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Background: ABO blood groups are associated with different risk of viral infections. In vitro studies demonstrated how anti-A and anti-B antibodies neutralized the infectious capacity of SARS-CoV-2. Therefore, here we describe the inflammatory response of COVID-19 patients in the context of the blood group aiming to assess the lower severity status found in group O patients. Methods: Prospective and consecutive study including blood samples from 108 adult patients diagnosed with COVID-19 and admitted to the “Hospital Clinico Universitario” Valladolid, Spain between March 24 and April 11 2020. Patients were divided according to their ABO blood group. Plasma aliquots were analyzed, in duplicate, for the quantification of 45 mediators by MAGPIX system (Luminex). Statistical analysis was performed using the R statistical package version 4.0.2 Findings: We found a lower risk (2.16 times) of mechanical ventilation or death in patients with blood group O [Log Rank: p=0.042, Hazard Ratio: 0.463, CI 95% (0.213-1.004), p=0.050]. Moreover, 15 cytokines were significantly over-expressed (and only one under-expressed) in blood group O. Last, a multivariate model found BDNF, IL-13 and IL-27 as the best cytokines able to differentiate the immune profile based on blood group. Interpretation: Our cohort showed how blood group O was associated with both lower rates of hospital admission and a lower risk of intubation or death. Indeed, these patients produced higher amounts of cytokines in response to SARS-CoV-2, hence mounting an effective immune response which allowed them to control the viral infection and therefore decrease the risk of further complications. Funding Statement: This research was funded by Instituto de Salud Carlos III, grant number COV20/00491. Declaration of Interests: Alvaro Tamayo-Velasco declares no conflict of interest. - Maria Jesus Penarrubia-Ponce declares no conflict of interest. - Francisco Javier Alvarez declares no conflict of interest. - Hugo Gonzalo-Benito declares no conflict of interest. - Ignacio de la Fuente declares no conflict of interest. - Sonia Perez Gonzalez declares no conflict of interest. - Lucia Rico declares no conflict of interest. - Maria Teresa Jimenez-Garcia declares no conflict of interest. - Alba Sanchez-Rodriguez declares no conflict of interest. - Milagros Hijas-Villaizan declares no conflict of interest. - Marta Martin Fernandez declares no conflict of interest. - Carlos Duenas declares no conflict of interest. - Esther Gomez-Sanchez declares no conflict of interest. - Maria Heredia-Rodriguez declares no conflict of interest. - Oscar Gorgojo-Galindo declares no conflict of interest. - Itziar Fernandez declares no conflict of interest. - Lourdes del Rio declares no conflict of interest. - Irene Carnicero-Frutos declares no conflict of interest. - Maria Fe Munoz-Moreno declares no conflict of interest. - Eduardo Tamayo declares no conflict of interest. - David Bernardo declares no conflict of interest. - Pedro Martinez-Paz declares no conflict of interest. Ethics Approval Statement: The study was approved by the Hospital's Clinical Ethics Committee (CEIm) and approval was obtained from all study participants (cod: PI 20-1717).

Background Numerous studies have evaluated the use of ultraviolet-C devices for terminal disinfection in hospitals, however, to date there is little information about the device's final impact on patients. We investigated the effect of an ultraviolet air sterilizer (UVAS) on the clinical outcomes of cardiac surgery patients. Materials and methods This random, prospective and non-interventional study included 1097 adult patients undergoing elective cardiac surgery: 522 stayed in an ICU room with UVAS (Medixair®) and 575 patients ICU room without UVAS and were used as a control. The primary outcome measure was to evaluate the effect of a UVAS on the overall prevalence of nosocomial infections in postoperative cardiac patients in ICUs. Results No significant differences in ventilator-associated pneumonia (4.6% vs. 5.0%, p = 0.77) and total infection (14.0% vs. 15.5%, p = 0.45) rates were detected in patients with and without the UVAS. The length of stay in the intensive care unit and at the hospital was similar in both groups, UVAS (4.6 (8.2) days and 18.3 (5.5) days) and without UVAS (4.6 (7.3) days and 19.2 (18.6) days). The 30-day in-hospital mortality rate was 5.3%, no significant differences between groups were observed (p = 0.053). Conclusion Novel ultraviolet-C technology has not been shown to significantly reduce nosocomial infections or mortality rates in cardiac surgery patients.

We intended to assess how acute kidney injuy impacts on procalcitonin levels in cardiac surgery patients, with or without infection, and whether procalcitonin might be used as a biomarker of infection in acute kidney injuy.A case-control study was designed which included patients that had had cardiac surgery between January 2011 and January 2015. Every patient developing severe sepsis or septic shock (n = 122; 5.5%) was enrolled. In addition, consecutive cardiac surgery patients during 2013 developing systemic inflammatory response syndrome (n = 318) were enrolled. Those recruited 440 patients were divided into 2 groups, according to renal function.Median procalcitonin levels were significantly higher during the 10 postoperative days in the acute kidney injury patients. Regression analysis showed that postoperatory day, creatinine, white blood cells and infection were significantly (P.0001) associated to serum procalcitonin level. In patients with creatinine ≥2, median procalcitonin levels were similar in infected and non-infected patients. Only when creatinine was less than 2 mg/L, the median procalcitonin levels were significantly higher in patients with infection, as compared to those with no infection.In acute kidney injuy patients, high procalcitonin levels are a marker of acute kidney injuy but will not be able to differentiate infected from non-infected patients.

Producción Científica, Purpose: Acute kidney injury (AKI) is a frequent complication after cardiac surgery and is associated with increased mortality. The aim was to design a nondialytic AKI score in patients with previously normal renal function undergoing cardiac surgery. Methods: Data were collected on 909 patients who underwent cardiac surgery with cardiopulmonary bypass between 2012 and 2014. A total of 810 patients fulfilled the inclusion criteria. Patients were classified as having AKI based on the RIFLE criteria. Postoperative AKI occurred in 137 patients (16.9%). Several parameters were recorded preoperatively, intraoperatively, and at intensive care unit admission, looking for a univariate andmultivariate associationwith AKI risk. A second data set of 741 patients, from2 different hospitals,was recorded as a validation cohort. Results: Four independent risk factors were included in the CRATE score: creatinine (odds ratio [OR], 9.66; 95% confidence interval [CI], 4.77-19.56; P b .001), EuroSCORE (OR, 1.40; CI, 1.29-1.52; P b .001), lactate (OR, 1.03; CI, 1.01- 1.04; P b .001), and cardiopulmonary bypass time (OR, 1.01; CI, 1.01-1.02; P b .001). The accuracy of the model was good, with an area under the curve of 0.89 (CI, 0.85-0.92). The CRATE score retained good discrimination in validation cohort, with an area under the curve of 0.81 (95% CI, 0.78-0.85). Conclusions: CRATE score is an accurate and easy to calculate risk score that uses affordable andwidely available variables in the routine care surgical patients.

Summary Objectives Sepsis is characterised by the frequent presence of organ failure and marked immunologic alterations. We studied the association between the extent of organ failure and the transcriptomic response of septic patients. Methods Gene expression profiles in the blood of 74 surgical patients with sepsis were compared with those of 30 surgical patients with no sepsis. Differentially expressed genes were assessed for their correlation with the sequential organ failure (SOFA) score. Results The expression levels of a group of genes participating in the cell cycle (HIST1H1C, CKS2, CCNA2, CDK1, CCNB2, CIT, CCNB1, AURKA, RAD51), neutrophil protease activity (ELANE, ADORA3, MPO, MMP8, CTSG), IL-1R and IL-18R response correlated directly with SOFA and mortality. Genes involved in T cell (LCK, CD3G, CD3D, ZAP70, ICOS, CD3E, CD28, IL2RB, CD8B, CD8A, CD40LG, IL23A, CCL5, SH2D1A, ITK, CD247, TBX21, GATA3, CCR7, LEF1, STAT4) and NK cell immunity (CD244, KLRK1, KLRD1) were inversely associated with SOFA and mortality. Conclusions The extent of organ failure in sepsis correlates directly with the existence of imbalanced innate and adaptive responses at the transcriptomic level. Quantification of the expression levels of the genes identified here could contribute to the simultaneous assessment of disease severity and immunological alterations in sepsis.

Purpose There is increasing evidence on the relationship between endogenously produced immunoglobulins and the clinical outcome in septic shock (SS). Materials and methods Levels of immunoglobulin G (IgG) subclasses, immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin E were measured in plasma from 42 patients with SS and in 36 patients with systemic inflammatory response syndrome at diagnosis. Association of immunoglobulins levels with disease severity and outcome was evaluated. Results Eighteen patients with SS finally died. Both patients with systemic inflammatory response syndrome and SS showed subnormal levels of total IgG, IgG2, and IgM. Patients with SS who died showed the lowest levels of total IgG and IgG1. Total IgG, IgG1, IgG2, IgG3, IgG4, and IgA correlated inversely with Acute Physiology and Chronic Health Evaluation II score in SS. Univariate Cox regression analysis showed that levels of IgG1, IgG2, IgG3, IgM, IgA, and total IgG were inversely associated to the probability of death at 28 days. Multivariate analysis showed that IgG1, total IgG, IgM, and IgA behaved as independent protective factors against mortality (hazard ratio, P ): 0.23, 0.026; 0.16, 0.028; 0.11, 0.042; 0.05, 0.010, respectively, whereas IgG3 showed a protective trend also. Conclusions Our study evidenced that, in addition to IgG1, other major endogenous immunoglobulins isotypes and subclasses seem to play a beneficial role in SS.

Background Persistent inflammation and fibrosis have been related to active progression of renal deterioration and reduced survival of kidney transplant. The aim of this study was to determine the impact of single-nucleotide polymorphisms (SNPs) located in regions related to inflammatory and immune processes on the development of chronic renal allograft dysfunction (CRAD). Methods A retrospective study was carried out on 276 patients who received kidney transplant (KT). SNPs were genotyped via the SNPlex platform. Statistical analysis was performed with SNPstat and regression logistic analyses were adjusted by age and gender of recipients and donors, cold ischemia time and the number of human leukocyte antigen (HLA) mismatches. Results From 276 patients with KT, 118 were non-CRAD and 158 were CRAD. Three SNPs showed significant associations with CRAD development: rs1800471 in transforming growth factor beta 1 (TGFB1), rs5186 in angiotensin II receptor type 1 (AGTR1), and rs699947 in vascular endothelial growth factor A (VEGFA). GC genotype of rs1800471 was associated with increased odds of CRAD compared to GG genotype (OR = 2.65 (95% confidence interval (CI) = 1.09; 6.47), p = 0.025), as well as AC and AA genotype of rs699947 assuming a dominant model (OR = 1.80 (95% CI = 1.02; 3.20), p = 0.044). Besides, AC and CC genotypes of rs5186 were associated with reduced odds of CRAD assuming a dominant model (OR = 0.56 (95% CI = 0.33; 0.96), p = 0.033). Conclusion Our findings suggest that three genes related to immunity and inflammation (rs1800471, rs5186 and rs699947) are associated to susceptibility or protection to CRAD, and might have diagnostic utility in predicting the likelihood of developing CRAD.

Introducción y objetivos: Los deportes de equipo requieren jugadores que puedan realizar un número elevado de sprints cortos, intercalados con períodos de recuperación o de intensidad, y a este tipo de esfuerzos se le ha denominado capacidad de realizar sprints repetidos (RSA). Aunque la importancia de estos esfuerzos está constatada en deportes de equipo, la diferencia entre deportistas de distintas disciplinas debe ser estudiada debido a la variabilidad de esfuerzos en los numerosos deportes colectivos. La presente investigación va encaminada a determinar las diferencias y analogías en test RSA entre deportistas amateurs y profesionales de deportes colectivos distintos como son el baloncesto y balonmano. Método: Se evaluaron 4 equipos, 2 de baloncesto y 2 de balonmano (divididos en amateurs y profesionales). El test RSA realizado fue 8 × 30 m con 25 s de recuperación, en pista con células fotoeléctricas. Resultados: Los resultados obtenidos no muestran diferencias significativas en las variables cinéticas entre los diferentes grupos. Sí se encontraron diferencias entre baloncesto profesional y balonmano profesional (p < 0,05) en las variables mejor sprint y aceleración 0-10 m. Se observó un descenso en la potencia (entre el 20,51 y el 23,37%) entre el sprint 1 y 8 en los 4 grupos, pero no hubo diferencias entre ellos. Conclusiones: El tipo de esfuerzos realizados por deportistas de deportes de cooperación y oposición de disciplinas semejantes (como baloncesto y balonmano) es similar en el test RSA, debido a que los esfuerzos realizados en competición se asemejan mucho entre deportes y con los esfuerzos realizados en el protocolo utilizado.