Relationship between Chronic Disease Conditions and Colorectal Cancer Screening: Results from the 2012 National Health Interview Survey Data

Background: Uptake of screening remains crucial in the prevention of both the incidence of colorectal cancer (CRC) and its mortality.Objectives: To estimate the prevalence of CRC screening and identify chronic conditions that predict CRC screening uptake among US adults using the 2012 National Health Interview Survey (NHIS) data.Materials and Methods: A cross-sectional analysis of the 2012 NHIS data. Chronic conditions examined were hypertension, cancer history, arthritis, ulcer, and high cholesterol level. A total of 21,511 participants were included in the analysis. Weighted univariate and multiple logistic regression analyses in SAS ver. 9.2 were used to estimate the odds ratios (ORs) with 95% confidence intervals (CIs).Results: The overall prevalence of CRC screening was 19%. The prevalence of CRC screening in adults with cancer history, hypertension, ulcer, high cholesterol, and arthritis was significantly higher than those without the chronic conditions (26% vs.18%, 23% vs.16%, 25% vs.18%, 23% vs. 16%, and 23% vs. 17%, respectively). After adjusting for potential factors, hypertension (OR=1.18, 95%CI=1.08-1.30), ulcer (OR=1.28, 95%CI=1.10-1.48), high cholesterol (OR=1.25, 95%CI=1.14-1.39), and arthritis (OR=1.24, 95%CI=1.12-1.37) were all positively associated with CRC screening (p0.05). Females were less likely to screen for CRC than to males (OR=0.72; 95% CI=0.65-0.80). Compared to young adults (18-44 years), screening was significantly higher in middle-aged (45-64 years) and elder adults (65+) (OR=2.60, 95%CI=2.11-3.21 and OR=2.67, 95%CI=2.13-3.33, respectively). African Americans were more likely to screen for CRC compared to their white counterparts (OR=1.61, 95% CI=1.44-1.81).  Conclusions: We have found significant associations between chronic conditions and CRC screening uptake. We also found higher uptake of CRC screen in African Americans than Whites, in contrast to earlier findings

Characterizing the Role of the Type VI Secretion System in Interbacterial Species Interactions and Pathogenesis

Bacteria require molecular mechanisms to properly sense and respond to their environment. This allows them to compete for specific niches, persist in polymicrobial communities, and contribute to virulence and pathogenesis. One mechanism Gram-negative bacteria have adapted is the use of type VI secretion systems (T6SS). The T6SS is a large needle complex that spans across the entire bacterial cell wall and functions through a contraction mechanism that results in the delivery of toxic effector proteins into neighbouring cells. Virulence is achieved through the targeting of essential components found in either eukaryotic or prokaryotic organisms, including cell wall, membrane lipids, and DNA. Despite the importance of the T6SS as an interbacterial weapon, there still exists an incomplete understanding of how T6SS expressing species can co-exist and the implications of antagonistic responses in shaping polymicrobial communities. Further, these species are often subject to a changing environment and yet, the role of environmental signals and their influence on interspecies interactions and the expression of the T6SS, remain largely unknown. Here, I examined the role of the T6SS in the context of multispecies communities. Using a mix of two antagonistic T6SS strains, Vibrio cholerae V52 and Aeromonas hydrophila SSU, both species co-existed despite active bacterial killing. Fluorescence microscopy analyses revealed survival was possible through the formation of sister-cell clusters. Cluster formation was dependent on T6SS effector delivery, highlighting a unique mechanism where destructive responses can mediate protection within a community. I also examined the environmental signals that activate the T6SS using Pseudomonas aeruginosa PAO1, a strain with a tightly regulated T6SS, as a model system. Results reveal that extracellular DNA, prevalent in cystic fibrosis sputum, activates the H1-T6SS cluster of P. aeruginosa. The addition of excess magnesium ions in the media negates the effect of eDNA on T6SS activation, suggesting eDNA may be a chelator of membrane ions and T6SS activation is a consequence of a perturbed membrane. Overall, I provide new insight into how bacterial communities are shaped, and the type of adaptations bacteria undergo to better survive and compete in the environment

State of the Science: The Relevance of Symptoms in Cardiovascular Disease and Research: A Scientific Statement From the American Heart Association

Symptoms of cardiovascular disease drive health care use and are a major contributor to quality of life. Symptoms are of fundamental significance not only to the diagnosis of cardiovascular disease and appraisal of response to medical therapy but also directly to patients’ daily lives. The primary purpose of this scientific statement is to present the state of the science and relevance of symptoms associated with cardiovascular disease. Symptoms as patient-reported outcomes are reviewed in terms of the genesis, manifestation, and similarities or differences between diagnoses. Specifically, symptoms associated with acute coronary syndrome, heart failure, valvular disorders, stroke, rhythm disorders, and peripheral vascular disease are reviewed. Secondary aims include (1) describing symptom measurement methods in research and application in clinical practice and (2) describing the importance of cardiovascular disease symptoms in terms of clinical events and other patient-reported outcomes as applicable

Inhibition of Pol I transcription treats murine and human AML by targeting the leukemia-initiating cell population

Despite the development of novel drugs, the prospects for many patients with acute myeloid leukemia (AML) remain dismal. This study reveals that the selective inhibitor of RNA polymerase I (Pol I) transcription, CX-5461, effectively treats aggressive AML, including mixed-lineage leukemia-driven AML, and outperforms standard chemotherapies. In addition to the previously characterized mechanism of action of CX-5461 (ie, the induction of p53-dependent apoptotic cell death), the inhibition of Pol I transcription also demonstrates potent efficacy in p53null AML in vivo. This significant survival advantage in both p53WT and p53null leukemic mice treated with CX-5461 is associated with activation of the checkpoint kinases 1/2, an aberrant G2/M cell-cycle progression and induction of myeloid differentiation of the leukemic blasts. The ability to target the leukemic-initiating cell population is thought to be essential for lasting therapeutic benefit. Most strikingly, the acute inhibition of Pol I transcription reduces both the leukemic granulocyte-macrophage progenitor and leukemia-initiating cell (LIC) populations, and suppresses their clonogenic capacity. This suggests that dysregulated Pol I transcription is essential for the maintenance of their leukemia-initiating potential. Together, these findings demonstrate the therapeutic utility of this new class of inhibitors to treat highly aggressive AML by targeting LICs.This work was supported by project grants from the National Health and Medical Research Council (NHMRC) of Australia (#1043884, 251608, 566702, 166908, 251688, 509087, 400116, 400120, and 566876) and an NHMRC program grant (#1053792), and the Cancer Council of Victoria grant-in-aid (#1084545). The researchers were funded by the following: NHMRC fellowships (R.D.H., R.B.P., R.W.J., and G.A.M.), Cancer Council of Victoria, Cancer Council of Australian Capital Territory, Sir Edward Weary Dunlop fellowship (G.A.M.), and the Leukemia Foundation of Australia (grant-in-aid to M.W., and Ph.D. scholarships to D.P.C. and J.D.)

Inhibition of Pol I transcription treats murine and human AML by targeting the leukemia-initiating cell population

Despite the development of novel drugs, the prospects for many patients with acute myeloid leukemia (AML) remain dismal. This study reveals that the selective inhibitor of RNA polymerase I (Pol I) transcription, CX-5461, effectively treats aggressive AML, including mixed-lineage leukemia-driven AML, and outperforms standard chemotherapies. In addition to the previously characterized mechanism of action of CX-5461 (ie, the induction of p53-dependent apoptotic cell death), the inhibition of Pol I transcription also demonstrates potent efficacy in p53null AML in vivo. This significant survival advantage in both p53WT and p53null leukemic mice treated with CX-5461 is associated with activation of the checkpoint kinases 1/2, an aberrant G2/M cell-cycle progression and induction of myeloid differentiation of the leukemic blasts. The ability to target the leukemic-initiating cell population is thought to be essential for lasting therapeutic benefit. Most strikingly, the acute inhibition of Pol I transcription reduces both the leukemic granulocyte-macrophage progenitor and leukemia-initiating cell (LIC) populations, and suppresses their clonogenic capacity. This suggests that dysregulated Pol I transcription is essential for the maintenance of their leukemia-initiating potential. Together, these findings demonstrate the therapeutic utility of thisnewclass of inhibitors to treat highly aggressive AML by targeting LICs

Quality of Care Initiative Improves Outcomes for Patients with Inflammatory Bowel Disease

There is significant variation in processes and outcomes of care for patients with inflammatory bowel disease (IBD), suggesting opportunities to improve quality of care. Recent efforts to define quality measures for IBD have identified emergency room (ER) visits, hospitalizations, corticosteroid use, and opioid use as indicators of care quality. We hypothesized that IBD care could be improved through a structured quality improvement (QI) program

Causes of Noncompliance with International Law: A Field Experiment on Anonymous Incorporation

20110302 into the Experiments on Governance and Politics Registry once that registry was begun at e-gap.org. Of those interventions registered, we report on the FATF, Premium, Corruption, and Terrorism conditions in this article. All other interventions outlined in the registered document are reported in other work. In our registration, we indicated that we would report results dichotomously as compliant or noncompliant, given a response. We still report response and nonresponse followed by a compliance level, but we expanded the set of possible types of compliance (nonresponse, noncompliance, partial compliance, compliance, and refusal). Presenting the information this way is more precise and is also consistent with the registry document because the fuller set of outcomes contains all information the dichotomized measures capture (se

Health-status outcomes with invasive or conservative care in coronary disease

BACKGROUND In the ISCHEMIA trial, an invasive strategy with angiographic assessment and revascularization did not reduce clinical events among patients with stable ischemic heart disease and moderate or severe ischemia. A secondary objective of the trial was to assess angina-related health status among these patients. METHODS We assessed angina-related symptoms, function, and quality of life with the Seattle Angina Questionnaire (SAQ) at randomization, at months 1.5, 3, and 6, and every 6 months thereafter in participants who had been randomly assigned to an invasive treatment strategy (2295 participants) or a conservative strategy (2322). Mixed-effects cumulative probability models within a Bayesian framework were used to estimate differences between the treatment groups. The primary outcome of this health-status analysis was the SAQ summary score (scores range from 0 to 100, with higher scores indicating better health status). All analyses were performed in the overall population and according to baseline angina frequency. RESULTS At baseline, 35% of patients reported having no angina in the previous month. SAQ summary scores increased in both treatment groups, with increases at 3, 12, and 36 months that were 4.1 points (95% credible interval, 3.2 to 5.0), 4.2 points (95% credible interval, 3.3 to 5.1), and 2.9 points (95% credible interval, 2.2 to 3.7) higher with the invasive strategy than with the conservative strategy. Differences were larger among participants who had more frequent angina at baseline (8.5 vs. 0.1 points at 3 months and 5.3 vs. 1.2 points at 36 months among participants with daily or weekly angina as compared with no angina). CONCLUSIONS In the overall trial population with moderate or severe ischemia, which included 35% of participants without angina at baseline, patients randomly assigned to the invasive strategy had greater improvement in angina-related health status than those assigned to the conservative strategy. The modest mean differences favoring the invasive strategy in the overall group reflected minimal differences among asymptomatic patients and larger differences among patients who had had angina at baseline

Initial invasive or conservative strategy for stable coronary disease

BACKGROUND Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, 121.8 percentage points; 95% CI, 124.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used