Cairo University

About: Cairo University is a education organization based out in Giza, Egypt. It is known for research contribution in the topics: Population & Medicine. The organization has 33532 authors who have published 55581 publications receiving 792654 citations. The organization is also known as: Fuad I University & King Fuad I University.

Syndecan-1 is a novel molecular marker for triple negative inflammatory breast cancer and modulates the cancer stem cell phenotype via the IL-6/STAT3, Notch and EGFR signaling pathways

Abstract: Inflammatory breast cancer (IBC), a particularly aggressive form of breast cancer, is characterized by cancer stem cell (CSC) phenotype. Due to a lack of targeted therapies, the identification of molecular markers of IBC is of major importance. The heparan sulfate proteoglycan Syndecan-1 acts as a coreceptor for growth factors and chemokines, modulating inflammation, tumor progression, and cancer stemness, thus it may emerge as a molecular marker for IBC. We characterized expression of Syndecan-1 and the CSC marker CD44, Notch-1 & -3 and EGFR in carcinoma tissues of triple negative IBC (n = 13) and non-IBC (n = 17) patients using qPCR and immunohistochemistry. Impact of siRNA-mediated Syndecan-1 knockdown on the CSC phenotype of the human triple negative IBC cell line SUM-149 and HER-2-overexpressing non-IBC SKBR3 cells employing qPCR, flow cytometry, Western blotting, secretome profiling and Notch pharmacological inhibition experiments. Data were statistically analyzed using Student’s t-test/Mann-Whitney U-test or one-way ANOVA followed by Tukey’s multiple comparison tests. Our data indicate upregulation and a significant positive correlation of Syndecan-1 with CD44 protein, and Notch-1 & -3 and EGFR mRNA in IBC vs non-IBC. ALDH1 activity and the CD44(+)CD24(-/low) subset as readout of a CSC phenotype were reduced upon Syndecan-1 knockdown. Functionally, Syndecan-1 silencing significantly reduced 3D spheroid and colony formation. Intriguingly, qPCR results indicate downregulation of the IL-6, IL-8, CCL20, gp130 and EGFR mRNA upon Syndecan-1 suppression in both cell lines. Moreover, Syndecan-1 silencing significantly downregulated Notch-1, -3, -4 and Hey-1 in SUM-149 cells, and downregulated only Notch-3 and Gli-1 mRNA in SKBR3 cells. Secretome profiling unveiled reduced IL-6, IL-8, GRO-alpha and GRO a/b/g cytokines in conditioned media of Syndecan-1 knockdown SUM-149 cells compared to controls. The constitutively activated STAT3 and NFκB, and expression of gp130, Notch-1 & -2, and EGFR proteins were suppressed upon Syndecan-1 ablation. Mechanistically, gamma-secretase inhibition experiments suggested that Syndecan-1 may regulate the expression of IL-6, IL-8, gp130, Hey-1, EGFR and p-Akt via Notch signaling. Syndecan-1 acts as a novel tissue biomarker and a modulator of CSC phenotype of triple negative IBC via the IL-6/STAT3, Notch and EGFR signaling pathways, thus emerging as a promising therapeutic target for IBC.

Search for new physics in events with same-sign dileptons and jets in pp collisions at √s = 8 TeV

Abstract: A search for new physics is performed based on events with jets and a pair of isolated, same-sign leptons. The results are obtained using a sample of proton-proton collision data collected by the CMS experiment at a centre-of-mass energy of 8 TeV at the LHC, corresponding to an integrated luminosity of 19.5 fb−1. In order to be sensitive to a wide variety of possible signals beyond the standard model, multiple search regions defined by the missing transverse energy, the hadronic energy, the number of jets and b-quark jets, and the transverse momenta of the leptons in the events are considered. No excess above the standard model background expectation is observed and constraints are set on a number of models for new physics, as well as on the same-sign top-quark pair and quadruple-top-quark production cross sections. Information on event selection efficiencies is also provided, so that the results can be used to confront an even broader class of new physics models.

Tamponade and injection sclerotherapy in the management of bleeding oesophageal varices.

Abstract: One hundred patients with bleeding oesophageal varices were randomized into two treatment groups after resuscitation. One group was managed by tamponade only (group 1); the other group (group 2) was treated by endoscopic injection of oesophageal varices. The patients in group 2 were further subdivided into 25 patients (group 2a), who had tamponade applied immediately after sclerotherapy, and 25 patients (group 2b), who had sclerotherapy without subsequent tamponade. Injection of varices controlled the acute bleeding episode more effectively than tamponade (74 per cent in group 2 v. 42 per cent in group 1). There was no significant difference in the overall mortality rate of the two groups, but group 2 had a significantly higher proportion of Child's grade C patients (38/50 v. 29/50 = 76 v. 58 per cent). If only Child's grade C patients are considered, 16 out of 29 (55 per cent) died in group 1, whereas only 12 out of 38 (32 per cent) died in group 2 (P less than 0.05). Tamponade applied after sclerotherapy had no demonstrable effect on the outcome of sclerotherapy. The long term follow-up of patients (maximum 4 years) showed that recurrence of bleeding was less in the sclerotherapy group (8.1 per cent) than in the tamponade only group (27.6 per cent; P less than 0.05).

Malarial acute renal failure.

Abstract: Malaria is an Italian word composed of “ mala ” and “ aria,” derived from malus (bad), and aeris (air). It was first used to describe a fever (miasma), which was wrongly attributed to exposure to poisonous air rising from marshes. Although the disease had been described in the Hippocratic Collection (460 to 377 BC) and its relation to mosquitoes suggested in the 5th century AD, by the Indian physician Susruta, it was only in 1880 that Charles Laveran, a French physician working in Algeria, discovered the true causative agent as being a sporozoan of the genus Plasmodium. More than a century later, we got to map the malaria genome, identifying a huge number of genes located on 14 chromosomes. Malaria is acquired through the sting of an infected Anopheles mosquito, which injects the sporozoites into the host’s dermis. These are carried with the blood stream to the liver, where they mature in the hepatocytes (extra-erythrocytic cycle) to tissue schizonts that release their merozoites into the hepatic sinusoids. The latter invade the red cells, starting the erythrocytic cycle, which comprises ring forms, trophozoites, and, subsequently, schizonts that contain a new generation of merozoites. The parasitized cells are induced by plasmodial DNA to develop a microtubular system that conveys nutrients to the parasite. They eventually rupture and release the merozoites, which repeat the same cycle. A few merozoites are sexually differentiated into male and female gametocytes, which are essential for the completion of the sexual cycle in the vector.