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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. [ABSTRACT FROM AUTHOR]

The C57 BL/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 C57 BL/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 C57 BL/6 lesion development and checked whether they are recognized or not by BALB/c mice. We demonstrate first that IgG2a predominance in C57 BL/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, C57 BL/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. [ABSTRACT FROM AUTHOR]

Objective: 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). Method: 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). Results: An increase in the levels of MDA-modified proteins and a decrease in the concentration of thiol groups among SLE patients (p < 0.05) were observed. IgG circulating autoantibodies in the sera of SLE patients exhibited a significant enhanced reactivity (p < 0.05) against catalase and SOD-modified proteins. The same data were observed in the different protein fractions extracted from cultured cells (p < 0.05). Conclusion: These data reinforce the role of oxidative stress and especially lipid peroxidation products in the progression of SLE disease. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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.