139 research outputs found

    The Soft Animal of Your Body: Seven Attempts to Explain Chronic Illness to Myself and to You

    Get PDF
    THE SOFT ANIMAL OF YOUR BODY – ARTIST’S STATEMENT If I knew how to explain vision loss or chronic pain, I wouldn’t have started this senior project. How do I communicate the knowledge that my body is slowly failing me, that even the best treatments aren’t guaranteed to work? With whom do I have to speak with to be heard and understood? I’ve previously attempted dictionary definitions, disability accommodation letters from the Bard Learning Commons, repeatedly cancelling plans with friends until they stop inviting me to things, and passive-aggressive conversations with my neurologist. None of these efforts have worked out so far as effective means of communication, but neither has wordless screaming, so I feel compelled to keep trying. The project is composed of eight pairs of one poem and one visual element - paintings, drawings, or ceramic sculpture. Each pair of works looks at chronic illness (mine, specifically) as experienced – or not experienced – through a different human organ or organ system. I don’t think I could literally vivisect myself and survive the process. This body of work is my earnest attempt at doing the next best thing. I wrote the first poem for the project on February 28, 2017. The title, “Self-Caregiver Fatigue” refers to the current trendiness of “self-care” as an industry as well as the sense of burnout or even resentment that can develop in a healthy adult caring for their sick relative. The relative can be a drain on financial and emotional resources as well as often being unhappy and ungrateful regardless of the quality of the care they receive; in a lot of ways it would be weirder if caregiver fatigue wasn’t a common occurrence. In Studio 16 of Bard UBS, in Kingston Neurology, alone in my room at three in the morning: I am my own miserable arthritic grandmother, my own resentful adult daughter. I pretend to be grateful for the opportunity to live; I pretend to be grateful for the responsibility to keep myself alive. I pretend that the awful task of giving voice to sickness can even be begun

    Certain Unramified Metabelian Extensions Using Lemmermeyer Factorizations

    Full text link
    We study solutions to the Brauer embedding problem with restricted ramification. Suppose GG and AA are a abelian groups, EE is a central extension of GG by AA, and f:Gal(Q‟/Q)→Gf:\text{Gal}(\overline{\mathbf{Q}}/\mathbf{Q})\rightarrow G a continuous homomorphism. We determine conditions on the discriminant of ff that are equivalent to the existence of an unramified lift f~:Gal(Q‟/Q)→E\widetilde{f}:\text{Gal}(\overline{\mathbf{Q}}/\mathbf{Q})\rightarrow E of ff. As a consequence of this result, we use conditions on the discriminant of KK for K/QK/\mathbf{Q} abelian to classify and count unramified nonabelian extensions L/KL/K normal over Q\mathbf{Q} where the (nontrivial) commutator subgroup of Gal(L/Q)\text{Gal}(L/\mathbf{Q}) is contained in its center. This generalizes a result due to Lemmermeyer, which states that a quadratic field Q(d)\mathbf{Q}(\sqrt{d}) has an unramified extension normal over Q\mathbf{Q} with Galois group H8H_8 the quaternion group if and only if the discriminant factors d=d1d2d3d=d_1 d_2 d_3 as a product of three coprime discriminants, at most one of which is negative, satisfying the following condition on Legendre symbols: (didjpk)=1 \left(\frac{d_i d_j}{p_k}\right)=1 for {i,j,k}={1,2,3}\{i,j,k\}=\{1,2,3\} and pip_i any prime dividing did_i

    Asthma-associated genetic variants induce IL33 differential expression through an enhancer-blocking regulatory region

    Get PDF
    Genome-wide association studies (GWAS) have implicated the IL33 locus in asthma, but the underlying mechanisms remain unclear. Here, we identify a 5 kb region within the GWAS-defined segment that acts as an enhancer-blocking element in vivo and in vitro. Chromatin conformation capture showed that this 5 kb region loops to the IL33 promoter, potentially regulating its expression. We show that the asthma-associated single nucleotide polymorphism (SNP) rs1888909, located within the 5 kb region, is associated with IL33 gene expression in human airway epithelial cells and IL-33 protein expression in human plasma, potentially through differential binding of OCT-1 (POU2F1) to the asthma-risk allele. Our data demonstrate that asthma-associated variants at the IL33 locus mediate allele-specific regulatory activity and IL33 expression, providing a mechanism through which a regulatory SNP contributes to genetic risk of asthma.This work was supported by NIH grants R01 HL118758, R01 HL128075, R01 HL119577, R01 HL085197, U19 AI095230, UG3 OD023282 and UM1 AI114271

    Stakeholder Priorities for Comparative Effectiveness Research in Chronic Obstructive Pulmonary Disease: A Workshop Report

    Get PDF
    Comparative effectiveness research (CER) is intended to address the expressed needs of patients, clinicians, and other stakeholders. Representatives of 54 stakeholder groups with an interest in chronic obstructive pulmonary disease (COPD) participated in workshops convened by the COPD Outcomes-based Network for Clinical Effectiveness and Research Translation (CONCERT) over a 2-year period. Year 1 focused on chronic care and care coordination. Year 2 focused on acute care and transitions in care between healthcare settings. Discussions and provisional voting were conducted via teleconferences and e-mail exchanges before the workshop. Final prioritization votes occurred after in-person discussions at the workshop. We used a modified Delphi approach to facilitate discussions and consensus building. To more easily quantify preferences and to evaluate the internal consistency of rankings, the Analytic Hierarchy Process was incorporated in Year 2. Results of preworkshop and final workshop voting often differed, suggesting that prioritization efforts relying solely on requests for topics from stakeholder groups without in-person discussion may provide different research priorities. Research priorities varied across stakeholder groups, but generally focused on studies to evaluate different approaches to healthcare delivery (e.g., spirometry for diagnosis and treatment, integrated healthcare strategies during transitions in care) rather than head-to-head comparisons of medications. This research agenda may help to inform groups intending to respond to CER funding opportunities in COPD. The methodologies used, detailed in the online supplement, may also help to inform prioritization efforts for CER in other health conditions

    Measuring health-related quality of life in chronic obstructive pulmonary disease: properties of the EQ-5D-5L and PROMIS-43 short form

    Get PDF
    Abstract Background The Patient Reported Outcomes Measurement Information System 43-item short form (PROMIS-43) and the five-level EQ-5D (EQ-5D-5L) are recently developed measures of health-related quality of life (HRQL) that have potentially broad application in evaluating treatments and capturing burden of respiratory-related diseases. The aims of this study were: (1) to examine their psychometric properties in patients with chronic obstructive pulmonary disease (COPD), and (2) to identify dimensions of HRQL that differ and do not differ by lung function. Methods We conducted a multi-center, cross-sectional study (“COPD Outcomes-based Network for Clinical Effectiveness & Research Translation” [CONCERT]). We analyzed patients who met spirometric criteria for COPD, and completed EQ-5D-5L and PROMIS questionnaires. Disease severity was graded based on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification. Pulmonary function test, PROMIS-43, EQ-5D (index score and EQ-Visual Analog Scale [EQ-VAS]), six minute walk test (6MWT), and three dyspnea scales (mMRC, Borg, FACIT-Dyspnea) were administered. Validity and reliability of EQ-5D-5L and PROMIS-43 were examined, and differences in HRQL by GOLD grade were assessed. Results Data from 670 patients with COPD were analyzed (mean age 68.5 years; 58% male). More severe COPD was associated with more problems with mobility, self-care and usual activities (all p-values <0.01) according to EQ-5D-5L. Related domains on EQ-5D-5L, PROMIS and clinical measures were moderately (r = 0.30-0.49) to strongly (r ≄ 0.50) correlated. A statistically significant trend of decreasing HRQL with more severe lung functions was observed for EQ-5D-5L index scores, EQ-VAS scores, and PROMIS physical function and social roles. Conclusions Results supported the validity of EQ-5D-5L and PROMIS-43 in COPD patients, and indicate that physical function and social activities decrease with level of lung function by GOLD grade, but not pain, mental health, sleep or fatigue as reported by patients

    Multicenter Study Comparing Case Definitions Used to Identify Patients with Chronic Obstructive Pulmonary Disease

    Get PDF
    Rationale: Clinical trials in chronic obstructive pulmonary disease (COPD) usually require evidence of airflow obstruction and clinical risk factors. International Classification of Diseases, Ninth Revision (ICD-9) diagnosis codes or patient-reported physician diagnoses are often used for epidemiologic studies and performance improvement programs

    Effects of Phosphodiesterase 4 Inhibition on Alveolarization and Hyperoxia Toxicity in Newborn Rats

    Get PDF
    International audienceBACKGROUND: Prolonged neonatal exposure to hyperoxia is associated with high mortality, leukocyte influx in airspaces, and impaired alveolarization. Inhibitors of type 4 phosphodiesterases are potent anti-inflammatory drugs now proposed for lung disorders. The current study was undertaken to determine the effects of the prototypal phosphodiesterase-4 inhibitor rolipram on alveolar development and on hyperoxia-induced lung injury. METHODOLOGY/FINDINGS: Rat pups were placed under hyperoxia (FiO2>95%) or room air from birth, and received rolipram or its diluent daily until sacrifice. Mortality rate, weight gain and parameters of lung morphometry were recorded on day 10. Differential cell count and cytokine levels in bronchoalveolar lavage and cytokine mRNA levels in whole lung were recorded on day 6. Rolipram diminished weight gain either under air or hyperoxia. Hyperoxia induced huge mortality rate reaching 70% at day 10, which was prevented by rolipram. Leukocyte influx in bronchoalveolar lavage under hyperoxia was significantly diminished by rolipram. Hyperoxia increased transcript and protein levels of IL-6, MCP1, and osteopontin; rolipram inhibited the increase of these proteins. Alveolarization was impaired by hyperoxia and was not restored by rolipram. Under room air, rolipram-treated pups had significant decrease of Radial Alveolar Count. CONCLUSIONS: Although inhibition of phosphodiesterases 4 prevented mortality and lung inflammation induced by hyperoxia, it had no effect on alveolarization impairment, which might be accounted for by the aggressiveness of the model. The less complex structure of immature lungs of rolipram-treated pups as compared with diluent-treated pups under room air may be explained by the profound effect of PDE4 inhibition on weight gain that interfered with normal alveolarization
    • 

    corecore