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Biomedical subjects

H Kaminski

Publications and source records attributed to H Kaminski.

9 recordsLinked to original sources
PubMed2006

Medical and surgical treatment for ocular myasthenia.

BACKGROUND: Approximately 50% of people with myasthenia gravis present initially with purely ocular symptoms, so called ocular myasthenia and between 50 to 60% of these people will progress to develop generalized disease. The vast majority will do so within the first one to two years. There is controversy surrounding the appropriate management of patients with ocular myasthenia. OBJECTIVES: To perform a systematic review of the literature relevant to the treatment of ocular myasthenia and to answer three specific questions. Are there any medical or surgical treatments that have an impact on the risk of progression from ocular to generalized myasthenia gravis? Are there any medical or surgical treatments that improve symptoms of diplopia or ptosis in ocular myasthenia? What is the frequency of side effects associated with treatments used in people with ocular myasthenia? SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register (searched December 2004), MEDLINE (1996 to 2004) and EMBASE (1980 to 2004) for randomized controlled trials as well as case-control and cohort studies. The titles and abstracts of all articles were read by both authors and the full text of all articles that were of possible relevance was reviewed in full. The references of all manuscripts included in the review were scanned to identify additional articles of relevance and experts in the field were contacted to identify additional published and unpublished data. Where necessary and possible, we contacted authors for further information. SELECTION CRITERIA: To be included in the review, studies had to meet three criteria: (a) randomized (or quasi-randomized) controlled study design; (b) active treatment compared to placebo, no treatment or some other treatment; and (c) results reported separately for patients with ocular myasthenia (grade 1) as defined by the Myasthenia Gravis Foundation of America. DATA COLLECTION AND ANALYSIS: We collected data regarding the risk of progression to generalized myasthenia gravis, improvement in ocular symptoms, and the frequency of treatment-related side effects. MAIN RESULTS: We identified two randomized controlled trials relevant to the treatment of ocular myasthenia, only one of which reported results in terms of the pre-specified outcome measures used in this review. This study included only three participants and was of limited methodological quality. In the absence of data from randomized controlled trials, we present a review of the available observational data. AUTHORS' CONCLUSIONS: There are no data from randomized controlled trials on the impact of any form of treatment on the risk of progression from ocular to generalized myasthenia gravis. The available randomized controlled literature does not permit any meaningful conclusions about the efficacy of any form of treatment for ocular myasthenia. Data from several reasonably good quality observational studies suggest that corticosteroids and azathioprine may be beneficial in reducing the risk of progression to generalized myasthenia gravis.

Adrenocorticotropic Hormone↗
PubMed2005

Simultaneous tomography and diffraction analysis of creep damage.

Creep damage by void nucleation and growth limits the lifetime of components subjected to loading at high temperatures. We report a combined tomography and diffraction experiment using high-energy synchrotron radiation that permitted us to follow in situ void growth and microstructure development in bulk samples. The results reveal that void growth versus time follows an exponential growth law. The formation of large void volumes coincides with texture evolution and dislocation density, reaching a steady state. Creep damage during a large proportion of sample creep life is homogeneous before damage localization occurs, which leads to rapid failure. The in situ determination of void evolution in bulk samples should allow for the assessment of creep damage in metallic materials and subsequently for lifetime predictions about samples and components that are subject to high-temperature loading.

Journal Article↗
PubMed2000

Identification of viral macrophage inflammatory protein (vMIP)-II as a ligand for GPR5/XCR1.

Lymphotactin is unique among chemokines in that it contains only two of four conserved cysteines and may possess a structure less constrained than other chemokines. The viral chemokine vMIP-II, which presumably has a structure similar to that of CC chemokines has been shown to inhibit many chemokine receptors, but its activity at GPR5/XCR1 has not been described. Interestingly, vMIP-II (but not vMIP-I) was found to be a potent antagonist of lymphotactin activity at GPR5/XCR1, extending the range of chemokine classes that this viral protein is known to inhibit to include the C class chemokine. In addition, we have extended previous analyses of GPR5/XCR1 expression and show that this receptor is expressed in leukocyte cells previously shown to be responsive to lymphotactin.

Animals↗
PubMed2000

Autoantibodies in thymoma-associated myasthenia gravis with myositis or neuromyotonia.

BACKGROUND: About 50% of patients with thymoma have paraneoplastic myasthenia gravis (MG). Myositis and myocarditis or neuromyotonia (NMT) will also develop in some. Patients with thymoma-associated MG produce autoantibodies to a variety of neuromuscular antigens, particularly acetylcholine receptor (AChR), titin, skeletal muscle calcium release channel (ryanodine receptor [RyR]), and voltage-gated potassium channels (VGKC). OBJECTIVE: To examine whether neuromuscular autoantibodies in patients with thymoma correlate with specific clinical syndromes. METHODS: Serum and plasma samples from 19 patients with thymoma-associated MG, of whom 5 had myositis and 6 had NMT, underwent testing for antibodies to AChR, titin, RyR, and VGKC. RESULTS: Antibodies to AChR and titin were found in 19 and 17 patients, respectively. Antibodies to RyR correlated with the presence of myositis (P = .03); they were found in all 5 patients with myositis and in only 1 patient with NMT, but also in 4 of 8 patients with neither disease. Antibodies to VGKC were found in 4 patients with NMT, 1 of 3 patients undergoing testing for myositis, and 2 of 7 patients undergoing testing with neither comorbidity. Presence of RyR antibodies correlated with high levels of titin antibodies. CONCLUSIONS: The results appear to distinguish partially between 3 groups of patients with thymoma-associated MG: the first with RyR antibodies and myositis or myocarditis, the second with NMT without RyR antibodies, and the third without RyR antibodies, myositis, or NMT. Differences in the thymoma may underlie these pathologic associations.

Adult↗
PubMed1999

Macrophage inflammatory protein-3 beta enhances IL-10 production by activated human peripheral blood monocytes and T cells.

We report that the addition of human macrophage inflammatory protein-3 beta (MIP-3 beta) to cultures of human PBMCs that have been activated with LPS or PHA results in a significant enhancement of IL-10 production. This effect was concentration-dependent, with optimal MIP-3 beta concentrations inducing more than a 5-fold induction of IL-10 from LPS-stimulated PBMCs and a 2- to 3-fold induction of IL-10 from PHA-stimulated PBMCs. In contrast, no significant effect on IL-10 production was observed when 6Ckine, the other reported ligand for human CCR7, or other CC chemokines such as monocyte chemoattractant protein-1, RANTES, MIP-1 alpha, and MIP-1 beta were added to LPS- or PHA-stimulated PBMCs. Similar results were observed using activated purified human peripheral blood monocytes or T cells. Addition of MIP-3 beta to nonactivated PBMCs had no effect on cytokine production. Enhancement of IL-10 production by MIP-3beta correlated with the inhibition of IL-12 p40 and TNF-alpha production by monocytes and with the impairment of IFN-gamma production by T cells, which was reversed by addition of anti-IL-10 Abs to the cultures. The ability of MIP-3 beta to augment IL-10 production correlated with CCR7 mRNA expression and stimulation of intracellular calcium mobilization in both monocytes and T cells. These data indicate that MIP-3 beta acts directly on human monocytes and T cells and suggest that this chemokine is unique among ligands binding to CC receptors due to its ability to modulate inflammatory activity via the enhanced production of the anti-inflammatory cytokine IL-10.

Adjuvants, Immunologic↗
PubMed1999

Cutting edge: species specificity of the CC chemokine 6Ckine signaling through the CXC chemokine receptor CXCR3: human 6Ckine is not a ligand for the human or mouse CXCR3 receptors.

The CC chemokine known as 6Ckine (SLC, Exodus-2, or TCA4) has been identified as a ligand for CCR7. Mouse 6Ckine has also been shown to signal through mouse CXCR3 and share some of the activities of IFN-gamma inducible protein 10 and monokine induced by IFN-gamma. Nonetheless, human 6Ckine has not been shown to bind CXCR3 receptor or have angiostatic activity. In this study, we report that human 6Ckine does not induce a calcium flux in either human CXCR3 or mouse CXCR3 transfected cells, although it is an equally potent agonist as mouse 6Ckine and human macrophage inflammatory protein-3beta in human CCR7 transfected cells. Mouse 6Ckine (but not human 6Ckine) is capable of competing with radiolabeled IFN-gamma inducible protein 10 for human CXCR3. In addition, radiolabeled human 6Ckine does not bind to either human CXCR3 or mouse CXCR3. Together these data suggest that human CC chemokine 6Ckine is not a ligand for the human or mouse CXC chemokine receptor CXCR3.

Animals↗