ABSTRACT
OBJECTIVES: The aim of the study was to identify covariates associated with 28-day mortality in septic patients admitted to the emergency department and derive and validate a score that stratifies mortality risk utilizing parameters that are readily available. METHODS: Patients with an admission diagnosis of suspected or confirmed infection and fulfilling at least two criteria for severe inflammatory response syndrome were included in this study. Patients' characteristics, vital signs, and laboratory values were used to identify prognostic factors for mortality. A scoring system was derived and validated. The primary outcome was the 28-day mortality rate. RESULTS: A total of 440 patients were included in the study. The 28-day hospital mortality rate was 32.4 and 25.2% for the derivation (293 patients) and validation (147 patients) sets, respectively. Factors associated with a higher mortality were immune-suppressed state (odds ratio 4.7; 95% confidence interval 2.0-11.4), systolic blood pressure on arrival less than 90 mmHg (3.8; 1.7-8.3), body temperature less than 36.0°C (4.1; 1.3-12.9), oxygen saturation less than 90% (2.3; 1.1-4.8), hematocrit less than 0.38 (3.1; 1.6-5.9), blood pH less than 7.35 (2.0; 1.04-3.9), lactate level more than 2.4 mmol/l (2.27; 1.2-4.2), and pneumonia as the source of infection (2.7; 1.5-5.0). The area under the receiver operating characteristic curve was 0.81 (0.75-0.86) in the derivation and 0.81 (0.73-0.90) in the validation set. The SPEED (sepsis patient evaluation in the emergency department) score performed better (P=0.02) than the Mortality in Emergency Department Sepsis score when applied to the complete study population with an area under the curve of 0.81 (0.76-0.85) as compared with 0.74 (0.70-0.79). CONCLUSION: The SPEED score predicts 28-day mortality in septic patients. It is simple and its predictive value is comparable to that of other scoring systems.
Subject(s)
Decision Support Techniques , Emergency Service, Hospital , Risk Assessment , Sepsis/diagnosis , Hospital Mortality , Humans , Middle Aged , Prognosis , Prospective Studies , Reproducibility of Results , Risk Assessment/methods , Risk Factors , Sepsis/mortality , Systemic Inflammatory Response Syndrome/diagnosis , Systemic Inflammatory Response Syndrome/mortality , Vital SignsABSTRACT
Native cartilage matrix derived (CMD) scaffolds from various animal and human sources have drawn attention in cartilage tissue engineering due to the demonstrable presence of bioactive components. Different chemical and physical treatments have been employed to enhance the micro-architecture of CMD scaffolds. In this study we have assessed the typical effects of physical cross-linking methods, namely ultraviolet (UV) light, dehydrothermal (DHT) treatment, and combinations of them on bovine articular CMD porous scaffolds with three different matrix concentrations (5%, 15% and 30%) to assess the relative strengths of each treatment. Our findings suggest that UV and UV-DHT treatments on 15% CMD scaffolds can yield architecturally optimal scaffolds for cartilage tissue engineering.
ABSTRACT
In humans, susceptibility to several immunopathologic diseases maps to a conserved block encompassing the polymorphic BAT1, NFKBIL1 (IKBL) and TNF genes in the central MHC. As a pre-requisite for studies of these genes in animal models, we characterized Bat1a and Nfkbil1 in inbred mice differing in their H2 haplotype. We identified two indels and nine single nucleotide polymorphisms (SNP) upstream of Nfkbil1, one indel, nine SNP upstream of Bat1a and a synonymous SNP in exon 2 of Bat1a. H2(g7) and H2(b) mice yielded identical Bat1a and Nfkbil1 sequences. Real time PCR (RT-PCR) showed Bat1a was expressed in adult brain, heart, kidney, liver, lung, pancreas and spleen. Expression of Bat1a was higher in brain and liver of 15-day embryos compared to 1-day old mice and increased moderately in liver and lung of adult mice 2-4 h after LPS challenge. Nfkbil1 expression was low or undetetectable in all tissues and cell lines.
