Research Spotlight

Warren, A. M., M. Reynolds, M. L. Foreman, M. M. Bennett, R. J. Weddle, J. D. Austin, K. Roden-Foreman and L. B. Petrey (2016). “Validation of a brief, two-question depression screen in trauma patients.” J Trauma Acute Care Surg 80(2): 318-323.

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BACKGROUND: Increasingly, depression following traumatic injury is recognized as a complication of injury. Unlike mandated screening for risky alcohol use in trauma centers, screening for psychological risks is not required by the American College of Surgeons’ Committee on Trauma. Limited resources and time constraints are commonly given reasons against routine screening. The purpose of this study was to determine if a two-item screen was as valid as an eight-question screen for depression. METHODS: A total of 421 patients were given the Patient Health Questionnaire 8 (PHQ-8) during initial hospitalization to assess depression in a prospective study at a Level I trauma center. A cutoff score of 10 or higher (possible range, 0-24) on the PHQ-8 is used as diagnostic for depression. The PHQ-2 (possible range, 0-6) is derived from the first two questions of the PHQ-8 and contains items assessing sad mood and loss of interest/pleasure during the previous 2 weeks. A cutoff score of 3 or higher was considered to be a positive screen result. Discriminatory ability of the PHQ-2 was calculated. RESULTS: The sample was predominantly male (65%) and white (67%). The majority (85%) sustained a blunt trauma, and the primary cause of injury was motor vehicle collision (37%), with a mean Injury Severity Score (ISS) of 11.6. A total of 142 patients (34%) were positive for depression on the PHQ-8. When comparing the PHQ-2 with the PHQ-8, a sensitivity of 76.1 and a specificity of 92.8 were found, as well as a positive predictive value of 84.4. CONCLUSION: The result of our study confirms that depression is a frequent condition (34%) among individuals who sustain physical injury. The PHQ-2 seems to have acceptable sensitivity and specificity to identify depression in this population. The use of a two-item screening questionnaire is a minimal addition to the evaluation of patients after injury, allowing for earlier intervention and better outcomes. LEVEL OF EVIDENCE: Diagnostic study, level IV; prognostic/epidemiologic study, level III.

Chung, J. R., B. Flannery, M. G. Thompson, M. Gaglani, M. L. Jackson, A. S. Monto, M. P. Nowalk, H. K. Talbot, J. J. Treanor, E. A. Belongia, K. Murthy, L. A. Jackson, J. G. Petrie, R. K. Zimmerman, M. R. Griffin, H. Q. McLean and A. M. Fry (2016). “Seasonal Effectiveness of Live Attenuated and Inactivated Influenza Vaccine.” Pediatrics 137(2): 1-10.

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BACKGROUND: Few observational studies have evaluated the relative effectiveness of live attenuated (LAIV) and inactivated (IIV) influenza vaccines against medically attended laboratory-confirmed influenza. METHODS: We analyzed US Influenza Vaccine Effectiveness Network data from participants aged 2 to 17 years during 4 seasons (2010-2011 through 2013-2014) to compare relative effectiveness of LAIV and IIV against influenza-associated illness. Vaccine receipt was confirmed via provider/electronic medical records or immunization registry. We calculated the ratio (odds) of influenza-positive to influenza-negative participants among those age-appropriately vaccinated with either LAIV or IIV for the corresponding season. We examined relative effectiveness of LAIV and IIV by using adjusted odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regression. RESULTS: Of 6819 participants aged 2 to 17 years, 2703 were age-appropriately vaccinated with LAIV (n = 637) or IIV (n = 2066). Odds of influenza were similar for LAIV and IIV recipients during 3 seasons (2010-2011 through 2012-2013). In 2013-2014, odds of influenza were significantly higher among LAIV recipients compared with IIV recipients 2 to 8 years old (OR 5.36; 95% CI, 2.37 to 12.13). Participants vaccinated with LAIV or IIV had similar odds of illness associated with influenza A/H3N2 or B. LAIV recipients had greater odds of illness due to influenza A/H1N1pdm09 in 2010-2011 and 2013-2014. CONCLUSIONS: We observed lower effectiveness of LAIV compared with IIV against influenza A/H1N1pdm09 but not A(H3N2) or B among children and adolescents, suggesting poor performance related to the LAIV A/H1N1pdm09 viral construct.

McMillin, M., G. Frampton, M. Quinn, S. Ashfaq, M. de Los Santos, 3rd, S. Grant and S. DeMorrow (2016). “Bile Acid Signaling Is Involved in the Neurological Decline in a Murine Model of Acute Liver Failure.” Am J Pathol 186(2): 312-323.

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Hepatic encephalopathy is a serious neurological complication of liver failure. Serum bile acids are elevated after liver damage and may disrupt the blood-brain barrier and enter the brain. Our aim was to assess the role of serum bile acids in the neurological complications after acute liver failure. C57Bl/6 or cytochrome p450 7A1 knockout (Cyp7A1(-/-)) mice were fed a control, cholestyramine-containing, or bile acid-containing diet before azoxymethane (AOM)-induced acute liver failure. In parallel, mice were given an intracerebroventricular infusion of farnesoid X receptor (FXR) Vivo-morpholino before AOM injection. Liver damage, neurological decline, and molecular analyses of bile acid signaling were performed. Total bile acid levels were increased in the cortex of AOM-treated mice. Reducing serum bile acids via cholestyramine feeding or using Cyp7A1(-/-) mice reduced bile acid levels and delayed AOM-induced neurological decline, whereas cholic acid or deoxycholic acid feeding worsened AOM-induced neurological decline. The expression of bile acid signaling machinery apical sodium-dependent bile acid transporter, FXR, and small heterodimer partner increased in the frontal cortex, and blocking FXR signaling delayed AOM-induced neurological decline. In conclusion, circulating bile acids may play a pathological role during hepatic encephalopathy, although precisely how they dysregulate normal brain function is unknown. Strategies to minimize serum bile acid concentrations may reduce the severity of neurological complications associated with liver failure.

Wolford, L. M. (2016). “Computer-Assisted Surgical Simulation for Concomitant Temporomandibular Joint Custom-Fitted Total Joint Reconstruction and Orthognathic Surgery.” Atlas Oral Maxillofac Surg Clin North Am 24(1): 55-66.

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Patients with temporomandibular joint (TMJ) conditions and coexisting dentofacial deformities can have these conditions corrected with concomitant TMJ and orthognathic surgery (CTOS) in 1 surgical stage or separated into 2 surgical stages. The 2-stage approach requires the patient to undergo 2 separate operations (surgery to correct the TMJ condition and a second operation to perform the orthognathic surgery) and 2 general anesthetics, significantly lengthening the overall treatment time. Performing CTOS in a single operation significantly decreases treatment time and provides better outcomes but requires careful treatment planning and surgical proficiency in the 2 surgical areas. Some TMJ conditions require total joint prostheses for best results. The application of computer technology for TMJ and orthognathic surgical planning and implementation has significantly improved the accuracy and predictability of treatment outcomes. This article presents the treatment planning and surgical protocol for the application of computer-assisted surgical simulation (CASS) for CTOS cases requiring TMJ reconstruction with patient-fitted total joint prostheses and orthognathic surgery. The CASS protocol decreases the preoperative workup time and increases the accuracy of model preparation and subsequent surgery.

Li, J., Q. Du, R. Hu, Y. Wang, X. Yin, H. Yu, P. Du, J. Plumas, L. Chaperot, Y. J. Liu and L. Zhang (2016). “Death receptor 6 is a novel plasmacytoid dendritic cell-specific receptor and modulates type I interferon production.” Protein Cell. Feb 24. [Epub ahead of print]

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Plasmacytoid dendritic cells (pDCs) are the professional type I interferon-producing cells of the immune system, which rapidly produce massive amounts of type I interferons (IFN-I) in response to viruses or other nucleic acids ligands through selectively expressed toll-like receptor (TLR)-7 and TLR9. The activation of pDCs not only inhibits virus replication, but also regulates the function of other immune cells and links the innate and adaptive immunity. The local accumulation of pDCs has been reported in both suppressive and overactive immune status (Swiecki and Colonna, 2010), which highlights the importance of characterizing the molecular mechanisms underlying the functional specialization of pDCs in IFN-I production. Death receptor 6 (DR6) is a member of death receptor family, which belongs to the tumor necrosis factor receptor superfamily (TNFRSF). It is reported that DR6 plays vital roles in axon pruning, neuron death, and negatively regulates oligodendrocyte survival, maturation and myelination in neural system. DR6-/- mice exhibit enhanced CD4+ T cell proliferation, Th2 cytokines production and B cell expansion, survival, and humoral responses, which imply that DR6 plays important roles in murine immune responses (Liu et al., 2001; Schmidt et al., 2003). However, the expression profiles and functions of DR6 in human immune system remain largely unknown. We found that DR6 was highly expressed in human pDCs comparing with other blood cells by microarray analysis. Additionally, we found that among the 6 death receptors, including TNFR1, CD95, DR3, DR4, DR5 and DR6, pDCs exclusively expressed DR6 but not others. To confirm the expression of DR6 in pDCs, we performed quantitative real time-PCR analysis on several cell types from peripheral blood. (Excerpt from text.)