The cloning and the characterization of the heat shock 70 (hsp70) genes of the medfly C. capitata, a major agricultural pest, are presented. Six genomic clones were isolated by screening a medfly genomic library with an hsp70 genomic fragment of Drosophila melanogaster. They form two 30 kb contigs, both of which map cytogenetically in a single major heat shock puff (3L:24C) of the salivary gland polytene chromosomes. Restriction mapping and blot hybridization indicated the presence of six putative hsp70 genes in these two closely linked regions. The sequence of one of these genes suggests that it is a heat-inducible hsp70 gene. The 638-codon open reading frame shows 84% identity at the amino acid level (73.5% at the nucleotide level), relative to corresponding D. melanogaster sequences. The 5' untranslated leader sequence, approximately 200 bp long, is not interrupted by introns and is very rich (48%) in adenine residues, resembling Drosophila heat-inducible hsp70 genes. Furthermore, the promoter of this gene contains two characteristic heat shock elements close upstream from the TATA box. The levels of the hsp70 transcripts are very low at 25-30 degrees C, increase significantly at 33 degrees C and reach maximum at 39 degrees C.
In group A streptococcal tonsillopharyngitis, 5 days of clarithromycin or amoxicillin/clavulanate treatment had clinical efficacy comparable with that of 10 days of penicillin V treatment; however, amoxicillin/clavulanate and penicillin V were bacteriologically more effective than clarithromycin because of its failure to eradicate the clarithromycin-resistant S. pyogenes isolates. The 5-day clarithromycin regimens are not recommended for treatment of streptococcal tonsillopharyngitis in areas where in vitro resistance of group A streptococci to clarithromycin is common.
OPG is increased, ADMA is decreased, but RANKL and Fetuin-A are unchanged in T1DM children. Whereas increased OPG has been firmly related to increased CVR, more studies, especially longitudinal studies, are needed to delineate the role and clinical significance of decreased ADMA and if Fetuin-A has any role in T1DM.
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