Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 998 children with recurrent respiratory diseases 26 children with selective IgA deficiency were found. Three groups were considered according to IgA level in serum: group I with IgA under 0.05 g per litre; group II with IgA between 0.05 and 0.3 g per litre; group III with IgA above 0.3 and under 1 g per litre. Non specific immunity was studied in these patients including immunoglobulin levels, alpha-1-antitrypsin (A.A.T.) phenotypes, phagocytosis of staphylococcus aureus by PMN, lysozyme level, complement system. Cellular immunity was evaluated by IDR tests and rosette forming cells (RE). Only non specific immune systems were disturbed in some patients and appeared as aggravating factors in IgA deficient patients. We found: Abnormal phenotypes of ATT in 11 cases; deficiencies of engulfment in 6 cases, of bactericidal activities of PMN in 7 cases out of 16 studied; decrease of lysozyme level in 4 cases out of 17 studied; increase of IgE level in 9 cases with atopic symptoms in 7 patients. In our experience the chief aggravating factor in IgA deficient patients is abnormal phenotype of AAT.
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PMID:[Non specific immunity of children with selective IgA deficiency. Aggravating role of abnormal phenotype of alpha-1-antitrypsin (author's transl)]. 31 58

66 patients with chronic urticaria were examined using a three-stage examination protocol. Stage I. consisted of case history, general dermatological and internal physical examination and routine laboratory tests. Stage II. comprised investigation for focal infections (dental, oto-laryngeal, gynecological, bile culture), determination of AST, acidity tests of the stomach and aimed radiological examinations. Stage III. consisted of immunological laboratory tests (immune complex, Igs, IgE, special IgE determination) and allergological examinations (epicutaneous, intracutaneous probes, Prick test).
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PMID:[Chronic urticaria]. 235 94

Liver function tests and immunoglobulin features of apparently 'healthy' blood donors were studied. Twenty-one (9.5%) subjects with HBsAg were observed. These subjects were found to have significantly higher mean and standard deviation of total serum bilirubin, alanine and aspartate aminotransferase levels than those of a randomly selected HBsAg-negative group. Serum urea was significantly lower (p less than 0.01) in the HBsAg-positive cases. Total serum IgE (IU/ml) was significantly higher in the HBsAg-positive cases (p less than 0.01). Comparison of laboratory findings of these cases and active hepatitis HBsAg-positive subjects showed that there were more elevated abnormalities in the latter.
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PMID:Biochemical studies of apparently 'healthy' blood donors with reference to liver function tests and immunoglobulins. 408 21

Hantaviruses cause an important human illness, HFRS. Blood samples from 22 HFRS-positive, six seronegative patients and 15 healthy controls were examined in 1995, during the largest HFRS epidemic in Croatia. Results of double- and triple-colour immunofluorescence analysis showed an increased percentage of cytotoxic T cells (CD3+CD8+) in seropositive patients compared with seronegatives and healthy controls. The majority of seropositive HFRS patients expressed activation and memory antigens on T and B lymphocytes. The percentage of CD23+ and CD21+ B lymphocytes was lower in seropositive patients. HFRS patients had elevated levels of sCD23 and five had elevated total IgE. The increased expression of both early and late T cell activation antigens, e.g. CD25, CD71 and HLA-DR, memory cells and sCD23 positively correlated with biochemical parameters (AST, ALT, urea, alpha2-globulin) during the acute phase of HFRS. The phenotypic changes observed, especially early and late T cell activation markers, as well as memory cells, could be useful parameters in the evaluation of HFRS course, and prognostic factors of HFRS severity. Additional attention should be paid to liver involvement in the pathogenesis of HFRS.
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PMID:Role of peripheral blood mononuclear cell (PBMC) phenotype changes in the pathogenesis of haemorrhagic fever with renal syndrome (HFRS). 993 61

The free radical nitric oxide (NO) is endogenously produced by enzymes known as NO synthases. NO in the airways is involved in a number of pathophysiological processes, such as airway inflammation, allergic reactions, and asthma. Asthma is a multifactorial disease that is caused by environmental and genetic factors. Genome wide screening approaches in families revealed evidence for linkage between chromosomal region 12q and allergic diseases, increased serum IgE levels as well as the development of asthma. The gene encoding for neuronal NOS (NOS1) is an attractive candidate gene for asthma, not only because it is localized in chromosomal region 12q24. Experimental studies in animals and humans suggest that NOS1 plays an important role in asthma. For instance, in a murine model of allergic asthma, NOS1 has been shown to be important for the development of bronchial hyperresponsiveness, since mice deficient for the nos1 gene were less responsive to airway challenge than both wild-type mice and mice deficient for the nos2 gene. Case-control studies in humans revealed allelic associations between polymorphic markers in the NOS1 gene and the diagnosis of asthma. Furthermore, increased concentrations of NO in the airways of asthmatics are closely related to the size of an intronic (AAT)(n)-repeat polymorphism in the NOS1 gene. The purpose of this review is to summarize studies that provide evidence for an involvement of NOS1 in the genetics of asthma.
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PMID:[Genetics of the neuronal NO synthase (NOS1) in the etiology of bronchial asthma]. 1150 91

Wolbachia are intracellular alpha-proteobacteria, closely related to Rickettsia, that infect various arthropods and filarial parasites. In the present study, the cDNA encoding the aspartate aminotransferase (AspAT) of Wolbachia from the human pathogenic filarial parasite Onchocerca volvulus (Ov-WolAspAT) was identified. At the amino acid level, the identity of the Ov-WolAspAT was 56% to Rickettsia prowazekii AspAT and 54% to the AspAT of the nitrogen-fixing bacterium Sinorhizobium meliloti, but the highest degree of identity was found to the putative AspAT of Wolbachia from Brugia malayi and Drosophila melanogaster (85%). All of these bacterial AspATs are members of the AspAT subclass Ib. A 35 kDa fragment of the Ov-WolAspAT was expressed in Escherichia coli, and immunolocalization using polyclonal antibodies against this antigen revealed that Ov-WolAspAT is present in a considerable proportion of the Wolbachia from O. volvulus, as well as in the endobacteria of several other filarial parasites. Western blot analysis using recombinant Ov-WolAspAT as antigen showed that IgG1 antibodies were present in 70 (51%) individuals living in areas endemic for O. volvulus, B. malayi or Wuchereria bancrofti and no IgG4 or IgE antibodies were found. Among 40 sera of persons from Uganda and Liberia who were putatively not infected with human filarial parasites, 11 (28%) individuals presented IgG1 antibodies, while none of the 33 sera from healthy Europeans and none of the 14 sera from patients with proven Rickettsia or Brucella infections reacted with the antigen. These results also show that an intracellular protein of Wolbachia endobacteria (WolAspAT) acts as antigen in human filariasis.
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PMID:An aspartate aminotransferase of Wolbachia endobacteria from Onchocerca volvulus is recognized by IgG1 antibodies from residents of endemic areas. 1274 2

X-linked hyper-immunoglobulin M (IgM) syndrome (XHIGM) is a rare genetic primary immunodeficiency disease caused by mutations of the CD40 ligand (CD40L) gene with normal or elevated levels of IgM and markedly decreased serum IgG, IgA, and IgE. Liver disease may occur as a clinical manifestation in XHIGM. This complication appears to increase with age. We report an 18-year-old male patient who had recurrent episodes of acalculous cholecystitis (AC) and sclerosing cholangitis (SC). The diagnosis of XHIGM was confirmed by the finding of CD40L expression < 1% of normal and a tyrosine 169 asparaginase (t526a) mutation in exon 5 (the tumor necrosis factor domain) of the CD40L gene. The patient had direct hyperbilirubinemia (direct bilirubin 5.5 mg/dL, total bilirubin 8.7 mg/dL), cholestasis (alkaline phosphatase 1133 U/L, gamma-glutamyl transferase 1019 U/L) and elevated transaminases (aspartate aminotransferase 70 U/L, alanine aminotransferase 101 U/L). Findings on abdominal ultrasound and abdominal computed tomography were compatible with AC. After the fourth episode of cholecystitis, cholecystectomy and liver biopsy were performed. Operative cholangiography revealed poor opacification of the hepatic duct and proximal common bile duct; the upstream intrahepatic bile ducts were not visualized. The biopsy specimen showed marked fibrosis of the portal areas. Enterococcus species was cultured from the bile. Children or adolescents with recurrent AC and SC should be evaluated for an underlying immunodeficiency syndrome such as XHIGM.
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PMID:Recurrent acalculous cholecystitis and sclerosing cholangitis in a patient with X-linked hyper-immunoglobulin M syndrome. 1603 32

Among proteins secreted from activated eosinophil granulocytes, eosinophil cationic protein (ECP) is the most useful tool for the follow-up of inflammatory diseases. Since ECP level reflects the eosinophil activation, it gives valuable information about disease activity. In this study, we aimed to investigate the possible relation between ECP levels and symptoms and laboratory findings of cystic echinococcosis (CE) and to evaluate the role of this protein in the diagnosis of CE. The study which was conducted at Clinical Microbiology Laboratory of Suleyman Demirel University Medical Faculty, Isparta, Turkey, included 58 patients with a pre-diagnosis of CE and 32 healthy individuals as control group. The diagnosis of CE was established serologically by modified enzyme-linked immunosorbent assay (ELISA) and indirect hemagglutination (IHA) test. The quantitative determination of ECP levels was done by fluoro-enzyme immunoassay (FEIA; Uni-CAP ECP, Pharmacia-Upjohn). The mean ECP level was 31.6 +/- 37 microg/ml in the patient group and 9.1 +/- 2.1 microg/ml in the control group, the difference being statistically significant (p = 0.001). Significant differences were also detected for erythrocyte sedimentation rate (ESR) (p = 0.001), total IgE level (p = 0.001), eosinophile count (p = 0.05) and CRP (p = 0.001) between the patient and the control groups. ECP was detected to be high in 35 (60%), IgE in 37 (63%), CRP in 29 (50%) and eosinophile count in 9 (15.5%) patients. While age, gender, ESR, IgE and CRP levels of patients with high ECP levels were not significantly different from levels of patients with normal ECP levels, significantly different eosinophil counts were detected among patients with high ECP values when compared to patients with normal ECP values. Furthermore, a correlation was detected between ECP levels and eosinophil rate, IgE and CRP levels of patients with CE (p = 0.01), while there was no correlation between ECP and ESR levels. Although high ECP level patients exhibited higher ALT and AST levels, no correlation was determined between liver enzyme levels and ECP levels (p > 0.05). The most common symtoms among CE patients were abdominal pain (41%), other gastrointestinal complaints (38%), shortness of breath (12%) and fever (10%). No statistically significant difference in terms of symptoms was detected between patients with high ECP levels and normal ECP levels. However, statistically significant difference was detected between ECP levels of patients with symptoms (except shortness of breath) and patients without symptoms (p < 0.05). In conclusion, ECP seems to be associated with the symptoms and signs of CE and it can be used as a valuable marker besides the other laboratory tests for the evaluation of patients with CE.
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PMID:[Evaluation of eosinophil cationic protein levels with clinical symptoms and laboratory findings of patients with cystic echinococcosis]. 1962 14

The aim of the study is to examine the relationship between toner-exposed work and health indices related to respiratory disorders and to confirm the baseline of a cohort study to clarify the effect of toner exposure in manufacturing plants. Subjects were 1614 male workers (809 toner-exposed workers and 805 referents) who were engaged in toner manufacturing plants in Japan (Fuji Xerox Co., Ltd). The age of subjects was from 19 to 59 years, and the average age was 40.2 years(median 40 years, SD 7.67). We conducted a pulmonary function test (PEFR, VC, FVC, FEV(1.0)%, V25/Ht) and a blood cell test (RBC, Hb, Hct, Plt, WBC, cell contents of WBC) and measured biochemical indices in blood (ALT, AST, gamma-GTP, CRP, IgE) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in urine. Student t-test and logistic regression analysis were applied to compare between the toner-exposed workers and the referents and to analyze the relationship among indices of effects and independent factors. There was no significant difference between the two groups in blood cell count and biochemical indices. Inflammation- and allergy-related markers such as 8OHdG and IgE also showed no significant difference between toner-exposed workers and the referents. The influence of smoking on pulmonary function indices was observed, but there was no relationship between the pulmonary function and toner-exposed work. In this article, we report a preliminary cross-sectional analysis in the subjects of a cohort study. No difference in pulmonary function indices was observed between the toner-exposed workers and the referents, and there was no consistent relationship between the exposure status and examined indices; however, the prevalence of subjective respiratory symptoms was higher in the exposed workers as presented in another report. Further analysis is important in the ongoing cohort study to clarify the effect of toner exposure on respiratory systems.
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PMID:Cross-sectional study on respiratory effect of toner-exposed work in manufacturing plants, Japan: pulmonary function, blood cells, and biochemical markers. 1975 44

ortho-Phthalaldehyde (OPA) has been used as a safe alternative disinfectant instead of glutaraldehyde; however, recently some adverse effects of OPA were reported in patients and medical professions. We examined the acute toxicity of OPA in male ICR mice injected with 0.125-0.5% OPA and killed some animals 1 day after a single OPA injection, and others 1 or 13 days after two OPA injections 5 days apart. Hematology, blood cell counts, specific antibody production, organ weights, hepatic enzymes, hepatic histopathology and gene expression of cytochrome P450 (CYP) mRNA in liver were examined. Single OPA injections elevated leukocyte counts, the proportion of neutrophils, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Two OPA injections dose-dependently increased leukocyte counts, the proportion of neutrophils, ALT and AST, and decreased alkaline phosphatase. Leukocyte counts and proportions of neutrophils normalized 13 days after the second of two injections. However, both ALT and AST remained high in mice given higher OPA doses. Significant increased liver-to-body weight ratio and mild hepatic lesions were observed. Gene expression of CYP1a1 and CYP2e1 revealed a tendency of up-regulation 1 day after two OPA injections. However, expression of these genes was then down-regulated 13 days after OPA injections. OPA induced specific IgE and IgG significantly in the sera, suggesting that OPA acts as a hapten. Overall, OPA caused acute inflammation and acted as a haptenic allergen, although it caused only mild liver injury. Such evidence suggested that careful washing and prevention of exposure were needed after OPA disinfection of medical instruments.
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PMID:Acute inflammation and immunoresponses induced by ortho-phthalaldehyde in mice. 2011 2


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