18 research outputs found

    Antineuronal antibodies in autistic children: relation to blood mercury

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    Background: It was recently suggested that autism, a severe neurodevelopmental disorder, may involve an autoimmune pathogenesis. Mercury (Hg) is a potential risk factor for autoimmunity in autistic children. Objective: We sought to investigate the expression of antineuronal antibodies, as an index of autoimmunity to brain, in autistic children. The potential relationship between blood mercury and these antibodies was also investigated. Methods: Forty autistic children (20 with mild to moderate and 20 with severe disease) were studied in comparison to 40 healthy children. After complete clinical and neuropsychiatric evaluation, serum antineuronal antibodies and blood Hg levels were estimated. Results: Autistic children had significantly higher seropositivity for antineuronal antibodies (67.5%) than healthy controls (5%). Similarly, the former group had significantly higher blood Hg levels than the latter (p < 0.0001). In addition, the two markers were positively associated with some parameters such as the family history of autoimmunity, autistic severity and some important clinical manifestations of autism (mental retardation, behavioral abnormalities and autistic regression) as well as EEG abnormalities. Conclusion: Autism may be, in part, one of the pediatric autoimmune neuropsychiatric disorders. Such autoimmunity may be triggered by environmental Hg exposure. Further studies are warranted to enforce these concepts. If these assumptions could be proved, routine assessment of serum antineuronal antibodies and blood mercury in autistic children would be mandatory. Studies assessing the role of immunotherapy and Hg chelators as new therapeutic modalities for autism are also recommended.Keywords: Antineuronal antibodies; autism; autoimmunity; children; heavy metals; EEG; mercuryEgypt J Pediatr Allergy Immunol 2007; 5(1): 21-3

    Ruminant Brucellosis in the Kafr El Sheikh Governorate of the Nile Delta, Egypt: Prevalence of a Neglected Zoonosis

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    Brucellosis is a zoonosis of mammals caused by bacteria of the genus Brucella. It is responsible for a vast global burden imposed on human health through disability and on animal productivity. In humans brucellosis causes a range of flu-like symptoms and chronic debilitating illness. In livestock brucellosis causes economic losses as a result of abortion, infertility and decreased milk production. The main routes for human infection are consumption of contaminated dairy products and contact with infected ruminants. The control of brucellosis in humans depends on its control in ruminants, for which accurate estimates of the frequency of infection are very useful, especially in areas with no previous frequency estimates. We studied the seroprevalence of brucellosis and its geographic distribution among domestic ruminants in one governorate of the Nile Delta region, Egypt. In the study area, the seroprevalence of ruminant brucellosis is very high and has probably increased considerably since the early 1990s. The disease is widespread but more concentrated around major animal markets. These findings question the efficacy of the control strategy in place and highlight the high infection risk for the animal and human populations of the area and the urgent need for an improved control strategy

    Global Transcriptome and Deletome Profiles of Yeast Exposed to Transition Metals

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    A variety of pathologies are associated with exposure to supraphysiological concentrations of essential metals and to non-essential metals and metalloids. The molecular mechanisms linking metal exposure to human pathologies have not been clearly defined. To address these gaps in our understanding of the molecular biology of transition metals, the genomic effects of exposure to Group IB (copper, silver), IIB (zinc, cadmium, mercury), VIA (chromium), and VB (arsenic) elements on the yeast Saccharomyces cerevisiae were examined. Two comprehensive sets of metal-responsive genomic profiles were generated following exposure to equi-toxic concentrations of metal: one that provides information on the transcriptional changes associated with metal exposure (transcriptome), and a second that provides information on the relationship between the expression of ∼4,700 non-essential genes and sensitivity to metal exposure (deletome). Approximately 22% of the genome was affected by exposure to at least one metal. Principal component and cluster analyses suggest that the chemical properties of the metal are major determinants in defining the expression profile. Furthermore, cells may have developed common or convergent regulatory mechanisms to accommodate metal exposure. The transcriptome and deletome had 22 genes in common, however, comparison between Gene Ontology biological processes for the two gene sets revealed that metal stress adaptation and detoxification categories were commonly enriched. Analysis of the transcriptome and deletome identified several evolutionarily conserved, signal transduction pathways that may be involved in regulating the responses to metal exposure. In this study, we identified genes and cognate signaling pathways that respond to exposure to essential and non-essential metals. In addition, genes that are essential for survival in the presence of these metals were identified. This information will contribute to our understanding of the molecular mechanism by which organisms respond to metal stress, and could lead to an understanding of the connection between environmental stress and signal transduction pathways

    Mammalian sex determination—insights from humans and mice

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    Disorders of sex development (DSD) are congenital conditions in which the development of chromosomal, gonadal, or anatomical sex is atypical. Many of the genes required for gonad development have been identified by analysis of DSD patients. However, the use of knockout and transgenic mouse strains have contributed enormously to the study of gonad gene function and interactions within the development network. Although the genetic basis of mammalian sex determination and differentiation has advanced considerably in recent years, a majority of 46,XY gonadal dysgenesis patients still cannot be provided with an accurate diagnosis. Some of these unexplained DSD cases may be due to mutations in novel DSD genes or genomic rearrangements affecting regulatory regions that lead to atypical gene expression. Here, we review our current knowledge of mammalian sex determination drawing on insights from human DSD patients and mouse models

    Model reference controlled separately excited DC motor

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    This research article proposes the speed control of a separately excited DC motor (SEDM) in the constant torque region. The novelty of this article lies in the application of artificial neural network-based model reference controller (MRC) for the speed control of SEDM. This paper also discusses and compares the speed control systems of SEDM using PI-controlled and fuzzy logic-controlled chopper circuit with MRC. The entire system has been modeled using MATLAB 7.0/SIMULINK toolbox. It has been observed that chopper-controlled speed control system could be eliminated by the use of MRC and the performance of the proposed system is comparable with speed control system using chopper circuit
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