The aim of this study was to compare two variants of a novel polycarbonate polyurethane prosthesis with polyethylene terephthalate (Dacron) prosthesis in an established sheep model of carotid patch angioplasty. Two variants of the polycarbonate polyurethane prosthesis were used: (1) Polycarbonate polyurethane equal (PCU-e) prosthesis consisted of a multilayered porous structure with equal internal and external layers; (2) Polycarbonate polyurethane with more porous inner layers (PCU-mp) prosthesis had more porous inner layers than external layers. Carotid patch angioplasty was performed in 12 sheep: in six sheep, the PCU-e variant and in the other six sheep, the PCU-mp variant was implanted. Dacron patches were implanted in the contralateral carotid artery of all sheep as a control. Half of the animals with each polycarbonate polyurethane variant were euthanized after two weeks and the other half after eight weeks. Cellular infiltration, endothelialization, and neointimal hyperplasia were examined. All grafts were patent, and no thrombus was seen in any of the harvested arteries. The pores of all the three patch materials allowed infiltration of inflammatory cells, capillaries, and connective tissue. After eight weeks, a nearly complete endothelialization was visible in all patch groups without an obvious difference between the three patch materials. The neointima was thinner in the PCU patches (PCU-e: 56 ± 13 µm, PCU-mp: 119 ± 60 µm) when compared to Dacron patches (156 ± 64 µm) after two weeks. After 8 weeks, a further neointimal growth was detectable, without any significant difference of neointimal thickness between the three patch materials (Dacron: 274 ± 82 µm, PCU-e: 324 ± 98 µm, PCU-mp: 235 ± 59 µm). With the novel polycarbonate polyurethane patch materials, we achieved promising functional and morphological results with 100% patency and nearly complete endothelialization. Our findings showed at least a non-inferiority of the novel polycarbonate polyurethane patch material compared to Dacron. There were no significant differences detected between the two polycarbonate polyurethane patch variants.

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Background11β HSD1 generates cortisol from cortisone. 11β HSD1 single-nucleotide polymorphism (SNP) was associated with metabolic syndrome (MeTS). Although the relation of acne vulgaris (AV) and skin tags (STs) with MeTS has been reported, the relationship between 11β HSD 1 SNP and cortisol activity in those patients has not studied till now.AimsTo investigate, two 11β-HSD1 SNPs (rs846910 and rs12086634), serum lipid profile and cortisol levels in patients with AV and STs in an Egyptian population.Patients and methodsThis case–control study was performed on 50 patients having STs and 50 complaining of AV and 50 sex- and age-matched controls. We searched for serum lipid profile, cortisol levels, and 11β-HSD1 rs846910 and rs12086634 SNPs using real time-PCR.ResultsCompared to controls,11β-HSD1 rs846910 GA genotype carriers had significantly higher risks for developing AV and STs by 3.4- and 4.9-fold, respectively, and its A allele increases these risks by 3.1 and 4.4 times, respectively. Also, 11β-HSD1 rs12086634 TG genotype increases the risk of AV by 3.2-fold, as well as STs by 3.5-fold, and its G allele increases the risk of AV by 3.2-fold and STs by 7-fold. In AV and ST patients, rs846910 GA genotype demonstrated significant associations with elevated body mass index (BMI), and cholesterol, low density lipoprotein (LDL), cortisol, and decreased high density lipoprotein serum levels, respectively. However, rs12086634 GG genotype was significantly associated with increased BMI, cholesterol, and LDL serum levels in patients with AV and STs, in addition to the number of STs and serum cortisol levels in ST patients.Conclusion11β-HSD1 rs846910 and rs12086634 gene polymorphisms may contribute to AV and STs pathogenesis, that may be mediated through enhancing the enzymatic activity (increasing cortisol levels). AV and STs are associated with obesity and atherogenic lipid profile. Diagnosis of AV and STs may play a role in early detection of the MeTS.

BackgroundLivin gene and Yes-Associated Protein 1 (YAP1 (play a pivotal role in organ size control and tumorigenesis.AimIn the present pilot study, we investigate the expression of Livin gene and YAP1 in hepatitis C virus (HCV) associated hepatocellular carcinoma (HCC) compared to other HCV patients and controls.Methods: the studied patients were divided into three groups 30 patients in each group in addition to 30 healthy subjects as a control group. Relative quantification of Livin gene and YAP-1 were assessed by quantitative Real Time RT-PCR (qPCR) in all studied patients and healthy controls. other laboratory investigations were done including complete blood count (CBC),international normalized ratio (INR) as well as liver function tests and tumor markers.ResultsSignificant overexpression of Livin gene and YAP-1 was detected in HCC group followed by Hepatitis C Virus (HCV) untreated group then HCV treated group. The relative quantitation (RQ) of both genes showed positive correlation to the carcinoembryonic antigen (CEA) level and a significant relation was found between higher level of Livin and YAP1 genes and tumor size. The overall survival rate was low in those patients with high levels of Livin and YAP 1 genes so they were considered as indicators of a bad prognosis.ConclusionThere is overexpression of Livin gene and YAP1 in hepatocellular carcinoma patients. They can be used as indicators of bad prognosis of the disease pathway together with low survival rate.