TNF-like ligand 1A (TL1A), a member of the TNF superfamily, is the ligand of DR3 and DcR3. Several types of cells, such as endothelial cells, monocytes/macrophages, dendritic cells, and CD4 and CD8 T cells, are capable of producing this cytokine. In present study, we demonstrated that TL1A aggravated collagen-induced arthritis in mice. It increased collagen-induced arthritis penetrance and clinical scores as well as the severity of the pathological findings. TL1A administration led to the occurrence of multiple enlarged germinal centers in the spleen, and it boosted serum anti-collagen Ab titers in vivo. In vitro, TL1A augmented TNF-α production by T cells upon TCR ligation, and it greatly enhanced Th17 differentiation and IL-17 production. We further showed that human rheumatoid arthritis (RA) synovial fluids had elevated TL1A titers, and human chrondrocytes and synovial fibroblasts were capable of secreting TL1A upon TNF-α or IL-1β stimulation. Taken together, these data suggest that TL1A secretion in lymphoid organs might contribute to RA initiation by promoting autoantibody production, and TL1A secretion stimulated by inflammatory cytokines in RA joints might be a part of a vicious circle that aggravates RA pathogenesis.
Objectives. Incidental findings on computed tomography (CT) scans are common. We sought to examine rates of findings and disclosure among discharged patients who received a CT scan in the ED. Methods. Retrospective chart review (Aug-Oct 2009) of 600 patients age 18 and older discharged home from an urban Level 1 trauma center. CT reports were used to identify incidental findings and discharge paperwork was used to determine whether the patient was informed of these findings. Results. There were 682 CT scans among 600 patients: 199 Abdomen & Pelvis, 405 Head, and 78 Thorax. A total of 348 incidental findings were documented in 228/682 (33.4%) of the scans, of which 34 (9.8%) were reported to patients in discharge paperwork. Patients with 1 incidental finding were less likely to receive disclosure than patients with 2 or more (P = .010). Patients age <60 were less likely to have incidental findings (P < .001). There was no significant disclosure or incidental finding difference by gender. Conclusions. While previous research suggests that CT incidental findings are often benign, reporting to patients is recommended but this is rarely happening.
A strong prediction model to identify those ED patients with mTBI at risk for PPCS was developed and could be easily implemented in the ED; therefore, helping to target those patients who would potentially benefit from close follow-up.
The objective of the current study was to determine the classification accuracy of serum S100B and apolipoprotein (apoA-I) for mild traumatic brain injury (mTBI) and abnormal initial head computed tomography (CT) scan, and to identify ethnic, racial, age, and sex variation in classification accuracy. We performed a prospective, multi-centered study of 787 patients with mTBI who presented to the emergency department within 6 h of injury and 467 controls who presented to the outpatient laboratory for routine blood work. Serum was analyzed for S100B and apoA-I. The outcomes were disease status (mTBI or control) and initial head CT scan. At cutoff values defined by 90% of controls, the specificity for mTBI using S100B (0.899 [95% confidence interval (CI): 0.78-0.92]) was similar to that using apoA-I (0.902 [0.87-0.93]), and the sensitivity using S100B (0.252 [0.22-0.28]) was similar to that using apoA-I (0.249 [0.22-0.28]). The area under the receiver operating characteristic curve (AUC) for the combination of S100B and apoA-I (0.738, 95% CI: 0.71, 0.77), however, was significantly higher than the AUC for S100B alone (0.709, 95% CI: 0.68, 0.74, p = 0.001) and higher than the AUC for apoA-I alone (0.645, 95% CI: 0.61, 0.68, p < 0.0001). The AUC for prediction of abnormal initial head CT scan using S100B was 0.694 (95%CI: 0.62, 0.77) and not significant for apoA-I. At a S100B cutoff of < 0.060 lg/L, the sensitivity for abnormal head CT was 98%, and 22.9% of CT scans could have been avoided. There was significant age and race-related variation in the accuracy of S100B for the diagnosis of mTBI. The combined use of serum S100B and apoA-I maximizes classification accuracy for mTBI, but only S100B is needed to classify abnormal head CT scan. Because of significant subgroup variation in classification accuracy, age and race need to be considered when using S100B to classify subjects for mTBI.
Literature on recruitment emphasizes processes and procedures under investigator control rather than understanding potential participants' judgments about the adequacy of their existing practices and the potential benefits of intervention participation relative to potential time and productivity trade-offs. Greater attention to such judgments may enhance recruitment and participation in under-studied and difficult to access populations.
Because hyperbaric oxygen treatment mobilizes bone marrow derived-stem/progenitor cells by a free radical mediated mechanism, we hypothesized that there may be differences in mobilization efficiency based on exposure to different oxygen partial pressures. Blood from twenty consecutive patients was obtained before and after the 1st, 10th and 20th treatment at two clinical centers using protocols involving exposures to oxygen at either 2.0 or 2.5 atmospheres absolute (ATA). Post-treatment values of CD34+, CD45-dim leukocytes were always 2-fold greater than the pre-treatment values for both protocols. Values for those treated at 2.5 ATA were significantly greater than the 2.0 ATA treatment group by factors of 1.9 to 3-fold after the 10th and before and after the 20th treatments. Intracellular content of hypoxia inducible factors -1,-2, and -3, thioredoxin-1 and poly-ADP-ribose polymerase assessed in permeabilized CD34+ cells with fluorophore-conjugated antibodies were twice as high in all post- versus pre-treatment samples with no significant differences between 2.0 and 2.5 ATA protocols. We conclude that putative progenitor cell mobilization is higher with 2.5 versus 2.0 ATA treatments, and all newly mobilized cells exhibit higher concentrations of an array of regulatory proteins.
BackgroundAmbulance offload delay (AOD) has been recognized by the National Association of EMS Physicians (NAEMSP) as an important quality marker. AOD is the time between arrival of a patient by EMS and the time that the EMS crew has given report and moved the patient off of the EMS stretcher, allowing the EMS crew to begin the process of returning to service. The AOD represents a potential delay in patient care and a delay in the availability of an EMS crew and their ambulance for response to emergencies. This pilot study was designed to assess the AOD at a university hospital utilizing direct observation by trained research assistants.FindingsA convenience sample of 483 patients was observed during a 12-month period. Data were analyzed to determine the AOD overall and for four groups of National Emergency Department Overcrowding Scale (NEDOCS) score ranges. The AOD ranged from 0 min to 157 min with a median of 11 min. When data were grouped by NEDOCS score, there was a statistically significant difference in median AOD between the groups (p < 0.001), indicating the relationship between ED crowding and AOD.ConclusionThe median AOD was considered significant and raised concerns related to patient care and EMS system resource availability. The NEDOCS score had a positive correlation with AOD and should be further investigated as a potential marker for determining diversion status or for destination decision-making by EMS personnel.
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