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  1. Book: Vili͡uĭskiĭ ėnt͡sefalomielit

    Goldfarb, Lev G

    2014  

    Title variant Viliuisk encephalomyelitis
    Author's details L.G. Golʹdfarb, V.A. Vladimirt͡sev, N.M. Renvik, F.A. Platonov = Viliuisk encephalomyelitis / L.G. Golfbarb, V.A. Vladimirtsev, N.M. Renwick, F.A. Platonov
    MeSH term(s) Encephalomyelitis
    Keywords Russia
    Language Russian ; English
    Size 254 pages :, illustrations, portraits ;, 21 cm
    Document type Book
    Note Text in Russian, table of contents and summary also in English.
    ISBN 9785769213922 ; 5769213922
    Database Catalogue of the US National Library of Medicine (NLM)

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  2. Article ; Online: The Location of Disease-Causing DES Variants Determines the Severity of Phenotype and the Morphology of Sarcoplasmic Aggregates.

    Silva, André Macedo Serafim / Rodrigo, Patricia / Moreno, Cristiane Araújo Martins / Mendonça, Rodrigo de Holanda / Estephan, Eduardo de Paula / Camelo, Clara Gontijo / Campos, Eliene Dutra / Dias, Alexandre Torchio / Nascimento, Amom Mendes / Kulikowski, Leslie Domenici / Oliveira, Acary Souza Bulle / Reed, Umbertina Conti / Goldfarb, Lev G / Olivé, Montse / Zanoteli, Edmar

    Journal of neuropathology and experimental neurology

    2022  Volume 81, Issue 9, Page(s) 746–757

    Abstract: Desmin (DES) is the main intermediate muscle filament that connects myofibrils individually and with the nucleus, sarcolemma, and organelles. Pathogenic variants of DES cause desminopathy, a disorder affecting the heart and skeletal muscles. We aimed to ... ...

    Abstract Desmin (DES) is the main intermediate muscle filament that connects myofibrils individually and with the nucleus, sarcolemma, and organelles. Pathogenic variants of DES cause desminopathy, a disorder affecting the heart and skeletal muscles. We aimed to analyze the clinical features, morphology, and distribution of desmin aggregates in skeletal muscle biopsies of patients with desminopathy and to correlate these findings with the type and location of disease-causing DES variants. This retrospective study included 30 patients from 20 families with molecularly confirmed desminopathy from 2 neuromuscular referral centers. We identified 2 distinct patterns of desmin aggregates: well-demarcated subsarcolemmal aggregates and diffuse aggregates with poorly delimited borders. Pathogenic variants located in the 1B segment and the tail domain of the desmin molecule are more likely to present with early-onset cardiomyopathy compared to patients with variants in other segments. All patients with mutations in the 1B segment had well-demarcated subsarcolemmal aggregates, but none of the patients with variants in other desmin segments showed such histological features. We suggest that variants located in the 1B segment lead to well-shaped subsarcolemmal desmin aggregation and cause disease with more frequent cardiac manifestations. These findings will facilitate early identification of patients with potentially severe cardiac syndromes.
    MeSH term(s) Cardiomyopathies/genetics ; Cardiomyopathies/pathology ; Desmin/genetics ; Humans ; Muscle, Skeletal/pathology ; Mutation/genetics ; Phenotype ; Retrospective Studies
    Chemical Substances Desmin
    Language English
    Publishing date 2022-09-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 3088-0
    ISSN 1554-6578 ; 0022-3069
    ISSN (online) 1554-6578
    ISSN 0022-3069
    DOI 10.1093/jnen/nlac063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Genetics and infectious disease: convergence at the prion.

    Goldfarb, Lev G

    Epidemiology (Cambridge, Mass.)

    2002  Volume 13, Issue 4, Page(s) 379–381

    MeSH term(s) Alleles ; Disease Outbreaks ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Humans ; Kuru/epidemiology ; Kuru/genetics ; Male ; Models, Genetic ; Mutation ; Papua New Guinea/epidemiology ; Polymorphism, Genetic ; Prions
    Chemical Substances Prions
    Language English
    Publishing date 2002-05-09
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 1053263-8
    ISSN 1531-5487 ; 1044-3983
    ISSN (online) 1531-5487
    ISSN 1044-3983
    DOI 10.1097/00001648-200207000-00003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Comorbidity screening in hidradenitis suppurativa: Evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations.

    Garg, Amit / Malviya, Neeta / Strunk, Andrew / Wright, Shari / Alavi, Afsaneh / Alhusayen, Raed / Alikhan, Ali / Daveluy, Steven D / Delorme, Isabelle / Goldfarb, Noah / Gulliver, Wayne / Hamzavi, Iltefat / Jaleel, Tarannum / Kimball, Alexa B / Kirby, Joslyn S / Kirchhof, Mark G / Lester, Janice / Lev-Tov, Hadar / Lowes, Michelle A /
    Micheletti, Robert / Orenstein, Lauren A / Piguet, Vincent / Sayed, Christopher / Tan, Jerry / Naik, Haley B

    Journal of the American Academy of Dermatology

    2021  Volume 86, Issue 5, Page(s) 1092–1101

    Abstract: Background: Hidradenitis suppurativa (HS) is associated with comorbidities that contribute to poor health, impaired life quality, and mortality risk.: Objective: To provide evidence-based screening recommendations for comorbidities linked to HS.: ... ...

    Abstract Background: Hidradenitis suppurativa (HS) is associated with comorbidities that contribute to poor health, impaired life quality, and mortality risk.
    Objective: To provide evidence-based screening recommendations for comorbidities linked to HS.
    Methods: Systematic reviews were performed to summarize evidence on the prevalence and incidence of 30 comorbidities in patients with HS relative to the general population. The screening recommendation for each comorbidity was informed by the consistency and quality of existing studies, disease prevalence, and magnitude of association, as well as benefits, harms, and feasibility of screening. The level of evidence and strength of corresponding screening recommendation were graded by using the Strength of Recommendation Taxonomy (SORT) criteria.
    Results: Screening is recommended for the following comorbidities: acne, dissecting cellulitis of the scalp, pilonidal disease, pyoderma gangrenosum, depression, generalized anxiety disorder, suicide, smoking, substance use disorder, polycystic ovary syndrome, obesity, dyslipidemia, diabetes mellitus, metabolic syndrome, hypertension, cardiovascular disease, inflammatory bowel disease, spondyloarthritis, and sexual dysfunction. It is also recommended to screen patients with Down syndrome for HS. The decision to screen for specific comorbidities may vary with patient risk factors. The role of the dermatologist in screening varies according to comorbidity.
    Limitations: Screening recommendations represent one component of a comprehensive care strategy.
    Conclusions: Dermatologists should support screening efforts to identify comorbid conditions in HS.
    MeSH term(s) Canada/epidemiology ; Comorbidity ; Female ; Hidradenitis Suppurativa/diagnosis ; Hidradenitis Suppurativa/epidemiology ; Hidradenitis Suppurativa/etiology ; Humans ; Metabolic Syndrome/epidemiology ; Pyoderma Gangrenosum/epidemiology
    Language English
    Publishing date 2021-01-23
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 603641-7
    ISSN 1097-6787 ; 0190-9622
    ISSN (online) 1097-6787
    ISSN 0190-9622
    DOI 10.1016/j.jaad.2021.01.059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Kuru: the old epidemic in a new mirror.

    Goldfarb, Lev G

    Microbes and infection

    2002  Volume 4, Issue 8, Page(s) 875–882

    Abstract: The kuru epidemic lasted almost a century; it started in 1901-1902, reached epidemic proportions in the mid-1950s, and disappeared in the 1990s. Kuru is the prototype member of a group of disorders known as transmissible spongiform encephalopathies (TSEs) ...

    Abstract The kuru epidemic lasted almost a century; it started in 1901-1902, reached epidemic proportions in the mid-1950s, and disappeared in the 1990s. Kuru is the prototype member of a group of disorders known as transmissible spongiform encephalopathies (TSEs) or prion diseases. Recent data on the genetics and pathogenesis of TSEs contribute to a better understanding of the documented kuru phenomena, and vice versa, observations made during the kuru epidemic are immensely helpful in understanding the epidemic of variant Creutzfeldt-Jakob disease that is currently developing in Europe. The major goal of this review is to identify and illustrate these points.
    MeSH term(s) Cannibalism/history ; Creutzfeldt-Jakob Syndrome/epidemiology ; Creutzfeldt-Jakob Syndrome/genetics ; Creutzfeldt-Jakob Syndrome/physiopathology ; History, 20th Century ; Humans ; Kuru/epidemiology ; Kuru/genetics ; Kuru/history ; Kuru/physiopathology ; New Guinea/ethnology ; Prions/physiology
    Chemical Substances Prions
    Language English
    Publishing date 2002-09-24
    Publishing country France
    Document type Historical Article ; Journal Article ; Review
    ZDB-ID 1465093-9
    ISSN 1769-714X ; 1286-4579
    ISSN (online) 1769-714X
    ISSN 1286-4579
    DOI 10.1016/s1286-4579(02)01608-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Tragedy in a heartbeat: malfunctioning desmin causes skeletal and cardiac muscle disease.

    Goldfarb, Lev G / Dalakas, Marinos C

    The Journal of clinical investigation

    2009  Volume 119, Issue 7, Page(s) 1806–1813

    Abstract: Muscle fiber deterioration resulting in progressive skeletal muscle weakness, heart failure, and respiratory distress occurs in more than 20 inherited myopathies. As discussed in this Review, one of the newly identified myopathies is desminopathy, a ... ...

    Abstract Muscle fiber deterioration resulting in progressive skeletal muscle weakness, heart failure, and respiratory distress occurs in more than 20 inherited myopathies. As discussed in this Review, one of the newly identified myopathies is desminopathy, a disease caused by dysfunctional mutations in desmin, a type III intermediate filament protein, or alphaB-crystallin, a chaperone for desmin. The range of clinical manifestations in patients with desminopathy is wide and may overlap with those observed in individuals with other myopathies. Awareness of this disease needs to be heightened, diagnostic criteria reliably outlined, and molecular testing readily available; this would ensure prevention of sudden death from cardiac arrhythmias and other complications.
    MeSH term(s) Animals ; Cardiomyopathies/diagnosis ; Cardiomyopathies/etiology ; Cardiomyopathies/therapy ; Desmin/chemistry ; Desmin/genetics ; Desmin/physiology ; Disease Models, Animal ; Humans ; Muscular Diseases/diagnosis ; Muscular Diseases/etiology ; Muscular Diseases/therapy ; Mutation ; Phenotype ; Protein Structure, Secondary ; alpha-Crystallin B Chain/genetics
    Chemical Substances CRYAB protein, human ; Desmin ; alpha-Crystallin B Chain
    Language English
    Publishing date 2009-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI38027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Myofibrillar myopathies: new developments.

    Olivé, Montse / Kley, Rudolf A / Goldfarb, Lev G

    Current opinion in neurology

    2013  Volume 26, Issue 5, Page(s) 527–535

    Abstract: Purpose of review: Myofibrillar myopathies (MFMs) are a heterogeneous group of skeletal and cardiac muscle diseases. In this review, we highlight recent discoveries of new genes and disease mechanisms involved in this group of disorders.: Recent ... ...

    Abstract Purpose of review: Myofibrillar myopathies (MFMs) are a heterogeneous group of skeletal and cardiac muscle diseases. In this review, we highlight recent discoveries of new genes and disease mechanisms involved in this group of disorders.
    Recent findings: The advent of next-generation sequencing technology, laser microdissection and mass spectrometry-based proteomics has facilitated the discovery of new MFM causative genes and pathomechanisms. New mutations have also been discovered in 'older' genes, helping to find a classification niche for MFM-linked disorders showing variant phenotypes. Cell transfection experiments using primary cultured myoblasts and newer animal models provide insights into the pathogenesis of MFMs.
    Summary: An increasing number of genes are involved in the causation of variant subtypes of MFM. The application of modern technologies in combination with classical histopathological and ultrastructural studies is helping to establish the molecular diagnosis and reach a better understanding of the pathogenic mechanisms of each MFM subtype, thus putting an emphasis on the development of specific means for prevention and therapy of these incapacitating and frequently fatal diseases.
    MeSH term(s) Animals ; Genetic Predisposition to Disease/genetics ; Humans ; Muscle Proteins/genetics ; Muscle Proteins/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Mutation/genetics ; Myopathies, Structural, Congenital/diagnosis ; Myopathies, Structural, Congenital/genetics ; Myopathies, Structural, Congenital/therapy ; Phenotype
    Chemical Substances Muscle Proteins
    Language English
    Publishing date 2013-09-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1182686-1
    ISSN 1473-6551 ; 1350-7540
    ISSN (online) 1473-6551
    ISSN 1350-7540
    DOI 10.1097/WCO.0b013e328364d6b1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Book: Bibliography of hemorrhagic fever with renal syndrome

    Gajdusek, Daniel Carleton / Goldfarb, Lev G. / Goldgaber, Dmitry

    (NIH publication ; 88-2603)

    1987  

    Author's details D. Carleton Gajdusek ; Lev G. Goldfarb ; Dmitry Goldgaber
    Series title NIH publication ; 88-2603
    Collection
    Keywords Hemorrhagic Fever with Renal Syndrome / bibliography ; Hämorrhagisches Fieber ; Nierenkrankheit
    Subject Nephropathie ; Nierenerkrankung ; Nierenerkrankungen ; Niere ; Renopathie
    Language English
    Size XIII, 290 S.
    Edition 2. ed.
    Publisher Laboratory of Central Nervous System Studies u.a.
    Publishing place Bethesda, Md
    Publishing country United States
    Document type Book
    HBZ-ID HT003273619
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Se 101 -(NIH) 88-2603- verfügbar in Königswinter Königswinter

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  9. Article ; Online: Genetic fitness and selection intensity in a population affected with high-incidence spinocerebellar ataxia type 1.

    Platonov, Fedor A / Tyryshkin, Kathrin / Tikhonov, Dmitriy G / Neustroyeva, Tatyana S / Sivtseva, Tatyana M / Yakovleva, Natalya V / Nikolaev, Valerian P / Sidorova, Oksana G / Kononova, Sardana K / Goldfarb, Lev G / Renwick, Neil M

    Neurogenetics

    2016  Volume 17, Issue 3, Page(s) 179–185

    Abstract: Spinocerebellar ataxia type 1 (SCA1) is the major and likely the only type of autosomal dominant cerebellar ataxia in the Sakha (Yakut) people of Eastern Siberia. The prevalence rate of SCA1 has doubled over the past 21 years peaking at 46 cases per 100, ... ...

    Abstract Spinocerebellar ataxia type 1 (SCA1) is the major and likely the only type of autosomal dominant cerebellar ataxia in the Sakha (Yakut) people of Eastern Siberia. The prevalence rate of SCA1 has doubled over the past 21 years peaking at 46 cases per 100,000 rural population. The age at death correlates closely with the number of CAG triplet repeats in the mutant ATXN1 gene (r = -0.81); most patients with low-medium (39-55) repeat numbers survived until the end of reproductive age. The number of CAG repeats expands in meiosis, particularly in paternal transmissions; the average total increase in intergenerational transmissions in our cohort was estimated at 1.6 CAG repeats. The fertility rates of heterozygous carriers of 39-55 CAG repeats in women were no different from those of the general Sakha population. Overall, the survival of mutation carriers through reproductive age, unaltered fertility rates, low childhood mortality in SCA1-affected families, and intergenerational transmission of increasing numbers of CAG repeats in the ATXN1 gene indicate that SCA1 in the Sakha population will be maintained at high prevalence levels. The low (0.19) Crow's index of total selection intensity in our SCA1 cohort implies that this mutation is unlikely to be eliminated through natural selection alone.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Ataxin-1/genetics ; Birth Rate ; Cohort Studies ; Female ; Genetic Fitness ; Heterozygote ; Humans ; Incidence ; Male ; Middle Aged ; Mutation ; Selection, Genetic ; Siberia/epidemiology ; Spinocerebellar Ataxias/epidemiology ; Spinocerebellar Ataxias/genetics
    Chemical Substances ATXN1 protein, human ; Ataxin-1
    Language English
    Publishing date 2016-04-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
    ZDB-ID 1339887-8
    ISSN 1364-6753 ; 1364-6745
    ISSN (online) 1364-6753
    ISSN 1364-6745
    DOI 10.1007/s10048-016-0481-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: A new disease allele for the p.C30071R mutation in titin causing hereditary myopathy with early respiratory failure.

    Pfeffer, Gerald / Sambuughin, Nyamkhishig / Olivé, Montse / Tyndel, Felix / Toro, Camilo / Goldfarb, Lev G / Chinnery, Patrick F

    Neuromuscular disorders : NMD

    2013  Volume 24, Issue 3, Page(s) 241–244

    Abstract: Hereditary myopathy with early respiratory failure is an autosomal dominant myopathy caused by mutations in the 119th fibronectin-3 domain of titin. To date all reported patients with the most common mutation in this domain (p.C30071R) appear to share ... ...

    Abstract Hereditary myopathy with early respiratory failure is an autosomal dominant myopathy caused by mutations in the 119th fibronectin-3 domain of titin. To date all reported patients with the most common mutation in this domain (p.C30071R) appear to share ancestral disease alleles. We undertook this study of two families with the p.C30071R mutation to determine whether they share the same haplotype as previously reported British families or whether the mutation arose as a de novo event. We sequenced the 119th fibronectin-3 domain in these two probands and flanking polymorphisms associated with the British haplotype in hereditary myopathy with early respiratory failure. A family of Indian descent had a haplotype that was not compatible with the British shared haplotype. Cloning of the 119th fibronectin-3 domain in this patient demonstrated polymorphisms rs191484894 and novel noncoding variant c.90225C>T on the same allele as the mutation, which is distinct from previously reported British families. This proves that the p.C30071R mutation itself (rather than the haplotype containing this mutation) causes hereditary myopathy with early respiratory failure and suggests its independent origin in different ethnic groups.
    MeSH term(s) Alleles ; Connectin/genetics ; Genetic Diseases, Inborn/genetics ; Haplotypes ; Humans ; Muscular Diseases/genetics ; Mutation ; Polymorphism, Genetic ; Respiratory Insufficiency/genetics
    Chemical Substances Connectin
    Language English
    Publishing date 2013-12-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; 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.2013.12.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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