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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.

The aim of this study was to evaluate the potential of a cross-linked pregelatinized potato starch (PREGEFLO® PI10) as matrix former for controlled release tablets. Different types of tablets loaded with diprophylline, diltiazem HCl or theophylline were prepared by direct compression of binary drug/polymer blends. The drug content was varied from 20 to 50%. Two hydroxypropyl methylcellulose grades (HPMC K100LV and K100M) were studied as alternative matrix formers. Drug release was measured in a variety of release media using different types of experimental set-ups. This includes 0.1 N HCl, phosphate buffer pH 6.8 and water, optionally containing different amounts of NaCl, sucrose, ethanol or pancreatin, fasted state simulated gastric fluid, fed state simulated gastric fluid, fasted state simulated intestinal fluid, fed state simulated intestinal fluid as well as media simulating the conditions in the colon of healthy subjects and patients suffering from Crohn's disease. The USP apparatuses I/II/III were used under a range of operating conditions and optionally coupled with the simulation of additional mechanical stress. Importantly, the drug release kinetics was not substantially affected by the investigated environmental conditions from tablets based on the cross-linked pregelatinized potato starch, similar to HPMC tablets. However, in contrast to the latter, the starch-based tablets roughly kept their shape upon exposure to the release media (they "only" increased in size) during the observation period, and the water penetration into the systems was much less pronounced. Thus, the investigated cross-linked pregelatinized potato starch offers an interesting potential as matrix former in controlled release tablets.

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.

International audience; The C57BL/6 mouse strain is resistant to Leishmania (L.) major infection and, unlike susceptible BALB/c, develops small self-healing cutaneous lesions. The specific antibody responses of C57BL/6 and BALB/c mice were previously characterized by the predominance of IgG2a (resistant' isotype associated with Th1) and IgG1 (pathogenic' isotype associated with Th2) antibodies, respectively. In this study, we looked for the presence of antigens able to elicit an exclusive or predominant IgG1 production during the early stages of C57BL/6 lesion development and checked whether they are recognized or not by BALB/c mice. We demonstrate first that IgG2a predominance in C57BL/6 sera occurs only late after infection, whereas in BALB/c, IgG1 antibodies dominate mostly in the early stages. Interestingly, soon after inoculation of live amastigotes, C57BL/6 displayed an exclusive IgG1 reactivity against particular L.major antigens but with MWs different from those identified in BALB/c. Furthermore, mice immunized with killed amastigotes displayed striking differences in their immunodetection profiles, particularly for the IgG1 isotype. Taken together, the observed differences in the specific antibody repertoires between infected mice resulted, at least in part, from immunological events independent from those triggered by the replicating parasite, and bring new insights into the selection of future vaccine candidates.

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.

Pendred syndrome comprises congenital sensorineural hearing loss, thyroid goiter, and positive perchlorate discharge test. Recently, this autosomal recessive disorder was shown to be caused by mutations in the PDS gene, which encodes an anion transporter called pendrin. Molecular analysis of the PDS gene was performed in two consanguineous large families from Southern Tunisia comprising a total of 23 individuals affected with profound congenital deafness; the same missense mutation, L445W, was identified in all affected individuals. A widened vestibular aqueduct was found in all patients who underwent computed tomography (CT) scan exploration of the inner ear. In contrast, goiter was present in only 11 affected individuals, who interestingly had a normal result of the perchlorate discharge test whenever performed. The present results question the sensitivity of the perchlorate test for the diagnosis of Pendred syndrome and support the use of a molecular analysis of the PDS gene in the assessment of individuals with severe to profound congenital hearing loss associated with inner ear morphological anomaly even in the absence of a thyroid goiter.

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.

We report the identification of a novel CC chemokine receptor 5 (CCR5) variant that seems associated with resistance to HIV-1 infection. The V130I mutation of the CCR5 receptor is located in the intracellular loop ICL2 known as DRY box and described in the literature as a nonsynonymous mutation present in nonhuman primates group. Extensive molecular modeling and dynamics simulations were performed to elucidate the mechanism by which the V130I mutation may induce conformational change of the CCR5 folding protein and prevent the interaction with the β-arrestin protein. Our study provides new mechanistic insight into how a specific mutation in the regulatory domain of CCR5 might alter the structural folding of the DRY box and the possible ICL2 loop binding with the β-arrestin protein, as described in our previous computational study. The results from our large-scale simulations complement recent experimental results and clinical features and offer useful insights into the mechanism behind CCR5 protein folding and signal transduction. In order for HIV, the entry of the virus to the cells must fuse with the CCR5 receptor that sits on the surface of T-helper immune cells. The described V130I mutation in the gene encoding the CCR5 protein may results in a defective CCR5-Arrestin binding complex that blocks entry of the virus.

Evaluation of the reactivity of autoantibodies of systemic lupus erythematosus (SLE) patients directed against malondialdehyde (MDA)-modified catalase, superoxide dismutase (SOD), and different Hep2 protein fractions (hydrophobic, hydrophilic, and nuclear).Thiol groups and MDA-protein adducts were first assessed among 65 SLE patients and 60 healthy controls. Then, the reactivities of SLE immunoglobulin (Ig)G autoantibodies towards MDA-modified and unmodified proteins were compared using a standard enzyme-linked immunosorbent assay (ELISA).An increase in the levels of MDA-modified proteins and a decrease in the concentration of thiol groups among SLE patients (p0.05) were observed. IgG circulating autoantibodies in the sera of SLE patients exhibited a significant enhanced reactivity (p0.05) against catalase and SOD-modified proteins. The same data were observed in the different protein fractions extracted from cultured cells (p0.05).These data reinforce the role of oxidative stress and especially lipid peroxidation products in the progression of SLE disease.

The aim of this paper is to study the relationship between the characteristics of board of directors and firm performance in a sample of 100 american firms, over the period 2001-2003. We particularly focus on board independence and CEO duality. Our results indicate a positive impact of board independence on the firm performance. We also find a negative relationship between CEO duality and performance. Finally we can indicate that Results of our empirical test fail to support stewardship theory and provide support for agency theory.

This paper presents a thorough review, including the authors' latest thinking, of one of the most persistent and troubling puzzles to the efficient market hypothesis: the closed-end fund puzzle. Financial economists have intensely scrutinised the economic explanations of the discount within the context of the efficient market hypothesis. Unfortunately, empirical evidence show that none of the traditional explanations individually accounts for all aspects of the closed-end fund discount. The failure of economic hypotheses to explain the closed-end fund discount leads many authors to explore behavioral explanations. We outline then the psychological evidence for this phenomenon and give a taxonomy for an array of factors that come under the common label of sentimental hypothesis.

This paper examines the investment-cash-flow sensitivity in a sample of 150 American firms over the period 1995-2004. Investment-cash-flow sensitivities can be attributed either to overinvestment resulting from the abuse of managerial discretion (Jensen [1986] and Stulz [1990]), or to underinvestment due to information problems (Myers et Majluf [1984]). We use Tobin's Q to discriminate between firms with these problems, where low Q firms face the managerial discretion problem and high Q firms the asymmetric information problem. Similarly to Degryse et De Jong [2006], we had found evidence which highlights substantially larger investment-cash-flow sensitivity for low Q firms. This finding shows that our empirical test provides support for managerial discretion hypothesis.

Arbitrage is widely considered as the central tenet of traditional finance that precludes the existence of disparities between prices and fundamentals. However, the real world arbitrage calls for large outlay of capital, entails some risk and is a lot more complex than the textbook definition suggests. The arbitrage appears therefore limited. The presence of risk will drastically reduce the arbitrageurs' ability to drive prices back in line with fundamentals. This paper outlines an overview of factors that lead to limits on arbitrage activities. Specifically, we study the properties of potential departures from the law of one price and discuss its impediments using two perspectives: the rational approach and the behavioural finance.

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.

Pendred syndrome comprises congenital sensorineural hearing loss, thyroid goiter, and positive perchlorate discharge test. Recently, this autosomal recessive disorder was shown to be caused by mutations in the PDS gene, which encodes an anion transporter called pendrin. Molecular analysis of the PDS gene was performed in two consanguineous large families from Southern Tunisia comprising a total of 23 individuals affected with profound congenital deafness; the same missense mutation, L445W, was identified in all affected individuals. A widened vestibular aqueduct was found in all patients who underwent computed tomography (CT) scan exploration of the inner ear. In contrast, goiter was present in only 11 affected individuals, who interestingly had a normal result of the perchlorate discharge test whenever performed. The present results question the sensitivity of the perchlorate test for the diagnosis of Pendred syndrome and support the use of a molecular analysis of the PDS gene in the assessment of individuals with severe to profound congenital hearing loss associated with inner ear morphological anomaly even in the absence of a thyroid goiter.

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.