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Sixu Chen,Daocheng Liu,Sihao He,Lei Yang,Quanwei Bao,Hao Qin,Huayu Liu,Yufeng Zhao,Zhaowen Zong 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Type 1 diabetes mellitus (T1DM) is a pathological condition associated with osteopenia. WNT/β-catenin signaling is implicated in this process. Trabecular and cortical bone respond differently to WNT/β-catenin signaling in healthy mice. We investigated whether this signaling has different effects on trabecular and cortical bone in T1DM. We first established a streptozotocin-induced T1DM mouse model and then constitutively activated β-catenin in osteoblasts in the setting of T1DM (T1-CA). The extent of bone loss was greater in trabecular bone than that in cortical bone in T1DM mice, and this difference was consistent with the reduction in the expression of β-catenin signaling in the two bone compartments. Further experiments demonstrated that in T1DM mice, trabecular bone showed lower levels of insulin-like growth factor-1 receptor (IGF-1R) than the levels in cortical bone, leading to lower WNT/β-catenin signaling activity through the inhibition of the IGF-1R/Akt/glycogen synthase kinase 3β (GSK3β) pathway. After β-catenin was activated in T1-CA mice, the bone mass and bone strength increased to substantially greater extents in trabecular bone than those in cortical bone. In addition, the cortical bone of the T1-CA mice displayed an unexpected increase in bone porosity, with increased bone resorption. The downregulated expression of WNT16 might be responsible for these cortical bone changes. In conclusion, we found that although the activation of WNT/ β-catenin signaling increased the trabecular bone mass and bone strength in T1DM mice, it also increased the cortical bone porosity, impairing the bone strength. These findings should be considered in the future treatment of T1DM-related osteopenia.
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Dynamic responses of a freestanding bridge tower under wave and wave-current loads
Chengxun Wei,Wenjing Wang,Daocheng Zhou 국제구조공학회 2022 Structural Engineering and Mechanics, An Int'l Jou Vol.82 No.4
A model experiment with a scale of 1:150 has been conducted to investigate the dynamic responses of a freestanding four-column bridge tower subjected to regular wave, random wave and coupled wave-current actions. The base shear forces of the caisson foundation and the dynamic behaviors of the superstructure were measured and analyzed. The comparisons of the test values with the theoretical values shows that wave-induced base shear forces on the bridge caisson foundation can be approximated by using a wave force calculation method in which the structure is assumed to be fixed and rigid. Although the mean square errors of the base shear forces excited by joint random wave and current actions are approximately equal to those excited by pure random waves, the existence of a forward current increases the forward base shear forces and decreases the backward base shear forces. The tower top displacements excited by wave-currents are similar to those excited by waves, suggesting that a current does not significantly affect the dynamic responses of the superstructure of the bridge tower. The experiment results can be used as a reference for similar engineering design.
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Kaixi Ren,Chao Jin,Pengfei Ma,Qinyou Ren,Zhansheng Jia,Daocheng Zhu 고려인삼학회 2016 Journal of Ginseng Research Vol.40 No.2
Background: Ginsenoside Rd (GSRd), a main component of the root of Panax ginseng, exhibits antiinflammation functions and decreases infarct size in many injuries and ischemia diseases such as focal cerebral ischemia. M1 Macrophages are regarded as one of the key inflammatory cells having functions for disease progression. Methods: To investigate the effect of GSRd on renal ischemia/reperfusion injury (IRI) and macrophage functional status, and their regulatory role on mouse polarized macrophages in vitro, GSRd (10e100 mg/ kg) and vehicle were applied to mice 30 min before renal IRI modeling. Renal functions were reflected by blood serum creatinine and blood urea nitrogen level and histopathological examination. M1 polarized macrophages infiltration was identified by flow cytometry analysis and immunofluorescence staining with CD11bþ, iNOSþ/interleukin-12/tumor necrosis factor-a labeling. For the in vitro study, GSRd (10 e100 mg/mL) and vehicle were added in the culture medium of M1 macrophages to assess their regulatory function on polarization phenotype. Results: In vivo data showed a protective role of GSRd at 50 mg/kg on Day 3. Serum level of serum creatinine and blood urea nitrogen significantly dropped compared with other groups. Reduced renal tissue damage and M1 macrophage infiltration showed on hematoxylineeosin staining and flow cytometry and immunofluorescence staining confirmed this improvement. With GSRd administration, in vitro cultured M1 macrophages secreted less inflammatory cytokines such as interleukin-12 and tumor necrosis factor-a. Furthermore, macrophage polarization-related pancake-like morphology gradually changed along with increasing concentration of GSRd in the medium. Conclusion: These findings demonstrate that GSRd possess a protective function against renal ischemia/ reperfusion injury via downregulating M1 macrophage polarization.
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Ren, Kaixi,Jin, Chao,Ma, Pengfei,Ren, Qinyou,Jia, Zhansheng,Zhu, Daocheng The Korean Society of Ginseng 2016 Journal of Ginseng Research Vol.40 No.2
Background: Ginsenoside Rd (GSRd), a main component of the root of Panax ginseng, exhibits anti-inflammation functions and decreases infarct size in many injuries and ischemia diseases such as focal cerebral ischemia. M1 Macrophages are regarded as one of the key inflammatory cells having functions for disease progression. Methods: To investigate the effect of GSRd on renal ischemia/reperfusion injury (IRI) and macrophage functional status, and their regulatory role on mouse polarized macrophages in vitro, GSRd (10-100 mg/kg) and vehicle were applied to mice 30 min before renal IRI modeling. Renal functions were reflected by blood serum creatinine and blood urea nitrogen level and histopathological examination. M1 polarized macrophages infiltration was identified by flow cytometry analysis and immunofluorescence staining with $CD11b^+$, $iNOS^+$/interleukin-12/tumor necrosis factor-${\alpha}$ labeling. For the in vitro study, GSRd ($10-100{\mu}g/mL$) and vehicle were added in the culture medium of M1 macrophages to assess their regulatory function on polarization phenotype. Results: In vivo data showed a protective role of GSRd at 50 mg/kg on Day 3. Serum level of serum creatinine and blood urea nitrogen significantly dropped compared with other groups. Reduced renal tissue damage and M1 macrophage infiltration showed on hematoxylin-eosin staining and flow cytometry and immunofluorescence staining confirmed this improvement. With GSRd administration, in vitro cultured M1 macrophages secreted less inflammatory cytokines such as interleukin-12 and tumor necrosis factor-${\alpha}$. Furthermore, macrophage polarization-related pancake-like morphology gradually changed along with increasing concentration of GSRd in the medium. Conclusion: These findings demonstrate that GSRd possess a protective function against renal ischemia/reperfusion injury via downregulating M1 macrophage polarization.
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