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Nero 7 startsmart 도웹음을 말씀하시면, 일단 리눅이 관련된 수정된 물에 깊슴한 브로드코딩이 있는 것들을 하위 윈도우에서 설치해준다면 그러는 거일 경우 있을 거에요. 된 브로드코딩을 깔고 ê·¸ 부분의 속을 보시면 되실듯해요 지우는게 아니고 안 된 것을 해ë�

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nerosmartstartfreedownloadfullversionThe 5′ and 3′ leader sequences and introns affect the translation of maize leaf rust resistance gene Lr33 in a 3′ proximal position.
The molecular basis of gene-for-gene interactions in host-pathogen resistance can be elucidated by cloning the corresponding resistance gene, the cytoplasmic and nuclear localization signals, its 5′ and 3′ leader sequences and introns. Maize leaf rust resistance gene Lr33 encodes a protein with two leucine-rich nuclear export signals (NESs), a single resistance gene-specific NES (RGS-NES) and a cytoplasmic retention NES. We have cloned and analyzed Lr33 gene sequences encoding the three NESs and their 3′ leader sequences from three inbred lines with different resistance. With native Lr33 gene sequences we compared the properties of the four NESs and those of a structural gene coding for the variable antigen RGA2. Changes in the leader sequences and intron positions that reduce translation efficiency in the coding sequence can be used to link the resistance gene to the protein and/or the antibody in the immune response.The expression of the large electrophoretic variant of the beta-2-glycoprotein I in atypical haemolytic uremic syndrome.
The expression of the large electrophoretic variant of beta-2-glycoprotein I (β2-GPI: GPI-Ib), the most important risk factor for atypical haemolytic uraemic syndrome (aHUS), has not been clarified in aHUS. In this study, we studied the expression of β2-GPI: GPI-Ib in patients with aHUS and determined whether β2-GPI: GPI-Ib mRNA and complement-mediated lysis of β2-GPI: GPI-Ib were increased in aHUS. Fifty-one aHUS patients and 38 non-aHUS patients were included. Seventeen healthy blood donors served as controls. Four groups were defined (three primary and one secondary aHUS) on the basis of clinical and laboratory findings at time of presentation: (i) aHUS caused by complement dysregulation (aHUS-Cdys


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