Table of contentsP001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP effluxR. M. Bateman, M. D. Sharpe, J. E. Jagger, C. G. EllisP002 - Lower serum immunoglobulin G2 level does not predispose to severe flu.J. Solé-Violán, M. López-Rodríguez, E. Herrera-Ramos, J. Ruíz-Hernández, L. Borderías, J. Horcajada, N. González-Quevedo, O. Rajas, M. Briones, F. Rodríguez de Castro, C. Rodríguez GallegoP003 - Brain protective effects of intravenous immunoglobulin through inhibition of complement activation and apoptosis in a rat model of sepsisF. Esen, G. Orhun, P. Ergin Ozcan, E. Senturk, C. Ugur Yilmaz, N. Orhan, N. Arican, M. Kaya, M. Kucukerden, M. Giris, U. Akcan, S. Bilgic Gazioglu, E. TuzunP004 - Adenosine a1 receptor dysfunction is associated with leukopenia: A possible mechanism for sepsis-induced leukopeniaR. Riff, O. Naamani, A. DouvdevaniP005 - Analysis of neutrophil by hyper spectral imaging - A preliminary reportR. Takegawa, H. Yoshida, T. Hirose, N. Yamamoto, H. Hagiya, M. Ojima, Y. Akeda, O. Tasaki, K. Tomono, T. ShimazuP006 - Chemiluminescent intensity assessed by eaa predicts the incidence of postoperative infectious complications following gastrointestinal surgeryS. Ono, T. Kubo, S. Suda, T. Ueno, T. IkedaP007 - Serial change of c1 inhibitor in patients with sepsis – A prospective observational studyT. Hirose, H. Ogura, H. Takahashi, M. Ojima, J. Kang, Y. Nakamura, T. Kojima, T. ShimazuP008 - Comparison of bacteremia and sepsis on sepsis related biomarkersT. Ikeda, S. Suda, Y. Izutani, T. Ueno, S. OnoP009 - The changes of procalcitonin levels in critical patients with abdominal septic shock during blood purificationT. Taniguchi, M. OP010 - Validation of a new sensitive point of care device for rapid measurement of procalcitoninC. Dinter, J. Lotz, B. Eilers, C. Wissmann, R. LottP011 - Infection biomarkers in primary care patients with acute respiratory tract infections – Comparison of procalcitonin and C-reactive proteinM. M. Meili, P. S. SchuetzP012 - Do we need a lower procalcitonin cut off?H. Hawa, M. Sharshir, M. Aburageila, N. SalahuddinP013 - The predictive role of C-reactive protein and procalcitonin biomarkers in central nervous system infections with extensively drug resistant bacteriaV. Chantziara, S. Georgiou, A. Tsimogianni, P. Alexandropoulos, A. Vassi, F. Lagiou, M. Valta, G. Micha, E. Chinou, G. MichaloudisP014 - Changes in endotoxin activity assay and procalcitonin levels after direct hemoperfusion with polymyxin-b immobilized fiberA. Kodaira, T. Ikeda, S. Ono, T. Ueno, S. Suda, Y. Izutani, H. ImaizumiP015 - Diagnostic usefullness of combination biomarkers on ICU admissionM. V. De la Torre-Prados, A. Garcia-De la Torre, A. Enguix-Armada, A. Puerto-Morlan, V. Perez-Valero, A. Garcia-AlcantaraP016 - Platelet function analysis utilising the PFA-100 does not predict infection, bacteraemia, sepsis or outcome in critically ill patientsN. Bolton, J. Dudziak, S. Bonney, A. Tridente, P. NeeP017 - Extracellular histone H3 levels are in...

Rheumatoid arthritis (RA) is a systemic autoimmune disorder affecting the peripheral joints. Different microRNAs had been investigated in RA including miRNA-146a meanwhile, miRNA-499 there were no studies to prove its expression in RA serum samples. This study was performed to investigate expression of both miRNAs-146a and -499 and their polymorphisms in Egyptian patients with RA and to evaluate their relationship with clinico-pathological data. The present study includes 108 subjects classified into two main groups: 52 RA patients and 56 unrelated healthy controls. RA patients were subclassified according to DAS28 score into inactive (23 patients) and active (29 patients). Quantitative expression of serum miRNA-146a, miRNA-499 as well as their Genotyping rs2910164 (C/G) and rs3746444 (T/C), respectively, were done to all subjects using real-time PCR. Serum miRNA-146a and -499 were significantly over expressed in RA patients, but they were not correlated to disease activity. Serum miRNA-146a was negatively correlated with anti-nuclear antibodies (ANA). miRNA-146a (rs2910164) genotyping revealed that the GG genotype and the frequency of the G allele were significantly higher in RA patients compared to the controls. miRNA-499 (rs3746444), genotyping revealed that the CC genotype and the frequency of the C allele were significantly higher. It can be concluded that both miRNAs-146a and -499 can be used as diagnostic markers for RA patients. Both miRNA-146a (rs2710164) and miRNA-499 (rs3746444) were significantly associated with RA susceptibility. The C allele of miRNA-146a (rs2710164) can be considered to be protective. On the other hand, the C allele of miRNA-499 (rs3746444) was significantly associated with RA susceptibility.

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BackgroundStent underexpansion is a major risk factor for in-stent restenosis and acute in-stent thrombosis1Intravascular ultrasound (IVUS) is one of the standards for detection of stent underexpansion (de Feyter et al. 1999; Mintz et al., 2001). StentBoost (SB) enhancement allows an improved angiographic visualization of the stent (Koolen et al., 2005).Aim of workComparison of stent expansion by IVUS and SB enhancement and detection of value of SB to guide dilatation post stent deployment.MethodologyIVUS, SB enhancement and QCA were done in 30 patients admitted for elective stenting procedures .We compared measurements of mean ±standard deviations of (Max SD, Min SD, Mean SD, stent symmetry index) using IVUS, SB and QCA after stent deployment and after postdilatation whenever necessary to optimize stent deployment. The Stent symmetry index was calculated [(maximum stent diameter minus minimum stent diameter) divided by maximum stent diameter].ResultsThe Max SD was (3.45 ± 0.62 vs 3.55 ± 0.56 vs 2.97 ± 0.59) by IVUS vs SB vs QCA respectively. Max SD was significantly higher by IVUS vs QCA (p .009) and between SB vs QCA (p .001) while there was nonsignificant difference between IVUS vs SB (p .53). The Min SD was (2.77 ± 0.53 vs 2.58 ± 0.56 vs 1.88 ± 0.60) by IVUS vs SB vs QCA respectively. Min SD was significantly higher by IVUS vs QCA (p .001) and between SB vs QCA (p .001) while there was nonsignificant difference between IVUS vs SB (p .07). The stent symmetry index was (0.24 ±0.09 vs 0.34 ± 0.09 vs 0.14 ±0.27) by IVUS vs SB vs QCA respectively. It was significantly higher by IVUS vs QCA (p .001) and between SB vs QCA (p .001) while there was nonsignificant difference between IVUS vs SB (p .32). SB was positively correlated with IVUS measurements of Max SD (p < .0001 & r 0.74) and Min SD (p < .0001 & r 0.68). QCA was positively correlated with IVUS measurements of Max SD correlation (p < .0001 & r 0.69) and Min SD (p < .0001 & r 0.63). QCA was positively correlated with SB measurements of Max SD (p < .0001 & r 0.61) and Min SD (p .003 & r 0.49).ConclusionsStentBoost enhancement has superior correlations for stent expansion measured by IVUS when compared with QCA. SB enhancement improved stent visualization and identification of stent underexpansion to guide stent postdilatation.

Background: The renin-angiotensin-aldosterone system plays a role in physiological and pathological responses of the heart to both static and dynamic exercise. Previous studies showed that the level of angiotensin II is determined by the angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism. Aim: We aimed in this study to determine the effect of ACE I/D gene polymorphism on the extent of functional and structural cardiac changes in response to one year of professional football training in young footballers. Methods and results:We studied 68 young male football players and a comparable control group. Besides medical history and clinical examination, 12 lead ECG and transthoracic 2D echocardiography examination were performed. Genotyping of ACE was analyzed using PCR-based technique. There was no statistically significant difference in distribution of genotypes among athletes compared with control subjects. D allele showed a graded effect on both EF (73.55, 67.5 and 60.2%, p=0.03) and PASP (37.6, 26.1 and 21.39 mmHg, p=0.02) in DD, ID and II subjects, respectively. Conclusion: Early cardiac changes in young footballers can be affected by ACE I/D polymorphism. There is a summative effect of the D allele in increasing EF and PASP in response to professional football training.

Background The characteristics, outcomes, and risk factors for in-hospital death of critically ill intensive care unit (ICU) patients with coronavirus disease-2019 (COVID-19) have been described in patients from Europe, North America and China, but there are few data from COVID-19 patients in Middle Eastern countries. The aim of this study was to investigate the characteristics, outcomes, and risk factors for in-hospital death of critically ill patients with COVID-19 pneumonia admitted to the ICUs of a University Hospital in Egypt. Methods Retrospective analysis of patients with COVID-19 pneumonia admitted between April 28 and July 29, 2020 to two ICUs dedicated to the isolation and treatment of patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections in Cairo University Hospitals. Diagnosis was confirmed in all patients using real-time reverse transcription polymerase chain reaction on respiratory samples and radiologic evidence of pneumonia. Results Of the 177 patients admitted to the ICUs during the study period, 160 patients had COVID-19 pneumonia and were included in the analysis (mean age: 60 ± 14 years, 67.5% males); 23% of patients had no known comorbidities. The overall ICU and hospital mortality rates were both 24.4%. The ICU and hospital lengths of stay were 7 (25–75% interquartile range: 4–10) and 10 (25–75% interquartile range: 7–14) days, respectively. In a multivariable analysis with in-hospital death as the dependent variable, ischemic heart disease, history of smoking, and secondary bacterial pneumonia were independently associated with a higher risk of in-hospital death, whereas greater PaO 2 /FiO 2 ratio on admission to the ICU was associated with a lower risk. Conclusion In this cohort of critically ill patients with COVID-19 pneumonia, ischemic heart disease, history of smoking, and secondary bacterial pneumonia were independently associated with a higher risk of in-hospital death.

Background/AimsA polymorphism in the microsomal triglyceride transfer protein (MTP) is associated with hepatic fibrosis, and carriers showed higher levels of steatosis, higher levels of hepatitis C virus (HCV) RNA and advanced fibrosis. The aim of this study was to study MTP expression pattern in HCV patients and impact of the MTP polymorphism on the response to antiviral therapy.MethodsOne hundred consecutive naive HCV genotype 4 patients were recruited to receive antiviral therapy, and 40 control subjects were also recruited. Demographic, laboratory, and histopathology data were collected. DNA was isolated, and the samples were subjected to polymerase chain reaction analysis and genotyping for MTP by restriction fragment length polymorphism analysis.ResultsPatients and controls were age- and sex-matched (male/female, 56/44, age, 39.2±7.8 years for patients with HCV; male/female, 18/22, age, 38.1±8.1 years for controls). MTP single nucleotide polymorphisms (SNPs) (GG, GT, TT) and alleles (G, T) in the patients versus the controls were 70%, 21%, 9% & 80.5%, 19.5% versus 10%, 87.5%, 2.5% & 53.8%, 46.3%, respectively (p=0.0001). The sustained viral response (SVR) of the patients was 60%. SNPs in MTP genotypes (GG, GT, and TT) and alleles (G and T) in the responders and nonresponders were 71.7%, 25%, 3.3% & 84.2%, 15.8% versus 67.5%, 15%, 17.5% & 75%, 25% (p=0.038 and p=0.109, respectively). A multivariate analysis showed that the GT genotype was an independent predictor of SVR (area under the curve 90% and p=0.0001).ConclusionsMTP could be a new predictor for SVR to antiviral therapy in patients with HCV genotype 4 infection.

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