Mitochondrial abnormalities in inclusion-body myositis
暂无分享,去创建一个
G. Kollberg | A. Oldfors | C. Lindberg | A. Oldfors | A. R. Moslemi | L. Jonasson | M. Ohlsson | G. Kollberg | C. Lindberg | A. Moslemi | M. Ohlsson | L. Jonasson
[1] A. Oldfors,et al. Inclusion body myositis: morphological clues to correct diagnosis , 2002, Neuromuscular Disorders.
[2] K. Nagaraju,et al. The Inhibition of Apoptosis in Myositis and in Normal Muscle Cells1 , 2000, The Journal of Immunology.
[3] S. Dimauro,et al. Distribution of wild-type and common deletion forms of mtDNA in normal and respiration-deficient muscle fibers from patients with mitochondrial myopathy. , 1994, Human molecular genetics.
[4] G Serratrice,et al. 31P NMR spectroscopy and ergometer exercise test as evidence for muscle oxidative performance improvement with coenzyme Q in mitochondrial myopathies , 1992, Neurology.
[5] S. Dimauro,et al. The genetics and pathology of oxidative phosphorylation , 2001, Nature Reviews Genetics.
[6] Richard J. Barohn,et al. Inclusion body myositis , 2000, Current treatment options in neurology.
[7] A. Pestronk,et al. Inflammatory myopathy with cytochrome oxidase negative muscle fibers: Methotrexate treatment , 1998, Muscle & nerve.
[8] S. Dimauro,et al. Mitochondrial encephalomyopathies. , 1989, Progress in clinical and biological research.
[9] S. McKiernan,et al. Mitochondrial DNA Deletion Mutations and Sarcopenia , 2002, Annals of the New York Academy of Sciences.
[10] N. Larsson,et al. Mitochondrial myopathies. , 2001, Acta physiologica Scandinavica.
[11] A. Pestronk,et al. Polymyositis with cytochrome oxidase negative muscle fibres. Early quadriceps weakness and poor response to immunosuppressive therapy. , 1997, Brain : a journal of neurology.
[12] W. Engel,et al. Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[13] C. van Broeckhoven,et al. Twinkle and POLG defects enhance age-dependent accumulation of mutations in the control region of mtDNA. , 2004, Nucleic acids research.
[14] A. Schapira. Mitochondrial myopathies. , 1989, BMJ.
[15] Z. Simmons,et al. Sporadic inclusion body myositis and hereditary inclusion body myopathy. , 2002, Journal of clinical neuromuscular disease.
[16] J. Müller‐Höcker. Cytochrome c oxidase deficient fibres in the limb muscle and diaphragm of man without muscular disease: An age-related alteration , 1990, Journal of the Neurological Sciences.
[17] E. Schon,et al. Two direct repeats cause most human mtDNA deletions. , 2004, Trends in genetics : TIG.
[18] C. Münscher,et al. The point mutation of mitochondrial DNA characteristic for MERRF disease is found also in healthy people of different ages , 1993, FEBS letters.
[19] E. Shoubridge,et al. Gene shifting: a novel therapy for mitochondrial myopathy. , 1999, Human molecular genetics.
[20] I. Nishino,et al. Thymidine phosphorylase gene mutations in MNGIE, a human mitochondrial disorder. , 1999, Science.
[21] R. Carrozzo,et al. Maternally‐inherited Leigh syndrome‐related mutations bolster mitochondrial‐mediated apoptosis , 2004, Journal of neurochemistry.
[22] Howard T. Jacobs,et al. Premature ageing in mice expressing defective mitochondrial DNA polymerase , 2004, Nature.
[23] W. Engel,et al. beta-Amyloid precursor protein mRNA is increased in inclusion-body myositis muscle. , 1993, Neuroreport.
[24] P. Nagley,et al. Age-related human mtDNA deletions: a heterogeneous set of deletions arising at a single pair of directly repeated sequences. , 1994, American journal of human genetics.
[25] A Seller,et al. Normal in vivo skeletal muscle oxidative metabolism in sporadic inclusion body myositis assessed by 31P-magnetic resonance spectroscopy. , 1998, Brain : a journal of neurology.
[26] H. Mandel,et al. Depletion of the other genome-mitochondrial DNA depletion syndromes in humans , 2002, Journal of Molecular Medicine.
[27] D. Wallace. Mitochondrial genetics: a paradigm for aging and degenerative diseases? , 1992, Science.
[28] Kristian Borg,et al. Sporadic inclusion body myositis: pilot study on the effects of a home exercise program on muscle function, histopathology and inflammatory reaction. , 2003, Journal of rehabilitation medicine.
[29] S. Dimauro,et al. Medicinal and genetic approaches to the treatment of mitochondrial disease. , 2003, Current medicinal chemistry.
[30] P. Nagley,et al. Multiple mitochondrial DNA deletions in an elderly human individual , 1992, FEBS letters.
[31] S. Dimauro,et al. Mitochondrial Encephalomyopathies: Therapeutic Approach , 2004, Annals of the New York Academy of Sciences.
[32] Jeong W. Pak,et al. Mitochondrial DNA mutations as a fundamental mechanism in physiological declines associated with aging , 2003, Aging cell.
[33] E. Holme,et al. Mitochondrial DNA Deletions in Muscle Fibers in Inclusion Body Myositis , 1995, Journal of neuropathology and experimental neurology.
[34] J. Schröder,et al. Pleomorphic mitochondrial and different filamentous inclusions in inflammatory myopathies associated with mtDNA deletions , 1998, Acta Neuropathologica.
[35] M. Fardeau,et al. Ageing muscle: clonal expansions of mitochondrial DNA point mutations and deletions cause focal impairment of mitochondrial function , 2002, Neuromuscular Disorders.
[36] W. Engel,et al. β‐Amyloid precursor epitopes in muscle fibers of inclusion body myositis , 1993 .
[37] E. Shoubridge,et al. Characterization of the mitochondrial DNA abnormalities in the skeletal muscle of patients with inclusion body myositis. , 1998, Journal of neuropathology and experimental neurology.
[38] Margaret A. Johnson,et al. Role of mitochondrial DNA mutations in human aging: Implications for the central nervous system and muscle , 1998, Annals of neurology.
[39] S. Dimauro,et al. Mitochondrial diseases. , 1989, Neurologic clinics.
[40] N. Chu,et al. Coenzyme Q10 treatment in mitochondrial encephalomyopathies. Short-term double-blind, crossover study. , 1997, European neurology.
[41] A. Oldfors,et al. Analysis of multiple mitochondrial DNA deletions in inclusion body myositis , 1997, Human mutation.
[42] T Yamamoto,et al. High-dose vitamin C therapy for inclusion body myositis. , 2001, Fukuoka igaku zasshi = Hukuoka acta medica.
[43] R. Hohlfeld,et al. Cytotoxic mechanisms in inflammatory myopathies. Co-expression of Fas and protective Bcl-2 in muscle fibres and inflammatory cells. , 1997, Brain : a journal of neurology.
[44] M. Falkenberg,et al. Reconstitution of a minimal mtDNA replisome in vitro , 2004, The EMBO journal.
[45] E. Holme,et al. Mitochondrial DNA deletions in inclusion body myositis. , 1993, Brain : a journal of neurology.
[46] A. Oldfors,et al. Expression of Bcl‐2 in inclusion body myositis , 2002, Acta neurologica Scandinavica.
[47] G. Comi,et al. Human mitochondrial DNA deletions associated with mutations in the gene encoding Twinkle, a phage T7 gene 4-like protein localized in mitochondria , 2001, Nature Genetics.
[48] E. Shoubridge,et al. Aerobic conditioning in patients with mitochondrial myopathies: Physiological, biochemical, and genetic effects , 2001, Annals of neurology.
[49] E. Holme,et al. Autosomal dominant progressive external ophthalmoplegia , 1999, Neurology.
[50] P. Tonin,et al. T-cell anti-apoptotic mechanisms in inflammatory myopathies , 2000, Journal of Neuroimmunology.
[51] A. Eisen,et al. Inclusion body myositis , 1978, Neurology.
[52] C. Broeckhoven,et al. Mutation of POLG is associated with progressive external ophthalmoplegia characterized by mtDNA deletions , 2001, Nature Genetics.
[53] S. Welle,et al. Ragged Red Fibers in Normal Aging and Inflammatory Myopathy , 1995, Annals of neurology.
[54] Margaret A. Johnson,et al. Reversal of a mitochondrial DNA defect in human skeletal muscle , 1997, Nature Genetics.
[55] S. Dimauro,et al. Multiple mitochondrial DNA deletions in sporadic inclusion body myositis: A study of 56 patients , 1996, Annals of neurology.
[56] E. Holme,et al. Clonal expansion of mitochondrial DNA with multiple deletions in autosomal dominant progressive external ophthalmoplegia , 1996, Annals of neurology.
[57] M. Nakagawa,et al. Apoptosis is suspended in muscle of mitochondrial encephalomyopathies , 2002, Acta Neuropathologica.
[58] L. Peltonen,et al. Role of adenine nucleotide translocator 1 in mtDNA maintenance. , 2000, Science.
[59] E. Shoubridge,et al. Late‐onset mitochondrial myopathy , 1995, Annals of neurology.
[60] N. Ashley,et al. Twinkle helicase is essential for mtDNA maintenance and regulates mtDNA copy number. , 2004, Human molecular genetics.
[61] W. Engel,et al. beta-Amyloid precursor epitopes in muscle fibers of inclusion body myositis. , 1993, Annals of neurology.
[62] P. Nagley,et al. Mutations in mitochondrial DNA accumulate differentially in three different human tissues during ageing. , 1998, Nucleic acids research.
[63] Kucharz Ej. [Inclusion body myositis]. , 1998, Polskie Archiwum Medycyny Wewnetrznej.