...
机译:由CLCN7的新型突变引起的II型良性骨质疏松症(Albers-Schönberg病)表现出异常的临床表现
Department of Clinical Science Division of Internal Medicine University of Rome “La Sapienza” Rome;
Istituto Dermopatico dell’Immacolata Rome;
Department of Medical Pathophysiology University of Rome “La Sapienza” RomeDepartment of Experimental Medicine University of L’Aquila L’Aquila;
Department of Clinical Science Division of Internal Medicine University of Rome “La Sapienza” Rome;
Department of Clinical Science Division of Internal Medicine University of Rome “La Sapienza” Rome;
Department of Clinical Science Division of Internal Medicine University of Rome “La Sapienza” Rome;
Department of Clinical Science Division of Internal Medicine University of Rome “La Sapienza” Rome;
Department of Pediatrics University of Rome “La Sapienza” Rome;
Department of Pediatrics University of Rome “La Sapienza” Rome;
Department of Medicine and Therapeutics University of Aberdeen Medical School Aberdeen Scotland;
Department of Medicine and Therapeutics University of Aberdeen Medical School Aberdeen Scotland;
Department of Experimental Medicine University of L’Aquila L’Aquila;
Autosomal dominant osteopetrosis; CLCN7; Chloride channel; Osteoclast;
机译:由CLCN7中的新突变引起的II型良性骨质疏松症(Albers-Schonberg病),具有异常的临床表现。
机译:Albers-Sch?nberg病(II型常染色体显性骨质疏松症)中的破骨细胞衍生的抗酒石酸血清磷酸酶5b
机译:Albers-Schonberg病(常染色体显性骨质疏松症,II型)是由ClCN7氯化物通道基因的突变引起的。
机译:因子vii缺乏:718个受试者的临床表现与FVII基因突变的临床表现和分子遗传学
机译:在原发性疾病突变的表型表现中的修饰基因。
机译:II型常染色体显性骨质疏松症(Albers-Schönberg病)到16p13.3染色体的定位
机译:II型常染色体显性骨质疏松症(Albers-Schönberg病)到16p13.3染色体的定位