| 1 | LA-ICP-MS zircon U-Pb dating and phenocryst EPMA of dikes, Guocheng, Jiaodong Peninsula: Implications for North China Craton lithosphere evolution显示文摘Widespread dike swarm, including diorite-, monzonite-porphyry and lamprophyre, intruded in the al- tered breccia gold deposits along basin marginal faults, Guocheng, Jiaodong Peninsula. Petrography exhibits biotite enclaves in amphibole phenocrysts and the presence of acicular apatites in these dikes. Electron probe microanalyses (EPMA) show that the amphibole and clinopyroxene phenocryst’s mantle in diorite porphyry and lamprophyre respectively has sharply higher MgO (Mg#) and Cr2O3 contents in contrast to their cores. The plagioclase phenocryst in monzonite porphyry has reverse zoning. These results indicate that the magma mixing between mantle-derived mafic and crust-derived felsic magmas occurred in the original process of the dikes. Zircon cathodoluminescence (CL) images show well-developed magmatic oscillatory zones and the acquired LA-ICP-MS zircon U-Pb weighted mean 206Pb/238U ages are 114±2 Ma (MSDW=1.5) for monzonite porphyry (GS1) and 116±1 Ma (MSDW=0.8) for diorite porphyry (GS2), respectively. Earlier magmatic events in the northwest Jiaodong Peninsula represented by some inherited or captured zircons also occur in these dikes. Magmatic zircons from GS1 and GS2 display consistent chondrite-normalized REE patterns and Nb/Ta values, implying that they may share a similar or same source. HREE enrichment and obvious negative Eu anomalies of these zircons preclude garnet presented in their source. Our results, combined with preciously pub- lished data, indicate that dike intrusion and gold mineralization among quartz vein, altered tectonite and altered breccia gold deposits are broadly contemporaneous throughout the Jiaodong Peninsula. These also imply that the intensive crust-mantle interaction and asthenospheric underplating had oc- curred in the Early Cretaceous in the Peninsula, together with foundering of lower crust in the early Mesozoic, representing the different stages of lithosphere thinning in the North China Craton (NNC). | TAN Jun WEI JunHao GUO LingLi ZHANG KeQing YAO ChunLiang LU JianPei LI HongMei | 2008 | Science China Earth Sciences2008，51，10： | 23 |
| 2 | HBB-deficient Macaca fascicularis monkey presents with human β-thalassemia显示文摘Dear Editor,β-Thalassemia is a common severe genetic disease caused by mutations in HBB and affects approximately 1.5% of the global population (Origa, 2017). In southern China, the carrier rate of β-thalassemia is as high as 6.43%, creating a high socio-economic burden (Xiong et al., 2010). In adult humans, there are three types of hemoglobin: HbA1 (~97%), HbA2 (~2%) and HbF (~1%). HbA1 (α2β2) is composed of two a-globin and two β-globi n sub units en coded by HBA and HBB, respectively;HbF (α2β2)is made up of two α-globin subunits and two β-globin sub units en coded by HBG. Mutations in the coding region or regulatory region of HBB are involved in β-thalassemia pathogenesis. Except for some rare dominant mutations, most HBB mutations are recessive (Origa, 2017). Depending on the mutation type, the β-globin level will either be reduced or completely depleted, resulting in α-globin accumulation and precipitation. These α-globin precipitates lead to red blood cell death, resulting in anemia and tissue damage, and even death in thalassemia major patients. Blood transfusions can help slow disease progression but lead to iron overload, ultimately resulting in iron toxicity. Bone marrow transfer is the only cure in the clinic and is available only to a small percentage of patients with human leukocyte antigervmatched donors. Recently, gene therapy and gene editing therapy have shown great promise in curing β-thalassemia (Glaser et al., 2015;Thompson et al., 2018). However, no appropriate animal models are available for evaluating the safety and efficacy of such advanced therapeutic strategies in vivo.β-thalassemia mice are the sole animal model available for research. However, substantial differences have been reported between the types and expressi on patter ns of human and mouse globins (McColl and Vadolas, 2016). Moreover, mice contain no fetal globin gene equivalent, and homozygous mutations of HBB in mouse for early models of β-thalassemia major or Cooley anemia are all embryonic lethal (Huo et al., 2009). Recently, significant phenotype and physiology differences have been reported between SIRT6- null mice and the non-human primate model (Zhang et al., 2018). Thus, an appropriate non-human primate model is needed for human β-thalassemia studies and treatments. | Yan Huang Chenhui Ding Puping Liang Duanduan Li Yu Tang Wei Meng Hongwei Sun Hongyu Lu Yu Chen Xueying Chen Qunshan Huang Jianpei Fang Canquan Zhou Shihua Yang Junjiu Huang | 2019 | Protein & Cell2019，10，7： | 4 |
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