Prevention of Intradialytic Hypotension in Patients with Acute Kidney Injury Submitted to Sustained Low-Efficiency Dialysis

Objectives: This study evaluated the effects of a protocol aiming to reduce hypotension in acute kidney injury (AKI) patients submitted to sustained low-efficiency dialysis (SLED). Methods: Patients were randomly assigned to two SLED prescriptions-control group, dialysate temperature was 37.0 degrees C with a fixed sodium concentration [138 mEq/L] and ultrafiltration (UF) rate; and profiling group, dialysate temperature was 35.5 degrees C with a variable sodium concentration [150-138 mEq/L] and UF rate. Results: Sixty-two SLED sessions were evaluated (34 in profiling and 28 in control). Patients (n = 31) were similar in terms of gender, age, and Sequential Organ Failure Assessment (SOFA) score. Dialysis time, dialysis dose, and post-dialysis serum sodium were similar in both groups. The profiling group had significantly less hypotension episodes (23% vs. 57% in control, p = 0.009) and achieved higher UF volume (2.23 +/- 1.25 L vs. 1.59 +/- 1.03 L in control, p = 0.04) when compared with control group. Conclusions: SLED protocol with modulation of dialysate temperature, sodium, and UF profiling showed similar efficacy but less intradialytic hypotension when compared with a standard SLED prescription.

A Systematic Mapping on the Role-Permission Relationship in Role Based Access Control Models

Access control is a key component of security in any computer system. In the last two decades, the research on Role Basead Access Control Models was intense. One of the most important components of a Role Based Model is the Role-Permission Relationship. In this paper, the technique of systematic mapping is used to identify, extract and analyze many approaches applied to establish the Role-Permission Relationship. The main goal of this mapping is pointing directions of significant research in the area of Role Based Access Control Models.

Retrospective Clinical Study of 988 Dual Acid-Etched Implants Placed in Grafted and Native Bone for Single-Tooth Replacement

Purpose: To evaluate the influence of sex, implant characteristics, and bone grafting on the survival rate of dual acid-etched (DAE) implants. Materials and Methods: Patients treated with internal-hex DAE implants for single-tooth replacement in a military dental clinic between January 2005 and December 2010 were included in this study. Clinical data related to implant characteristics, implant location, presence of grafted bone, and implant failures were collected. The primary outcome was implant loss. The survival rate was analyzed using the Kaplan-Meier method. Cox regression modeling was used to determine which factors would predict implant failure. Results: DAE implants were evaluated in a total of 988 patients (80.3% men). Twenty-four (2.4%) implants failed, most were cylindric (54.2%) with regular platforms (70.8%) and were 10 mm long (58.3%). The failure rate was 2.4% for the anterior maxilla, 3.3% for the posterior maxilla, 1.6% for the anterior mandible, and 2.0% for posterior mandible. The cumulative survival rate was 97.6%. The failure rate was 8.8% in implants placed after sinus augmentation, 7.3% in bone block-grafted areas, and 1.6% in native bone. Based on multivariable analysis (Cox regression), sinus augmentation and bone block grafting had a statistically significant effect on implant failure; the hazard ratios were 5.5 and 4.6, respectively. Conclusion: The results revealed that DAE implants had high survival rates, and no influence of sex, location, shape, diameter, or length on failure rates could be observed. However, a significant association was observed between failure and presence of bone graft in the implant area. Int J Oral Maxillofac Implants 2012;27:1243-1248

Mutations in ADAR1 cause Aicardi-Goutieres syndrome associated with a type I interferon signature

Adenosine deaminases acting on RNA (ADARs) catalyze the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) and thereby potentially alter the information content and structure of cellular RNAs. Notably, although the overwhelming majority of such editing events occur in transcripts derived from Alu repeat elements, the biological function of non-coding RNA editing remains uncertain. Here, we show that mutations in ADAR1 (also known as ADAR) cause the autoimmune disorder Aicardi-Goutieres syndrome (AGS). As in Adar1-null mice, the human disease state is associated with upregulation of interferon-stimulated genes, indicating a possible role for ADAR1 as a suppressor of type I interferon signaling. Considering recent insights derived from the study of other AGS-related proteins, we speculate that ADAR1 may limit the cytoplasmic accumulation of the dsRNA generated from genomic repetitive elements.

Murine Dendritic Cells Transcriptional Modulation upon Paracoccidioides brasiliensis Infection

Limited information is available regarding the modulation of genes involved in the innate host response to Paracoccidioides brasiliensis, the etiologic agent of paracoccidioidomycosis. Therefore, we sought to characterize, for the first time, the transcriptional profile of murine bone marrow-derived dendritic cells (DCs) at an early stage following their initial interaction with P. brasiliensis. DCs connect innate and adaptive immunity by recognizing invading pathogens and determining the type of effector T-cell that mediates an immune response. Gene expression profiles were analyzed using microarray and validated using real-time RT-PCR and protein secretion studies. A total of 299 genes were differentially expressed, many of which are involved in immunity, signal transduction, transcription and apoptosis. Genes encoding the cytokines IL-12 and TNF-alpha, along with the chemokines CCL22, CCL27 and CXCL10, were up-regulated, suggesting that P. brasiliensis induces a potent proinflammatory response in DCs. In contrast, pattern recognition receptor (PRR)-encoding genes, particularly those related to Toll-like receptors, were down-regulated or unchanged. This result prompted us to evaluate the expression profiles of dectin-1 and mannose receptor, two other important fungal PRRs that were not included in the microarray target cDNA sequences. Unlike the mannose receptor, the dectin-1 receptor gene was significantly induced, suggesting that this beta-glucan receptor participates in the recognition of P. brasiliensis. We also used a receptor inhibition assay to evaluate the roles of these receptors in coordinating the expression of several immune-related genes in DCs upon fungal exposure. Altogether, our results provide an initial characterization of early host responses to P. brasiliensis and a basis for better understanding the infectious process of this important neglected pathogen.