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Various Infections (various + infections)
Selected AbstractsPhotoprotein aequorin as a novel reporter for SNP genotyping by primer extension,application to the variants of mannose-binding lectin gene,HUMAN MUTATION, Issue 3 2006Panayotis G. Zerefos Abstract Mannose-binding lectin (MBL) is a key component of the innate immune system, and its deficiency is associated with increased susceptibility to various infections and autoimmune disorders. Since several nucleotide variations in the mannose-binding lectin 2 gene (MBL2) have been associated with the functional deficiency of MBL, there is a growing need to screen its allelic variants and develop genotyping methods for MBL2. In this context we propose a rapid, robust, cost-efficient, and automatable method for detecting all known allelic variants of MBL2. This report introduces for the first time the photoprotein aequorin as a reporter in genotyping by primer extension (PEXT) reactions. The method involves a single PCR amplification of a genomic region that spans all six variant nucleotide sites, i.e., three structural mutations in exon 1 (c.154C>T, pArg52Cys; c.161A>G, p.Gly54Asp; and c.170A>G, p.Gly57Glu), two single nucleotide polymorphisms (SNPs) at positions c.,619G>C and c.,290G>C (promoter region), and one SNP at position c.,66C>T of the 5, untranslated region. PCR is followed by PEXT reactions for each site. Biotin-dUTP is incorporated in the extended primer. The genotyping primers contain a poly(dA) segment at their 5, end. The products are captured by hybridization on the surface of microtiter wells that are coated with a poly(dT)-albumin. The extended primers only are detected by reaction with a streptavidin-aequorin conjugate. The bound photoprotein aequorin is measured within 3,sec by simply adding Ca2+. We carried out extensive optimization studies of the PEXT reaction and genotyped the six nucleotide variant sites using blood specimens from 27 normal DNA samples. The results of the proposed method agreed entirely with the sequencing data. Hum Mutat 27(3), 279,285, 2006. © 2006 Wiley-Liss, Inc. [source] Ceftriaxone-associated biliary pseudolithiasis in childrenJOURNAL OF CLINICAL ULTRASOUND, Issue 5 2006Betül Biner MD Abstract Purpose. Ceftriaxone is known to induce reversible precipitations, known as pseudolithiasis, in the gallbladder and urinary tract. The aim of this study was to investigate the incidence and predisposing factors that contribute to this side effect. Methods. A prospective study was conducted in 156 children admitted for the treatment of various infections with different daily ceftriaxone doses (50 mg/kg, 75 mg/kg, and 100 mg/kg). Sonographic examinations of the gallbladder and urinary tract were performed before treatment on the third and seventh day of therapy, and at the first and second month after the end of treatment. Patients with positive findings were followed with weekly sonographic examinations until the abnormality resolved. Results. Abnormal gallbladder sonograms were demonstrated in 27 children (17%); 16 of them (10%) had gallbladder lithiasis, 11 had gallbladder sludge (7%) (n = 4 on the third day, n = 23 on the seventh day), and 1 developed urolithiasis (0.6%). Five children (19%) were symptomatic. The abnormalities resolved after a mean of 16 days (range 10,30 days). Patients with pseudolithiasis were older and treated with higher drug doses than those with normal sonographic findings (P < 0.01 and P < 0.05, respectively). Conclusions. Biliary pseudolithiasis (and infrequently nephrolithiasis) usually occurs in children receiving high doses of ceftriaxone. It is generally asymptomatic. When this reversible complication becomes symptomatic, unnecessary cholecystectomy should be avoided. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:217,222, 2006 [source] Molecular detection of hepatitis B, hepatitis C, and torque teno viruses in drug users in Saudi ArabiaJOURNAL OF MEDICAL VIROLOGY, Issue 8 2009Alhusain J. Alzahrani Abstract Injecting drug users are at increased risk of infection with hepatitis viruses and blood-borne pathogens. The aim of this study was to examine HBV, HCV, HDV, and TTV infections in Saudi drug users (N,=,344). Extraction of nucleic acid from serum, reverse-transcription, amplification of viral nucleic acids, and HBV and HCV genotyping were done using established techniques. Of the analyzed samples, 41 (12%) contained detectable HBV DNA, 131 (38%) contained detectable HCV RNA, and 174 (51%) had detectable TTV DNA. The predominant HBV genotype was found to be genotype D and the predominant HCV genotype was found to be genotype 1b. All the samples were negative for HDV. Twelve samples (3.5%) were found to contain mixed HBV and HCV genomes, 24 samples (7%) were found to contain mixed HBV and TTV genomes, 82 samples (24%) were found to contain mixed HCV and TTV genomes, and 9 samples (2.6%) were found to contain mixed HBV, HCV, and TTV genomes. Identification of various infections in drug users will help the control of these infections in this group as well as in the community. J. Med. Virol. 81:1343,1347, 2009. © 2009 Wiley-Liss, Inc. [source] The expanding realm of heterologous immunity: friend or foe?CELLULAR MICROBIOLOGY, Issue 2 2006Kathleen R. Page Summary Antecedent or current infections can alter the immunopathologic outcome of a subsequent unrelated infection. Immunomodulation by co-infecting pathogens has been referred to as ,heterologous immunity' and has been postulated to play a role in host susceptibility to disease, tolerance to organ transplant, and autoimmune disease. The effect of various infections on heterologous immune responses has been well studied in the context of shared epitopes and cross-reactive T cells. It has been shown that prior infections can modulate protective immunity and immunopathology by forming a pool of memory T cells that can cross-react with antigens from heterologous organisms or through the generation of a network of regulatory cells and cytokines. While it is not feasible to alter a host's history of prior infection, understanding heterologous immune responses in the context of simultaneous unrelated infections could have important therapeutic implications. Here, we outline key evidence from animal and human studies demonstrating the effect of heterologous immunity on the outcome of disease. We briefly review the role of T cells, but expand our discussion to explore other immune mechanisms that may modulate the response to concurrent active infections. In particular, we underscore the role of the innate immune system, polarized responses and regulatory mechanisms on heterologous immune responses. [source] | ||||||||||