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Affected Organs (affected + organ)
Selected AbstractsSoluble protein oligomers as emerging toxins in alzheimer's and other amyloid diseasesIUBMB LIFE, Issue 4-5 2007Sergio T. Ferreira Abstract Amyloid diseases are a group of degenerative disorders characterized by cell/tissue damage caused by toxic protein aggregates. Abnormal production, processing and/or clearance of misfolded proteins or peptides may lead to their accumulation and to the formation of amyloid aggregates. Early histopathological investigation of affected organs in different amyloid diseases revealed the ubiquitous presence of fibrillar protein aggregates forming large deposits known as amyloid plaques. Further in vitro biochemical and cell biology studies, as well as studies using transgenic animal models, provided strong support to what initially seemed to be a solid concept, namely that amyloid fibrils played crucial roles in amyloid pathogenesis. However, recent studies describing tissue-specific accumulation of soluble protein oligomers and their strong impact on cell function have challenged the fibril hypothesis and led to the emergence of a new view: Fibrils are not the only toxins derived from amyloidogenic proteins and, quite possibly, not the most important ones with respect to disease etiology. Here, we review some of the recent findings and concepts in this rapidly developing field, with emphasis on the involvement of soluble oligomers of the amyloid-, peptide in the pathogenesis of Alzheimer's disease. Recent studies suggesting that soluble oligomers from different proteins may share common mechanisms of cytotoxicity are also discussed. Increased understanding of the cellular toxic mechanisms triggered by protein oligomers may lead to the development of rational, effective treatments for amyloid disorders. IUBMB Life, 59: 332-345, 2007 [source] Pathological and epidemiological observations on rickettsiosis in cultured sea bass (Dicentrarchus labrax L.) from GreeceJOURNAL OF APPLIED ICHTHYOLOGY, Issue 6 2004F. Athanassopoulou Summary A systemic infection of a Rickettsia -like organism (RLO) in cultured sea bass is described for the first time. In hatcheries, clinical signs were lethargy, inappetence and discoloration. Twenty days after transfer to sea cages from hatcheries where the disease existed, fish showed erratic and abnormal swimming behaviour, loss of orientation, and lethargy. Cumulative mortality in colder months of the year reached 30% in hatcheries and 80% in cages. Surviving fish in cages did not show any clinical signs of RLO infection in the subsequent year. Evidence for a systemic distribution of RLO was supported by histolopathological lesions in both infected hatchery and caged fish, where the lesion profile included cranial sensory, central nervous, integumental and alimentary organ systems. Intracranial lesions were primarily characterized by an ascending histiocytic perineuritis and necrotizing congestive meningoencephalitis, with evidence for transfer of infective agents across the blood,brain barrier confirmed by the presence of RLOs within capillary endothelium and histiocytes in inflamed regions of the optic tectum and the cerebellum. In the most severe cases, infection spread to the statoacoustical (semicircular) canal system and the ependymal lining of ventricles, with marked rickettsial-laden histiocytic infiltration of the canal lumen. Integumental lesions were restricted to the oral submucosa, nares and integumental dermis of the cranium. Alimentary lesions were noted in both the liver parenchyma and mucosa/submucosa of the stomach. In all affected organs the RLOs were found by immunohistochemistry to be related to Piscirickettsia salmonis. [source] Development of liver dysfunction after delivery is possibly due to postpartum autoimmune hepatitis.JOURNAL OF INTERNAL MEDICINE, Issue 4 2002A report of three cases Autoimmune diseases, especially autoimmune thyroid disease, frequently develop after delivery due to the immune rebound mechanism. Most cases involve transient dysfunction of affected organs. Weexamined three patients who developed liver dysfunction after delivery. They were all diagnosed with definite or probable autoimmune hepatitis using the scoring system of the International Autoimmune Hepatitis Group. Moreover, all of them had anti-CYP2D6 antibodies detected by a sensitive radioligand assay. Our findings strongly suggest that liver dysfunction is induced by postpartum autoimmune hepatitis, and clinicians should be aware of this disease. [source] Quantitative temporal and spatial distribution of adenovirus type 2 correlates with disease manifestations and organ failure during disseminated infectionJOURNAL OF MEDICAL VIROLOGY, Issue 2 2008Dirk Forstmeyer Abstract Disseminated adenovirus (HAdV) infections are serious complications in allogenic stem cell transplant (SCT) recipients. Quantitative HAdV DNA detection in blood samples demonstrated the association of high virus loads with disease and improved early diagnosis. However, the pathogenesis of disseminated HAdV disease, for example sources of HAdV DNA shedding in the blood stream and association of HAdV replication sites with disease manifestations, remained obscure. In this report, 24 bioptic and autoptic organ and tissue samples of an adult SCT recipient suffering from disseminated infection were quantitatively analyzed for HAdV DNA. Results indicate subsequent virus replication in the colon, bone marrow and liver as origin of HAdV DNAemia, which increased from 1.4,×,104 copies/ml to a peak of 2,×,109 copies/ml over a period of 84 days in spite of antiviral therapy. Symptoms as diarrhoea, bone marrow failure and hepatic failure were clearly linked to high HAdV DNA concentrations in affected organs. For example, the HAdV DNA level was 2.2,× 103 copies/cell in a colon biopsy when the patient suffered from diarrhoea whereas only 1.1,× 101 copies/cell were detected when symptoms had improved. Focal HAdV infection of the liver as demonstrated by laser microdissection was followed by fulminant virus replication with 1.3,×,105 copies of HAdV DNA/cell causing terminal hepatic failure. In conclusion, pathogenesis of disseminated HAdV disease was associated with virus replication in affected organs and not immune mediated as suggested recently by a fatal case of gene therapy with a non-replication competent HAdV-C5 vector. J. Med. Virol. 80:294,297, 2008. © 2007 Wiley-Liss, Inc. [source] Interleukin-12 induces salivary gland dysfunction in transgenic mice, providing a new model of Sjögren's syndromeARTHRITIS & RHEUMATISM, Issue 12 2009Jelle L. Vosters Objective Interleukin-12 (IL-12) is a pleiotropic cytokine that is elevated in the affected organs of patients with Sjögren's syndrome (SS). We have previously reported that overexpression of IL-12 in CBA mice leads to mononuclear infiltration of salivary and lacrimal glands, as well as to expansion of bronchial lymphoid tissue and decreased mucociliary clearance. Because xerostomia is one of the most important clinical features in SS patients, our main objective in the current study was to evaluate salivary gland function in IL-12,transgenic mice. Our secondary objective was to further characterize this animal model and to determine if the changes observed in these mice are representative of those observed in patients with SS overall. Methods Pilocarpine-stimulated salivary flow was used to address salivary gland function in a large group of IL-12,transgenic mice bred onto the autoimmune-prone SJL background. Furthermore, salivary glands were removed to assess the formation of infiltrates in the glands and gland morphology. Serum was also collected from these animals to investigate the formation of autoantibodies. Results Pilocarpine-stimulated salivary flow was significantly lower in IL-12,transgenic mice than in wild-type controls. Salivary glands from transgenic mice exhibited an increase in both the number and the size of lymphocytic foci, versus glands from age-matched controls. Furthermore, the acini in transgenic mice were fewer in number and larger in size compared with acini in controls. An age-dependent increase in anti-SSB/La antibodies was observed in IL-12,transgenic mice and was accompanied by an increase in antinuclear antibodies. Conclusion Our findings indicate that a number of conditions associated with SS are exhibited by IL-12,transgenic SJL mice and that this model might be useful in researching multiple aspects of the disease. [source] Lactate dehydrogenase predicts hypoxic ischaemic encephalopathy in newborn infants: a preliminary studyACTA PAEDIATRICA, Issue 8 2010Mathias Karlsson Abstract Background:, Enzyme leakage as a result of hypoxia-ischaemia induced cell damage in affected organs is seen together with hypoxic ischaemic encephalopathy (HIE) after perinatal asphyxia. Aim:, To investigate whether plasma lactate dehydrogenase [LDH], alanine aminotransferase [ALT] and aspartate aminotransferase [AST] during the first 12 h after birth predict HIE and adverse neurodevelopment outcome in newborn term infants with intra-partum signs of foetal distress. Methods:, Enzymes were measured within 12 h post partum in newborn infants with differing degree of HIE (n = 41) and in infants with signs of foetal distress during birth (n = 205) without HIE (non-HIE group). All infants were randomized into two groups. One group (n = 123) was used for calculation of cut off limits for the enzymes studied and the other group (n = 123) was used for calculation of the predictive value of the enzymes for detection of HIE. Results:, Using ROC curves, a cut off level of 1049 U/L for [LDH] was the best predictor of HIE (sensitivity 100% and specificity 97%) but also for long term outcome after HIE. Conclusion: [LDH] is a good predictor of HIE during the first 12 h after birth. This result is of clinical interest offering a potential inexpensive and safe prognostic marker in newborn infants with perinatal asphyxia. [source] | |||||||||||||