics of FOGs. Analytical and multiphysics simulations uncover two significant new predictions. First, changes in environmental temperature can lead to misalignment of the coupling structure between the chip and fiber, which is the main reason for the deterioration of the MIOC wavelength temperature stability. Second, misalignment caused by temperature changes is related to the initial alignment parameters of the coupling structure. Therefore, we can effectively improve the wavelength temperature stability of an MIOC by correctly choosing the initial alignment state of the coupling structure. Space coupling experiments are also presented to verify these predictions, and the experimental and simulation results are in good agreement.
Keyword ：
Fiber optic gyroscope (FOG) LiNbO3 waveguide multifunctional integrated optical chip (MIOC)
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| GB/T 7714 | Yao, Junjie , Li, Ke , Li, Bei et al. Study of Wavelength Temperature Stability of Multifunctional Integrated Optical Chips Applied on Fiber Optic Gyroscopes [J]. | Journal of Lightwave Technology , 2018 , 36 (23) : 5528-5535 . |
| MLA | Yao, Junjie et al. "Study of Wavelength Temperature Stability of Multifunctional Integrated Optical Chips Applied on Fiber Optic Gyroscopes" . | Journal of Lightwave Technology 36 . 23 (2018) : 5528-5535 . |
| APA | Yao, Junjie , Li, Ke , Li, Bei , Wang, Chenge , Kan, Chen , She, Xuan et al. Study of Wavelength Temperature Stability of Multifunctional Integrated Optical Chips Applied on Fiber Optic Gyroscopes . | Journal of Lightwave Technology , 2018 , 36 (23) , 5528-5535 . |
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Abstract ：
Recent work in a murine model of ascending urinary tract infection has suggested that C5a/C5aR1 interactions play a pathogenic role in the development of renal infection through enhancement of bacterial adhesion/colonization to renal tubular epithelial cells (RTECs). In the present study, we extended these observations to human. We show that renal tubular epithelial C5aR1 signaling is involved in promoting uropathogenic Escherichia coil (UPEC) adhesion/invasion of host cells. Stimulation of primary cultures of RTEC with C5a resulted in significant increases in UPEC adhesion/invasion of the RTEC. This was associated with enhanced expression of terminal oc-mannosyl residues (Man) (a ligand for type 1 fimbriae of E. cols) in the RTEC following C5a stimulation. Mechanism studies revealed that C5aR1-mediated activation of ERK1/2/NF-kappa B and upregulation of proinflammatory cytokine production (i.e., INF-alpha) is at least partly responsible for the upregulation of Man expression and bacterial adhesion. Clinical sample studies showed that C5aR1 and Man were clearly detected in the renal tubular epithelium of normal human kidney biopsies, and UPEC bound to the epithelium in a D-mannose-dependent manner. Additionally, C5a levels were significantly increased in urine of urinary tract infection patients compared with healthy controls. Our data therefore demonstrate that, in agreement with observations in mice, human renal tubular epithelial C5aR1 signaling can upregulate Man expression in RTEC, which enhances UPEC adhesion to and invasion of RTEC. It also suggests the in vivo relevance of upregulation of Man expression in renal tubular epithelium by C5a/C5aR1 interactions and its potential impact on renal infection.
Keyword ：
renal tubular epithelial cell mannosyl residues C5aR1 uropathogenic Escherichia coli bacterial adhesion/invasion
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| GB/T 7714 | Song, Yun , Wu, Kun-Yi , Wu, Weiju et al. Epithelial C5aR1 Signaling Enhances Uropathogenic Escherichia coil Adhesion to Human Renal Tubular Epithelial Cells [J]. | FRONTIERS IN IMMUNOLOGY , 2018 , 9 . |
| MLA | Song, Yun et al. "Epithelial C5aR1 Signaling Enhances Uropathogenic Escherichia coil Adhesion to Human Renal Tubular Epithelial Cells" . | FRONTIERS IN IMMUNOLOGY 9 (2018) . |
| APA | Song, Yun , Wu, Kun-Yi , Wu, Weiju , Duan, Zhao-Yang , Gao, Ya-Feng , Zhang, Liang-Dong et al. Epithelial C5aR1 Signaling Enhances Uropathogenic Escherichia coil Adhesion to Human Renal Tubular Epithelial Cells . | FRONTIERS IN IMMUNOLOGY , 2018 , 9 . |
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Abstract ：
Collectin-11 is a recently described soluble C-type lectin, a pattern recognition molecule of the innate immune system that has distinct roles in host defense, embryonic development, and acute inflammation. However, little is known regarding the role of collectin-11 in tissue fibrosis. Here, we investigated collectin-11 in the context of renal ischemia-reperfusion injury. Compared with wild-type littermate controls, Collec11 deficient (CL-11(-/-)) mice had significantly reduced renal functional impairment, tubular injury, renal leukocyte infiltration, renal tissue inflammation/fibrogenesis, and collagen deposition in the kidneys after renal ischemia-reperfusion injury. In vitro, recombinant collectin-11 potently promoted leukocyte migration and renal fibroblast proliferation in a carbohydrate-dependent manner. Additionally, compared with wild-type kidney grafts, CL-11(-/-) mice kidney grafts displayed significantly reduced tubular injury and collagen deposition after syngeneic kidney transplant. Our findings demonstrate a pathogenic role for collectin-11 in the development of tubulointerstitial fibrosis and suggest that local collectin-11 promotes this fibrosis through effects on leukocyte chemotaxis and renal fibroblast proliferation. This insight into the pathogenesis of tubulointerstitial fibrosis may have implications for CKD mediated by other causes as well.
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| GB/T 7714 | Wu, Weiju , Liu, Chengfei , Farrar, Conrad A. et al. Collectin-11 Promotes the Development of Renal Tubulointerstitial Fibrosis [J]. | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY , 2018 , 29 (1) : 168-181 . |
| MLA | Wu, Weiju et al. "Collectin-11 Promotes the Development of Renal Tubulointerstitial Fibrosis" . | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 29 . 1 (2018) : 168-181 . |
| APA | Wu, Weiju , Liu, Chengfei , Farrar, Conrad A. , Ma, Liang , Dong, Xia , Sacks, Steven H. et al. Collectin-11 Promotes the Development of Renal Tubulointerstitial Fibrosis . | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY , 2018 , 29 (1) , 168-181 . |
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