tbuckley/cabot-search huggingface dataset:
Pulmonary Function Reduction in Diabetes With and Without Chronic Obstructive Pulmonary Disease
Authors: Gregory L. Kinney, Jennifer L. Black-Shinn, Emily S. Wan, Barry Make, Elizabeth Regan, Sharon Lutz, Xavier Soler, Edwin K. Silverman, James Crapo, John E. Hokanson
Journal: Diabetes Care (2013)

Diabetes damages major organ systems through disrupted glycemic control and increased inflammation. The effects of diabetes on the lung have been of interest for decades, but the modest reduction in pulmonary function and its nonprogressive nature have limited its investigation. A recent systematic review found that diabetes was associated with reductions in forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and diffusing capacity for carbon monoxide of the lung and increased FEV1/FVC. They reported pooled results including few smokers. This study will examine measures of pulmonary function in participants with extensive smoking exposure.We examined pulmonary function in participants with a >10-pack-year history of smoking with and without diabetes with and without chronic obstructive pulmonary disease (COPD). We measured pulmonary function, exercise capacity, and pulmonary-related quality of life in 10,129 participants in the Genetic Epidemiology of Chronic Obstructive Pulmonary Disease (COPDGene) Study.Participants with diabetes were observed to have reduced pulmonary function after controlling for known risk factors and also significant reductions in exercise capacity and quality of life across functional stages of COPD.Pulmonary function in patients with ≥10 pack-years of smoking and diabetes is reduced, and this decrease is associated with significant reductions in activity-related quality of life and exercise capacity.
Control of Epstein-Barr virus infection in vitro by T helper cells specific for virion glycoproteins
Authors: Dinesh Adhikary, Uta Behrends, Andreas Moosmann, Klaus Witter, Georg W. Bornkamm, Josef Mautner
Journal: The Journal of Experimental Medicine (2006)

Epstein-Barr virus (EBV) establishes lifelong persistent infections in humans by latently infecting B cells, with occasional cycles of reactivation, virus production, and reinfection. Protective immunity against EBV is mediated by T cells, but the role of EBV-specific T helper (Th) cells is still poorly defined. Here, we study the Th response to the EBV lytic cycle proteins BLLF1 (gp350/220), BALF4 (gp110), and BZLF1 and show that glycoprotein-specific Th cells recognize EBV-positive cells directly; surprisingly, a much higher percentage of target cells than those expressing lytic cycle proteins were recognized. Antigen is efficiently transferred to bystander B cells by receptor-mediated uptake of released virions, resulting in recognition of target cells incubated with &amp;lt;1 virion/cell. T cell recognition does not require productive infection and occurs early after virus entry before latency is established. Glycoprotein-specific Th cells are cytolytic and inhibit proliferation of lymphoblastoid cell lines (LCL) and the outgrowth of LCL after infection of primary B cells with EBV. These results establish a novel role for glycoprotein-specific Th cells in the control of EBV infection and identify virion proteins as important immune targets. These findings have implications for the treatment of diseases associated with EBV and potentially other coated viruses infecting MHC class II–positive cells.
Two patients with the same type of iatrogenic disease
Authors: B. Vandooren, C. Haenebalcke, Y. Bogaerts
Journal: European Respiratory Journal (2005)

Case 1 A 67-yr-old female, who was recently diagnosed as having multiple myeloma, presented with dyspnoea on exertion of ,3 months' duration (fig.1).The day before presentation, the patient had developed a cough productive of green-brown sputa and increasing dyspnoea.On clinical examination, a tachypnoeic patient with bibasal crepitations on lung auscultation and without fever was observed.Arterial blood analysis showed an arterial oxygen tension (Pa,O 2 ) of 8.71 kPa and an arterial carbon dioxide tension (Pa,CO 2 ) of 5.32 kPa.
Family history of prostate cancer in patients with localized prostate cancer: an independent predictor of treatment outcome.
Authors: P A Kupelian, V A Kupelian, J S Witte, R Macklis, E A Klein
Journal: Journal of Clinical Oncology (1997)

To determine if familial prostate cancer patients have a less favorable prognosis than patients with sporadic prostate cancer after treatment for localized disease with either radiotherapy (RT) or radical prostatectomy (RP).One thousand thirty-eight patients treated with either RT (n = 583) or RP (n = 455) were included in this analysis. These patients were noted as having a positive family history if they confirmed the diagnosis of prostate cancer in a first-degree relative. The outcome of interest was biochemical relapse-free survival (bRFS). We used proportional hazards to analyze the effect of the presence of family history and other potential confounding variables (ie, age, treatment modality, stage, biopsy Gleason sum [GS], and initial prostate-specific antigen [iPSA] levels) on treatment outcome.Eleven percent of all patients had a positive family history. The 5-year bRFS rates for patients with negative and positive family histories were 52% and 29%, respectively (P < .001). The potential confounders with bRFS rates were iPSA levels, biopsy GS, and clinical tumor stage; treatment modality and age did not appear to be associated with outcome. After adjusting for potential confounders, family history of prostate cancer remained strongly associated with biochemical failure.This is the first study to demonstrate that the presence of a family history of prostate cancer correlates with treatment outcome in a large unselected series of patients. Our findings suggest that familial prostate cancer may have a more aggressive course than nonfamilial prostate cancer, and that clinical and/or pathologic parameters may not adequately predict this course.
The Definition of Primary and Secondary Glioblastoma
Authors: Hiroko Ohgaki, Paul Kleihues
Journal: Clinical Cancer Research (2012)

Glioblastoma is the most frequent and malignant brain tumor. The vast majority of glioblastomas (~90%) develop rapidly de novo in elderly patients, without clinical or histologic evidence of a less malignant precursor lesion (primary glioblastomas). Secondary glioblastomas progress from low-grade diffuse astrocytoma or anaplastic astrocytoma. They manifest in younger patients, have a lesser degree of necrosis, are preferentially located in the frontal lobe, and carry a significantly better prognosis. Histologically, primary and secondary glioblastomas are largely indistinguishable, but they differ in their genetic and epigenetic profiles. Decisive genetic signposts of secondary glioblastoma are IDH1 mutations, which are absent in primary glioblastomas and which are associated with a hypermethylation phenotype. IDH1 mutations are the earliest detectable genetic alteration in precursor low-grade diffuse astrocytomas and in oligodendrogliomas, indicating that these tumors are derived from neural precursor cells that differ from those of primary glioblastomas. In this review, we summarize epidemiologic, clinical, histopathologic, genetic, and expression features of primary and secondary glioblastomas and the biologic consequences of IDH1 mutations. We conclude that this genetic alteration is a definitive diagnostic molecular marker of secondary glioblastomas and more reliable and objective than clinical criteria. Despite a similar histologic appearance, primary and secondary glioblastomas are distinct tumor entities that originate from different precursor cells and may require different therapeutic approaches.
Dyspnoea assessed by visual analogue scale in patients with chronic obstructive lung disease during progressive and high intensity exercise.
Authors: A Noseda, J P Carpiaux, J Schmerber, J C Yernault
Journal: Thorax (1992)

<h3>Background and objectives</h3> Black patients have a higher incidence of kidney failure but lower rate of deceased- and living-donor kidney transplantation compared with White patients, even after taking differences in comorbidities into account. We assessed whether social determinants of health (<i>e.g</i>., demographics, cultural, psychosocial, knowledge factors) could account for race differences in receiving deceased- and living-donor kidney transplantation. <h3>Design, setting, participants, &amp; measurements</h3> <i>Via</i> medical record review, we prospectively followed 1056 patients referred for kidney transplant (2010–2012), who completed an interview soon after kidney transplant evaluation, until their kidney transplant. We used multivariable competing risk models to estimate the cumulative incidence of receipt of any kidney transplant, deceased-donor transplant, or living-donor transplant, and the factors associated with each outcome. <h3>Results</h3> Even after accounting for social determinants of health, Black patients had a lower likelihood of kidney transplant (subdistribution hazard ratio, 0.74; 95% confidence interval, 0.55 to 0.99) and living-donor transplant (subdistribution hazard ratio, 0.49; 95% confidence interval, 0.26 to 0.95), but not deceased-donor transplant (subdistribution hazard ratio, 0.92; 95% confidence interval, 0.67 to 1.26). Black race, older age, lower income, public insurance, more comorbidities, being transplanted before changes to the Kidney Allocation System, greater religiosity, less social support, less transplant knowledge, and fewer learning activities were each associated with a lower probability of any kidney transplant. Older age, more comorbidities, being transplanted before changes to the Kidney Allocation System, greater religiosity, less social support, and fewer learning activities were each associated with a lower probability of deceased-donor transplant. Black race, older age, lower income, public insurance, higher body mass index, dialysis before kidney transplant, not presenting with a potential living donor, religious objection to living-donor transplant, and less transplant knowledge were each associated with a lower probability of living-donor transplant. <h3>Conclusions</h3> Race and social determinants of health are associated with the likelihood of undergoing kidney transplant.
Circumvention of Normal Constraints on Granule Protein Gene Expression in Peripheral Blood Neutrophils and Monocytes of Patients with Antineutrophil Cytoplasmic Autoantibody–Associated Glomerulonephritis
Authors: Jia Jin Yang, William F. Pendergraft, David A. Alcorta, Patrick H. Nachman, Susan L. Hogan, Robin P. Thomas, Pamela Sullivan, J. Charles Jennette, Ronald J. Falk, Gloria A. Preston
Journal: Journal of the American Society of Nephrology (2004)

Granulopoiesis-related genes are distinctively upregulated in peripheral leukocytes of patients with antineutrophil cytoplasmic autoantibodies (ANCA)-associated glomerulonephritis. Affymetrix microarrays identified the upregulation of nine neutrophilic primary granule genes, including myeloperoxidase (MPO) and proteinase 3 (PR3), plus five secondary granule genes. Coordinate expression of granulocyte maturation marker CD35, measured by TaqMan PCR, and positive in situ staining for PR3 transcripts in polymorphic neutrophils and monocytes indicate that these genes are expressed in "mature" cells. Increased transcripts correlated with disease activity and absolute neutrophil values but not with "left shift," drug regimen, cytokine levels, hematuria, proteinuria, ANCA titer, serum creatinine, gender, or age. Upregulation of PR3 and MPO transcripts was specifically associated with ANCA disease (n = 56) as these changes were not detected in patients with ESRD (n = 25) or systemic lupus erythematosus (n = 17), as determined by TaqMan PCR. This is the first report of this phenomenon in nonneoplastic cells. The data raise the hypothesis that, in addition to the presence of anti-MPO or anti-PR3 autoantibodies, a second critical component in the cause of this disease is the reactivation of once-silenced genes leading to increased antigen availability.
T Cells and NKT Cells in the Pathogenesis of Asthma
Authors: Everett H. Meyer, Rosemarie H. DeKruyff, Dale T. Umetsu
Journal: Annual Review of Medicine (2007)

Asthma is an immunological disease with multiple inflammatory and clinical phenotypes, characterized by symptoms of wheezing, shortness of breath, and coughing due to airway hyperreactivity (AHR) and reversible airway obstruction. In allergic asthma, the most common form of asthma, airway inflammation is mediated by adaptive immune recognition of protein allergens by Th2 cells, resulting in airway eosinophilia. However, in other forms of asthma, inflammation is associated with immune responses to respiratory infections and airway neutrophilia. A central feature common to all forms of asthma is AHR, the heightened responsiveness of the airways to nonspecific stimuli. AHR has been shown recently in animal models of asthma to require the presence of CD1d-restricted, invariant T cell receptor-positive, natural killer T (iNKT) cells. Although allergen-specific Th2 cells and iNKT cells have many phenotypic similarities (e.g., expression of CD4 and production of Th2 cytokines), they have complementary activities, such as production of Th2 cytokines under different conditions, differential sensitivity to corticosteroids, and responsiveness to different classes of antigen (proteins versus glycolipids). We hypothesize that Th2 cells and iNKT cells interact synergistically to induce asthma but that different forms of asthma result from distinct roles of CD4 + iNKT cells versus Th2 cells.
Glucosamine, Chondroitin Sulfate, and the Two in Combination for Painful Knee Osteoarthritis
Authors: Daniel O. Clegg, Domenic J. Reda, Crystal L. Harris, Marguerite A. Klein, James R. O'Dell, Michele M. Hooper, John D. Bradley, Clifton O. Bingham, Michael H. Weisman, Christopher G. Jackson, Nancy E. Lane, John J. Cush, Larry W. Moreland, H. Ralph Schumacher, Chester V. Oddis, Frederick Wolfe, Jerry A. Molitor, David E. Yocum, Thomas J. Schnitzer, Daniel E. Furst, Allen D. Sawitzke, Helen Shi, Kenneth D. Brandt, Roland W. Moskowitz, H. James Williams
Journal: New England Journal of Medicine (2006)

Glucosamine and chondroitin sulfate are used to treat osteoarthritis. The multicenter, double-blind, placebo- and celecoxib-controlled Glucosamine/chondroitin Arthritis Intervention Trial (GAIT) evaluated their efficacy and safety as a treatment for knee pain from osteoarthritis.We randomly assigned 1583 patients with symptomatic knee osteoarthritis to receive 1500 mg of glucosamine daily, 1200 mg of chondroitin sulfate daily, both glucosamine and chondroitin sulfate, 200 mg of celecoxib daily, or placebo for 24 weeks. Up to 4000 mg of acetaminophen daily was allowed as rescue analgesia. Assignment was stratified according to the severity of knee pain (mild [N=1229] vs. moderate to severe [N=354]). The primary outcome measure was a 20 percent decrease in knee pain from baseline to week 24.The mean age of the patients was 59 years, and 64 percent were women. Overall, glucosamine and chondroitin sulfate were not significantly better than placebo in reducing knee pain by 20 percent. As compared with the rate of response to placebo (60.1 percent), the rate of response to glucosamine was 3.9 percentage points higher (P=0.30), the rate of response to chondroitin sulfate was 5.3 percentage points higher (P=0.17), and the rate of response to combined treatment was 6.5 percentage points higher (P=0.09). The rate of response in the celecoxib control group was 10.0 percentage points higher than that in the placebo control group (P=0.008). For patients with moderate-to-severe pain at baseline, the rate of response was significantly higher with combined therapy than with placebo (79.2 percent vs. 54.3 percent, P=0.002). Adverse events were mild, infrequent, and evenly distributed among the groups.Glucosamine and chondroitin sulfate alone or in combination did not reduce pain effectively in the overall group of patients with osteoarthritis of the knee. Exploratory analyses suggest that the combination of glucosamine and chondroitin sulfate may be effective in the subgroup of patients with moderate-to-severe knee pain. (ClinicalTrials.gov number, NCT00032890.).
The Right Care in the Right Place
Authors: William J. Hall
Journal: JAMA Internal Medicine (2013)

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AAV-mediated factor IX gene transfer to skeletal muscle in patients with severe hemophilia B
Authors: C. S. Manno, A. J. Chew, S. Hutchison, P. J. Larson, R. W. Herzog, V. R. Arruda, S. J. Tai, M. V. Ragni, A. Thompson, M. Ozelo, L. B. Couto, D. G. B. Leonard, F. A. Johnson, A. McClelland, C. Scallan, E. Skarsgard, A. W. Flake, M. A. Kay, K. A. High, B. Glader
Journal: Blood (2003)
Inhibition by red wine extract, resveratrol, of cytokine release by alveolar macrophages in COPD
Authors: S V Culpitt
Journal: Thorax (2003)

<b>Background:</b> The pathophysiology of chronic obstructive pulmonary disease (COPD) features pulmonary inflammation with a predominant alveolar macrophage involvement. Bronchoalveolar macrophages from patients with COPD release increased amounts of inflammatory cytokines in vitro, an effect that is not inhibited by the glucocorticosteroid dexamethasone. Resveratrol (3,5,4′-trihydroxystilbene) is a component of red wine extract that has anti-inflammatory and antioxidant properties. A study was undertaken to determine whether or not resveratrol would inhibit cytokine release in vitro by alveolar macrophages from patients with COPD. <b>Methods:</b> Alveolar macrophages were isolated from bronchoalveolar lavage (BAL) fluid from cigarette smokers and from patients with COPD (n=15 per group). The macrophages were stimulated with either interleukin (IL)-1β or cigarette smoke media (CSM) to release IL-8 and granulocyte macrophage-colony stimulating factor (GM-CSF). The effect of resveratrol was examined on both basal and stimulated cytokine release. <b>Results:</b> Resveratrol inhibited basal release of IL-8 in smokers and patients with COPD by 94% and 88% respectively, and inhibited GM-CSF release by 79% and 76% respectively. Resveratrol also inhibited stimulated cytokine release. Resveratrol reduced IL-1β stimulated IL-8 and GM-CSF release in both smokers and COPD patients to below basal levels. In addition, resveratrol inhibited CSM stimulated IL-8 release by 61% and 51% respectively in smokers and COPD patients, and inhibited GM-CSF release by 49% for both subject groups. <b>Conclusions:</b> Resveratrol inhibits inflammatory cytokine release from alveolar macrophages in COPD. Resveratrol or similar compounds may be effective pharmacotherapy for macrophage pathophysiology in COPD.
XIII. Prognostic Significance of Negative U Waves in the Electrocardiogram in Hypertension
Authors: ROBERT L. KEMP, BORYS SURAWICZ, JOHN C. BETTINGER, HARRY GOTTLIEB, SAMUEL BELLET
Journal: Circulation (1957)

Negative U waves were found in 23 per cent of 287 electrocardiograms of hypertensive patients. The group of patients with negative U waves showed higher average diastolic and mean blood pressures, more advanced congestive heart failure, a higher incidence of marked cardiomegaly and uremia, more serious cerebrovascular complications, and a higher mortality than the group with positive U waves. Normal heart size, normal electrocardiographic patterns, and absence of evidence of renal impairment or congestive heart failure occurred more commonly in the group with positive U waves. Negative U waves were found in 43 per cent of 114 cases of "left ventricular strain" pattern in hypertensive patients. In the presence of "left ventricular strain" pattern, the patients with negative U waves had more advanced congestive heart failure, a higher incidence of marked cardiomegaly and uremia, and a higher mortality than the patients with positive or isoelectric U waves. A concept has been advanced that in the evolution of the "left ventricular strain" pattern, the inversion of the U wave is a late event that follows the inversion of the T wave by a certain time lag. In the few cases in which an inverted U wave followed a positive T wave, the morbidity and mortality were very high. A negative U wave constituted the only abnormal finding in 1 case.
Mechanical Ventilation with or without Daily Changes of In-Line Suction Catheters
Authors: MARIN H. KOLLEF, DONNA PRENTICE, STEVEN D. SHAPIRO, VICTORIA J. FRASER, PATRICIA SILVER, ELLEN TROVILLION, PAMELA WEILITZ, BENJAMIN VON HARZ, ROBERT ST. JOHN
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

The purpose of this study was to determine the safety and cost-effectiveness of not routinely changing in-line suction catheters for patients requiring mechanical ventilation. Patients were randomly assigned to receive either no routine in-line suction catheter changes (n = 258) or in-line suction catheter changes every 24 h (n = 263). The main outcome measure was the incidence of ventilator-associated pneumonia. Other outcomes evaluated included hospital mortality, acquired organ system derangements, duration of mechanical ventilation, lengths of intensive care and hospital stay, and the cost for in-line suction catheters. Ventilator-associated pneumonia was seen in 38 patients (14.7%) receiving no routine in-line suction catheter changes and in 39 patients (14.8%) receiving in-line suction catheter changes every 24 h (relative risk, 0.99; 95% CI, 0.66 to 1.50). No statistically significant differences for hospital mortality, lengths of stay, the number of acquired organ system derangements, death in patients with ventilator-associated pneumonia, or mortality directly attributed to ventilator-associated pneumonia were found between the two treatment groups. Patients receiving in-line suction catheter changes every 24 h had 1,224 catheter changes costing a total of $11,016; patients receiving no routine in-line suction catheter changes had a total of 93 catheter changes costing $837. Our findings suggest that the elimination of routine in-line suction catheter changes is safe and can reduce the costs associated with providing mechanical ventilation.