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Study was conducted to assess two enzyme detoxifying activities and insecticide-resistance gene expression quantitation using real-time (PCR). Four populations of pink bollworm were compared with baseline laboratory strain. Field populations showed higher levels of enzymatic activity, glutathione-S-transferase and β–esterases, than those of the laboratory strain. The amplification curves scored a cycle threshold (Ct) value of 25 for the ribosomal protein subunit7 (rps7). For the BtR gene, the Ct values of analyzed biological groups ranged from 20 for laboratory strain to 24 for Fayoum group. For Cad1, the Ct values ranged from 19 for laboratory strain to 23 for Fayoum and Qalubia populations. Therefore, the present work introduces a method for the challenge of monitoring resistance to Bt toxins in crops which require, according to IPM (Integrated pest management) program, a wise insecticide application. [ABSTRACT FROM AUTHOR]

Abstract Background Hearing loss is a clinically and genetically heterogeneous disorder. Mutations in the DFNB1 locus have been reported to be the most common cause of autosomal recessive non-syndromic hearing loss worldwide. Apart from DFNB1, many other loci and their underlying genes have also been identified and the basis of our study was to provide a comprehensive introduction to the delineation of the molecular basis of non-syndromic hearing loss in the Saudi Arabian population. This was performed by screening DFNB1 and to initiate prioritized linkage analysis or homozygosity mapping for a pilot number of families in which DFNB1 has been excluded. Methods Individuals from 130 families of Saudi Arabian tribal origin diagnosed with an autosomal recessive non-syndromic sensorineural hearing loss were screened for mutations at the DFNB1 locus by direct sequencing. If negative, genome wide linkage analysis or homozygosity mapping were performed using Affymetrix GeneChip® Human Mapping 250K/6.0 Arrays to identify regions containing any known-deafness causing genes that were subsequently sequenced. Results Our results strongly indicate that DFNB1 only accounts for 3% of non-syndromic hearing loss in the Saudi Arabian population of ethnic ancestry. Prioritized linkage analysis or homozygosity mapping in five separate families established that their hearing loss was caused by five different known-deafness causing genes thus confirming the genetic heterogeneity of this disorder in the kingdom. Conclusion The overall results of this study are highly suggestive that underlying molecular basis of autosomal recessive non-syndromic deafness in Saudi Arabia is very genetically heterogeneous. In addition, we report that the preliminary results indicate that there does not seem to be any common or more prevalent loci, genes or mutations in patients with autosomal recessive non-syndromic hearing loss in patients of Saudi Arabian tribal origin.