Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
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Polyarthritis was induced in lambs via the i/v infection with 2 cm3 of 24-hour Erysipelothrix rhusiopathiae broth culture, which led to distinctive morphologic and biochemical changes in the peripheral blood. The hemoglobin content, the erythrocyte count, and the hematocrit value dropped, while ESR rose with the development of the infection process. The white blood picture presented transient and slight drop of the leukocyte count followed by leukocytosis with shifting to the left, aneosinophilia, lympho- and monopenia in the acute stage, and well manifested eosinophilia in the chronic stage of the infection. The changes in the total protein and the protein fractions consisted in hypoproteinemia in the first days following infection, hypoalbuminemia during the entire period, and hyperproteinemia and hypergammaglobulinemia in the chronic stage. The changes in the blood electrolites consisted in the rise of Ca and K, the drop of Na, and transient changes in the level of P, tending toward a rise in the chronic stage. It was also established that the values of sialic acid were raised in the entire period of polyarthritis development, while those of aspartate aminotransferase and alanine aminotransferase were higher in the first seven-day period only.
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PMID:[Morphological and biochemical changes in the blood of lambs with experimental Erysipelothrix polyarthritis]. 403 95

Case 1. A 23-year-old white housewife presented with an erythematous violaceous rash on her face, neck, chest, and limbs, particularly over the dorsum of the hands and fingers; diffuse alopecia; and an inability to climb stairs and get up from a low seat. The clinical examination showed red to violaceous well-demarcated plaques on sun-exposed areas on the dorsum of the fingers and hands, with periungual erythema and telangiectasia; facial erythema; and heliotrope rash. There was also symmetric involvement of proximal muscles of the limbs. Laboratory examination showed hypergammaglobulinemia, elevated serum aspartate aminotransferase, and serum alanine aminotransferase; normal activities of creatinokinase, lactate dehydrogenase, and aldolase; an antinuclear antibody titer of 1:40 with a speckled pattern; negative anti-DNA and anti-Scl70; and normal serum complement levels (C3, C4, and CH50). Urinalysis results were within normal limits. Skin biopsy histopathology showed hyperkeratosis, edema of the upper epidermis, scattered inflammatory infiltrate, and focal accumulation of mucin in the form of acid mucopolysaccharides. Deep asymptomatic nodules on the inner upper limbs appeared later. Histopathology of these lesions showed focal areas of lobular panniculitis in the subcutaneous tissue, with lymphoplasmocytic inflammatory infiltrate without vasculitis (Figure 1 and Figure 2). Case 2. A 29-year-old white housewife presented with an erythematous violaceous rash on her face, neck, chest, and lower extremities. Clinical examination showed red to violaceous well-demarcated aching plaques on the internal surface of the thighs and tips of the fingers; periungual erythema and digital petechiae; Raynaud's phenomenon; and bilateral ulnar and cervical enlarged lymph nodes. Laboratory examination showed elevated serum aspartate aminotransferase, alanine aminotransferase, creatinokinase, lactate dehydrogenase, and aldolase; negative venereal disease research test results; an antinuclear antibody titer of 1:1024 with speckled pattern; negative anti-DNA and anti-Scl70; and normal serum complement levels (C3, C4, and CH50). Urinalysis results were within normal limits. Histopathology of the deep asymptomatic nodule on the inner left thigh showed lobular panniculitis with a scattered inflammatory infiltrate and diffuse fat necrosis, in addition to calcium deposition between the lipocytes and microcysts without vasculitis (Figure 3).
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PMID:Dermatomyositis with panniculitis. 1721 24

Sarcocystosis in psittaciform birds occurs in several different presentations, making ante-mortem diagnosis challenging without specific laboratory tests. This study followed the course of 11 birds diagnosed with sarcocystosis by serologic analysis and/or post-mortem examinations during a 10-month period in 2006-07. The disease presented in three different clinical forms: an acute pulmonary disease (three birds), muscular disease (five), and neurological disease (three). Early diagnosis of sarcocystosis was possible through the combined used of plasma protein electrophoresis and indirect fluorescent antibody serology in birds presented with the neurological and muscular forms of the disease. In three of these birds the plasma electrophoretic patterns revealed marked hypergammaglobulinemia. All of the birds that presented with the acute pulmonary form developed similar gross and microscopic lesions. Definitive diagnosis was ultimately made by microscopic observation of intravascular pulmonary schizonts containing merozoites. Schizonts were identified in the cerebellum and brainstem in two birds with the neurological form of disease. Those birds that initially presented with severe lethargy and weakness were considered to suffer from the muscular form of disease if they had extreme elevations of muscle enzyme activities (creatine phosphokinase, aspartate aminotransferase) and beta and gamma globulins concentrations, and were seropositive for antibodies to Sarcocystis falcatula. In this group the progression of the disease varied. Two birds recovered completely, and secondary aspergillosis was diagnosed in three birds. The histopathological lesions observed are discussed and interpreted in light of earlier findings from experimental infections in budgerigars, which provide insights into the natural course of sarcocystosis in psittaciform birds.
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PMID:Clinical presentation and pathology of sarcocystosis in psittaciform birds: 11 cases. 1845 22