WordNet

the spontaneous emission of a stream of particles or electromagnetic rays in nuclear decay (同)radioactivity
energy that is radiated or transmitted in the form of rays or waves or particles
the act of spreading outward from a central source
a radial arrangement of nerve fibers connecting different parts of the brain
the spread of a group of organisms into new habitats
emit a sound; "bells and gongs chimed"
a percussion instrument consisting of a set of tuned bells that are struck with a hammer; used as an orchestral instrument (同)bell, gong
a grotesque product of the imagination (同)chimaera
(Greek mythology) fire-breathing female monster with a lions head and a goats body and a serpents tail; daughter of Typhon (同)Chimaera

PrepTutorEJDIC

〈U〉(光・熱・放射能などの)発散,放射 / 〈C〉放射物;放射線;輻射(ふくしゃ)熱 / 〈C〉(喜び・幸福感などの)発散《+『of』+『名』》 / =radioactivity
《複数形で》(一組の)『鐘』(さまざまな音階の音を組み合わせた鐘楼の鐘,玄関のチャイムなど) / 《複数形で》チャイム(鐘の組み合わせによる楽器) / 〈C〉チャイムによる音(音楽);チャイムを鳴らしたような音 / 〈U〉〈C〉《文》調和,一致 / 〈鐘・チャイム〉'を'『鳴らす』 / …'を'鐘を鳴らして告げる / …'を'声をそろえて言う / 〈鐘・チャイムが〉鳴る / (…と)調和する《+『with』+『名』》
《C-》キメラ(ライオンの頭とヤギの体と竜または蛇の尾を持つギリシア神話の動物) / 〈C〉(一般に想像上の)怪物,寄怪な幻想
鐘を鳴らす人

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1. 放射線療法誘発性肺障害 radiation induced lung injury
2. Radiation-related risks of imaging studies
3. 小児における放射線被曝の臨床的特徴 clinical features of radiation exposure in children
4. 成人における放射線障害の生物学および臨床的特徴 biology and clinical features of radiation injury in adults
5. 黒色腫（メラノーマ）のマネージメントにおける放射線療法 radiation therapy in the management of melanoma

English Journal

Crystallization and preliminary X-ray diffraction analysis of domain-chimeric L-(2S,3S)-butanediol dehydrogenase.

Shimegi T1, Ooyama T1, Ohtsuki T1, Kurisu G2, Kusunoki M1, Ui S1.Author information 1Graduate School of Medical and Engineering Science, Department of Education, University of Yamanashi, Japan.2Division of Structural Biology, Institute for Protein Research, Osaka University, Japan.AbstractA domain-chimeric L-2,3-butanediol dehydrogenase (chimera L-BDH), which was designed to possess both the S-configuration specificity of L-BDH and the stability of meso-BDH, was constructed by exchanging the respective domains of these two BDHs. However, chimera L-BDH possessed a lower enzymatic function than expected based on the two original enzymes. To elucidate the causes of the decreased stability and substrate specificity, crystallization of the protein was performed. Chimera L-BDH was purified to homogeneity via ammonium sulfate fractionation and three column-chromatography steps, and was crystallized using the hanging-drop vapour-diffusion method. The crystals belonged to space group C2221, diffracted synchrotron radiation to 1.58 Å resolution and were most likely to contain two molecules in the asymmetric unit.
Acta crystallographica. Section F, Structural biology communications.Acta Crystallogr F Struct Biol Commun.2014 Apr;70(Pt 4):461-3. doi: 10.1107/S2053230X13032755. Epub 2014 Mar 25.
A domain-chimeric L-2,3-butanediol dehydrogenase (chimera L-BDH), which was designed to possess both the S-configuration specificity of L-BDH and the stability of meso-BDH, was constructed by exchanging the respective domains of these two BDHs. However, chimera L-BDH possessed a lower enzymatic func
PMID 24699738

High-resolution intravital imaging reveals that blood-derived macrophages but not resident microglia facilitate secondary axonal dieback in traumatic spinal cord injury.

Evans TA1, Barkauskas DS2, Myers JT3, Hare EG4, You JQ5, Ransohoff RM6, Huang AY7, Silver J8.Author information 1Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: teresa.evans@case.edu.2Department of Biomedical Engineering, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: deborah.sim@case.edu.3Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: jay.myers@case.edu.4Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: ehare@laurelschool.org.5Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: jxy268@case.edu.6Department of Neurosciences, Neuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. Electronic address: ransohr@ccf.org.7Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: ayh3@case.edu.8Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: jxs10@case.edu.AbstractAfter traumatic spinal cord injury, functional deficits increase as axons die back from the center of the lesion and the glial scar forms. Axonal dieback occurs in two phases: an initial axon intrinsic stage that occurs over the first several hours and a secondary phase which takes place over the first few weeks after injury. Here, we examine the secondary phase, which is marked by infiltration of macrophages. Using powerful time-lapse multi-photon imaging, we captured images of interactions between Cx3cr1(+/GFP) macrophages and microglia and Thy-1(YFP) axons in a mouse dorsal column crush spinal cord injury model. Over the first few weeks after injury, axonal retraction bulbs within the lesion are static except when axonal fragments are lost by a blebbing mechanism in response to physical contact followed by phagocytosis by mobile Cx3Cr1(+/GFP) cells. Utilizing a radiation chimera model to distinguish marrow-derived cells from radio-resistant CNS-resident microglia, we determined that the vast majority of accumulated cells in the lesion are derived from the blood and only these are associated with axonal damage. Interestingly, CNS-resident Cx3Cr1(+/GFP) microglia did not increasingly accumulate nor participate in neuronal destruction in the lesion during this time period. Additionally, we found that the blood-derived cells consisted mainly of singly labeled Ccr2(+/RFP) macrophages, singly labeled Cx3Cr1(+/GFP) macrophages and a small population of double-labeled cells. Since all axon destructive events were seen in contact with a Cx3Cr1(+/GFP) cell, we infer that the CCR2 single positive subset is likely not robustly involved in axonal dieback. Finally, in our model, deletion of CCR2, a chemokine receptor, did not alter the position of axons after dieback. Understanding the in vivo cellular interactions involved in secondary axonal injury may lead to clinical treatment candidates involving modulation of destructive infiltrating blood monocytes.
Experimental neurology.Exp Neurol.2014 Apr;254:109-20. doi: 10.1016/j.expneurol.2014.01.013. Epub 2014 Jan 24.
After traumatic spinal cord injury, functional deficits increase as axons die back from the center of the lesion and the glial scar forms. Axonal dieback occurs in two phases: an initial axon intrinsic stage that occurs over the first several hours and a secondary phase which takes place over the fi
PMID 24468477

Macrophages control vascular stem/progenitor cell plasticity through tumor necrosis factor-α-mediated nuclear factor-κB activation.

Wong MM1, Chen Y, Margariti A, Winkler B, Campagnolo P, Potter C, Hu Y, Xu Q.Author information 1From the Cardiovascular Division, King's College London BHF Centre, London, United Kingdom (M.M.W., A.M., B.W., P.C., C.P., Y.H., Q.X.); and Department of Vascular Surgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China (Y.C.).AbstractOBJECTIVE: Vascular lineage differentiation of stem/progenitor cells can contribute to both tissue repair and exacerbation of vascular diseases such as in vein grafts. The role of macrophages in controlling vascular progenitor differentiation is largely unknown and may play an important role in graft development. This study aims to identify the role of macrophages in vascular stem/progenitor cell differentiation and thereafter elucidate the mechanisms that are involved in the macrophage- mediated process.
Arteriosclerosis, thrombosis, and vascular biology.Arterioscler Thromb Vasc Biol.2014 Mar;34(3):635-43. doi: 10.1161/ATVBAHA.113.302568. Epub 2014 Jan 23.
OBJECTIVE: Vascular lineage differentiation of stem/progenitor cells can contribute to both tissue repair and exacerbation of vascular diseases such as in vein grafts. The role of macrophages in controlling vascular progenitor differentiation is largely unknown and may play an important role in graf
PMID 24458710

Japanese Journal

Depletion of Primordial Germ Cells (PGCs) by X-irradiation to Extraembryonic Region of Chicken Embryos and Expression of Xenotransplanted Quail PGCs

ATSUMI Yusuke,YAZAWA Shigenobu,USUI Fumitake,NAKAMURA Yoshiaki,YAMAMOTO Yasuhiro,TAGAMI Takahiro,HIRAMATSU Kohzy,KAGAMI Hiroshi,ONO Tamao
The journal of poultry science 46(2), 136-143, 2009-04-25
… Exposure of chicken embryos to similar to 7.2 Gy of x-radiation at stage 13 with the application of a lead shield to the embryo proper is thus a feasible approach to depletion of endogenous germ cells and the production of chicken-quail germline chimeras. …
NAID 10024799460

Staphylokinase-Annexin XI Chimera Exhibited Efficient in Vitro Thrombolytic Activities

CHIOU Jeng-Fong,WOON Ming-Dar,CHENG Shin-Nan,HSU Chih-Hsueng,CHERNG Shiou-Chi,HSIEH Feng-Ken,LIN Shou-Ming,SHIAU Chia-Yang
Bioscience, biotechnology, and biochemistry 71(5), 1122-1129, 2007-05-23
… Hence, a new option other than the most committed ANXV for the ANX based chimera without elaboration of linker construction is presented. …
NAID 10027514184