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Introduction: In diabetes mellitus the increase of AgII (Angiotensin II), IGF-1(insulin like growth factor-1) and growth hormone induce kidney lesions especially changes in content and thickness of GBM and widening and fusion of podocyte pedicles. In this research for the first time the combination of Losartan (AT1 receptor blocker) and Octreotide (Somatostatin analogue) were used in order to prevent glomerular epithelial lesions.
Materials & Methods: In this experimental study 15 male rats (2 months age) were uninephrectomised from left flank and divided in 5 groups (3 per group). 7 days later diabetes was induced in 2th, 3th, 4th and 5th group by Alloxan (120mg/kg) subcutaneously. 5 days after diabetes induction, the third group received Losartan (5mg/kg/day) orally, 4th group Octretide (10 ŭg/day) subcutaneously and 5th group both two drugs with the mentioned doses for 8 weeks. The 2th group was served as diabetic non treatment group. Kidneys of all groups were fixed by perfusion technique. After second fixation of 1 mm3 cortex parts in Osmium Tetroxide, they were processed in TAAB812 resin for embedding. Thin sections (600 nm thickness) were prepared and investigated by transmission electron microscope qualitatively.
Results: Losartan inhibited fusion and thickening of podocyte pedicles but in some cases couldn,t maintain the 3 layer form of GBM. Octreotide had little effect on inhibition of fusion and thickening of podocyte pedicles and no effect in 3 layer form maintaining of GBM. Combined therapy inhibited fusion and thickening of podocyte pedicles and maintained 3 layer form of GBM but in some cases the lamina rara near endothelium was not seen.
Conclusion: Octreotide have little effect on prevention of glomerular epithelium lesions. However Losartan could prevent glomerular epithelium lesions well, but combined drug therapy showed better results comparing Losartan.

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Background: Hearing loss is a common sensory impairment in humans which half of its causes are genetic reasons. Genetic hearing loss can be divided into the two types of syndromic and non-syndromic, which 80% of non-syndromic cases is Autosomal Recessive Non-Syndromic Hearing Loss. The aim of the present research is to determine the contribution of DFNB2 locus (MYO7A gene) in causing an autosomal recessive hearing loss in the one group of the deaf families of Khuzestan province.

Materials and Methods: This study was conducted on 26 families with autosomal recessive hearing loss (with 4 patients) and negative for GJB2 mutations in Khuzestan province. 22 families suffered from ARNSHL and 4 families suffered from Usher syndrome. Linkage analysis was performed by using STR (Short Tandem Repeat) markers related to DFNB2 locus. Each family’s genotype was determined by PCR-PAGE method. Furthermore, haplotypes drawing and LOD score calculations were performed.

Results: From 26 families with hearing loss participating in this research, following genetic linkage analysis and haplotypes drawing, two families (7.7% of the families) showed linkage to DFNB2 locus. One family (4.5%) suffered from ARNSHL and another family suffered from Usher syndrome.

Conclusion: The results of the present research show that the contribution of DFNB2 locus in causing hearing loss in the population of Khuzestan province was similar to other studies conducted in Iran and this locus with other important loci should be considered to check in the hearing loss panel.

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Abstract

Background: Hearing loss (HL) is the most common congenital defect in humans. One or two in thousand newborn babies have prelingual hearing loss. Autosomal recessive non-syndromic hearing loss (ARNSHL) is the most common form of hereditary deafness. Hearing loss is more common in the developing countries which is due to genetic and environmental (cultural -health factors) reasons. HL has a wide range of clinical demonstrations including: congenital or late onset, conductive or sensory-neural, syndromic or non-syndromic hearing loss. The goal of this project is to determine the portion of the DFNB21 (TECTA) in ARNSHL in families with negative GJB2 gene in Khuzestan province.

Materials and Methods: We studied 21 families with ARNSHL with at least 4 patients and negative for GJB2 mutations from Khuzestan province. Genetic linkage analysis was performed using STR markers linked to DFNB21 locus.

Results: Following genetic linkage analysis and haplotyping, out of 21 families with ARNSHL, one family showed linkage to the DFNB21 (TECTA) locus.

Conclusion: The results of this project confirm other studies in Iran and give insight into the most common loci causing ARNSHL in Iran which could be helpful in research and clinic.