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  1. Article: Causalgia: redefinition as a clinical pain syndrome.

    Tahmoush, Albert J

    Pain

    1981  Volume 10, Issue 2, Page(s) 187–197

    Abstract: In this report, the following criteria were used for the diagnosis of causalgia: (a) the presence of continuous, burning pain distal to a site of injury; (b) hyperalgesia and allodynia in the painful area; and (c) a traumatic event occurring proximal in ... ...

    Abstract In this report, the following criteria were used for the diagnosis of causalgia: (a) the presence of continuous, burning pain distal to a site of injury; (b) hyperalgesia and allodynia in the painful area; and (c) a traumatic event occurring proximal in the painful area and within weeks prior to the onset of pain. The McGill pain questionnaire was used to test the selected pain population for homogeneity. The scores were similar among the patients and different from the scores in other pain syndromes. It is concluded that the above criteria are sufficient to make the diagnosis of causalgia. In addition, it appears that a central nervous system abnormality best accounts for the clinical features of causalgia.
    MeSH term(s) Adult ; Causalgia/diagnosis ; Causalgia/physiopathology ; Central Nervous System/physiopathology ; Female ; Humans ; Male ; Middle Aged ; Military Medicine ; Neuralgia/diagnosis ; Peripheral Nerves/physiopathology ; Prospective Studies ; Surveys and Questionnaires ; Terminology as Topic
    Language English
    Publishing date 1981-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 193153-2
    ISSN 1872-6623 ; 0304-3959
    ISSN (online) 1872-6623
    ISSN 0304-3959
    DOI 10.1016/0304-3959(81)90194-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1158: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Mutation in the novel nuclear-encoded mitochondrial protein CHCHD10 in a family with autosomal dominant mitochondrial myopathy.

    Ajroud-Driss, Senda / Fecto, Faisal / Ajroud, Kaouther / Lalani, Irfan / Calvo, Sarah E / Mootha, Vamsi K / Deng, Han-Xiang / Siddique, Nailah / Tahmoush, Albert J / Heiman-Patterson, Terry D / Siddique, Teepu

    Neurogenetics

    2014  Volume 16, Issue 1, Page(s) 1–9

    Abstract: Mitochondrial myopathies belong to a larger group of systemic diseases caused by morphological or biochemical abnormalities of mitochondria. Mitochondrial disorders can be caused by mutations in either the mitochondrial or nuclear genome. Only 5% of all ... ...

    Abstract Mitochondrial myopathies belong to a larger group of systemic diseases caused by morphological or biochemical abnormalities of mitochondria. Mitochondrial disorders can be caused by mutations in either the mitochondrial or nuclear genome. Only 5% of all mitochondrial disorders are autosomal dominant. We analyzed DNA from members of the previously reported Puerto Rican kindred with an autosomal dominant mitochondrial myopathy (Heimann-Patterson et al. 1997). Linkage analysis suggested a putative locus on the pericentric region of the long arm of chromosome 22 (22q11). Using the tools of integrative genomics, we established chromosome 22 open reading frame 16 (C22orf16) (later designated as CHCHD10) as the only high-scoring mitochondrial candidate gene in our minimal candidate region. Sequence analysis revealed a double-missense mutation (R15S and G58R) in cis in CHCHD10 which encodes a coiled coil-helix-coiled coil-helix protein of unknown function. These two mutations completely co-segregated with the disease phenotype and were absent in 1,481 Caucasian and 80 Hispanic (including 32 Puerto Rican) controls. Expression profiling showed that CHCHD10 is enriched in skeletal muscle. Mitochondrial localization of the CHCHD10 protein was confirmed using immunofluorescence in cells expressing either wild-type or mutant CHCHD10. We found that the expression of the G58R, but not the R15S, mutation induced mitochondrial fragmentation. Our findings identify a novel gene causing mitochondrial myopathy, thereby expanding the spectrum of mitochondrial myopathies caused by nuclear genes. Our findings also suggest a role for CHCHD10 in the morphologic remodeling of the mitochondria.
    MeSH term(s) Chromosomes, Human, Pair 22 ; Family ; Female ; Genes, Dominant ; Humans ; Male ; Mitochondria/genetics ; Mitochondria/ultrastructure ; Mitochondrial Myopathies/genetics ; Mitochondrial Proteins/genetics ; Mutation ; Puerto Rico
    Chemical Substances CHCHD10 protein, human ; Mitochondrial Proteins
    Language English
    Publishing date 2014-09-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1339887-8
    ISSN 1364-6753 ; 1364-6745
    ISSN (online) 1364-6753
    ISSN 1364-6745
    DOI 10.1007/s10048-014-0421-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5295: Show issues Location:
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  3. Article: CSF-ACE activity in probable CNS neurosarcoidosis.

    Tahmoush, Albert J / Amir, Mary S / Connor, William W / Farry, James K / Didato, Sevastian / Ulhoa-Cintra, Alice / Vasas, Jennifer M / Schwartzman, Robert J / Israel, Harold L / Patrick, Herbert

    Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG

    2002  Volume 19, Issue 3, Page(s) 191–197

    Abstract: Objective: To redefine the utility of CSF-ACE as a selective indicator of probable CNS neurosarcoidosis.: Methods: The diagnosis of probable CNS neurosarcoidosis required: (a) biopsy evidence of systemic sarcoidosis, (b) cortical, brainstem, and/or ... ...

    Abstract Objective: To redefine the utility of CSF-ACE as a selective indicator of probable CNS neurosarcoidosis.
    Methods: The diagnosis of probable CNS neurosarcoidosis required: (a) biopsy evidence of systemic sarcoidosis, (b) cortical, brainstem, and/or spinal cord deficits, (c) enhancing lesions on brain and/or spinal cord MRI, and (d) exclusion of other etiologies which could account for the neurological deficits. Radioassay measurement of CSF-ACE activity was performed in 11 patients who met our criteria for probable CNS neurosarcoidosis and 207 control patients.
    Results: The M +/- SD for CSF-ACE activity was significantly higher (p < 0.05) for the 11 probable CNS neurosarcoidosis patients (9.5 +/- 6.9 nmol/mL/min) than for the control patients (2.9 +/- 2.7 nmol/mL/min). The optimal CSF-ACE activity discriminator value was 8 nmol/mL/min. At this value, the sensitivity and specificity of CSF-ACE activity was 55% and 94%, respectively.
    Conclusions: CSF-ACE activity is a useful biochemical marker of probable CNS neurosarcoidosis when brain and/or spinal cord MRI show diffuse enhancing lesions.
    MeSH term(s) Adult ; Aged ; Biomarkers/cerebrospinal fluid ; Central Nervous System/pathology ; Central Nervous System Diseases/cerebrospinal fluid ; Central Nervous System Diseases/diagnosis ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Peptidyl-Dipeptidase A/cerebrospinal fluid ; Retrospective Studies ; Sarcoidosis/cerebrospinal fluid ; Sarcoidosis/diagnosis ; Sensitivity and Specificity
    Chemical Substances Biomarkers ; Peptidyl-Dipeptidase A (EC 3.4.15.1)
    Language English
    Publishing date 2002-10
    Publishing country Italy
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1339192-6
    ISSN 1124-0490
    ISSN 1124-0490
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2076: Show issues Location:
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