Citations

Hispanics bear a disproportionate burden of diabetes in the United States, yet relations of structural, socio-cultural and behavioral factors linked to diabetes are not fully understood across all of their communities. The current study examines disparities and factors associated with diabetes in adult Hispanics of Mexican-descent (N = 648) participating in a population survey of an underserved rural U.S.-Mexico border community. The overall rate of diabetes prevalence rate in the sample, based on self-report and a glucose testing, was 21%; much higher than rates reported for U.S. adults overall, for all Hispanic adults, or for Mexican American adults specifically. Acculturation markers and social determinants of health indicators were only significantly related to diabetes in models not accounting for age. Older age, greater BMI (>30), greater waist-to-hip ratio as well as lower fruit and vegetable consumption were significantly related to increased likelihood of diabetes when all structural, cultural, behavioral, and biological factors were considered. Models with sets of behavioral factors and biological factors each significantly improved explanation of diabetes relative to prior social ecological theory-guided models. The findings show a critical need for diabetes prevention efforts in this community and suggest that health promotion efforts should particularly focus on increasing fruit and vegetable consumption.

Background The national waste rate for hospital‐issued blood products ranges from 0% to 6%, with operating room–responsible waste representing up to 70% of total hospital waste. A common reason for blood product waste is inadequate intraoperative storage. Study Design and Methods Our transfusion service database was used to quantify and categorize red blood cell ( RBC ) and fresh‐frozen plasma ( FFP ) units issued for intraoperative transfusion that were wasted over a 27‐month period. Two cohorts were created: 1) before implementation of a blood transport and storage initiative ( BTSI )— RBC and plasma waste J anuary 1, 2011‐ M ay 31, 2012; 2) after implementation of BTSI — RBC and plasma waste J une 1, 2012, to M arch 31, 2013. The BTSI replaced existing storage coolers (8‐hr coolant life span with temperature range of 1‐10°C) with a cooler that had a coolant life span of 18 hours and a temperature range of 1 to 6°C and included an improved educational cooler placard and an alert mechanism in the electronic health record. Monthly median RBC and plasma waste and its associated cost were the primary outcomes. Results An intraoperative BTSI significantly reduced median monthly RBC (1.3% vs. 0.07%) and FFP (0.4% vs. 0%) waste and its associated institutional cost. The majority of blood product waste was due to an unacceptable temperature of unused returned blood products. Conclusion An intraoperative BTSI significantly reduced median monthly RBC and FFP waste. The cost to implement this initiative was small, resulting in a significant estimated return on investment that may be reproducible in institutions other than ours.

AbstractTraumatic brain injury (TBI) and post‐traumatic stress disorder (PTSD) are signature injuries of the wars in Iraq and Afghanistan and have been linked to an increased risk of Alzheimer's disease (AD) and other dementias. A meeting hosted by the Alzheimer's Association and the Veterans' Health Research Institute (NCIRE) in May 2012 brought together experts from the U.S. military and academic medical centers around the world to discuss current evidence and hypotheses regarding the pathophysiological mechanisms linking TBI, PTSD, and AD. Studies underway in civilian and military populations were highlighted, along with new research initiatives such as a study to extend the Alzheimer's Disease Neuroimaging Initiative (ADNI) to a population of veterans exposed to TBI and PTSD. Greater collaboration and data sharing among diverse research groups is needed to advance an understanding and appropriate interventions in this continuum of military injuries and neurodegenerative disease in the aging veteran.

Background— Radial access for percutaneous coronary intervention (r-PCI) is associated with reduced vascular complications; however, previous reports have shown that <2% of percutaneous coronary intervention (PCI) procedures in the United States are performed via the radial approach. Our aims were to evaluate temporal trends in r-PCI and compare procedural outcomes between r-PCI and transfemoral PCI. Methods and Results— We conducted a retrospective cohort study from the CathPCI registry (n=2 820 874 procedures from 1381 sites) between January 2007 and September 2012. Multivariable logistic regression models were used to evaluate the adjusted association between r-PCI and bleeding, vascular complications, and procedural success, using transfemoral PCI as the reference. Outcomes in high-risk subgroups such as age ≥75 years, women, and patients with acute coronary syndrome were also examined. The proportion of r-PCI procedures increased from 1.2% in quarter 1 2007 to 16.1% in quarter 3 2012 and accounted for 6.3% of total procedures from 2007 to 2012 (n=178 643). After multivariable adjustment, r-PCI use in the studied cohort of patients was associated with lower risk of bleeding (adjusted odds ratio, 0.51; 95% confidence interval, 0.49–0.54) and lower risk of vascular complications (adjusted odds ratio, 0.39; 95% confidence interval, 0.31–0.50) in comparison with transfemoral PCI. The reduction in bleeding and vascular complications was consistent across important subgroups of age, sex, and clinical presentation. Conclusions— There has been increasing adoption of r-PCI in the United States. Transradial PCI now accounts for 1 of 6 PCIs performed in contemporary clinical practice. In comparison with traditional femoral access, transradial PCI is associated with lower vascular and bleeding complication rates.

ObjectiveTo evaluate the reasons that complete remission is not achieved or maintained with original treatment in some patients with antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis (AAV) treated with rituximab (RTX) or with cyclophosphamide/azathioprine (CYC/AZA).MethodsThe Rituximab in AAV trial was a randomized, double‐blind, placebo‐controlled trial comparing the rate of remission induction among patients treated with RTX (n = 99) and patients treated with CYC followed by AZA (n = 98). Glucocorticoids were tapered over a period of 5 months. The primary outcome measure was lack of disease activity without glucocorticoid treatment at 6 months. To determine the most important reason for failure to achieve the primary outcome, 7 hierarchical categories of reasons were defined retrospectively (uncontrolled disease, adverse event leading to therapy discontinuation, severe flare, limited flare, Birmingham Vasculitis Activity Score for Wegener's Granulomatosis >0, prednisone treatment at any dosage, and other).ResultsAlthough remission (lack of disease activity) was achieved in 170 of the 197 patients (86%) in the first 6 months, the primary outcome measure was not achieved in 42%. There were 3 deaths. Twenty‐four percent of the patients failed to achieve the primary end point due to active disease: 10 (5%) experienced uncontrolled disease in the first month and 37 (19%) experienced flares after initial improvement. In the majority of such patients, treatment with blinded crossover or according to best medical judgment led to disease control. Ninety‐one percent of patients who had uncontrolled disease or experienced a severe flare had proteinase 3 (PR3)–ANCA. When patients with uncontrolled disease were excluded from analysis, those who were PR3‐ANCA positive were found to experience fewer flares when treated with RTX compared to CYC/AZA (8 of 59 [14%] versus 20 of 62 [32%]; P = 0.02). Neither ANCA titers nor B cell counts predicted disease flare.ConclusionCurrent treatment regimens are largely successful in controlling AAV, but in approximately one‐fourth of patients, active disease persists or recurs in the first 6 months despite treatment. PR3‐ANCA positivity is a risk factor for recurrence or persistence of severe disease. ANCA titers and B cell detectability are poor predictors of both disease relapse and disease quiescence in the first 6 months.

Severe aplastic anemia (AA) is a bone marrow (BM) failure (BMF) disease frequently caused by aberrant immune destruction of blood progenitors. Although a Th1-mediated pathology is well described for AA, molecular mechanisms driving disease progression remain ill defined. The NOTCH signaling pathway mediates Th1 cell differentiation in the presence of polarizing cytokines, an action requiring enzymatic processing of NOTCH receptors by γ-secretase. Using a mouse model of AA, we demonstrate that expression of both intracellular NOTCH1IC and T-BET, a key transcription factor regulating Th1 cell differentiation, was increased in spleen and BM-infiltrating T cells during active disease. Conditionally deleting Notch1 or administering γ-secretase inhibitors (GSIs) in vivo attenuated disease and rescued mice from lethal BMF. In peripheral T cells from patients with untreated AA, NOTCH1IC was significantly elevated and bound to the TBX21 promoter, showing NOTCH1 directly regulates the gene encoding T-BET. Treating patient cells with GSIs in vitro lowered NOTCH1IC levels, decreased NOTCH1 detectable at the TBX21 promoter, and decreased T-BET expression, indicating that NOTCH1 signaling is responsive to GSIs during active disease. Collectively, these results identify NOTCH signaling as a primary driver of Th1-mediated pathogenesis in AA and may represent a novel target for therapeutic intervention.

AbstractThis study investigated causal attributions and attitudes toward a hypothetical lung cancer patient. Participants included 147 undergraduate students who read 1 of 3 vignettes about a man recently diagnosed with lung cancer. The vignettes were identical except for the causal description of the patient's lung cancer (genetic, smoking, or combined). Compared with the other 2 conditions, participants in the genetic condition believed the hypothetical patient had less control and less responsibility for his illness; they also noted more pity and less anger. There were no significant differences in these variables between the smoking and combined conditions. Information about genetic information appears to trigger more positive perceptions of lung cancer patients, but only in the absence of smoking histories.

Abstract Aims The proteasome prevents the intracellular accumulation of proteins and its impairment can lead to structural and functional alterations, as noted for the coronary vasculature in a previous study. Utilizing the same model, this study was designed to test the hypothesis that chronic proteasome inhibition (PSI) also leads to structural and functional changes of the heart. Methods and results Female domestic pigs were randomized to a normal diet without (N) or with twice-weekly subcutaneous injections of the proteasome inhibitor MLN-273 (0.08 mg/kg, N + PSI, n = 5 each group). In vivo data on cardiac structure and function as well as myocardial perfusion and microvascular permeability response to adenosine and dobutamine were obtained by electron beam computed tomography after 11 weeks. Subsequent ex vivo myocardial analyses included immunoblotting, immunostaining, TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labelling), Masson trichrome, and Congo red staining. Compared with N, an increase in LV mass was observed in N + PSI (106.5 ± 16.4 g vs. 183.1 ± 24.2 g, P &lt; 0.05). The early to late diastolic filling ratio was increased in N + PSI vs. N (3.5 ± 0.6 vs. 1.8 ± 0.1, P &lt; 0.05). The EF tended to be lower (46 ± 12% and 53 ± 9%, respectively) and cardiac output was significantly lower in N + PSI than in N (2.9 ± 1.1 vs. 4.7 ± 1.1 L/min, P &lt; 0.05). Tissue analyses demonstrated an accumulation of proteasome substrates, apoptosis, and fibrosis in the PSI group. Compared with N, the myocardial perfusion response was reduced and microvascular permeability was increased in N + PSI. Conclusion The current study demonstrates that chronic proeasome inhibition affects the cardiovascular system, leading to functional and structural alteration of the heart consistent with a hypertrophic–restrictive cardiomyopathy phenotype.