107,955 research outputs found
Uveo-Meningeal Syndromes: Vogt-Koyanagi-Harada (VKH) Disease
Ocular inflammatory symptoms with concurrent neuro-ophthalmologic manifestations can be diagnostically challenging. We provide a general overview of uveo-meningeal syndromes, which comprises a heterogeneous group of disorders that involve inflammation of the uveal tract, retina, and meninges. The presentation focuses on the uveomeningeal syndrome of Vogt-Koyanagi-Harada (VKH) Disease by providing a comprehensive overview of diagnostic criteria, pathogenesis, clinical course, and management. To demonstrate the heterogeneous clinical presentations and possible neuro-ophthalmological manifestations that can challenge diagnosis, we chronicle three cases of VKH seen at our institution and highlight the diagnostic work-up, management, and outcomes. This presentation summarizes a practical strategy for approaching the clinical heterogeneity of VKH.[1] Brazis PW, Stewart M, Lee A. The Uveo-Meningeal Syndromes. The Neurologist 2004, 10(4):171-184; [2] Tsuboyama M, Chandler JV, Scharf E, et al. Neurologic Complications of Acute Posterior Multifocal Placoid Pigment Epitheliopathy: A Case Series of 4 Patients. Neurohospitalist 2018; 8(3):146-151.; [3] Allegri P, Risotto R, Herbort CP, Murialdo U. CNS Disease and Uveitis. J Ophthalmic Vis Res. 2011; 6(4): 284-308.; [4] Lavezzo MM, Sakata VM, et al. Vogt-Koyanagi-Harada disease: review of a rare autoimmune disease targeting antigens of melanocytes. Ophanet Journal of Rare Diseases. 2016; 11: 29; [5] Read RW, Rao NA: Utility of existing Vogt-Koyanagi-Harada syndrome diagnostic criteria at initial evaluation of the individual patient: a retrospective analysis. Ocul Immunol Inflamm 2000; 8: pp. 227-234.; [6] Read RW, Rao NA, Cunningham ET. Vogt-Koyanagi-Harada Disease. Curr Opin Ophthal. 2000; 11(6):437-442; [7] Read RW, Holland GN, Rao NA, et. al.: Revised diagnostic criteria for Vogt-Koyanagi-Harada disease: report of an international committee on nomenclature. Am J Ophthalmol 2001; 131: pp. 647-652.; [8] Goto, Rao, and Rao. Ryan\u27s Retina 7th Edition 2022; 76, 1577-1589; [9] Feldman BH, O\u27Keefe GD, Salcedo HR, et al. Vogt-Koyanagi-Harada Disease. Eyewiki 2023. https://eyewiki.aao.org/Vogt-Koyanagi-Harada_Disease; [10] Dogan B, Erol MK, Cengiz A. Vogt-Koyanagi-Harada disease following BCG vaccination and tuberculosis. Springerplus. 2016; 5: 603; [11] Ferriera FT, Araujo DC, et al. Possible Association between Vogt-Koyanagi-Harada Disease and Coronavirus Disease Vaccine: A report for Four Cases. Ocul Immunol Inflamm. 2022; 1-7; [12] Rao NA, Gupta A, Dustin L, et al. Frequency of distinguishing clinical features in Vogt-Koyanagi-Harada disease. Ophthalmology 2010;117:591-9; [13] Weisz JM, Holland GN, Roer LN, et. al.: Association between Vogt-Koyanagi-Harada syndrome and HLA-DR1 and DR4 in Hispanic patients living in Southern California. Ophthalmology 1995; 102: pp. 1012-1015.; [14] Shi T, Lv W, Zhang L, Chen J, Chen H. Association of HLA-DR4/HLA-DRB1*04 with Vogt-Koyanagi-Harada disease: a systematic review and meta-analysis. Sci Rep. 2014 Nov 10;4:6887
Vogt-Koyanagi-Harada disease.
Vogt-Koyanagi-Harada disease is a rare, multisystem, autoimmune disorder with numerous clinical manifestations, mediated through a T-helper 1 response against melanocytes in the eye, inner ear, central nervous system, hair and skin. We describe a 20-year-old British-Honduran man with recent worsening headache and photophobia, vomiting and visual blurring. On examination, his pupils reacted sluggishly and visual acuities were bilaterally reduced. Optical coherence tomography showed gross retinal swelling and neurosensory detachments. MR scan of the brain was normal, but cerebrospinal fluid showed a reactive picture with 258 ×10 lymphocytes./L (normal ≤5×10/L). Following treatment with immunosuppression (prednisolone, tacrolimus, mycophenolate mofetil, adalimumab), he made a full recovery. Clinicians should consider Vogt-Koyanagi-Harada disease in patients presenting with headache with acute profound visual loss. A prompt diagnosis and immunosuppressive therapy can lead to complete resolution
Chiral approach to phi radiative decays
The radiative decays of the phi meson are known to be a good source of information about the a0(980) and f0(980) scalar mesons. We discuss these decays starting from a nonlinear model Lagrangian which maintains the (broken) chiral symmetry for the pseudoscalar (P), scalar (S) and vector (V) nonets involved. The characteristic feature is derivative coupling for the SPP interaction. In an initial approximation which models all the scalar nonet radiative processes together with the help of a pointlike vertex, it is noted that the derivative coupling prevents the a0 and f0 resonance peaks from getting washed out (by falling phase space). However, the shapes of the invariant two final PP mass distributions do not agree well with the experimental ones. For improving the situation we verify that inclusion of the charged K meson loop diagrams in the model does reproduce the experimental spectrum shapes in the resonance region. The derivative coupling introduces quadratic as well as logarithmic divergences in this calculation. Using dimensional regularization we show in detail that these divergences actually cancel out among the four diagrams, as expected from gauge invariance. We point out the features which are expected to be important for further work on this model and for learning more about the puzzling scalar mesons
Letter, [Author unclear] to Paulina T. Merritt
Handwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
Novos conhecimentos sobre a doença de Vogt-Koyanagi-Harada
Vogt-Koyanagi-Harada disease (VKH), a well-established multiorgan disorder affecting pigmented structures, is an autoimmune disorder of melanocyte proteins in genetically susceptible individuals. Several clinical and experimental data point to the importance of the effector role of CD4+ T cells and Th1 cytokines, the relevance of searching a target protein in the melanocyte, and the relevance of the HLA-DRB1*0405 in the pathogenesis of the disease. Vogt-Koyanagi-Harada disease has a benign course when early diagnosed and adequatey treated. Full-blown recurrences are rare after the acute stage of Vogt-Koyanagi-Harada disease is over. On the other hand, clinical findings, such as progressive tissue depigmentation (including sunset glow fundus) and uveitis recurrence, indicate that ocular inflammation may persist after the acute phase. Additionally, indocyanine green angiography findings suggest the presence of choroidal inflammation in eyes without clinically detectable inflammation. The aim of this paper is to review the latest research results on Vogt-Koyanagi-Harada disease pathogenesis and chronic/convalescent stages, which may help to better understand this potentially blinding disease and to improve its treatment.A doença de Vogt-Koyanagi-Harada (VKH) afeta vários órgãos que têm em comum a presença de pigmento. É doença autoimune que agride os melanócitos de indivíduos geneticamente susceptíveis. Inúmeras evidências clínicas e experimentais demonstram a importância de células T CD4+ como células efetoras da resposta imune celular, das citocinas pró-inflamatórias Th1, da procura da proteína-alvo dentro do melanócito, e da relevância do HLA-classe II DRB1*0405 na patogênese desta doença. A doença de Vogt-Koyanagi-Harada apresenta bom prognóstico visual desde que o diagnóstico seja precoce e o tratamento instituído seja adequado. Recidivas com acometimento do segmento posterior são raras após a fase aguda da doença. No entanto, achados clínicos como a progressiva despigmentação do fundo, incluindo o aspecto em por do sol, e as recidivas da uveíte indicam que a inflamação ocular pode persistir mesmo após a fase aguda da doença. Os achados da angiografia com indocianina verde também sugerem a presença de inflamação da coróide mesmo em olhos sem inflamação clinicamente detectável. O objetivo do presente trabalho é rever os mais recentes estudos sobre a patogênese da doença Vogt-Koyanagi-Harada e sobre os aspectos clínicos da fase crônica e/ou convalescente da doença, permitindo melhores conhecimentos sobre esta doença potencialmente mórbida e oferecendo terapias mais adequadas
Antigen-specific electrophoretic cell separation for immunological investigations
Preincubation of human blood lymphocytes with cell surface antigen specific antibodies under non-capping conditions reduces the electrophoretic mobility of the corresponding lymphocyte subpopulation. Antigen-positive and antigen-negative cells can be separated by free flow electrophoresis with high yield, purity and viability. The use of fluorescence-labelled second antibodies augments the induced decrease in net surface charge density, and allows rapid detection of antigen-positive cells in the fractions of electrophoresis. Carrier-free cell electrophoresis of human peripheral blood lymphocytes after reaction with anti-IgM-antibody or the monoclonal antibodies OKT4 or OKT8, and sandwich staining with tetrarhodamine isothiocyanate-labelled anti-IgG resulted in the large-scale separation of high pure human B and T lymphocyte subpopulations. Their functional integrity was shown in assays of lymphocyte transformation and of antigen-specific induction and regulation of antibody synthesis in vitro. These separate lymphocyte subpopulations are useful tools for immunological investigations. While, for instance, the effects of drugs on human lymphocytes are obscured by coincident changes in cell composition of the peripheral blood tested that do not by themselves reflect whole body immunocompetence, the cell separation and in vitro assays at a defined cell number and cell composition allow the recording of quantitative changes in the function of different cell subpopulations. We studied the influence of the anesthetic thiopental on separated human lymphocyte subsets. In both polyclonal lectin stimulation and in vitro antibody production, thiopental exhibited a noncytotoxic suppression of lymphocyte functions. B-Cells, T-helper and T-suppressor cells were equally affected and showed the same dose response.(ABSTRACT TRUNCATED AT 250 WORDS
Model of superconducting vortices in layered materials for the interpretation of transmission electron microscopy images
More realistic simulations of the magnetic field and electron optical phase shift associated to pancake vortices in layered high-T-c superconducting specimen require a number of layers larger than 7, the practical upper limit set by the discrete algebraic approach followed so far. This goal can be achieved by resorting to a continuum approximation of the screening layers above and below the one containing the pancake vortex. It is thus possible to increase the number of layers and to investigate more exotic vortex core structures than those represented by the pancakes pinned at tilted columnar defects. In particular it will be shown how recently observed dumbbell-like contrast features in the out-of-focus images of superconducting vortices forming a large angle with the specimen surfaces can be interpreted as due to a kinked structure of the pancakes
Vogt-Koyanagi-Harada syndrome. .
OBJECTIVES: The objectives of this study are to review our current knowledge of the aetiopathogenesis of Vogt-Koyanagi-Harada syndrome, including viral infection, genetic factors and immunomediated mechanisms, and to discuss pathogenesis and its relevance to pharmacotherapy. SYSTEMATIC REVIEW METHODOLOGY: Relevant publications from 1965 to 2012 on the aetiopathogenesis and pharmacotherapy of VKHS were analysed. RESULTS AND CONCLUSION: Vogt-Koyanagi-Harada syndrome (VKHS) is a rare multisystemic autoimmune disease that affects tissues containing melanin, including the eye, inner ear, meninges, and skin. The disease is characterised by bilateral uveitis associated with a varying constellation of auditory, neurological and cutaneous manifestations. The disease occurs more frequently among people with darker skin pigmentation. Asians, Native Americans, and Hispanics are most frequently affected. It predominates in patients aged between 20 and 50years, and females are affected more frequently, with a female:male ratio of 2:1. The classic clinical course is characterised by bilateral panuveitis, hypoacusis, and meningitis, in addition to cutaneous involvement with poliosis, vitiligo, and alopecia. Although the exact cause of VKH disease remains unknown, it is thought to be a T-cell-mediated autoimmune process directed against melanocytes. VKHS classically begins with vague systemic symptoms suggestive of a viral infection, although a clear association between a specific viral agent and the disease has not been established. Genetic factors may play an important role in the loss of self-tolerance in VKHS. The HLA-DRB1*0405 allele is the main susceptibility allele for VKHS. Early and aggressive systemic corticosteroids are still the primary initial therapy for VKHS. Ocular complications may require an intravitreous injection of corticosteroids. Despite proper treatment with steroids, a number of patients experience recurrent attacks or steroid-associated complications. Thus, non steroid immunomodulatory therapy (IMT) has become necessary for the treatment of VKHS
Upregulation of T-bet expression in peripheral blood mononuclear cells during Vogt-Koyanagi-Harada disease
Aim: To test the hypothesis that T-bet expression is altered in patients with Vogt-Koyanagi-Harada (VKH) disease. Methods: Peripheral blood was withdrawn from 16 VKH patients before and after immunosuppressive treatment and from 16 healthy individuals. IFN-, IL-2, and IL-4 in the serum and the supernatants of peripheral blood mononuclear cells (PBMC) cultured with or without phytohaemagglutinin (PHA) were measured by ELISA. T-bet mRNA and protein expression in PBMC cultured with or without PHA was detected by RT-PCR and western blot, respectively. Results: The level of IFN-, but not IL-2 and IL-4, was significantly higher in the supernatants of stimulated PBMC in patients than in controls. A significantly increased T-bet mRNA was found in VKH patients during an active uveitis episode, but not in quiescent patients, compared to controls. T-bet protein was detectable in VKH patients during an active uveitis episode, but not in quiescent patients nor in the healthy controls. Stimulation of PBMC with PHA resulted in a marked upregulation of T-bet mRNA and protein expression for both patients and controls with no significant difference between the two groups. Conclusions: Upregulation of T-bet may be associated with the development of a Th1 mediated immune response in VKH diseas
Handwritten biographical information on Paulina T. McClung Merritt
A handwritten biography of Paulina T. McClung Merritt by an unknown author, 1892.
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