Addressing anxiety in college: A mindfulness group for use in college counseling centers

This project proposes a mindfulness group to address anxiety in college counseling settings. As will be discussed, anxiety is often cited as the most common presenting concern in college counseling centers, and as the need for mental health services in college is increasing, the necessity for cost effective and timely interventions (i.e., groups) becomes apparent. Research on the efficacy of mindfulness as a treatment for generalized anxiety disorder and social anxiety disorder is reviewed, as is the potential for self-compassion to be used as a complement to learning mindfulness skills to address anxiety. Finally, an eight-session group protocol that incorporates this literature is presented, and guidelines and suggestions are offered

Risk of Lower Extremity Amputation Revision in Patients with Peripheral Vascular Disease Adjusting for a Competing Risk of Death

Indiana University-Purdue University Indianapolis (IUPUI)Objectives: The aims of this study are to estimate the cumulative incidence of lower extremity amputation (LEA) revision and reamputation adjusting for a competing risk of death, estimate the one-year event-free mortality rates for patients with peripheral vascular disease undergoing LEA, and develop predictive models for LEA revision and reamputation adjusting for a competing risk of death. Methods: This was a retrospective review of the prospectively collected Vascular Quality Initiative (VQI) registry between 2013 and 2018. Adults undergoing unilateral LEA were included. Demographics, comorbidities, medications, smoking status, history of vascular procedures and revascularization attempts, and procedure urgency were considered. Models to predict LEA revision and reamputation were developed using multivariable regression on the interval-censored competing risks data using semiparametric regression on the cumulative incidence function. Results: The cumulative incidences of LEA revision and revision-free mortality within one year of index amputation are 14.9% and 15.5% respectively. Patient BMI, smoking status, aspirin use, history of revascularization, and level of planned LEA are significantly associated with the odds of LEA revision. Age, amputation urgency, dialysis, and level of planned LEA are associated with the one-year odds of revision-free mortality. A patient receiving an index above knee amputation (AKA) has 61% lower odds of LEA revision (p < 0.0001) but 51% higher odds of revision-free mortality following LEA (p < 0.0001). Previous revascularization procedures increase the odds of revision by 23% (p < 0.0001). The cumulative incidences of reamputation and one-year reamputation-free mortality following LEA are 11.5% and 16.9% respectively. Urgency of the procedure, history of revascularization procedures, and level of planned LEA are statistically associated with the odds of reamputation when adjusting for the competing risk of death. Patients receiving index AKA have 62% lower odds of reamputation (p < 0.0001) compared to BKA. Dialysis is the strongest predictor of one-year mortality (OR 2.576, p < 0.0001). Conclusions: Patients with appropriately managed PVD, which still progresses to amputation have higher odds of LEA revision and reamputation. Revision risk can be predicted and compared on the basis of patient factors and the planned index amputation

Modulating Glutathione Thiol Status Alters Pancreatic β-cell Morphogenesis in the Developing Zebrafish (Danio rerio) Embryo

Emerging evidence suggests that redox-active chemicals perturb pancreatic islet development. To better understand potential mechanisms for this, we used zebrafish (Danio rerio) embryos to investigate roles of glutathione (GSH; predominant cellular redox buffer) and the transcription factor Nrf2a (Nfe2l2a; zebrafish Nrf2 coortholog) in islet morphogenesis. We delineated critical windows of susceptibility to redox disruption of beta-cell morphogenesis, interrogating embryos at 24, 48 and 72 h post fertilization (hpf) and visualized Nrf2a expression in the pancreas using whole-mount immunohistochemistry at 96 hpf. Chemical GSH modulation at 48 hpf induced significant islet morphology changes at 96 hpf. Pro-oxidant exposures to tert-butylhydroperoxide (77.6 mu M; 10-min at 48 hpf) or tert-butylhydroquinone (1 mu M; 48-56 hpf) decreased beta-cell cluster area at 96 hpf. Conversely, exposures to antioxidant N-acetylcysteine (bolsters GSH pools; 100 mu M; 48-72 hpf) or sulforaphane (activates Nrf2a; 20 mu M; 48-72 hpf) significantly increased islet areas. Nrf2a was also stabilized in beta-cells: 10-min exposures to 77.6 mu M tert-butylhydroperoxide significantly increased Nrf2a protein compared to control islet cells that largely lack stabilized Nrf2a; 10-min exposures to higher (776 mu M) tert-butylhydroperoxide concentration stabilized Nrf2a throughout the pancreas. Using biotinylated-GSH to visualize in situ protein glutathionylation, islet cells displayed high protein glutathionylation, indicating oxidized GSH pools. The 10-min high (776 mu M) tert-butylhydroperoxide exposure (induced Nrf2a globally) decreased global protein glutathionylation at 96 hpf. Mutant fish expressing inactive Nrf2a were protected against tert-butylhydroperoxide-induced abnormal islet morphology. Our data indicate that disrupted redox homeostasis and Nrf2a stabilization during pancreatic beta-cell development impact morphogenesis, with implications for disease states at later life stages. Our work identifies a potential molecular target (Nrf2) that mediates abnormal beta-cell morphology in response to redox disruptions. Moreover, our findings imply that developmental exposure to exogenous stressors at distinct windows of susceptibility could diminish the reserve redox capacity of beta-cells, rendering them vulnerable to later-life stresses and disease

Perceived loss of social support after non-neurologic injury negatively impacts recovery

Background: Traumatic injury is not only physically devastating, but also psychologically isolating, potentially leading to poor quality of life, depression and posttraumatic stress disorder (PTSD). Perceived social support (PSS) is associated with better outcomes in some populations. What is not known is if changes in PSS influence long-term outcomes following nonneurologic injury. We hypothesized that a single drop in PSS during recovery would be associated with worse quality of life. Methods: This is a post hoc analysis of a prospectively collected database that included patients 18 years or older admitted to a Level I trauma center with Injury Severity Score (ISS) of 10 or higher, and no traumatic brain or spinal cord injury. Demographic and injury data were collected at the initial hospital admission. Screening for depression, PTSD, and Medical Outcomes Study Short Form 36 Mental Composite Score (MCS) were obtained at the initial hospitalization, 1, 2, 4, and 12 months postinjury. The Multidimensional Scale of Perceived Social Support (MSPSS) was obtained at similar time points. Patients with high MSPSS (>5) at baseline were included and grouped by those that ever reported a score ≤5 (DROP), and those that remained high (STABLE). Outcomes were determined at 4 and 12 months. Results: Four hundred eleven patients were included with 96 meeting DROP criteria at 4 months, and 97 at 1 years. There were no differences in sex, race, or injury mechanism. The DROP patients were more likely to be single (p = 0.012 at 4 months, p = 0.0006 at 1 year) and unemployed (p = 0.016 at 4 months, and p = 0.026 at 1 year) compared with STABLE patients. At 4 months and 1 year, DROP patients were more likely to have PTSD, depression, and a lower MCS (p = 0.0006, p < 0.0001). Conclusion: Patients who have a drop in PSS during the first year of recovery have significantly higher odds of poor psychological outcomes. Identifying these socially frail patients provides an opportunity for intervention to positively influence an otherwise poor quality of life. Level of evidence: Therapeutic, Prognostic and Epidemiological, Level III

Financial Toxicity Is Associated With Worse Physical and Emotional Long-term Outcomes After Traumatic Injury

Background Increasing healthcare costs and high deductible insurance plans have shifted more responsibility for medical costs to patients. After serious illnesses, financial responsibilities may result in lost wages, forced unemployment, and other financial burdens, collectively described as financial toxicity. Following cancer treatments, financial toxicity is associated with worse long-term health related quality of life outcomes (HRQOL). The purpose of this study was to determine the incidence of financial toxicity following injury, factors associated with financial toxicity, and the impact of financial toxicity on long-term HRQOL. Methods Adult patients with an injury severity score of 10 or greater and without head or spinal cord injury were prospectively followed for 1 year. The Short-Form-36 was used to determine overall quality of life at 1, 2, 4 and 12 months. Screens for depression and post-traumatic stress syndrome (PTSD) were administered. The primary outcome was any financial toxicity. A multivariable generalized estimating equation was used to account for variability over time. Results 500 patients were enrolled and 88% suffered financial toxicity during the year following injury (64% reduced income, 58% unemployment, 85% experienced stress due to financial burden). Financial toxicity remained stable over follow-up (80–85%). Factors independently associated with financial toxicity were lower age (OR 0.96 [0.94–0.98]), and lack of health insurance (OR 0.28 [0.14–0.56]) and larger household size (OR 1.37 [1.06–1.77]). After risk adjustment, patients with financial toxicity had worse HRQOL, and more depression and PTSD in a step-wise fashion based on severity of financial toxicity. Conclusions Financial toxicity following injury is extremely common and is associated with worse psychological and physical outcomes. Age, lack of insurance, and large household size are associated with financial toxicity. Patients at risk for financial toxicity can be identified and interventions to counteract the negative effects should be developed to improve long-term outcomes. Level of Evidence Prognostic/epidemiologic study, level II

Treatment of asymptomatic blunt cerebrovascular injury (BCVI): a systematic review

Background The management of asymptomatic blunt cerebrovascular injury (BCVI) with respect to stroke prevention and vessel healing is challenging.Objectives The aim of this systematic review was to determine if a specific treatment results in lower stroke rates and/or improved vessel healing in asymptomatic BCVI.Data sources An electronic literature search of MEDLINE, EMBASE, Cochrane Library, CINAHL, SCOPUS, Web of Science, and ClinicalTrials.gov performed from inception to March 2020.Study eligibility criteria Studies were included if they reported on a comparison of any treatment for BCVI and stroke and/or vessel healing rates.Participants and interventions Adult patients diagnosed with asymptomatic BCVI(s) who were treated with any preventive medication or procedure.Study appraisal and synthesis methods All studies were systematically reviewed and bias was evaluated by the Newcastle-Ottawa Scale. No meta-analysis was performed secondary to significant heterogeneity across studies in patient population, screening protocols, and treatment selection. The main outcomes were stroke and healing rate.Results Of 8781 studies reviewed, 19 reported on treatment effects for asymptomatic BCVI and were included for review. Any choice of medical management was better than no treatment, but no specific differences between choice of medical management and stroke outcomes were found. Vessel healing was rare and the majority of healed vessels were following low-grade injuries.Limitations Majority of the included studies were retrospective and at high risk of bias.Conclusions or implications of key findings Asymptomatic BCVI should be treated medically using a consistent, local protocol. High-quality studies on the effect of individual antithrombotic agents on stroke rates and vessel healing for asymptomatic BCVI are required

Feo - Transport of ferrous iron into bacteria

Bacteria commonly utilise a unique type of transporter, called Feo, to specifically acquire the ferrous (Fe2+) form of iron from their environment. Enterobacterial Feo systems are composed of three proteins: FeoA, a small, soluble SH3-domain protein probably located in the cytosol; FeoB, a large protein with a cytosolic N-terminal G-protein domain and a C-terminal integral inner-membrane domain containing two 'Gate' motifs which likely functions as the Fe2+ permease; and FeoC, a small protein apparently functioning as an [Fe-S]-dependent transcriptional repressor. We provide a review of the current literature combined with a bioinformatic assessment of bacterial Feo systems showing how they exhibit common features, as well as differences in organisation and composition which probably reflect variations in mechanisms employed and function