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Background: Cesarean section is the most performed major abdominal surgery. While cesarean delivery is usually an uncomplicated procedure, up to 20% of patients can experience a complication following cesarean delivery with infectious complications being the most common. Nosocomial infections represent one of the major sources of morbidity and mortality in hospitalized patients around the world. Objective: The aim of the current work was to evaluate if the different scrubbing methods of surgical team before cesarean section by different materials change the rates of post-operative surgical site infection or not. Patient and methods: This randomized controlled trial (RCT) study included a total of 278 pregnant women, attending at Departments of Obstetrics and Gynecology, Menouf General Hospital and Menoufia University Hospitals, during the period of September 2019 till August 2020. Result: there was no statistically significant difference between the studied groups regarding their demographic and clinical data. There was no statistically significant difference between group A and group B regarding offensive odor at day 10 and 15 post-operatively. No offensive odor reported after day 25 or 30 postoperative (p> 0.05). Also, there was no statistically significant difference between group A and group B regarding approximation at day 10, 20, 25 and 30 post-operatively (p> 0.05. There was no statistically significant difference between group A and group B regarding hotness, redness, tenderness, swelling, discharge and offensive odor at day 10, 20, 25 and 30 post-operatively (p> 0.05). Conclusion: It could be concluded that for the increasing rates of CS being performed without a clear medical indication; new practice protocols should be implemented to reduce the rate of cesarean deliveries as CS surgery has a 5–20 times higher risk of post-partum infection as compared to vaginal deliveries.

Different types of starches were used to prepare controlled release tablets loaded with diprophylline by direct compression. The impact of the natural origin of the starch, potential chemical modifications (e.g., cross-linking with phosphate or adipate, hydroxypropylation, acetylation to different degrees, partial hydrolysis) and type of pre-gelatinization process (laboratory scale with ethanol and oven drying versus industrial scale drum drying) on the resulting drug release kinetics were studied. Texture analysis of the hydrogels created upon exposure to the release medium, optical and scanning electron microscopy as well as X-ray powder diffraction measurements were used to better understand the observations. Also, a “quick test” using a texture analyzer to rapidly estimate the capacity of a specific starch type to control the resulting drug release rate was proposed. Two types of hydroxypropyl methylcellulose (HPMC K100 M and K100 LV) were studied for reasons of comparison. Interestingly, the “quick test” allowed to detect differences in the mechanical strength of the hydrogels formed upon contact with aqueous fluids, which correlated well with the observed drug release patterns from tablets when measured using a USP III (“Bio’-Dis”) apparatus at 30 rpm. However, diprophylline release was not very much affected by the investigated starch types when using a USP basket apparatus at 75 rpm. This can be attributed to the much lower mechanical stress experienced by the hydrogels under these conditions. Furthermore, caution must be paid when studying starch types, which are pre-gelatinized at the laboratory scale using ethanol precipitation and oven drying. The obtained starch granules can have significantly different key properties compared to granules obtained by industrial scale drum drying, resulting in substantially different drug release patterns.

Geographically isolated populations have been successfully used to localize genes for recessive inherited diseases, including non-syndromic sensorineural recessive deafness (NSRD). To date, 25 loci for NSRD have been localized on human chromosomes (DFNB loci), and six of the corresponding genes have been identified. Here, we report on the contribution of the DFNB1 locus (GJB2 gene) to NRSD in seven affected families living in three northern Tunisian geographic isolates, and we provide evidence for genetic heterogeneity within isolates. This finding challenges the classical view of a single 'founder' mutation segregating in such isolates.

Prelingual non-syndromic (isolated) deafness is the most frequent hereditary sensory defect. In >80% of the cases, the mode of transmission is autosomal recessive. To date, 14 loci have been identified for the recessive forms (DFNB loci). For two of them, DFNB1 and DFNB2, the genes responsible have been characterized; they encode connexin 26 and myosin VIIA, respectively. In order to evaluate the extent to which the connexin 26 gene (Cx26) contributes to prelingual deafness, we searched for mutations in this gene in 65 affected Caucasian families originating from various countries, mainly tunisia, France, New Zealand and the UK. Six of these families are consanguineous, and deafness was shown to be linked to the DFNB1 locus, 10 are small non consanguineous families in which the segregation of the trait has been found to be compatible with the involvement of DFNB1, and in the remaining 49 families no linkage analysis has been performed. A total of 62 mutant alleles in 39 families were identified. Therefore, mutations in Cx26 represent a major cause of recessively inherited prelingual deafness since according to the present results they would underlie approximately half of the cases. In addition, one specific mutation, 30delG, accounts for the majority (approximately 70%) of the Cx26 mutant alleles. It is therefore one of the most frequent disease mutations so far identified. Several lines of evidence indicate that the high prevalence of the 30delG mutation arises from a mutation hot spot rather than from a founder effect. Genetic counseling for prelingual deafness has been so far considerably impaired by the difficulty in distinguishing genetic and non genetic deafness in families presenting with a single deaf child. Based on the results presented here, the development of a simple molecular test could be designed which should be of considerable help.

Usher syndrome (USH) is an autosomal recessive disorder characterised by hearing impairment and retinitis pigmentosa (RP). The prevalence of USH varies from one population to another, for example, 3-4.4 per 100 000 in Scandinavian and North American populations1,2 and 6.2-10 per 100 000 in the city of Birmingham, UK.3 This syndrome is clinically heterogeneous and three clinical forms have been described4: (1) USH type I (USH1) is characterised by severe to profound congenital deafness, constant vestibular dysfunction, and prepubertal onset of RP; (2) USH type II (USH2) is characterised by congenital moderate to severe deafness, absence of vestibular dysfunction, and onset of RP usually in the late second to early third decade; (3) USH type III (USH3) is characterised by postlingual progressive deafness, occasional vestibular dysfunction, and progressive RP with a variable age of onset (see also http://www.ncbi.nlm.nih.gov/omim). Usher syndrome is also genetically heterogeneous; at least six distinct loci are responsible for USH1 (USH1A-F), three for USH2 (USH2A-C), and one for USH35 (Hereditary hearing loss homepage at URL, http://dnalab.www.uia.ac.be/dnalab/hhh). Usher syndrome type II (USH2) appears to be the commonest clinical form of the disorder in the American population, accounting for more than 50% of all USH cases.3,6 This clinical form tends to be rare in other populations.7 In the Tunisian population, only two USH2 families, Us8 and Z (this work), have been identified so far. These families were ascertained from villages from the south and the north of Tunisia, respectively, where endogamous marriage is relatively common for social and cultural reasons. Of all the USH2 subtypes, USH2A seems to be the most frequent. According to a study performed in various ethnic populations, USH2A is responsible for more than 85% of USH2 cases.9 This genetic form showed considerable phenotypic …

Geographically isolated populations have been successfully used to localize genes for recessive inherited diseases, including non-syndromic sensorineural recessive deafness (NSRD). To date, 25 loci for NSRD have been localized on human chromosomes (DFNB loci), and six of the corresponding genes have been identified. Here, we report on the contribution of the DFNB1 locus (GJB2 gene) to NRSD in seven affected families living in three northern Tunisian geographic isolates, and we provide evidence for genetic heterogeneity within isolates. This finding challenges the classical view of a single 'founder' mutation segregating in such isolates.

Usher type II syndrome is defined by the association of retinitis pigmentosa, appearing in the late second to early third decade of life, with congenital moderate to severe non-progressive hearing loss. This double sensory impairment is not accompanied by vestibular dysfunction. To date, only one Usher type II locus, USH2A, at chromosome band 1q41, has been defined. Here, we demonstrate by linkage analysis, that the gene responsible for Usher type II syndrome in a Tunisian consanguineous family maps to chromosome 3 at position p23-24.2, thus providing definitive evidence for the genetic heterogeneity of the syndrome. A maximum lod score of 4.3 was obtained with the polymorphic microsatellite markers corresponding to loci D3S1578, D3S3647 and D3S3658. This maps the gene underlying USH2B to a chromosomal region which overlaps the interval defined for the non-syndromic sensorineural recessive deafness DFNB6, raising the possibility that a single gene underlies both defects. However, the audiometric features in the patients affected by USH2B and DFNB6 are very different.

Editor—Congenital deafness occurs in approximately 1 in 1000 live births and at least 50% of these cases are hereditary.1 Among the prelingual genetic forms of deafness, the autosomal recessive forms ( DFNB ) are frequent (80% of the cases) and in most cases are sensorineural and severe.1 Twenty eight loci that cause autosomal recessive non-syndromic hearing loss (ARNSHL) have been identified (http://dnalab-www.uia.ac.be./dnalab/hhh/index.html). The first locus defined for recessive deafness ( DFNB1 ) is linked to chromosome 13q12-13 and was identified by homozygosity mapping in two large consanguineous families from Tunisia.2 This initial report was followed by the identification of other consanguineous families of different ethnic origins which were linked to the DFNB1 locus and of several non-consanguineous white families in which the ARNSHL phenotype cosegregated with markers from chromosome 13q12-13.3-6Mutations in connexin26 ( Cx26 ), a gene that encodes gap junction protein beta-2 (GJB-2), have been shown to result in autosomal recessive ( DFNB1 ) and dominant ( DFNA3 ) non-syndromic sensorineural deafness.7 Mutations in the Cx26 gene have been found to be the most common cause of autosomal recessive deafness and the most frequently observed mutation is 35delG.8-12 The high prevalence of Cx26 mutations and their importance as a cause of ARNSHL have prompted the development of several different mutation detection assays to screen the single Cx26 coding exon.13-16 A rapid method to detect mutations in the GJB2 …

Bladder cancer is the first most common urogenital cancer in men in Tunisia, with a high recurrence rate. Patients with muscle-invasive disease develop metastasis. The need for expensive continuous surveillance. In this thesis we try to search some candidate biomarkers. Their use for cancer staging and personalization of therapy at the time of diagnosis in order to identify a better treatment could improve patient care. The aim of this first part of our study was to investigate the clinical significance of three immune cell-related transcription factors, T-bet, GATA-3 and Bcl-6 in Tunisian patients with bladder cancer. We found that T-bet level was significantly higher in invasive carcinoma with high- grade. However, T-bet is predictive of response to BCG. On the contrary, the expression of GATA-3 and Bcl-6 was significantly higher in non-invasive carcinoma with low grade. We furthermore studied the effect of activation of soluble FasL and TRAIL molecule in bladder cancer. We demonstrate that the mean serum level of sFasL was higher in patients than in normal donors. sFasL was only higher than in sera of healthy donors where patients had superficial stage and low- and medium-grade cancer. sTRAIL was significantly lower in sera from patients with invasive and high-grade bladder carcinoma than in controls. Finally, we demonstrate that p-Akt levels in patients with invasive carcinoma and high-grade bladder cancer were significantly elevated compared to patients with non-invasive and low grade bladder cancer. Altogether, our results suggest that Akt activation can provide useful prognostic information., Le cancer de la vessie représente un vrai problème de santé publique, avec une surveillance et suivi clinique à long terme en raison de l’importance des fréquences de récidives. La chimiothérapie reste souvent inefficace. L’objectif de cette thèse est donc la recherche de marqueurs sérologiques et moléculaires à valeur pronostique dans le cancer de la vessie qui peuvent servir à prédire la maladie. D’abord, nous avons étudié trois facteurs de transcriptions des lymphocytes T activées qui sont T-bet, GATA-3 et Bcl-6. Nous avons montré une surexpression de T-bet chez les malades à stade invasif et de haut grade, cependant, la surexpression de GATA-3 et Bcl-6 a été corrélée au stade superficiel et de bas grade. La survie a été corrélée avec le groupe des malades sans histoires de récidive ou progression et avec la surexpression de Bcl-6 et GATA-3. Cependant les malades qui expriment fortement T-bet répondent mieux au BCG. Ensuite, nous avons visé la détection de FasL et TRAIL solubles dans le sérum des malades atteints du cancer vésicale. Nous avons montré une surexpression de sFasL et sTRAIL chez les malades à stade superficiel et de bas grade. Le rôle anti-tumoral de ces cytokines a été confirmé sur deux lignées du cancer de la vessie montrant que le traitement avec le sérum riche en sFasL ou en sTRAIL diminue la viabilité cellulaire in vitro. A la fin de cette thèse, nous avons testé l’activation p-Akt dans la tumeur vésicale. Nous avons montré une surexpression de p-Akt au sein des tumeurs comparées au tissu sain adjacent, et au sein des malades à stade invasif et de haut grade. Akt semble être un marqueur de progression tumorale dans le cancer de la vessie.