Iranian

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The relationship between the immunoglobulin (Ig) nucleotide sequence and the ability of a B cell to develop into a malignant cell was studied in a subset of B cells, B-1 cells. B-1 cells become malignant in chronic lymphocytic leukemia (CLL) and are responsible for the production of "natural autoanti‌bodies". The autoimmune NZB mouse has been known as a human malignancy and CLL model, be‌cause of the age-dependent onset of clonally expanded hyperdiploid B-1 cells in these mice. The Ig heavy chain variable region in hyperdiploid B-1 clones from several NZB mice showed common char‌acteristics in the CDR3 shared with fetal B cells: lack of N base insertions and presence of homology sequences at the VH-D-JH junctions that can be encoded by either of the two joined gene segments. Using a degenerative oligoprimer was shown no significant differences in expression of the restricted CDR3/DFL16 region in newborns or in the liver of either strain of mice as young adults. However, the expression of the restricted CDR3/DFL16 in the spleens of young adult NZB was remarkably ele‌vated and showed significant differences from the expression in newborn NZB as well as from young adult and newborn BALB/c mice. It appears that malignant hyperdiploid B-1 cells are derived from fetal B cells. This technique can be used as a molecular marker to demonstrate a relative increase in the expression of this CDR3 in animals pre-destined to develop B-malignancies.

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Accurate and rapid diagnosis of human cytomegalovirus (HCMV) disease in immunocompromised patients has remained as a challenge. Quantitative competitive PCR (QC-PCR) methods for detection of HCMV in these individuals have improved the positive and negative predictive values of PCR for diagnosis of HCMV disease. In this study we used QC-PCR assay, using a co-amplified DNA standard, to quantitate the HCMV glycoprotein B (gB) gene in different samples. A DNA internal standard (IS) was designed by replacing HCMV primer binding site at 5' ends of primers that amplifies a 156-bp fragment of lambda genome, and a 200 bp amplicon was produced. Two DNA fragments of 257 bp wild type and 200-bp (IS) were co-amplified with the same oligonucleotide primer sets, analyzed by gel electrophoresis and used for construction of a standard curve. From this, the copy number of the gB gene present in different samples could be determined. Co-amplification with 1,000 copies of IS, allowed quantitation of 10-100,000 of HCMV DNA in a single PCR. This rapid assay avoids using radioactive components and other less efficient quantitative systems. It has the potential for early identification of patients at high risk of development of HCMV disease, and is useful for therapeutic monitoring. Iran. Biomed. J. 9 (4): 187-191, 2005

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Background: Quantitation of Helicobacter pylori (Hp) in the gastric tissue is essential for assessment of vaccination/therapeutic regimens. Methods & Results: Here, the inhibitory effect of mouse gastric DNA (MgDNA) on amplification of Hp genomic DNA (HpDNA) was evaluated by spiking HpDNA with serial dilutions of MgDNA, which yielded concentrations of >10 ng/µl and >0.63-10 ng/µl of MgDNA, as inhibition and interference zones, respectively. Mice were then inoculated with varying doses of Hp and assessed at the inhibition-free concentration of 0.63 ng/µl. The average Hp copy numbers per microgram of gastric tissue discriminated mice having received high vs. low dose inoculums (p < 0.001). Secondly, Hp copy numbers were quantitated in immunized mice, which demonstrated significantly lower numbers, in reference to controls (p = 0.006). Conclusion: Our method, bypassing the inhibition and/or interference imposed by MgDNA, was able to quantitate gastric tissue-colonizing Hp, segregating mice inoculated with low vs. high doses of Hp, as well as those immunized from controls.