目的探讨Fox M1、Cep55及c-Myc蛋白在基底细胞样型乳腺癌(BLBC)中的表达及临床意义。方法采用免疫组化方法检测66例BLBC、70例NON-BLBC和66例癌旁正常乳腺组织中Fox M1、Cep55及c-Myc蛋白的表达情况及三者间的相互关系。结果 Fox M1蛋白...目的探讨Fox M1、Cep55及c-Myc蛋白在基底细胞样型乳腺癌(BLBC)中的表达及临床意义。方法采用免疫组化方法检测66例BLBC、70例NON-BLBC和66例癌旁正常乳腺组织中Fox M1、Cep55及c-Myc蛋白的表达情况及三者间的相互关系。结果 Fox M1蛋白在BLBC、NON-BLBC和癌旁正常乳腺组织中的阳性表达率分别为77.3%(51/66)、60.0%(42/70)、13.6%(9/66),Cep55蛋白在BLBC、NON-BLBC和癌旁正常乳腺组织中的阳性表达率分别为74.2%(49/66)、57.1%(40/70)、16.7%(11/66),c-Myc蛋白在BLBC、NON-BLBC和癌旁正常乳腺组织中的阳性表达率分别为71.2%(47/66)、54.3%(38/70)、22.7%(15/66),差异均有统计学意义(P<0.05)。Fox M1、Cep55及c-Myc蛋白的表达与BLBC的TNM分期及淋巴结转移情况密切相关(P<0.05),而与年龄、绝经与否、肿块大小无关(P>0.05)。Fox M1和Cep55蛋白在BLBC中的表达呈正相关关系(P<0.05),Fox M1和c-Myc蛋白在BLBC中的表达呈正相关关系(P<0.05),而Cep55与c-Myc的表达没有相关性(P>0.05)。结论 Fox M1、Cep55及c-Myc蛋白可能参与了BLBC的发生、发展,并且Fox M1分别与Cep55及c-Myc在BLBC发生发展过程中可能有一定的协同作用;Cep55蛋白与c-Myc蛋白在BLBC中的表达没有相关性,说明Cep55及c-Myc可能通过不同的作用对BLBC的发生发展过程产生影响。展开更多
目的：研究中国人群对氧磷酯酶1（PON1）基因L55M多态性与冠状动脉粥样硬化性心脏病（冠心病）相关性。方法全面检索关于PON1基因L55M多态性与冠心病关联性的原始研究，纳入符合入选标准研究，并进行数据合并。利用PON1基因的不同的遗...目的：研究中国人群对氧磷酯酶1（PON1）基因L55M多态性与冠状动脉粥样硬化性心脏病（冠心病）相关性。方法全面检索关于PON1基因L55M多态性与冠心病关联性的原始研究，纳入符合入选标准研究，并进行数据合并。利用PON1基因的不同的遗传模型OR值及其95%CI作为效应指标进行分析。结果6个原始研究共计2338例对象[其中冠心病患者组1229例，健康对照组1109例]进入最后的数据合并。Meta分析表明PON1基因L55M多态性与冠心病易感性无统计学意义[纯合子比较模型（MM vs. LL）：OR=0.57，95%CI：0.26~1.25，P=0.16；杂合子比较模型（LM vs. LL）：OR=1.46，95%CI：0.79~2.71， P=0.22；显性遗传模型（MM＋LM vs. LL）：OR=1.32，95%CI：0.73~2.38，P=0.35；隐性遗传模型（MM vs. LM＋LL）：OR=0.56，95%CI：0.26~1.21，P=0.14]。结论中国人群冠心病易感性与PON1基因L55M多态性无关。展开更多
We report a multi-wavelength study of two evolved planetary nebulae(PNs)M 2–55 and Abell 2.Deep optical narrow-band images([O III],Hα,and[N II])of M 2–55 reveal two pairs of bipolar lobes and a new faint arc-like s...We report a multi-wavelength study of two evolved planetary nebulae(PNs)M 2–55 and Abell 2.Deep optical narrow-band images([O III],Hα,and[N II])of M 2–55 reveal two pairs of bipolar lobes and a new faint arc-like structure.This arc-shaped filament around M 2–55 appears as a well-defined boundary from southwest to southeast,strongly suggesting that this nebula is in interaction with its surrounding interstellar medium.From the imaging data of Wide-field Infrared Survey Explorer(WISE)all-sky survey,we discovered extensive mid-infrared halos around these PNs,which are approximately twice the size of their main nebulae seen in the visible.We also present a mid-resolution optical spectrum of M 2–55,which shows that it is a high-excitation evolved PN with a low electron density of 250 cm^-3.Furthermore,we investigate the properties of these nebulae from their spectral energy distributions(SEDs)by means of archival data.展开更多
Due to its difficulty in early diagnosis and lack of sensitivity to chemotherapy and radiotherapy,renal cell carcinoma(RCC)remains to be a frequent cause of cancer-related death.Here,we probed into new targets for its ...Due to its difficulty in early diagnosis and lack of sensitivity to chemotherapy and radiotherapy,renal cell carcinoma(RCC)remains to be a frequent cause of cancer-related death.Here,we probed into new targets for its early diagnosis and treatment for RCC.microRNA(miRNA)data of M2-EVs and RCC were searched on the Gene Expression Omnibus database,followed by the prediction of the potential downstream target.Expression of target genes was measured via RT-qPCR and Western blot,respectively.M2 macrophage was obtained viaflow cytometry with M2-EVs extracted.The binding ability of miR-342-3p to NEDD4L and to CEP55 ubiquitination was studied with their roles in the physical abilities of RCC cells assayed.Subcutaneous tumor-bearing mouse models and lung metastasis models were prepared to observe in vivo role of target genes.M2-EVs induced RCC growth and metastasis.miR-342-3p showed high expression in both M2-EVs and RCC cells.M2-EVs carrying miR-342-3p promoted RCC cell abilities to proliferate,invade and migrate.In RCC cells,M2-EV-derived miR-342-3p could specifically bind to NEDD4L and consequently elevate CEP55 protein expression via suppressing NEDD4L,thereby exerting tumor-promoting effects.CEP55 could be degraded by ubiquitination under the function of NEDD4L,and miR-342-3p delivered by M2-EVs facilitated the RCC occurrence and development by activating the PI3K/AKT/mTOR signaling pathway.In conclusion,M2-EVs promote RCC growth and metastasis by delivering miR-342-3p to suppress NEDD4L and subsequently inhibit CEP55 ubiquitination and degradation via activation of the PI3K/AKT/mTOR signaling pathway,strongly driving the proliferative,migratory and invasive of RCC cells.展开更多
文摘目的：研究中国人群对氧磷酯酶1（PON1）基因L55M多态性与冠状动脉粥样硬化性心脏病（冠心病）相关性。方法全面检索关于PON1基因L55M多态性与冠心病关联性的原始研究，纳入符合入选标准研究，并进行数据合并。利用PON1基因的不同的遗传模型OR值及其95%CI作为效应指标进行分析。结果6个原始研究共计2338例对象[其中冠心病患者组1229例，健康对照组1109例]进入最后的数据合并。Meta分析表明PON1基因L55M多态性与冠心病易感性无统计学意义[纯合子比较模型（MM vs. LL）：OR=0.57，95%CI：0.26~1.25，P=0.16；杂合子比较模型（LM vs. LL）：OR=1.46，95%CI：0.79~2.71， P=0.22；显性遗传模型（MM＋LM vs. LL）：OR=1.32，95%CI：0.73~2.38，P=0.35；隐性遗传模型（MM vs. LM＋LL）：OR=0.56，95%CI：0.26~1.21，P=0.14]。结论中国人群冠心病易感性与PON1基因L55M多态性无关。
基金supported by MoST grant(108-2112-M-008-001)support of the staff of the Lijiang 2.4m telescope+4 种基金Funding for the telescope has been provided by Chinese Academy of Sciences and the People’s Government of Yunnan ProvinceFinancial support for this work is supported by the grants from The Science and Technology Development Fund,Macao SAR(file no061/2017/A2and 0007/2019/A)the Faculty Research Grants of Macao University of Science and Technology(project codeFRG-19-004-SSI)supported by the National Natural Science Foundation of China(NSFC,Grant No.U1731122)NSFC(Grant No.11973099)for financial support
文摘We report a multi-wavelength study of two evolved planetary nebulae(PNs)M 2–55 and Abell 2.Deep optical narrow-band images([O III],Hα,and[N II])of M 2–55 reveal two pairs of bipolar lobes and a new faint arc-like structure.This arc-shaped filament around M 2–55 appears as a well-defined boundary from southwest to southeast,strongly suggesting that this nebula is in interaction with its surrounding interstellar medium.From the imaging data of Wide-field Infrared Survey Explorer(WISE)all-sky survey,we discovered extensive mid-infrared halos around these PNs,which are approximately twice the size of their main nebulae seen in the visible.We also present a mid-resolution optical spectrum of M 2–55,which shows that it is a high-excitation evolved PN with a low electron density of 250 cm^-3.Furthermore,we investigate the properties of these nebulae from their spectral energy distributions(SEDs)by means of archival data.
基金supported by the Science and Technology Department of Sichuan Province(2015SZ0117,2019YJ0701,and 2021YJ0239).
文摘Due to its difficulty in early diagnosis and lack of sensitivity to chemotherapy and radiotherapy,renal cell carcinoma(RCC)remains to be a frequent cause of cancer-related death.Here,we probed into new targets for its early diagnosis and treatment for RCC.microRNA(miRNA)data of M2-EVs and RCC were searched on the Gene Expression Omnibus database,followed by the prediction of the potential downstream target.Expression of target genes was measured via RT-qPCR and Western blot,respectively.M2 macrophage was obtained viaflow cytometry with M2-EVs extracted.The binding ability of miR-342-3p to NEDD4L and to CEP55 ubiquitination was studied with their roles in the physical abilities of RCC cells assayed.Subcutaneous tumor-bearing mouse models and lung metastasis models were prepared to observe in vivo role of target genes.M2-EVs induced RCC growth and metastasis.miR-342-3p showed high expression in both M2-EVs and RCC cells.M2-EVs carrying miR-342-3p promoted RCC cell abilities to proliferate,invade and migrate.In RCC cells,M2-EV-derived miR-342-3p could specifically bind to NEDD4L and consequently elevate CEP55 protein expression via suppressing NEDD4L,thereby exerting tumor-promoting effects.CEP55 could be degraded by ubiquitination under the function of NEDD4L,and miR-342-3p delivered by M2-EVs facilitated the RCC occurrence and development by activating the PI3K/AKT/mTOR signaling pathway.In conclusion,M2-EVs promote RCC growth and metastasis by delivering miR-342-3p to suppress NEDD4L and subsequently inhibit CEP55 ubiquitination and degradation via activation of the PI3K/AKT/mTOR signaling pathway,strongly driving the proliferative,migratory and invasive of RCC cells.
