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Search Results: 1 - 10 of 297508 matches for " Connett J "
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Mannose-binding lectin deficiency and acute exacerbations of chronic obstructive pulmonary disease
Albert RK,Connett J,Curtis JL,Martinez FJ
International Journal of COPD , 2012,
Abstract: Richard K Albert,1 John Connett,2 Jeffrey L Curtis,3,4 Fernando J Martinez,3 MeiLan K Han,3 Stephen C Lazarus,5 Prescott G Woodruff51Medicine Service, Denver Health and Department of Medicine, University of Colorado Denver, Denver, CO, 2Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, 3Pulmonary and Critical Care Medicine, Department of Medicine, University of Michigan, Ann Arbor, MI, 4Pulmonary and Critical Care Medicine, VA Medical Center, Ann Arbor, MI, 5Pulmonary and Critical Care Medicine, Department of Medicine, and Cardiovascular Research Institute, University of California, San Francisco, CA, USABackground: Mannose-binding lectin is a collectin involved in host defense against infection. Whether mannose-binding lectin deficiency is associated with acute exacerbations of chronic obstructive pulmonary disease is debated.Methods: Participants in a study designed to determine if azithromycin taken daily for one year decreased acute exacerbations had serum mannose-binding lectin concentrations measured at the time of enrollment.Results: Samples were obtained from 1037 subjects (91%) in the trial. The prevalence of mannose-binding lectin deficiency ranged from 0.5% to 52.2%, depending on how deficiency was defined. No differences in the prevalence of deficiency were observed with respect to any demographic variable assessed, and no differences were observed in time to first exacerbation, rate of exacerbations, or percentage of subjects requiring hospitalization for exacerbations in those with deficiency versus those without, regardless of how deficiency was defined.Conclusion: In a large sample of subjects with chronic obstructive pulmonary disease selected for having an increased risk of experiencing an acute exacerbation of chronic obstructive pulmonary disease, only 1.9% had mannose-binding lectin concentrations below the normal range and we found no association between mannose-binding lectin concentrations and time to first acute exacerbation or frequency of acute exacerbations during one year of prospective follow-up.Keywords: COPD, acute exacerbations, mannose-binding lectin
Mannose-binding lectin deficiency and acute exacerbations of chronic obstructive pulmonary disease
Albert RK, Connett J, Curtis JL, Martinez FJ, Han MK, Lazarus SC, Woodruff PG
International Journal of Chronic Obstructive Pulmonary Disease , 2012, DOI: http://dx.doi.org/10.2147/COPD.S33714
Abstract: nnose-binding lectin deficiency and acute exacerbations of chronic obstructive pulmonary disease Original Research (852) Total Article Views Authors: Albert RK, Connett J, Curtis JL, Martinez FJ, Han MK, Lazarus SC, Woodruff PG Published Date November 2012 Volume 2012:7 Pages 767 - 777 DOI: http://dx.doi.org/10.2147/COPD.S33714 Received: 09 May 2012 Accepted: 09 July 2012 Published: 23 November 2012 Richard K Albert,1 John Connett,2 Jeffrey L Curtis,3,4 Fernando J Martinez,3 MeiLan K Han,3 Stephen C Lazarus,5 Prescott G Woodruff5 1Medicine Service, Denver Health and Department of Medicine, University of Colorado Denver, Denver, CO, 2Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, 3Pulmonary and Critical Care Medicine, Department of Medicine, University of Michigan, Ann Arbor, MI, 4Pulmonary and Critical Care Medicine, VA Medical Center, Ann Arbor, MI, 5Pulmonary and Critical Care Medicine, Department of Medicine, and Cardiovascular Research Institute, University of California, San Francisco, CA, USA Background: Mannose-binding lectin is a collectin involved in host defense against infection. Whether mannose-binding lectin deficiency is associated with acute exacerbations of chronic obstructive pulmonary disease is debated. Methods: Participants in a study designed to determine if azithromycin taken daily for one year decreased acute exacerbations had serum mannose-binding lectin concentrations measured at the time of enrollment. Results: Samples were obtained from 1037 subjects (91%) in the trial. The prevalence of mannose-binding lectin deficiency ranged from 0.5% to 52.2%, depending on how deficiency was defined. No differences in the prevalence of deficiency were observed with respect to any demographic variable assessed, and no differences were observed in time to first exacerbation, rate of exacerbations, or percentage of subjects requiring hospitalization for exacerbations in those with deficiency versus those without, regardless of how deficiency was defined. Conclusion: In a large sample of subjects with chronic obstructive pulmonary disease selected for having an increased risk of experiencing an acute exacerbation of chronic obstructive pulmonary disease, only 1.9% had mannose-binding lectin concentrations below the normal range and we found no association between mannose-binding lectin concentrations and time to first acute exacerbation or frequency of acute exacerbations during one year of prospective follow-up.
The Algebra and Geometry of Isometries
John E. Connett
Mathematics , 2014,
Abstract: An expository approach is given on the relationship between algebraic and geometric approaches to properties of isometries in the plane and the 2-sphere.
Studying bacteria in respiratory specimens by using conventional and molecular microbiological approaches
Geraint B Rogers, Thomas WV Daniels, Andrew Tuck, Mary P Carroll, Gary J Connett, Gondi JP David, Kenneth D Bruce
BMC Pulmonary Medicine , 2009, DOI: 10.1186/1471-2466-9-14
Abstract: Six different media used in routine diagnostic microbiology were inoculated with sputum from twelve patients. Bacterial growth on these plates was harvested and both RNA and DNA extracted. DNA and RNA were also extracted directly from the same sample of sputum. All nucleic acids served as templates for PCR and reverse transcriptase-PCR amplification of "broad range" bacterial 16S rRNA gene regions. The regions amplified were separated by Terminal Restriction Fragment Length Polymorphism (T-RFLP) profiling and compared to assess the degree of overlap between approaches.A mean of 16.3 (SD 10.0) separate T-RF band lengths in the profiles from each sputum sample by Direct Molecular Analysis, with a mean of 8.8 (SD 5.8) resolved by DNA profiling and 13.3 (SD 8.0) resolved by RNA profiling. In comparison, 8.8 (SD 4.4) T-RF bands were resolved in profiles generated by Culture-derived Molecular Analysis. There were a total of 184 instances of T-RF bands detected in the direct sputum profiles but not in the corresponding culture-derived profiles, representing 83 different T-RF band lengths. Amongst these were fifteen instances where the T-RF band represented more than 10% of the total band volume (with a mean value of 23.6%). Eight different T-RF band lengths were resolved as the dominant band in profiles generated directly from sputum. Of these, only three were detected in profiles generated from the corresponding set of cultures.Due to their focus on isolation of a small group of recognised pathogens, the use of culture-dependent methods to analyse samples from chronic respiratory infections can provide a restricted understanding of the bacterial species present. The use of a culture-independent molecular approach here identifies that there are many bacterial species in samples from CF and COPD patients that may be clinically relevant.Sputum culture has been used by the respiratory physician to provide insight into the bacteria present in many airway diseases such as pneum
Risk for Hospital Readmission following Bariatric Surgery
Robert B. Dorman, Christopher J. Miller, Daniel B. Leslie, Federico J. Serrot, Bridget Slusarek, Henry Buchwald, John E. Connett, Sayeed Ikramuddin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0032506
Abstract: Background and Objectives Complications resulting in hospital readmission are important concerns for those considering bariatric surgery, yet present understanding of the risk for these events is limited to a small number of patient factors. We sought to identify demographic characteristics, concomitant morbidities, and perioperative factors associated with hospital readmission following bariatric surgery. Methods We report on a prospective observational study of 24,662 patients undergoing primary RYGB and 26,002 patients undergoing primary AGB at 249 and 317 Bariatric Surgery Centers of Excellence (BSCOE), respectively, in the United States from January 2007 to August 2009. Data were collected using standardized assessments of demographic factors and comorbidities, as well as longitudinal records of hospital readmissions, complications, and mortality. Results The readmission rate was 5.8% for RYGB and 1.2% for AGB patients 30 days after discharge. The greatest predictors for readmission following RYGB were prolonged length of stay (adjusted odds ratio [OR], 2.3; 95% confidence interval [CI], 2.0–2.7), open surgery (OR, 1.8; CI, 1.4–2.2), and pseudotumor cerebri (OR, 1.6; CI, 1.1–2.4). Prolonged length of stay (OR, 2.3; CI, 1.6–3.3), history of deep venous thrombosis or pulmonary embolism (OR, 2.1; CI, 1.3–3.3), asthma (OR, 1.5; CI, 1.1–2.1), and obstructive sleep apnea (OR, 1.5; CI, 1.1–1.9) were associated with the greatest increases in readmission risk for AGB. The 30-day mortality rate was 0.14% for RYGB and 0.02% for AGB. Conclusion Readmission rates are low and mortality is very rare following bariatric surgery, but risk for both is significantly higher after RYGB. Predictors of readmission were disparate for the two procedures. Results do not support excluding patients with certain comorbidities since any reductions in overall readmission rates would be very small on the absolute risk scale. Future research should evaluate the efficacy of post-surgical managed care plans for patients at higher risk for readmission and adverse events.
Effect of heme oxygenase-1 polymorphisms on lung function and gene expression
Goh Tanaka, Farzian Aminuddin, Loubna Akhabir, Jian-Qing He, Karey Shumansky, John E Connett, Nicholas R Anthonisen, Raja T Abboud, Peter D Paré, Andrew J Sandford
BMC Medical Genetics , 2011, DOI: 10.1186/1471-2350-12-117
Abstract: We genotyped five single nucleotide polymorphisms (SNPs) in the HMOX1 gene in Caucasians who had the fastest (n = 278) and the slowest (n = 304) decline of FEV1 % predicted, selected from smokers in the NHLBI Lung Health Study. These SNPs were also studied in Caucasians with the lowest (n = 535) or the highest (n = 533) baseline lung function. Reporter genes were constructed containing three HMOX1 promoter polymorphisms and the effect of these polymorphisms on H2O2 and hemin-stimulated gene expression was determined. The effect of the HMOX1 rs2071749 SNP on gene expression in alveolar macrophages was investigated.We found a nominal association (p = 0.015) between one intronic HMOX1 SNP (rs2071749) and lung function decline but this did not survive correction for multiple comparisons. This SNP was in perfect linkage disequilibrium with rs3761439, located in the promoter of HMOX1. We tested rs3761439 and two other putatively functional polymorphisms (rs2071746 and the (GT)n polymorphism) in reporter gene assays but no significant effects on gene expression were found. There was also no effect of rs2071749 on HMOX1 gene expression in alveolar macrophages.We found no association of the five HMOX1 tag SNPs with lung function decline and no evidence that the three promoter polymorphisms affected the regulation of the HMOX1 gene.Oxidative stress induced by smoking is considered to play a role in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). Oxidant compounds in cigarette smoke cause an excess of oxidants in the lung, and lead to direct cell injury, lung extracellular matrix damage, inactivation of antiproteinases, and induction of proinflammatory mediators [1].Heme oxygenase-1 (HMOX1) is an essential enzyme in heme catabolism and is induced by oxidative stress. HMOX1 catalyzes the conversion of heme to biliverdin, carbon monoxide and iron. Subsequent to the reaction, biliverdin is converted to bilirubin by biliverdin reductase. Biliverdin and bilirubin
Contribution of alpha- and beta-defensins to lung function decline and infection in smokers: an association study
Alison M Wallace, Jian-Qing He, Kelly M Burkett, Jian Ruan, John E Connett, Nicholas R Anthonisen, Peter D Paré, Andrew J Sandford
Respiratory Research , 2006, DOI: 10.1186/1465-9921-7-76
Abstract: Subjects were genotyped for the alpha-defensin-1/alpha-defensin-3 copy number polymorphism and four beta-defensin-1 polymorphisms (G-20A, C-44G, G-52A and Val38Ile).There were no associations between individual polymorphisms or imputed haplotypes and rate of decline in lung function or susceptibility to infection.These findings suggest that, in a white population, the defensin polymorphisms tested may not be of importance in determining who develops abnormally rapid lung function decline or is susceptible to developing lower respiratory infections.Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow obstruction due to chronic inflammation. COPD is closely related to cigarette smoking, which is the main environmental risk factor. Longitudinal studies show that only a minority of cigarette smokers develop airflow limitation,[1] suggesting that other environmental or genetic factors are important. Family and twin studies provide further evidence that genetic factors play a key role in the etiology of this disease.[2,3] Inherited deficiency of alpha-1 antitrypsin is associated with COPD; other genetic risk factors remain to be identified.Defensins are small (29–47 amino acids) cationic microbicidal peptides that form part of both the innate and adaptive immune responses. Defensins show activities against Gram-positive and Gram-negative bacteria, fungi, yeast, and enveloped viruses.[4] Defensins are known primarily for their antimicrobial activities; however, the scope of their activities extends beyond immune responses and some of these functions could contribute to lung injury. [5-9]Based on a characteristic three-dimensional fold and a 6-cysteine/3-disulfide pattern, human defensins are divided into two groups, alpha-defensins and beta-defensins.[10] Three closely related alpha-defensins, alpha-defensin-1 (DEFA1), DEFA2, and DEFA3, are major constituents of neutrophil azurophilic granules (30–50% of the total protein content)[11] and p
Fluorine in medicine
Anna Strunecka,Jiri Patocka,Paul Connett
Journal of Applied Biomedicine , 2004,
Abstract: Fluoride has long been known to influence the activity of various enzymes in vitro. Latterly it hasbeen demonstrated that many effects primarily attributed to fluoride are caused by a synergisticaction of fluoride plus aluminum. Fluorinated chemicals are of growing importance, withapplications in medicine. Fluorine substitution has profound effects on the properties of organiccompounds. The very high electronegativity of fluorine can modify electron distribution in themolecule, affecting its absorption, distribution and metabolism. Fluorine-containing drugs are used inmedicine as anesthetics, antibiotics, anti-cancer and anti-inflammatory agents,psychopharmaceuticals, and in many other applications. The potential contribution of fluorinatingpharmaceuticals to human fluoride exposure is discussed.
Combining parametric, semi-parametric, and non-parametric survival models with stacked survival models
Andrew Wey,John Connett,Kyle Rudser
Statistics , 2013,
Abstract: For estimating conditional survival functions, non-parametric estimators can be preferred to parametric and semi-parametric estimators due to relaxed assumptions that enable robust estimation. Yet, even when misspecified, parametric and semi-parametric estimators can possess better operating characteristics in small sample sizes due to smaller variance than non-parametric estimators. Fundamentally, this is a bias-variance tradeoff situation in that the sample size is not large enough to take advantage of the low bias of non-parametric estimation. Stacked survival models estimate an optimally weighted combination of models that can span parametric, semi-parametric, and non-parametric models by minimizing prediction error. An extensive simulation study demonstrates that stacked survival models consistently perform well across a wide range of scenarios by adaptively balancing the strengths and weaknesses of individual candidate survival models. In addition, stacked survival models perform as good as, or better than, the model selected through cross-validation. Lastly, stacked survival models are applied to a well-known German breast cancer study.
The Relationship between Telomere Length and Mortality in Chronic Obstructive Pulmonary Disease (COPD)
Jee Lee, Andrew J. Sandford, John E. Connett, Jin Yan, Tammy Mui, Yuexin Li, Denise Daley, Nicholas R. Anthonisen, Angela Brooks-Wilson, S. F. Paul Man, Don D. Sin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035567
Abstract: Some have suggested that chronic obstructive pulmonary disease (COPD) is a disease of accelerated aging. Aging is characterized by shortening of telomeres. The relationship of telomere length to important clinical outcomes such as mortality, disease progression and cancer in COPD is unknown. Using quantitative polymerase chain reaction (qPCR), we measured telomere length of peripheral leukocytes in 4,271 subjects with mild to moderate COPD who participated in the Lung Health Study (LHS). The subjects were followed for approximately 7.5 years during which time their vital status, FEV1 and smoking status were ascertained. Using multiple regression methods, we determined the relationship of telomere length to cancer and total mortality in these subjects. We also measured telomere length in healthy “mid-life” volunteers and patients with more severe COPD. The LHS subjects had significantly shorter telomeres than those of healthy “mid-life” volunteers (p<.001). Compared to individuals in the 4th quartile of relative telomere length (i.e. longest telomere group), the remaining participants had significantly higher risk of cancer mortality (Hazard ratio, HR, 1.48; p = 0.0324) and total mortality (HR, 1.29; p = 0.0425). Smoking status did not make a significant difference in peripheral blood cells telomere length. In conclusion, COPD patients have short leukocyte telomeres, which are in turn associated increased risk of total and cancer mortality. Accelerated aging is of particular relevance to cancer mortality in COPD.
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