Impact Of Hospital Infections On Patients Outcomes Undergoing Cardiac Surgery At Santa Casa De Misericórdia De Marília [impacto Das Infecções Hospitalares Na Evolução De Pacientes Submetidos à Cirurgia Cardíaca Na Santa Casa De Misericórdia De Marília]

Objective: this study aimed to determine the incidence of nosocomial infections, the risk factors and the impact of these infections on mortality among patients undergoing to cardiac surgery. Methods: Retrospective cohort study of 2060 consecutive patients from 2006 to 2012 at the Santa Casa de Misericórdia de Marília. Results: 351 nosocomial infections were diagnosed (17%), 227 non-surgical infections and 124 surgical wound infections. Major infections were mediastinitis (2.0%), urinary tract infection (2.8%), pneumonia (2.3%), and bloodstream infection (1.7%). The in-hospital mortality was 6.4%. Independent variables associated with non-surgical infections were age ≥ 60 years (OR 1.59, 95% CI 1.09 to 2.31), ICU stay ≥ 2 days (OR 5, 49, 95% CI 2.98 to 10, 09), mechanical ventilation ≥ 2 days (OR11, 93, 95% CI 6.1 to 23.08), use of urinary catheter ≥ 3 days (OR 4.85 95% CI 2.95-7.99). Non-surgical nosocomial infections were more frequent in patients with surgical wound infection (32.3% versus 7.2%, OR 6.1, 95% CI 4.03 to 9.24). Independent variables associated with mortality were age greater than 60 years (OR 2.0; 95% CI 1.4 to3.0), use of vasoactive drugs (OR 3.4, 95% CI 1.9 to 6, 0), insulin use (OR 1.8; 95% CI 1.2 to 2.8), surgical reintervention (OR 4.4; 95% CI 2.1 to 9.0) pneumonia (OR 4.3; 95% CI 2.1 to 8.9) and bloodstream infection (OR = 4.7, 95% CI 2.0 to 11.2). Conclusion: Non-surgical hospital infections are common in patients undergoing cardiac surgery; they increase the chance of surgical wound infection and mortality.292167176(2011), World Health Organization. Report on the burden of endemic health care-associated infection worldwide. 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Tissue-specific sensitivity to AID expression in transgenic mouse models

Activation-induced cytidine deaminase (AID), an enzyme with homology to members of the APOBEC family, is involved in somatic hypermutation (SHM) of immunoglobulin (Ig) genes, either by direct deamination of DNA or by an indirect action through its putative RNA editing activity. AID is able to mutate both Ig-like reporter constructs and selected non-Ig genes in normal B cells and in other cells when ectopically overexpressed in mammalian cells and transgenic mice. However, in spite of the fact that in these transgenic animals AID activity was driven by an ubiquitous promoter, only T lymphomas and lung adenomas occurred. In the present work, we constructed three sets of transgenic mice in which AID was under the control of lck, HTLV-I and MMTV promoters, respectively. The lck/AID mice developed thymic lymphomas with variable but high efficiency, while no tumor was detected in HTLV-I/AID mice after two years of monitoring. Four MMTV/AID founder mice died with an atypical clinical picture, although no mammary tumor was found. These findings suggest that additional factors, present in thymocytes but not in other tissues or in lymphoid cells at different stages of differentiation, are needed for AID to fully manifest its tumorigenic potential in mouse. Alternatively, the display of full AID mutagenic and transforming activity could be related to the existence of physiologic DSBs which occur in both thymocytes and switching B cells