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  1. Article: A 72-year-old woman with right frontal extra-axial mass.

    Bodi, Istvan / Hortobágyi, Tibor / Buk, Stefan

    Brain pathology (Zurich, Switzerland)

    2008  Volume 18, Issue 2, Page(s) 279–282

    Abstract: We present a case of plasma cell predominant lymphoplasmacyte-rich meningioma with numerous crystalline inclusions. A 72-year-old woman presented with 1-year history of memory disturbance and an MRI revealing a right frontal extra-axial mass. Histology ... ...

    Abstract We present a case of plasma cell predominant lymphoplasmacyte-rich meningioma with numerous crystalline inclusions. A 72-year-old woman presented with 1-year history of memory disturbance and an MRI revealing a right frontal extra-axial mass. Histology showed a benign meningioma with multifocal accumulation of numerous large cells with abundant eosinophilic cytoplasm, filled with lamellar inclusions and bipyramidal crystals. In addition, some classic plasma cells, mastocytes and lymphocytes were also detected. The crystal-containing cells were positive by CD79a and PGM1 and expressed polyclonal light chains, with kappa predominance. Electron microscopy showed crystals with needle or rectangular shape in plasma cells. Plasma cell inclusions have been reported occasionally in reactive inflammatory lesions but more frequently in plasma cell tumors and lymphoplasmacytic lymphoma, maybe associated with crystal-storing histiocytosis. Although plasma cell predominant lymphoplasmacyte-rich meningioma is not uncommon, to our knowledge, similar crystalline inclusions in plasma cells have not been reported previously in meningioma.
    MeSH term(s) Aged ; Brain Neoplasms/pathology ; Brain Neoplasms/surgery ; Female ; Frontal Lobe/pathology ; Frontal Lobe/surgery ; Frontal Lobe/ultrastructure ; Humans ; Magnetic Resonance Imaging/methods ; Meningeal Neoplasms/pathology ; Meningeal Neoplasms/surgery ; Meningioma/pathology ; Meningioma/surgery ; Microscopy, Electron, Transmission ; Neurosurgical Procedures/methods
    Language English
    Publishing date 2008-03-25
    Publishing country Switzerland
    Document type Case Reports ; Letter
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/j.1750-3639.2008.00143.x
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    Zs.A 3585: Show issues Location:
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  2. Article ; Online: Clinical and neuropathological features of X-linked spinal muscular atrophy (SMAX2) associated with a novel mutation in the UBA1 gene.

    Dlamini, Nomazulu / Josifova, Dragana J / Paine, Simon M L / Wraige, Elizabeth / Pitt, Matthew / Murphy, Amanda J / King, Andrew / Buk, Stefan / Smith, Frances / Abbs, Stephen / Sewry, Caroline / Jacques, Thomas S / Jungbluth, Heinz

    Neuromuscular disorders : NMD

    2013  Volume 23, Issue 5, Page(s) 391–398

    Abstract: Infantile-onset X-linked spinal muscular atrophy (SMAX2) is a rare lethal disorder linked to mutations in the UBA1 (previously UBE1) gene, encoding ubiquitin-activating enzyme 1 that has an important role in the ubiquitin-proteasome pathway. Published ... ...

    Abstract Infantile-onset X-linked spinal muscular atrophy (SMAX2) is a rare lethal disorder linked to mutations in the UBA1 (previously UBE1) gene, encoding ubiquitin-activating enzyme 1 that has an important role in the ubiquitin-proteasome pathway. Published pathological reports are scarce. Here we report a male infant who presented from birth with predominantly truncal hypotonia following an antenatal history of reduced fetal movements. He had a myopathic face, profound weakness, multiple contractures and areflexia. Creatine kinase was moderately raised. Brain MRI showed non-specific symmetrical periventricular white matter changes. Neurophysiology revealed evidence of motor and sensory involvement and muscle biopsy showed marked inflammatory changes with subtle features suggestive of acute denervation. UBA1 sequencing revealed a novel hemizygous missense mutation (c.1670A>T; p.Glu557Val). He died from progressive respiratory failure at 4 months. On post mortem assessment, in addition to severe ventral motor neuron pathology, there was widespread involvement of the sensory system, as well as developmental and degenerative cerebellar abnormalities. In contrast to typical SMN1-associated SMA, the thalamus was unaffected. These findings indicate that SMAX2 is more accurately classified as a motor sensory neuronopathy rather than a pure anterior horn cell disorder. Ubiquitin-proteasome pathway defects may not only cause neurodegeneration but also affect normal neuronal development.
    MeSH term(s) Arthrogryposis/genetics ; Fatal Outcome ; Genes, X-Linked/genetics ; Genetic Diseases, X-Linked/genetics ; Humans ; Infant, Newborn ; Male ; Mutation/genetics ; SMN Complex Proteins/genetics ; Spinal Muscular Atrophies of Childhood/complications ; Spinal Muscular Atrophies of Childhood/diagnosis ; Spinal Muscular Atrophies of Childhood/physiopathology ; Ubiquitin-Activating Enzymes/genetics
    Chemical Substances SMN Complex Proteins ; UBA1 protein, human ; Ubiquitin-Activating Enzymes (EC 6.2.1.45)
    Language English
    Publishing date 2013-03-18
    Publishing country England
    Document type Case Reports ; Journal Article
    ZDB-ID 1077681-3
    ISSN 1873-2364 ; 0960-8966
    ISSN (online) 1873-2364
    ISSN 0960-8966
    DOI 10.1016/j.nmd.2013.02.001
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  3. Article ; Online: Congenital muscular dystrophy, myasthenic symptoms and epidermolysis bullosa simplex (EBS) associated with mutations in the PLEC1 gene encoding plectin.

    Forrest, Katharine / Mellerio, Jemima E / Robb, Stephanie / Dopping-Hepenstal, Patricia J C / McGrath, John A / Liu, Lu / Buk, Stefan J A / Al-Sarraj, Safa / Wraige, Elizabeth / Jungbluth, Heinz

    Neuromuscular disorders : NMD

    2010  Volume 20, Issue 11, Page(s) 709–711

    Abstract: Mutations in the PLEC1 gene encoding plectin have been reported in neonatal epidermolysis bullosa simplex with muscular dystrophy of later-onset (EBS-MD). A neuromuscular transmission defect has been reported in one previous patient. We report a boy ... ...

    Abstract Mutations in the PLEC1 gene encoding plectin have been reported in neonatal epidermolysis bullosa simplex with muscular dystrophy of later-onset (EBS-MD). A neuromuscular transmission defect has been reported in one previous patient. We report a boy presenting from birth with features of a congenital muscular dystrophy and late-onset myasthenic symptoms. Repetitive nerve stimulation showed significant decrement, and strength improved with pyridostigmine. Subtle blistering noticed only retrospectively prompted further genetic testing, revealing recessive PLEC1 mutations. We conclude that PLEC1 should be considered in the differential diagnosis of congenital muscular dystrophies and myasthenic syndromes, even in the absence of prominent skin involvement.
    MeSH term(s) Child ; Epidermolysis Bullosa Simplex/genetics ; Humans ; Male ; Muscular Dystrophies/congenital ; Muscular Dystrophies/genetics ; Mutation ; Plectin/genetics
    Chemical Substances PLEC protein, human ; Plectin
    Language English
    Publishing date 2010-11
    Publishing country England
    Document type Case Reports ; Journal Article
    ZDB-ID 1077681-3
    ISSN 1873-2364 ; 0960-8966
    ISSN (online) 1873-2364
    ISSN 0960-8966
    DOI 10.1016/j.nmd.2010.06.003
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  4. Article ; Online: King-Denborough syndrome with and without mutations in the skeletal muscle ryanodine receptor (RYR1) gene.

    Dowling, James J / Lillis, Suzanne / Amburgey, Kimberley / Zhou, Haiyan / Al-Sarraj, Safa / Buk, Stefan J A / Wraige, Elizabeth / Chow, Gabby / Abbs, Stephen / Leber, Steven / Lachlan, Katherine / Baralle, Diana / Taylor, Alexandra / Sewry, Caroline / Muntoni, Francesco / Jungbluth, Heinz

    Neuromuscular disorders : NMD

    2011  Volume 21, Issue 6, Page(s) 420–427

    Abstract: King-Denborough syndrome (KDS), first described in 1973, is a rare condition characterised by the triad of dysmorphic features, myopathy, and malignant hyperthermia susceptibility (MHS). Autosomal dominant inheritance with variable expressivity has been ... ...

    Abstract King-Denborough syndrome (KDS), first described in 1973, is a rare condition characterised by the triad of dysmorphic features, myopathy, and malignant hyperthermia susceptibility (MHS). Autosomal dominant inheritance with variable expressivity has been reported in several cases. Mutations in the skeletal muscle ryanodine receptor (RYR1) gene have been implicated in a wide range of myopathies such as central core disease (CCD), the malignant hyperthermia (MH) susceptibility trait and one isolated patient with KDS. Here we report clinical, pathologic and genetic features of four unrelated patients with KDS. Patients had a relatively uniform clinical presentation but muscle biopsy findings were highly variable. Heterozygous missense mutations in RYR1 were uncovered in three out of four families, of which one mutation was novel and two have previously been reported in MH. Further RyR1 protein expression studies performed in two families showed marked reduction of the RyR1 protein, indicating the presence of allelic RYR1 mutations not detectable on routine sequencing and potentially explaining marked intrafamilial variability. Our findings support the hypothesis that RYR1 mutations are associated with King-Denborough syndrome but that further genetic heterogeneity is likely.
    MeSH term(s) Adolescent ; Biopsy ; Child ; Female ; Humans ; Male ; Malignant Hyperthermia/genetics ; Malignant Hyperthermia/pathology ; Microscopy, Electron ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Mutation, Missense/genetics ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism
    Chemical Substances Ryanodine Receptor Calcium Release Channel
    Language English
    Publishing date 2011-04-22
    Publishing country England
    Document type Case Reports ; Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1077681-3
    ISSN 1873-2364 ; 0960-8966
    ISSN (online) 1873-2364
    ISSN 0960-8966
    DOI 10.1016/j.nmd.2011.03.006
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  5. Article ; Online: Infantile onset myofibrillar myopathy due to recessive CRYAB mutations.

    Forrest, Katharine M L / Al-Sarraj, Safa / Sewry, Caroline / Buk, Stefan / Tan, S Veronica / Pitt, Matthew / Durward, Andrew / McDougall, Marilyn / Irving, Melita / Hanna, Michael G / Matthews, Emma / Sarkozy, Anna / Hudson, Judith / Barresi, Rita / Bushby, Kate / Jungbluth, Heinz / Wraige, Elizabeth

    Neuromuscular disorders : NMD

    2010  Volume 21, Issue 1, Page(s) 37–40

    Abstract: Mutations in the αB-crystallin (CRYAB) gene, encoding a small heat shock protein with chaperone function, are a rare cause of myofibrillar myopathy with autosomal-dominant inheritance, late-onset and moderate severity. We report a female infant ... ...

    Abstract Mutations in the αB-crystallin (CRYAB) gene, encoding a small heat shock protein with chaperone function, are a rare cause of myofibrillar myopathy with autosomal-dominant inheritance, late-onset and moderate severity. We report a female infant presenting from 4 months with profound muscle stiffness, persistent creatine kinase elevation and electromyography characterized by spontaneous electrical activity and pseudomyotonic discharges. Muscle biopsy suggested a myofibrillar myopathy and genetic testing revealed homozygosity for the CRYAB mutation c.343delT (p.Ser115ProfsX14). These findings suggest a severe, recessively inherited form of CRYAB-related myofibrillar myopathy. Profound muscle stiffness as the main presenting feature indicates αB-crystallin as a potent modifier of muscle contractility.
    MeSH term(s) Connectin ; Cytoskeletal Proteins/metabolism ; Electromyography ; Female ; Genes, Recessive/genetics ; Humans ; Infant ; Microfilament Proteins ; Microscopy, Electron, Transmission ; Muscle Proteins/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscle, Skeletal/ultrastructure ; Muscular Diseases/genetics ; Muscular Diseases/pathology ; Muscular Diseases/physiopathology ; Mutation/genetics ; Myofibrils/pathology ; Neural Conduction/physiology ; Peripheral Nerves/physiopathology ; alpha-Crystallin B Chain/genetics ; alpha-Crystallin B Chain/metabolism
    Chemical Substances CRYAB protein, human ; Connectin ; Cytoskeletal Proteins ; MYOT protein, human ; Microfilament Proteins ; Muscle Proteins ; alpha-Crystallin B Chain
    Language English
    Publishing date 2010-12-03
    Publishing country England
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1077681-3
    ISSN 1873-2364 ; 0960-8966
    ISSN (online) 1873-2364
    ISSN 0960-8966
    DOI 10.1016/j.nmd.2010.11.003
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  6. Article ; Online: Multi-minicore disease and atypical periodic paralysis associated with novel mutations in the skeletal muscle ryanodine receptor (RYR1) gene.

    Zhou, Haiyan / Lillis, Suzanne / Loy, Ryan E / Ghassemi, Farshid / Rose, Michael R / Norwood, Fiona / Mills, Kerry / Al-Sarraj, Safa / Lane, Russell J M / Feng, Lucy / Matthews, Emma / Sewry, Caroline A / Abbs, Stephen / Buk, Stefan / Hanna, Michael / Treves, Susan / Dirksen, Robert T / Meissner, Gerhard / Muntoni, Francesco /
    Jungbluth, Heinz

    Neuromuscular disorders : NMD

    2010  Volume 20, Issue 3, Page(s) 166–173

    Abstract: The skeletal muscle ryanodine receptor plays a crucial role in excitation-contraction (EC) coupling and is implicated in various congenital myopathies. The periodic paralyses are a heterogeneous, dominantly inherited group of conditions mainly associated ...

    Abstract The skeletal muscle ryanodine receptor plays a crucial role in excitation-contraction (EC) coupling and is implicated in various congenital myopathies. The periodic paralyses are a heterogeneous, dominantly inherited group of conditions mainly associated with mutations in the SCN4A and the CACNA1S genes. The interaction between RyR1 and DHPR proteins underlies depolarization-induced Ca(2+) release during EC coupling in skeletal muscle. We report a 35-year-old woman presenting with signs and symptoms of a congenital myopathy at birth and repeated episodes of generalized, atypical normokalaemic paralysis in her late teens. Genetic studies of this patient revealed three heterozygous RYR1 substitutions (p.Arg2241X, p.Asp708Asn and p.Arg2939Lys) associated with marked reduction of the RyR1 protein and abnormal DHPR distribution. We conclude that RYR1 mutations may give rise to both myopathies and atypical periodic paralysis, and RYR1 mutations may underlie other unresolved cases of periodic paralysis with unusual features.
    MeSH term(s) Adult ; Arginine/genetics ; Caffeine/pharmacology ; Calcium/metabolism ; Calcium Channels/genetics ; Calcium Channels, L-Type/genetics ; Calcium Channels, L-Type/metabolism ; Cell Line, Transformed ; DNA Mutational Analysis/methods ; Electron Transport Complex IV/drug effects ; Family Health ; Female ; Humans ; Lysine/genetics ; Male ; Membrane Potentials/drug effects ; Membrane Potentials/genetics ; Muscle, Skeletal/pathology ; Muscular Diseases/classification ; Muscular Diseases/genetics ; Muscular Diseases/pathology ; Mutation/genetics ; NAV1.4 Voltage-Gated Sodium Channel ; Patch-Clamp Techniques ; Phosphodiesterase Inhibitors/pharmacology ; Ryanodine/metabolism ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sodium Channels/genetics ; Transfection/methods ; Tritium/metabolism
    Chemical Substances CACNA1S protein, human ; Calcium Channels ; Calcium Channels, L-Type ; NAV1.4 Voltage-Gated Sodium Channel ; Phosphodiesterase Inhibitors ; Ryanodine Receptor Calcium Release Channel ; SCN4A protein, human ; Sodium Channels ; Tritium (10028-17-8) ; Ryanodine (15662-33-6) ; Caffeine (3G6A5W338E) ; Arginine (94ZLA3W45F) ; Electron Transport Complex IV (EC 1.9.3.1) ; Lysine (K3Z4F929H6) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2010-01-18
    Publishing country England
    Document type Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1077681-3
    ISSN 1873-2364 ; 0960-8966
    ISSN (online) 1873-2364
    ISSN 0960-8966
    DOI 10.1016/j.nmd.2009.12.005
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  7. Article ; Online: Recessive mutations in EPG5 cause Vici syndrome, a multisystem disorder with defective autophagy.

    Cullup, Thomas / Kho, Ay Lin / Dionisi-Vici, Carlo / Brandmeier, Birgit / Smith, Frances / Urry, Zoe / Simpson, Michael A / Yau, Shu / Bertini, Enrico / McClelland, Verity / Al-Owain, Mohammed / Koelker, Stefan / Koerner, Christian / Hoffmann, Georg F / Wijburg, Frits A / ten Hoedt, Amber E / Rogers, R Curtis / Manchester, David / Miyata, Rie /
    Hayashi, Masaharu / Said, Elizabeth / Soler, Doriette / Kroisel, Peter M / Windpassinger, Christian / Filloux, Francis M / Al-Kaabi, Salwa / Hertecant, Jozef / Del Campo, Miguel / Buk, Stefan / Bodi, Istvan / Goebel, Hans-Hilmar / Sewry, Caroline A / Abbs, Stephen / Mohammed, Shehla / Josifova, Dragana / Gautel, Mathias / Jungbluth, Heinz

    Nature genetics

    2012  Volume 45, Issue 1, Page(s) 83–87

    Abstract: Vici syndrome is a recessively inherited multisystem disorder characterized by callosal agenesis, cataracts, cardiomyopathy, combined immunodeficiency and hypopigmentation. To investigate the molecular basis of Vici syndrome, we carried out exome and ... ...

    Abstract Vici syndrome is a recessively inherited multisystem disorder characterized by callosal agenesis, cataracts, cardiomyopathy, combined immunodeficiency and hypopigmentation. To investigate the molecular basis of Vici syndrome, we carried out exome and Sanger sequence analysis in a cohort of 18 affected individuals. We identified recessive mutations in EPG5 (previously KIAA1632), indicating a causative role in Vici syndrome. EPG5 is the human homolog of the metazoan-specific autophagy gene epg-5, encoding a key autophagy regulator (ectopic P-granules autophagy protein 5) implicated in the formation of autolysosomes. Further studies showed a severe block in autophagosomal clearance in muscle and fibroblasts from individuals with mutant EPG5, resulting in the accumulation of autophagic cargo in autophagosomes. These findings position Vici syndrome as a paradigm of human multisystem disorders associated with defective autophagy and suggest a fundamental role of the autophagy pathway in the immune system and the anatomical and functional formation of organs such as the brain and heart.
    MeSH term(s) Agenesis of Corpus Callosum/genetics ; Antigens, Neoplasm/genetics ; Autophagy/genetics ; Autophagy-Related Proteins ; Biopsy ; Cataract/genetics ; Consanguinity ; Exome ; Family ; Genes, Recessive ; Humans ; Intracellular Signaling Peptides and Proteins ; Lysosomal Membrane Proteins ; Lysosomes/metabolism ; Muscle, Skeletal/pathology ; Muscle, Skeletal/ultrastructure ; Mutation ; Proteins/metabolism ; Vesicular Transport Proteins
    Chemical Substances Antigens, Neoplasm ; Autophagy-Related Proteins ; EPG5 protein, human ; Intracellular Signaling Peptides and Proteins ; Lysosomal Membrane Proteins ; NBR1 protein, human ; Proteins ; Vesicular Transport Proteins
    Language English
    Publishing date 2012-12-09
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/ng.2497
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