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Xingsong Qin,Muwen Yang,Xinyu Zheng 대한외과학회 2019 Annals of Surgical Treatment and Research(ASRT) Vol.97 No.1
Purpose: The combination of indocyanine green and methylene blue (ICG + MB) was reported to be an efficient tracer method in sentinel lymph node biopsy (SLNB). However, whether this method is superior to MB only or carbon nanoparticles (CN) is controversial. This study was to evaluate the efficacy of the three methods in SLNB for breast cancer, and to analyze its influencing factors. Methods: One hundred eighty patients with early breast cancer were recruited and randomly divided into 3 groups. Each group comprising of 60 patients with SLNB using ICG + MB, MB, and CN, respectively. Then the 3 groups were compared in detection rate, mean number of SLNs, and the detection rates and number of metastatic sentinel lymph nodes (SLNs). Results: The detection rate of SLNs was 100% (60 of 60) in ICG + MB group, 96.7% (58 of 60), and 98.3% (59 of 60) in MB and CN group, respectively, with no significant difference (P = 0.362). Totally, 204 SLNs (mean ± standard deviation [SD] [range], 3.4 ± 1.4 [2–8]) were detected in ICG + MB group, 102 (1.7 ± 0.7 [0–3]) and 145 (2.4 ± 0.7 [0–6]) in MB and CN group, indicating significant difference (P < 0.001). The detection rate of metastatic SLN was 23.3% (14 of 60) in ICG + MB group, which was higher than 18.3% (11 of 60) and 20% (11 of 60) in MB and CN group, respectively, but showed no statistical significance (P = 0.788). Conclusion: ICG + MB method was superior to MB only and CN only methods in the mean number of SLNs, thus predicting axillary lymph node metastasis more accurately. Therefore, in areas where the standard method is not available, ICG + MB may be more suitable as an alternative tracer for SLNB.
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Low dose Emodin induces tumor senescence for boosting breast cancer chemotherapy via silencing NRARP
Zu, Cong,Qin, Guangyuan,Yang, Chunshu,Liu, Ning,He, Anning,Zhang, Mingdi,Zheng, Xinyu Elsevier 2018 Biochemical and biophysical research communication Vol.505 No.4
<P><B>Abstract</B></P> <P><B>Purpose</B></P> <P>The resistance to 5-FU often limits its clinical effectiveness on breast cancer treatment. Combination therapy thus is employed to overcome this treatment resistance. We here report a potent antitumor effect of Emodin at low dose on chemotherapy sensitivity of MCF-7 breast cancer cells.</P> <P><B>Methods</B></P> <P>Cell viability, apoptosis, glutathiones (GSH) concentration and Reactive oxygen species (ROS) activity following Emodin and 5-FU treatment was assessed. Cellular senescence following combined treatment and silence of NRARP was examined by senescence-associated β-galactosidase analysis. Western blot analysis was used to determine changes in the expression of p21, p16, p27, E2F1 and NRARP.</P> <P><B>Results</B></P> <P>Low dose Emodin potentiates 5-FU-induced apoptosis of breast cancer cells, in association with inhibition of NRARP, resulting in cellular senescence. RNA interference of NRARP induced cellular senescence in MCF-7 breast cancer cells. Furthermore, the cellular senescence induced by Emodin and 5-FU treatment could be reverted by pcDNA–NRARP.</P> <P><B>Conclusion</B></P> <P>These findings provide preclinical evidence for repurposing use of Emodin in combination with chemotherapeutic agents to treat breast cancer as an alternative salvage regimen.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The chemoresistance often limits clinical effectiveness of chemotherapy on breast cancer treatment. </LI> <LI> Emodin potentiates 5-FU-induced apoptosis of breast cancer cells. </LI> <LI> Low dose Emodin induces cellular senescence in breast cancer cells by inhibition of Nrarp. </LI> </UL> </P>
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Min Li,Lujun Song,Xiaodong Gao,Wenju Chang,Xinyu Qin 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.4
Type 1 diabetes mellitus is caused by the autoimmune destruction of β cells within the islets. In recent years,innate immunity has been proposed to play a key role in this process. High-mobility group box 1 (HMGB1), an inflammatory trigger in a number of autoimmune diseases,activates proinflammatory responses following its release from necrotic cells. Our aim was to determine the significance of HMGB1 in the natural history of diabetes in non-obese diabetic (NOD) mice. We observed that the rate of HMGB1 expression in the cytoplasm of islets was much greater in diabetic mice compared with non-diabetic mice. The majority of cells positively stained for toll-like receptor 4 (TLR4) were βcells; few α cells were stained for TLR4. Thus, we examined the effects of anti-TLR4 antibodies on HMGB1 cell surface binding, which confirmed that HMGB1 interacts with TLR4 in isolated islets. Expression changes in HMGB1 and TLR4 were detected throughout the course of diabetes. Our findings indicate that TLR4 is the main receptor on β cells and that HMGB1 may signal via TLR4 to selectively damage β cells rather than αcells during the development of type 1 diabetes mellitus.
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