// +author:k arlt +author:arlt var _ajax_res = { hits: 7, first: 0, results: [ {userid:"julia.kehr", "articletype":"article","pages":"319-325","author":"K Arlt, S Brandt, J Kehr","year":"2001","title":"Amino acid analysis in five pooled single plant cell samples using capillary electrophoresis coupled to laser-induced fluorescence detection.","month":"Aug","journal":"J Chromatogr A","publisher":"","volume":"926","number":"2","note":"","tags":"Amino Acids,Cucurbita,Electrophoresis, Capillary,Lasers,Sensitivity and Specificity,Spectrometry, Fluorescence","booktitle":"","editor":"","abstract":"In this study 21 amino acid standards, samples of pure phloem sap and samples of pooled mesophyll cells were derivatized with fluorescein isothiocyanate, separated by capillary electrophoresis and detected with laser-induced fluorescence at 488 nm. Two different background electrolytes, a sodium borate buffer containing sodium dodecyl sulfate and a sodium borate buffer containing alpha-cyclodextrin, were used for the separation. Using the sodium dodecyl sulfate buffer, 14 amino acid standards could be separated, spiking identified 12 amino acids in pure phloem sap and 13 amino acids in pooled mesophyll cells. With the alpha-cyclodextrin containing background electrolyte, a resolution of 20 amino acid standards could be attained, 17 amino acids in pure phloem sap and 10 amino acids in mesophyll cells could be assigned. Leucine and isoleucine comigrated in both buffer systems. All separations were performed with a voltage of +20 kV and completed within 30 min. The detection limits obtained were in the fmol range for the sodium dodecyl sulfate and in the pmol range for the alpha-cyclodextrin background electrolyte. Compared to the one published capillary electrophoresis-based method for the determination of amino acids from few plant cells, the procedure described here allows very high sensitivity due to the use of laser-induced fluorescence detection and opens the possibility to dilute and measure pl samples with an fully automated, commercially available CE system.","address":"","school":"","issn":"0021-9673","doi":"","isi":"","pubmed":"11556336","key":"Arlt2001","howpublished":"","urllink":"","refid":22} , {userid:"m.biehl", "articletype":"inproceedings","pages":"","author":"S Ghosh, E S Baranowski, M Biehl, W Arlt, P Tino, K Bunte","year":"2017","title":"Computer aided diagnosis of inborn steroidegenic disorders (abstract)","month":"","journal":"","publisher":"","volume":"MLR-01-2017","number":"","note":"","tags":"","booktitle":"Proc. Mittweida Workshop on Computational Intelligence MiWoCI","editor":"F.-M. Schleif, T Villmann","abstract":"","address":"","school":"","issn":"","doi":"","isi":"","pubmed":"","key":"ghosh2017miwoci","howpublished":"","urllink":"","refid":1074,"weight":1074} , {userid:"m.biehl", "articletype":"inproceedings","pages":"","author":"S Ghosh, E S Baranowski, R van Veen, G.-J. de Vries, M Biehl, W Arlt, P Tino, K Bunte","year":"2017","title":"Computer aided diagnosis under the influence of heterogeneous data and imbalanced classes","month":"","journal":"","publisher":"","volume":"","number":"","note":"","tags":"","booktitle":"ICT.Open 2017","editor":"","abstract":"","address":"","school":"","issn":"","doi":"","isi":"","pubmed":"","key":"ghosh2017computer","howpublished":"","urllink":"","refid":1073,"weight":1073} , {userid:"m.biehl", "articletype":"article","pages":"","author":"E Baranowski, K Bunte, C H L Shackleton, A E Tayler, B A Hughes, M Biehl, P Tino, T Guran, W Arlt","year":"2017","title":"Steroid metabolomics for accurate and rapid diagnosis of inborn steroidogenic disorders","month":"","journal":"Endocrine Abstracts","publisher":"","volume":"49","number":"","note":"","tags":"","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"","doi":"","isi":"","pubmed":"","key":"Baranowski2017","howpublished":"","urllink":"","refid":1079,"weight":1079} , {userid:"m.biehl", "articletype":"inproceedings","pages":"199-204","author":"S Ghosh, E Baranowski, R van Veen, G.-J. de Vries, M Biehl, W Arlt, P Tino, K Bunte","year":"2017","title":"Comparison of strategies to learn from imbalanced classes for computer aided diagnosis of inborn steroidogenic disorders","month":"","journal":"","publisher":"Ciaco - i6doc.com","volume":"","number":"","note":"","tags":"","booktitle":"25th European Symposium on Artificial Neural Networks, Computational Intelligence and Machine Learning, ESANN 2017","editor":"M Verleysen","abstract":"","address":"","school":"","issn":"","doi":"","isi":"","pubmed":"","key":"ghosh2017comparison","howpublished":"","urllink":"","refid":1071,"weight":1071} , {userid:"m.biehl", "articletype":"article","pages":"","author":"I Bancos, A Taylor, V Chortis, A Sitch, K Lank, A Prete, M Terzolo, M Fassnacht, M Quinkler, D Kastelan, D Vassiliadi, F Beuschlein, U Ambroziak, M Biehl, J Deeks, W Arlt","year":"2018","title":"Urine steroid metabolomics as a diagnostic tool for detection of adrenocortical malignancy - a prospective test validation study","month":"","journal":"Endocrine Abstracts","publisher":"","volume":"56","number":"","note":"","tags":"","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"","doi":"","isi":"","pubmed":"","key":"Bancos2018","howpublished":"","urllink":"","refid":1063,"weight":1063} , {userid:"m.biehl", "refid":"1058","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Steroid metabolome analysis reveals prevalent glucocorticoid excess in primary aldosteronism","year":"2017","author":"Wiebke Arlt, Katharina Lang, Alice J Sitch, Anna S Dietz, Yara Rhayem, Irina Bancos. Annette Feuchtinger, Vasileios Chortis, Lorna C Gilligan, Philippe Ludwig, Anna Riester, Evelyn Asbach, Beverly A Hughes, Donna M O'\u0099Neil, Martin Bidlingmaier, Jeremy W Tomlinson, Zaki K Hassan-Smith, D Aled Rees, Christian Adolf, Stefanie Hahner, Marcus Quinkler, Tanja Dekkers, Jaap Deinum, Michael Biehl, Brian G Keevil, Cedric H L Shackleton, Jonathan J Deeks, Axel K Walch, Felix Beuschlein, Martin Reincke","journal":"JCI Insight","volume":"2","number":"8","pages":"","month":"05","doi":"10.1172\/jci.insight.93136","pubmed":"","pdflink":"","urllink":"http:\/\/insight.jci.org\/articles\/view\/93136","abstract":"BACKGROUND. Adrenal aldosterone excess is the most common cause of secondary hypertension and is associated with increased cardiovascular morbidity. However, adverse metabolic risk in primary aldosteronism extends beyond hypertension, with increased rates of insulin resistance, type 2 diabetes, and osteoporosis, which cannot be easily explained by aldosterone excess. METHODS. We performed mass spectrometry\u00e2\u0080\u0093based analysis of a 24-hour urine steroid metabolome in 174 newly diagnosed patients with primary aldosteronism (103 unilateral adenomas, 71 bilateral adrenal hyperplasias) in comparison to 162 healthy controls, 56 patients with endocrine inactive adrenal adenoma, 104 patients with mild subclinical, and 47 with clinically overt adrenal cortisol excess. We also analyzed the expression of cortisol-producing CYP11B1 and aldosterone-producing CYP11B2 enzymes in adenoma tissue from 57 patients with aldosterone-producing adenoma, employing immunohistochemistry with digital image analysis. RESULTS. Primary aldosteronism patients had significantly increased cortisol and total glucocorticoid metabolite excretion (all P < 0.001), only exceeded by glucocorticoid output in patients with clinically overt adrenal Cushing syndrome. Several surrogate parameters of metabolic risk correlated significantly with glucocorticoid but not mineralocorticoid output. Intratumoral CYP11B1 expression was significantly associated with the corresponding in vivo glucocorticoid excretion. Unilateral adrenalectomy resolved both mineralocorticoid and glucocorticoid excess. Postoperative evidence of adrenal insufficiency was found in 13 (29%) of 45 consecutively tested patients. CONCLUSION. Our data indicate that glucocorticoid cosecretion is frequently found in primary aldosteronism and contributes to associated metabolic risk. Mineralocorticoid receptor antagonist therapy alone may not be sufficient to counteract adverse metabolic risk in medically treated patients with primary aldosteronism. FUNDING. Medical Research Council UK, Wellcome Trust, European Commission.","note":"","tags":"","weight":1058,"publisher":"The American Society for Clinical Investigation","booktitle":"","editor":"","address":"","school":"","issn":"","isi":"","key":"ref10.1172\/jci.insight.93136","howpublished":"http:\/\/insight.jci.org\/articles\/view\/93136"} ] } ; ajaxResultsLoaded(_ajax_res);