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1. Unpacking Healthcare Professionals’ Work to Achieve Coherence in the Healthcare Journey of Elderly Patients: An Interview Study

Author

Kumlin M, Berg GV, Kvigne K, and Hellesø R

Subjects
older, care trajectory, complex healthcare, health personnel, interdisciplinary, Medicine (General), R5-920
Abstract

Marianne Kumlin,1– 3 Geir Vegar Berg,2,4 Kari Kvigne,1 Ragnhild Hellesø3 1Department of Health and Nursing Sciences, Inland Norway University of Applied Sciences Elverum, Elverum, Norway; 2Innlandet Hospital Trust, Lillehammer, Norway; 3Department of Nursing Science, Institute of Health and Society, Faculty of Medicine, University of Oslo, Oslo, Norway; 4Department of Health Sciences, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Gjøvik, NorwayCorrespondence: Marianne Kumlin Tel +47 91594685Email marianne.kumlin@inn.noAim: Today, seamless, person-centered healthcare is emphasized when dealing with elderly patients with comprehensive needs. Studies have uncovered a complex healthcare terrain. Despite a great deal of effort on the part of policy makers and healthcare providers, the work healthcare professionals undertake to develop seamless healthcare is still unclear. Therefore, the aim of this study was to uncover the work that healthcare professionals undertake to achieve coherent and comprehensive healthcare for elderly patients with multiple health problems during their journey through the complex healthcare terrain.Methods: This study has an explorative design with individual interviews. Twenty-five healthcare professionals from primary and specialist care agreed to participate. A thematic analysis method was employed.Results: The analyses revealed three central themes in the healthcare professionals’ work to build coherence in the patients’ care trajectory: Working to manage a patient’s illness trajectory during the course of the patient’s life, working to achieve a comprehensive overall picture, and considering multiple options in a “patchwork” terrain.Conclusion: Healthcare professionals have a common understanding that hospital stays are a short part of the elderly person’s journey in the healthcare system. In the comprehensive work to obtain the overall picture of the illness trajectory within the patient’s life story, healthcare professionals emphasized the importance of working in an interdisciplinary manner. Interprofessional consulting and collaboration should be strengthened to build coherence in the older patient’s complex care trajectory.Keywords: older, care trajectory, complex healthcare, health personnel, interdisciplinary

Published
2021

4. Plasma proteins elevated in severe asthma despite oral steroid use and unrelated to Type-2 inflammation

Author

Mikus, M.S. Kolmert, J. Andersson, L.I. Östling, J. Knowles, R.G. Gómez, C. Ericsson, M. Thörngren, J.-O. Khoonsari, P.E. Dahlén, B. Kupczyk, M. de Meulder, B. Auffray, C. Bakke, P.S. Beghe, B. Bel, E.H. Caruso, M. Chanez, P. Chawes, B. Fowler, S.J. Gaga, M. Geiser, T. Gjomarkaj, M. Horváth, I. Howarth, P.H. Johnston, S.L. Joos, G. Krug, N. Montuschi, P. Musial, J. Niżankowska-Mogilnicka, E. Olsson, H.K. Papi, A. Rabe, K.F. Sandström, T. Shaw, D.E. Siafakas, N.M. Uhlén, M. Riley, J.H. Bates, S. Middelveld, R.J.M. Wheelock, C.E. Chung, K.F. Adcock, I.M. Sterk, P.J. Djukanovic, R. Nilsson, P. Dahlén, S.-E. James, A. Ahmed, H. Balgoma, D. Bansal, A.T. Baribaud, F. Bigler, J. Billing, B. Bisgaard, H. Boedigheimer, M.J. Bønnelykke, K. Brandsma, J. Brinkman, P. Bucchioni, E. Burg, D. Bush, A. Chaiboonchoe, A. Checa, T. Compton, C.H. Corfield, J. Cunoosamy, D. D’Amico, A. Emma, R. Erpenbeck, V.J. Erzen, D. Fichtner, K. Fitch, N. Fleming, L.J. Formaggio, E. Frey, U. Gahlemann, M. Goss, V. Guo, Y.-K. Hashimoto, S. Haughney, J. Hedlin, G. Hekking, P.-P.W. Higenbottam, T. Hohlfeld, J.M. Holweg, C.T.J. Knox, A.J. Konradsen, J. Lazarinis, N. Lefaudeux, D. Li, T. Loza, M.J. Lutter, R. Manta, A. Masefield, S. Matthews, J.G. Mazein, A. Meiser, A. Miralpeix, M. Mores, N. Murray, C.S. Myles, D. Naz, S. Nordlund, B. Pahus, L. Pandis, I. Pavlidis, S. Postle, A. Powel, P. Rao, N. Reinke, S. Roberts, A. Roberts, G. Rowe, A. Schofield, J.P.R. Seibold, W. Selby, A. Sigmund, R. Singer, F. Sjödin, M. Skipp, P.J. Sousa, A.R. Sun, K. Thornton, B. Uddin, M. van Aalderen, W.M. van Geest, M. Vestbo, J. Vissing, N.H. Wagener, A.H. Wagers, S.S. Weiszhart, Z. Wheelock, C.E. Wheelock, Å. Wilson, S.J. Yasinska, V. Brusselle, G.G. Campbell, D.A. Contoli, M. Damm, K. de Rudder, I. Delin, I. Devautour, C. Duplaga, M. Eduards, M. Ek, A. Ekström, T. Figiel, E. Gaber, F. Gauw, S. Gawlewicz-Mroczka, A. Gerding, D. Haque, S. Hewitt, L. Hiemstra, P.S. Holgate, S.T. Holloway, J. Kania, A. Kanniess, F. Karlsson, Ö. Kips, J.C. Kumlin, M. Lantz, A.-S. Lazarinis, N. Magnussen, H. Mallia, P. Martling, I. Meziane, L. Oikonomidou, E. Olsson, M. Pace, E. Papadopouli, E. Papadopoulos, N. Plataki, M. Profita, M. Reinius, L.E. Richter, K. Robinson, D.S. Romagnoli, M. Samara, K. Schelfhout, V. Skedinger, M. Stamataki, E. ten Brinke, A. Vachier, I. Wallén-Nielsen, E. van Veen, I. Weersink, E. Wilson, S.J. Yasinska, V. Zervas, E. Ziolkowska-Graca, B. U-BIOPRED (Unbiased Biomarkers for the Prediction of Respiratory Disease outcome) Study Group BIOAIR (Longitudinal Assessment of Clinical Course Biomarkers in Severe Chronic Airway Disease) Consortium

Abstract

Rationale Asthma phenotyping requires novel biomarker discovery. Objectives To identify plasma biomarkers associated with asthma phenotypes by application of a new proteomic panel to samples from two well-characterised cohorts of severe (SA) and mild-to-moderate (MMA) asthmatics, COPD subjects and healthy controls (HCs). Methods An antibody-based array targeting 177 proteins predominantly involved in pathways relevant to inflammation, lipid metabolism, signal transduction and extracellular matrix was applied to plasma from 525 asthmatics and HCs in the U-BIOPRED cohort, and 142 subjects with asthma and COPD from the validation cohort BIOAIR. Effects of oral corticosteroids (OCS) were determined by a 2-week, placebo-controlled OCS trial in BIOAIR, and confirmed by relation to objective OCS measures in U-BIOPRED. Results In U-BIOPRED, 110 proteins were significantly different, mostly elevated, in SA compared to MMA and HCs. 10 proteins were elevated in SA versus MMA in both U-BIOPRED and BIOAIR (alpha-1-antichymotrypsin, apolipoprotein-E, complement component 9, complement factor I, macrophage inflammatory protein-3, interleukin-6, sphingomyelin phosphodiesterase 3, TNF receptor superfamily member 11a, transforming growth factor-β and glutathione S-transferase). OCS treatment decreased most proteins, yet differences between SA and MMA remained following correction for OCS use. Consensus clustering of U-BIOPRED protein data yielded six clusters associated with asthma control, quality of life, blood neutrophils, high-sensitivity C-reactive protein and body mass index, but not Type-2 inflammatory biomarkers. The mast cell specific enzyme carboxypeptidase A3 was one major contributor to cluster differentiation. Conclusions The plasma proteomic panel revealed previously unexplored yet potentially useful Type-2independent biomarkers and validated several proteins with established involvement in the pathophysiology of SA. © 2022 European Respiratory Society. All rights reserved.

Published
2022

5. Plasma proteins elevated in severe asthma despite oral steroid use and unrelated to Type-2 inflammation

Author

Mikus, M. S., Kolmert, J., Andersson, L. I., Ostling, J., Knowles, R. G., Gomez, C., Ericsson, M., Thorngren, J. -O., Khoonsari, P. E., Dahlen, B., Kupczyk, M., de Meulder, B., Auffray, C., Bakke, P. S., Beghe, Bianca, Bel, E. H., Caruso, M., Chanez, P., Chawes, B., Fowler, S. J., Gaga, M., Geiser, T., Gjomarkaj, M., Horvath, I., Howarth, P. H., Johnston, S. L., Joos, G., Krug, N., Montuschi, P., Musial, J., Nizankowska-Mogilnicka, E., Olsson, H. K., Papi, A., Rabe, K. F., Sandstrom, T., Shaw, D. E., Siafakas, N. M., Uhlen, M., Riley, J. H., Bates, S., Middelveld, R. J. M., Wheelock, C. E., Chung, K. F., Adcock, I. M., Sterk, P. J., Djukanovic, R., Nilsson, P., Dahlen, S. -E., James, A., Ahmed, H., Balgoma, D., Bansal, A. T., Baribaud, F., Bigler, J., Billing, B., Bisgaard, H., Boedigheimer, M. J., Bonnelykke, K., Brandsma, J., Brinkman, P., Bucchioni, E., Burg, D., Bush, A., Chaiboonchoe, A., Checa, T., Compton, C. H., Corfield, J., Cunoosamy, D., D'Amico, A., Emma, R., Erpenbeck, V. J., Erzen, D., Fichtner, K., Fitch, N., Fleming, L. J., Formaggio, E., Frey, U., Gahlemann, M., Goss, V., Guo, Y. -K., Hashimoto, S., Haughney, J., Hedlin, G., Hekking, P. -P. W., Higenbottam, T., Hohlfeld, J. M., Holweg, C. T. J., Knox, A. J., Konradsen, J., Lazarinis, N., Lefaudeux, D., Li, T., Loza, M. J., Lutter, R., Manta, A., Masefield, S., Matthews, J. G., Mazein, A., Meiser, A., Miralpeix, M., Mores, N., Murray, C. S., Myles, D., Naz, S., Nordlund, B., Pahus, L., Pandis, I., Pavlidis, S., Postle, A., Powel, P., Rao, N., Reinke, S., Roberts, A., Roberts, G., Rowe, A., Schofield, J. P. R., Seibold, W., Selby, A., Sigmund, R., Singer, F., Sjodin, M., Skipp, P. J., Sousa, A. R., Sun, K., Thornton, B., Uddin, M., van Aalderen, W. M., van Geest, M., Vestbo, J., Vissing, N. H., Wagener, A. H., Wagers, S. S., Weiszhart, Z., Wheelock, A., Wilson, S. J., Yasinska, V., Brusselle, G. G., Campbell, D. A., Contoli, M., Damm, K., de Rudder, I., Delin, I., Devautour, C., Duplaga, M., Eduards, M., Ek, A., Ekstrom, T., Figiel, E., Gaber, F., Gauw, S., Gawlewicz-Mroczka, A., Gerding, D., Haque, S., Hewitt, L., Hiemstra, P. S., Holgate, S. T., Holloway, J., Kania, A., Kanniess, F., Karlsson, O., Kips, J. C., Kumlin, M., Lantz, A. -S., Magnussen, H., Mallia, P., Martling, I., Meziane, L., Oikonomidou, E., Olsson, M., Pace, E., Papadopouli, E., Papadopoulos, N., Plataki, M., Profita, M., Reinius, L. E., Richter, K., Robinson, D. S., Romagnoli, M., Samara, K., Schelfhout, V., Skedinger, M., Stamataki, E., ten Brinke, A., Vachier, I., Wallen-Nielsen, E., van Veen, I., Weersink, E., Zervas, E., and Ziolkowska-Graca, B.

Subjects
Blood Proteins, Humans, Inflammation, Proteomics, Severity of Illness Index, Steroids, Asthma, Quality of Life
Published
2022

23. Detection of exacerbations in asthma based on electronic diary data : results from the 1-year prospective BIOAIR study

Author

Kupczyk, M., Haque, S., Sterk, P. J., Nizankowska-Mogilnicka, E., Papi, A., Bel, E. H., Chanez, P., Dahlen, B., Gaga, M., Gjomarkaj, M., Howarth, P. H., Johnston, S. L., Joos, G. F., Kanniess, F., Tzortzaki, E., James, A., Middelveld, R. J. M., Dahlen, S.-E., Weersink, E., Papadopoulos, N., Oikonomidou, E., Zervas, E., Contoli, M., Pauwels, R. A., Brusselle, G., de Rudder, I., Schelfhout, V., Richter, K., Gerding, D., Magnussen, H., Siafakas, N. M., Samara, K., Plataki, M., Papadopouli, E., Szczeklik, A., Ziolkowska-Graca, B., Kania, A., Gawlewicz-Mroczka, A., Duplaga, M., Figiel, E., Rabe, K. F., Hiemstra, P. S., Gauw, S., van Veen, I., Kips, J. C., Mallia, P., Campbell, D. A., Robinson, D. S., Fabbri, L. M., Romagnoli, M., Vachier, I., Devautour, C., Meziane, L., Maurizio Vignola, A., Pace, E., Profita, M., Holgate, S. T., Wilson, S. J., Hewitt, L., Holoway, J., Damm, K., Delin, I., Eduards, M., Ek, A., Ekstrom, T., Gulich, A., Johansson, L. E., Karlsson, O., Kumlin, M., Martling, I., Skedinger, M., Amsterdam institute for Infection and Immunity, and Pulmonology

Subjects
2. Zero hunger, Pulmonary and Respiratory Medicine, Pediatrics, medicine.medical_specialty, Exacerbation, business.industry, medicine.disease, Electronic diary, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, 030228 respiratory system, Asthma Control Questionnaire, medicine, Sputum, Medical history, 030212 general & internal medicine, medicine.symptom, business, Body mass index, Lung function, Asthma
Abstract

Background Objective measures are required that may be used as a proxy for exacerbations in asthma. The aim was to determine the sensitivity and specificity of electronic diary data to detect severe exacerbations (SEs) of asthma. A secondary aim was to identify phenotypic variables associated with a higher risk of exacerbation. Methods In the BIOAIR study, 169 patients with asthma (93 severe (SA); 76 mild to moderate (MA)) recorded lung function, symptoms and medication use in electronic diaries for 1 year. Data were analysed using receiver-operator characteristics curves and related to physician-diagnosed exacerbations. Medical history and baseline clinical data were used to assess risk of exacerbation. Results Of 122 physician-diagnosed exacerbations, 104 occurred in the SA group (1.1 per patient/year), 18 in the MA group (0.2 per patient/year) and 63 were severe using American Thoracic Society/European Respiratory Society criteria. During exacerbations, peak expiratory flow (PEF) and forced expiratory volume in 1 s significantly decreased, whereas day and night symptoms significantly increased. An algorithm combining a 20% decrease in PEF or a 20% increase in day symptoms on 2 consecutive days was able to detect SEs with 65% sensitivity and 95% specificity. The strongest risk factors for SEs were low Asthma Control Questionnaire score, sputum eosinophils ≥3%, body mass index >25 and low quality of life (St George9s Respiratory Questionnaire), with ORs between 3.61 and 2.22 (p Conclusions Regular electronic monitoring of PEF and asthma symptoms provides an acceptable sensitivity and specificity for the detection of SEs and may be suitable for personal internet-based monitoring of asthma control.

Published
2013

37. Release of prostaglandin D2 and leukotriene C4 in response to hyperosmolar stimulation of mast cells.

Author

Gulliksson, M., Palmberg, L., Nilsson, G., Ahlstedt, S., and Kumlin, M.

Subjects
MAST cells, PROSTAGLANDINS, LEUKOTRIENES, HISTAMINE, IMMUNOGLOBULIN E
Abstract

Background: Mannitol-induced bronchoconstriction in subjects with exercise-induced asthma is associated with increased urinary excretion of 9 α, 11 β-PGF2, a metabolite of prostaglandin D2 (PGD2) serving as a mast cell marker. It has however been questioned whether or not human mast cells release PGD2 and leukotriene C4 (LTC4) after osmotic challenge with mannitol in vitro. Methods: Cord blood-derived human mast cells were stimulated osmotically, immunologically or with a combination of both. Supernatants were analysed for PGD2, LTC4 and histamine contents with enzyme immunoassays. Results: Significant release of de novo synthesized eicosanoids, predominantly PGD2 [12 (8.8, 14) pmol/106cells; median (25th, 75th percentile) but also LTC4 (0.1 (0.08, 0.15) pmol/106 cells] were found in mast cells in vitro in response to 0.7 M mannitol stimulation. A massive release of histamine [70 (5.3)% of total; mean (SEM)] was also found. There were no correlations between the levels of released mediators after mannitol stimulation. In contrast, there was a correlation between release of PGD2 and LTC4, following immunological stimulation. Conclusion: The findings support that hyperosmolar challenge activates mast cells, but different than antigen stimulation. [ABSTRACT FROM AUTHOR]

Published
2006
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39. Relation between bronchial responsiveness to inhaled leukotriene D4 and markers of leukotriene biosynthesis.

Author

Gyllfors, P., Kumlin, M., Dahlén, S.-E., Gaber, F., Ehrs, P.-O., and Dahlén, B.

Subjects
*LEUKOTRIENES, *ARACHIDONIC acid, *EICOSANOIC acid derivatives, *OBSTRUCTIVE lung diseases, *CLINICAL trials, *MEDICAL research
Abstract

Background: While clinical trials with antileukotrienes have shown overall beneficial effects in asthma, the factors that determine leukotriene dependent asthma are still unclear. A study was undertaken to determine whether or not leukotriene responsiveness in the airways correlates with endogenous leukotriene biosynthesis. Methods: Bronchial responsiveness to leukotriene (LT) D4 was assessed as PD20FEV1 in 20 subjects with mild asthma and 10 healthy controls, and compared with bronchial responsiveness to methacholine and two global measures of leukotriene production-urinary LTB4 and ex vivo production of LTB4 in whole blood. Results: In patients with asthma the bronchoconstrictor activity of LTD4 was about 1300 times greater than methacholine (geometric mean PD20 0.69 nmol v 887 nmol). Ihose who were most responsive to LTD4 were relatively less responsive to methacholine (p<0.01). There was, however, no correlation between bronchial responsiveness to LTD4 and urinary LTE< or blood ex vivo LTB4 levels in asthmatic subjects or healthy controls. Subjects with asthma treated with inhaled corticosteroids produced higher levels of LTB4 (p<0.05). Conclusions: General measures of leukotriene production cannot predict bronchial responsiveness to LTD4. The unique bronchoconstrictive potency of LTD4 on human airways may relate to the locally regulated expression of the cysteinyl LT1 receptor. [ABSTRACT FROM AUTHOR]

Published
2005
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41. Validation and application of a new simple strategy for measurements of urinary leukotriene E4 in humans.

Author

Kumlin, M., Stensvad, F., Larsson, L., Dahlén, B., and Dahlen, S.-E.

Subjects
*LEUKOTRIENES, *ENZYME-linked immunosorbent assay, *URINALYSIS, *ASTHMATICS, *ANTIGENS, *ALLERGIES
Abstract

To monitor endogenous production of cysteinyl-containing leukotrienes, the end- metabolite leukotriene F4 (LTF4) was analysed in urine. Results obtained with a sensitive enzyme immunoassay (EIA), performed on crude urine samples correlated well with data obtained from a previously reported radioimmunoassay. Enzyme immunoassay analysis of unextracted urine was justified by an excellent agreement between analyses in crude samples and measurements achieved after purification on solid phase extraction followed by separation on reversed-phase high performance liquid chromatography. Moreover, LTF4 was stable in urine samples stored at -20°C, for months without the addition of preservatives. The stability of LTE4 in urine was not improved by addition of the antioxidant 4-hydroxy-TEMPO and pH adjustment to 9. As assessed by EIA analysis in crude urine samples. baseline values for urinary leukotriene E4 were not significantly different between atopic asthmatic subjects and non-asthmatic individuals, and there was no diurnal variation in urinary excretion of LTE4 in healthy subjects. However, we confirmed earlier data on significantly higher basal levels of urinary LTE4 in aspirin-intolerant asthmatics. In addition, a post- challenge increase in urinary LTE4 levels was detected in association with allergen-induced airway obstruction in atopic asthmatics. The per cent increase in urinary LTE4 was similar, irrespective of whether the samples were purified or not prior to EIA. Thus, combined with random validation by high performance liquid chromatography. the strategy of direct EIA of serially diluted urine samples was found to he a good index of in vivo production of leukotrienes. This was further reinforced by the demonstration that pretreatment with the leukotriene biosynthesis inhibitor Bay × 1005 inhibited the post allergen-challenge increase in urinary LTE4 as shown both with unpurified and purified samples. [ABSTRACT FROM AUTHOR]

Published
1995
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43. Identification and biological activity of dihydro-leukotriene B4: A prominent metabolite of leukotriene B4in the human lung

Author

Kumlin, M., Falck, J.R., Raud, J., Harada, Y., Dahlén, S.-E., and Granström, E.

Abstract

Exogenous [3H]leukotriene B4(LTB4) was converted into several polar and non-polar metabolites in the chopped human lung. One of the major metabolites was identified as 5(S),12-dihydroxy-6,8,14-eicosatrienoic acid (10,11-dihydro-LTB4) by means of co-chromatography with authentic standards, ultraviolet spectrometry and gas chromatography-mass spectrometry. Analysis on chiral straight phase HPLC revealed the presence of both the 12(S) and 12(R) epimers of dihydro-LTB4. Dihydro-LTB4was also formed from endogenously generated LTB4in ionophore A23187 stimulated incubations. The dihydro metabolites were approximately 100 times less potent than LTB4in causing guinea pig lung strip contraction and leukocyte-dependent inflammation in the hamster cheek pouch in vivo.

Published
1990
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44. Increased urinary excretion of the prostaglandin D"2 metabolite 9@a,11@b-prostaglandin F"2 after aspirin challenge supports mast cell activation in aspirin-induced airway obstruction

Author

O'Sullivan, S., Dahlen, B., Dahlen, S.E., and Kumlin, M.

Abstract

Prostaglandin (PG)D"2 is a major product of arachidonic acid metabolism in pulmonary mast cells. We therefore attempted to determine whether measurement of the stable urinary metabolite of PGD"2, 9@a,11@b-PGF"2, could serve as a marker of mast cell activation in the lungs. A commercially available enzyme immunoassay was validated and found to be specific and sensitive when applied to unpurified urine. There was no diurnal variation in the levels of 9@a,11@b-PGF"2 in healthy volunteers. Morning baseline values of urinary 9@a,11@b-PGF"2 were measured in three groups-healthy volunteers (n = 9), patients with atopic asthma (n = 14), and aspirin-intolerant patients with asthma (n = 12)-and found to be very similar, 54 +/- 9, 62 +/- 6, and 71 +/- 15 ng/mmol creatinine, respectively (means +/- SEM). Urinary excretion of 9@a,11@b-PGF"2 was increased threefold immediately after allergen-induced bronchoconstriction in nine patients with atopic asthma. Bronchial challenge with inhaled lysine aspirin in eight aspirin-intolerant patients with asthma produced bronchoconstriction without extrapulmonary symptoms and was also followed by a significant increase in the urinary excretion of 9@a,11@b-PGF"2. In addition, challenge with a higher dose of aspirin produced an even greater increase in urinary 9@a,11@b-PGF"2, supporting dose-dependent release of PGD"2 during aspirin-induced bronchoconstriction. In contrast, the postchallenge levels of urinary 9@a,11@b-PGF"2 were not increased when bronchoconstriction was induced by histamine challenge in the aspirin-intolerant patients with asthma. The study confirms mast cell involvement in allergen-induced bronchoconstriction and provides novel data, which strongly support the hypothesis that pulmonary mast cells are activated during aspirin-induced airway obstruction. It is finally suggested that measurement of urinary 9@a,11@b-PGF"2 with enzyme immunoassay may be used as a new noninvasive strategy to monitor mast cell activation in vivo. (J ALLERGY CLIN IMMUNOL 1996;98:421-32.)

Published
1996
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45. Distribution of Edwardsiella ictaluriin California

Author

Chen, M. F., Henry-Ford, D., Kumlin, M. E., Key, M. L., Light, T. S., Cox, W. T., and Modin, J. C.

Abstract

Wild and domestic populations of channel catfish Ictalurus punctatuswere examined to determine the distribution of the disease called enteric septicemia of catfish (ESC) in California. The causative agent of ESC, Edwardsiella ictaluri, was isolated from five separate sites in California. Two of these isolations were from rectal swabs of asymptomatic fish, confirming that a carrier state may exist. Normal-appearing fish with serum antibody titer to E. ictaluriwere commonly found in domestic channel catfish populations, suggesting that many fish become infected but recover. Wild channel catfish with antibody to E. ictaluriwere also found in major reservoirs and water distribution canals. Edwardsiella ictaluriappears to be widely distributed within California.

Published
1994
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48. Acute BVDV-2 infection in beef calves delays humoral responses to a non-infectious antigen challenge

Author

Mccorkell, R., Horsman, S. R., Wynne-Edwards, K., Muench, G., Drunen Littel-Van Den Hurk, S., Waeckerlin, R., Eschbaumer, M., Dardari, R., Chaiyakul, M., Gajda, P., Czub, M., Frank van der Meer, Bauer, A., Brown, D., Burn, J., Duke, I., Ford, K., Frey, C., Gordon, H., Graham, E., Houston, I., Janzen, S., Knoll, H., Kumlin, M., Lam, W., Lockhart, S., Lowe, E., Mcdonal, K., Mcmurray, J., Mitchell, K., Mizen, K., Neat, S., Oliver, V., Radics, S., Riphagen, K., Risling, M., Robinson, A., Romanow, J., Schonknecht, J., Spence, E., Stalwick, J., Stephens, H., Weleschuc, M., Woodman, J., Wilson, J., Biernaskie, J., Caulkett, J., Chernick, A., Colangeli, L., Dow, N., Finney, C., Hawes, W., Hecker, K., Kozak, K., Law, S., Mowat, D., O Brien, N., Pinkham, S., Sooley, T., Stevens, T., Windeyer, C., Wolfe, S., and Yates, R.

49. Use of tritium labeled amino acid conjugates of prostaglandins and thromboxanes as labeled ligands in prostanoid radioimmunoassay

Author

Lidia Sautebin, Maria Kumlin, Hans Kindahl, Elisabeth Granström, Sautebin, Lidia, Kindahl, H., Kumlin, M., and Granstrom, E.

Subjects
Thromboxane, Radioimmunoassay, Heterologous, Prostaglandin, Ligands, Tritium, Binding, Competitive, Biochemistry, chemistry.chemical_compound, Endocrinology, Amino Acids, Chromatography, High Pressure Liquid, chemistry.chemical_classification, Chromatography, Thromboxanes, Prostanoid, respiratory system, Amino acid, chemistry, Eicosanoid, Prostaglandins, lipids (amino acids, peptides, and proteins), Chromatography, Thin Layer, circulatory and respiratory physiology
Abstract

Conjugates of prostaglandins and thromboxanes with tritium labeled amino acids were prepared and employed as labeled ligands in prostaglandin and thromboxane radioimmunoassays. Assays for PGF2 alpha, 15-keto-13, 14-dihydro-PGF2 alpha, TXB2 and 15-keto-13,14-dihydro-TXB2 were evaluated in comparative studies using either these heterologous ligands or the corresponding homologous tritiated eicosanoid as tracers. Binding properties for the respective antibodies were found to be similar using either tracer. Three biological studies were also conducted, viz. study of the release of TXB2 during collagen induced platelet aggregation, of 15-keto-13,14-dihydro-TXB2 during guinea pig pulmonary anaphylaxis, and of PGF2 alpha (measured as 15-keto-13,14-dihydro-PGF2 alpha in peripheral plasma) during bovine luteolysis. The analyses gave comparable results using either the heterologous or the homologous assay. Thus, this type of labeled prostanoid conjugates may serve as a convenient alternative to homologous tracers in radioimmunoassay. Heterologous tracers may even in certain cases provide the only simple solution to the problem of preparing a labeled ligand of high specific activity.

Published
1985
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50. Mucosal LTE 4 , PGD 2 and 15(S)-HETE as potential prognostic markers for polyp recurrence in chronic rhinosinusitis.

Author

Nordström A, Jangard M, Ryott M, Tang X, Svedberg M, and Kumlin M

Subjects
Humans, Female, Male, Middle Aged, Chronic Disease, Adult, Prognosis, Nasal Mucosa metabolism, Nasal Mucosa pathology, Eosinophils metabolism, Eosinophils pathology, Mast Cells metabolism, Mast Cells pathology, Rhinosinusitis, Sinusitis metabolism, Sinusitis pathology, Sinusitis surgery, Sinusitis diagnosis, Nasal Polyps metabolism, Nasal Polyps pathology, Nasal Polyps surgery, Nasal Polyps genetics, Leukotriene E4 metabolism, Hydroxyeicosatetraenoic Acids metabolism, Rhinitis metabolism, Rhinitis pathology, Rhinitis diagnosis, Rhinitis surgery, Biomarkers metabolism, Recurrence, Prostaglandin D2 metabolism
Abstract

Background: Altered biosynthesis of eicosanoids is linked to type 2 inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP), but their role in recalcitrant NPs is unclear., Objectives: We sought to identify endotypes that are linked to recalcitrant CRSwNP, based on eicosanoids, their biosynthetic enzymes, and receptors as well as cytokines and the presence of eosinophils and mast cells in recurrent NPs., Methods: Mucosal tissue collected at the time of sinus surgery from 54 patients with CRSwNP and 12 non-CRS controls were analysed for leukotriene (LT) E4, prostaglandin (PG) D2, 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) and 17 cytokines with ELISAs and Bio-Plex immunoassays. Patient subgroups were identified by cluster analysis and the probability of NP recurrence were tested with logistic regression analyses. Gene expressions were analysed with qPCR. Tryptase and eosinophil-derived neurotoxin (EDN) were measured with ELISAs as indications of the presence of mast cells and eosinophils, respectively., Results: Clustering of patients showed that an inflammatory signature characterised by elevated LTE 4 , PGD 2 , 15(S)-HETE and IL-13 was associated with NP recurrence. Previous NP surgery as well as aspirin-exacerbated respiratory disease were significantly more common among these patients. Expression of cyclooxygenase 1 was the only gene associated with NP recurrence. Levels of EDN, but not tryptase, were significantly higher in patients with recurrent NPs., Conclusion: Distinguishing endotypes that include LTE 4 , PGD 2 , 15HETE and conventional biomarkers of type 2 inflammation could help predict recurrent nasal polyposis and thus identify cases of recalcitrant CRSwNP., Competing Interests: Declaration of Competing Interest None of the authors have any conflict of interest to declare., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2024
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