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1. Rivaroxaban Compared with Standard Anticoagulants for the Treatment of Acute Venous Thromboembolism in Children: a Randomised, Controlled, Phase 3 Trial

Author

Male, C., Lensing, A. W. A., Palumbo, J. S., Kumar, R., Nurmeev, I., Hege, K., Bonnet, D., Connor, P., Hooimeijer, H. L., Torres, M., Chan, A. K. C., Kenet, G., Holzhauer, S., Santamaría, A., Amedro, P., Chalmers, E., Simioni, P., Bhat, R. V., Yee, D. L., Lvova, O., Beyer-Westendorf, J., Biss, T. T., Martinelli, I., Saracco, P., Peters, M., Kállay, K., Gauger, C. A., Massicotte, M. P., Young, G., Pap, A. F., Majumder, M., Smith, W. T., Heubach, J. F., Berkowitz, S. D., Thelen, K., Kubitza, D., Crowther, M., Prins, M. H., Monagle, P., Molinari, A. C., Nowak, Göttl, U., Chain, J., Robertson, J., Thom, K., Streif, W., Schwarz, R., Schmitt, K., Grangl, G., Van Damme, A., Maes, P., Labarque, V., Petrilli, A., Loggeto, S., Azeka, E., Brandao, L., Le, D., Sabapathy, C., Giordano, P., Wu, R., Ding, J., Huang, W., Mao, J., Lähteenmäki, P., Decramer, S., Bernig, T., Chada, M., Chan, G., Kally, K., Nolan, B., Revel-Vilk, S., Tamary, H., Levin, C., Tormene, D., Abbattista, M., Artoni, A., Ikeyama, T., Inuzuka, R., Yasukochi, S., Morales Soto, M., Solis Labastida, K. A., Suijker, M. H., Bartels, M., Tamminga, R. Y., Van Ommen, C. H., Te Loo, D. M., Anjos, R., Zubarovskaya, L., Popova, N., Samochatova, E., Belogurova, M., Svirin, P., Shutova, T., Lebedev, V., Barbarash, O., Koh, P. L., Mei, J. C., Podracka, L., Berrueco, R., Fernandez, M. F., Frisk, T., Grunt, S., Rischewski, J., Albisetti-Pedroni, M., Antmen, A., Tokgoz, H., Karakas, Z., Motwani, J., Williams, M., Grainger, J., Payne, J., Richards, M., Baird, S., Bhatnagar, N., Aramburo, A., Crary, S., Wynn, T., Carpenter, S., Ahuja, S., Goldenberg, N., Woods, G., Godder, K., Scott-Emuakpor, A., Roach, G., Raffini, L., Shah, N., Shah, S., Thornburg, C., Zia, A., Berkow, R., Male, C., Lensing, A. W. A., Palumbo, J. S., Kumar, R., Nurmeev, I., Hege, K., Bonnet, D., Connor, P., Hooimeijer, H. L., Torres, M., Chan, A. K. C., Kenet, G., Holzhauer, S., Santamaría, A., Amedro, P., Chalmers, E., Simioni, P., Bhat, R. V., Yee, D. L., Lvova, O., Beyer-Westendorf, J., Biss, T. T., Martinelli, I., Saracco, P., Peters, M., Kállay, K., Gauger, C. A., Massicotte, M. P., Young, G., Pap, A. F., Majumder, M., Smith, W. T., Heubach, J. F., Berkowitz, S. D., Thelen, K., Kubitza, D., Crowther, M., Prins, M. H., Monagle, P., Molinari, A. C., Nowak, Göttl, U., Chain, J., Robertson, J., Thom, K., Streif, W., Schwarz, R., Schmitt, K., Grangl, G., Van Damme, A., Maes, P., Labarque, V., Petrilli, A., Loggeto, S., Azeka, E., Brandao, L., Le, D., Sabapathy, C., Giordano, P., Wu, R., Ding, J., Huang, W., Mao, J., Lähteenmäki, P., Decramer, S., Bernig, T., Chada, M., Chan, G., Kally, K., Nolan, B., Revel-Vilk, S., Tamary, H., Levin, C., Tormene, D., Abbattista, M., Artoni, A., Ikeyama, T., Inuzuka, R., Yasukochi, S., Morales Soto, M., Solis Labastida, K. A., Suijker, M. H., Bartels, M., Tamminga, R. Y., Van Ommen, C. H., Te Loo, D. M., Anjos, R., Zubarovskaya, L., Popova, N., Samochatova, E., Belogurova, M., Svirin, P., Shutova, T., Lebedev, V., Barbarash, O., Koh, P. L., Mei, J. C., Podracka, L., Berrueco, R., Fernandez, M. F., Frisk, T., Grunt, S., Rischewski, J., Albisetti-Pedroni, M., Antmen, A., Tokgoz, H., Karakas, Z., Motwani, J., Williams, M., Grainger, J., Payne, J., Richards, M., Baird, S., Bhatnagar, N., Aramburo, A., Crary, S., Wynn, T., Carpenter, S., Ahuja, S., Goldenberg, N., Woods, G., Godder, K., Scott-Emuakpor, A., Roach, G., Raffini, L., Shah, N., Shah, S., Thornburg, C., Zia, A., and Berkow, R.

Abstract

Background: Treatment of venous thromboembolism in children is based on data obtained in adults with little direct documentation of its efficacy and safety in children. The aim of our study was to compare the efficacy and safety of rivaroxaban versus standard anticoagulants in children with venous thromboembolism. Methods: In a multicentre, parallel-group, open-label, randomised study, children (aged 0–17 years) attending 107 paediatric hospitals in 28 countries with documented acute venous thromboembolism who had started heparinisation were assigned (2:1) to bodyweight-adjusted rivaroxaban (tablets or suspension) in a 20-mg equivalent dose or standard anticoagulants (heparin or switched to vitamin K antagonist). Randomisation was stratified by age and venous thromboembolism site. The main treatment period was 3 months (1 month in children <2 years of age with catheter-related venous thromboembolism). The primary efficacy outcome, symptomatic recurrent venous thromboembolism (assessed by intention-to-treat), and the principal safety outcome, major or clinically relevant non-major bleeding (assessed in participants who received ≥1 dose), were centrally assessed by investigators who were unaware of treatment assignment. Repeat imaging was obtained at the end of the main treatment period and compared with baseline imaging tests. This trial is registered with ClinicalTrials.gov, number NCT02234843 and has been completed. Findings: From Nov 14, 2014, to Sept 28, 2018, 500 (96%) of the 520 children screened for eligibility were enrolled. After a median follow-up of 91 days (IQR 87–95) in children who had a study treatment period of 3 months (n=463) and 31 days (IQR 29–35) in children who had a study treatment period of 1 month (n=37), symptomatic recurrent venous thromboembolism occurred in four (1%) of 335 children receiving rivaroxaban and five (3%) of 165 receiving standard anticoagulants (hazard ratio [HR] 0·40, 95% CI 0·11–1·41). Repeat imaging showed an improved eff

Published
2020

3. Dynamic changes of orexin A and leptin in obese children during body weight reduction

Author

Zamrazilová H, K Kotaska, Nevoral J, Jiří Bronský, Nedvídková J, Chada M, M Pechová, and R Průsa

Subjects
Leptin, Male, medicine.medical_specialty, Aging, Adolescent, Physiology, Body height, Radioimmunoassay, Neuropeptide, Nutritional Status, Body weight, Body Mass Index, Orexin-A, Internal medicine, Weight Loss, Medicine, Humans, Obesity, Insulin-Like Growth Factor I, Child, Orexins, business.industry, digestive, oral, and skin physiology, Body Weight, Neuropeptides, Intracellular Signaling Peptides and Proteins, Nutritional status, General Medicine, Plasma levels, medicine.disease, Body Height, Endocrinology, Female, business, hormones, hormone substitutes, and hormone antagonists
Abstract

In this study, we describe changes of plasma levels of the hypothalamic neuropeptide orexin A in obese children during the reduction of body weight and its relationship to other biochemical and anthropometrical parameters. We measured orexin A fasting plasma levels by the RIA method in 58 obese children--33 girls and 25 boys; mean age 13.1+/-0.38 years (range 7-18.5) before and after 5 weeks of weight-reduction therapy. Leptin, IGF-1, and IGFBP-3 levels were measured in all the subjects and were compared to orexin A levels and anthropometrical data. Average weight in subjects before weight-reduction was 74.2+/-2.79 kg and after weight-loss 67.4+/-2.60 kg (p

Published
2006

7. Improved measurement of the pseudoscalar decay constant [Formula Presented]

Author

Chada, M. (M.), Chan, S. (S.), Eigen, G. (G.), Miller, J.S. (J. S.), O’Grady, C. (C.), Schmidtler, M. (M.), Urheim, J. (J.), Weinstein, A.J. (A. J.), Würthwein, F. (F.), Bliss, D.W. (D. W.), Masek, G. (G.), Paar, H.P. (H. P.), Prell, S. (S.), Sharma, V. (V.), Asner, D.M. (D. M.), Gronberg, J. (J.), Hill, T.S. (T. S.), Lange, D.J. (D. J.), Morrison, R.J. (R. J.), Nelson, H.N. (H. N.), Nelson, T.K. (T. K.), Roberts, D. (D.), Ryd, A. (A.), Balest, R. (R.), Behrens, B.H. (B. H.), Ford, W.T. (W. T.), Park, H. (H.), Roy, J. (J.), Smith, J.G. (J. G.), Alexander, J.P. (J. P.), Baker, R. (R.), Bebek, C. (C.), Berger, B.E. (B. E.), Berkelman, K. (K.), Bloom, K. (K.), Boisvert, V. (V.), Cassel, D.G. (D. G.), Crowcroft, D.S. (D. S.), Dickson, M. (M.), von Dombrowski, S. (S.), Drell, P.S. (P. S.), Ecklund, K.M. (K. M.), Ehrlich, R. (R.), Foland, A.D. (A. D.), Gaidarev, P. (P.), Gibbons, L. (L.), Gittelman, B. (B.), Gray, S.W. (S. W.), Hartill, D.L. (D. L.), Heltsley, B.K. (B. K.), Hopman, P.I. (P. I.), Kandaswamy, J. (J.), Kim, P.C. (P. C.), Kreinick, D.L. (D. L.), Lee, T. (T.), Liu, Y. (Y.), Mistry, N.B. (N. B.), Ng, C.R. (C. R.), Nordberg, E. (E.), Ogg, M. (M.), Patterson, J.R. (J. R.), Peterson, D. (D.), Riley, D. (D.), Soffer, A. (A.), Valant-Spaight, B. (B.), Ward, C. (C.), Athanas, M. (M.), Avery, P. (P.), Jones, C.D. (C. D.), Lohner, M. (M.), Patton, S. (S.), Prescott, C. (C.), Yelton, J. (J.), Zheng, J. (J.), Brandenburg, G. (G.), Briere, R.A. (R. A.), Ershov, A. (A.), Gao, Y.S. (Y. S.), Kim, D.Y.-J. (D. Y.J.), Wilson, R. (R.), Yamamoto, H. (H.), Browder, T.E. (T. E.), Li, Y. (Y.), Rodriguez, J.L. (J. L.), Bergfeld, T. (T.), Eisenstein, B.I. (B. I.), Ernst, J. (J.), Gladding, G.E. (G. E.), Gollin, G.D. (G. D.), Hans, R.M. (R. M.), Johnson, E. (E.), Karliner, I. (I.), Marsh, M.A. (M. A.), Palmer, M. (M.), Selen, M. (M.), Thaler, J.J. (J. J.), Edwards, K.W. (Kenneth W.), Bellerive, A. (Alain), Janicek, R. (R.), MacFarlane, D.B. (D. B.), Patel, P.M. (P. M.), Sadoff, A.J. (A. J.), Ammar, R. (R.), Baringer, P. (P.), Bean, A. (A.), Besson, D. (D.), Coppage, D. (D.), Darling, C. (C.), Davis, R. (R.), Kotov, S. (S.), Kravchenko, I. (I.), Kwak, N. (N.), Zhou, L. (L.), Anderson, S. (S.), Kubota, Y. (Y.), Lee, S.J. (S. J.), O’Neill, J.J. (J. J.), Poling, R. (R.), Riehle, T. (T.), Smith, A. (A.), Alam, M.S. (M. S.), Athar, S.B. (S. B.), Ling, Z. (Z.), Mahmood, A.H. (A. H.), Timm, S. (S.), Wappler, F. (F.), Anastassov, A. (A.), Duboscq, J.E. (J. E.), Fujino, D. (D.), Gan, K.K. (K. K.), Hart, T. (T.), Honscheid, K. (K.), Kagan, H. (H.), Kass, R. (R.), Lee, J. (J.), Spencer, M.B. (M. B.), Sung, M. (M.), Undrus, A. (A.), Wolf, A. (A.), Zoeller, M.M. (M. M.), Nemati, B. (B.), Richichi, S.J. (S. J.), Ross, W.R. (W. R.), Severini, H. (H.), Skubic, P. (P.), Bishai, M. (M.), Fast, J. (J.), Hinson, J.W. (J. W.), Menon, N. (N.), Miller, D.H. (D. H.), Shibata, E.I. (E. I.), Shipsey, I.P.J. (I. P.J.), Yurko, M. (M.), Glenn, S. (S.), Johnson, S.D. (S. D.), Kwon, Y. (Y.), Roberts, S. (S.), Thorndike, E.H. (E. H.), Jessop, C.P. (C. P.), Lingel, K. (K.), Marsiske, H. (H.), Perl, M.L. (M. L.), Savinov, V. (V.), Ugolini, D. (D.), Wang, R. (R.), Zhou, X. (X.), Coan, T.E. (T. E.), Fadeyev, V. (V.), Korolkov, I. (I.), Maravin, Y. (Y.), Narsky, I. (I.), Shelkov, V. (V.), Staeck, J. (J.), Stroynowski, R. (R.), Volobouev, I. (I.), Ye, J. (J.), Artuso, M. (M.), Azfar, F. (F.), Efimov, A. (A.), Goldberg, M. (M.), He, D. (D.), Kopp, S. (S.), Moneti, G.C. (G. C.), Mountain, R. (R.), Schuh, S. (S.), Skwarnicki, T. (T.), Stone, S. (S.), Viehhauser, G. (G.), Xing, X. (X.), Bartelt, J. (J.), Csorna, S.E. (S. E.), Jain, V. (V.), McLean, K.W. (K. W.), Marka, S. (S.), Godang, R. (R.), Kinoshita, K. (K.), Lai, I.C. (I. C.), Pomianowski, P. (P.), Schrenk, S. (S.), Bonvicini, G. (G.), Cinabro, D. (D.), Greene, R. (R.), Perera, L.P. (L. P.), Zhou, G.J. (G. J.), Chada, M. (M.), Chan, S. (S.), Eigen, G. (G.), Miller, J.S. (J. S.), O’Grady, C. (C.), Schmidtler, M. (M.), Urheim, J. (J.), Weinstein, A.J. (A. J.), Würthwein, F. (F.), Bliss, D.W. (D. W.), Masek, G. (G.), Paar, H.P. (H. P.), Prell, S. (S.), Sharma, V. (V.), Asner, D.M. (D. M.), Gronberg, J. (J.), Hill, T.S. (T. S.), Lange, D.J. (D. J.), Morrison, R.J. (R. J.), Nelson, H.N. (H. N.), Nelson, T.K. (T. K.), Roberts, D. (D.), Ryd, A. (A.), Balest, R. (R.), Behrens, B.H. (B. H.), Ford, W.T. (W. T.), Park, H. (H.), Roy, J. (J.), Smith, J.G. (J. G.), Alexander, J.P. (J. P.), Baker, R. (R.), Bebek, C. (C.), Berger, B.E. (B. E.), Berkelman, K. (K.), Bloom, K. (K.), Boisvert, V. (V.), Cassel, D.G. (D. G.), Crowcroft, D.S. (D. S.), Dickson, M. (M.), von Dombrowski, S. (S.), Drell, P.S. (P. S.), Ecklund, K.M. (K. M.), Ehrlich, R. (R.), Foland, A.D. (A. D.), Gaidarev, P. (P.), Gibbons, L. (L.), Gittelman, B. (B.), Gray, S.W. (S. W.), Hartill, D.L. (D. L.), Heltsley, B.K. (B. K.), Hopman, P.I. (P. I.), Kandaswamy, J. (J.), Kim, P.C. (P. C.), Kreinick, D.L. (D. L.), Lee, T. (T.), Liu, Y. (Y.), Mistry, N.B. (N. B.), Ng, C.R. (C. R.), Nordberg, E. (E.), Ogg, M. (M.), Patterson, J.R. (J. R.), Peterson, D. (D.), Riley, D. (D.), Soffer, A. (A.), Valant-Spaight, B. (B.), Ward, C. (C.), Athanas, M. (M.), Avery, P. (P.), Jones, C.D. (C. D.), Lohner, M. (M.), Patton, S. (S.), Prescott, C. (C.), Yelton, J. (J.), Zheng, J. (J.), Brandenburg, G. (G.), Briere, R.A. (R. A.), Ershov, A. (A.), Gao, Y.S. (Y. S.), Kim, D.Y.-J. (D. Y.J.), Wilson, R. (R.), Yamamoto, H. (H.), Browder, T.E. (T. E.), Li, Y. (Y.), Rodriguez, J.L. (J. L.), Bergfeld, T. (T.), Eisenstein, B.I. (B. I.), Ernst, J. (J.), Gladding, G.E. (G. E.), Gollin, G.D. (G. D.), Hans, R.M. (R. M.), Johnson, E. (E.), Karliner, I. (I.), Marsh, M.A. (M. A.), Palmer, M. (M.), Selen, M. (M.), Thaler, J.J. (J. J.), Edwards, K.W. (Kenneth W.), Bellerive, A. (Alain), Janicek, R. (R.), MacFarlane, D.B. (D. B.), Patel, P.M. (P. M.), Sadoff, A.J. (A. J.), Ammar, R. (R.), Baringer, P. (P.), Bean, A. (A.), Besson, D. (D.), Coppage, D. (D.), Darling, C. (C.), Davis, R. (R.), Kotov, S. (S.), Kravchenko, I. (I.), Kwak, N. (N.), Zhou, L. (L.), Anderson, S. (S.), Kubota, Y. (Y.), Lee, S.J. (S. J.), O’Neill, J.J. (J. J.), Poling, R. (R.), Riehle, T. (T.), Smith, A. (A.), Alam, M.S. (M. S.), Athar, S.B. (S. B.), Ling, Z. (Z.), Mahmood, A.H. (A. H.), Timm, S. (S.), Wappler, F. (F.), Anastassov, A. (A.), Duboscq, J.E. (J. E.), Fujino, D. (D.), Gan, K.K. (K. K.), Hart, T. (T.), Honscheid, K. (K.), Kagan, H. (H.), Kass, R. (R.), Lee, J. (J.), Spencer, M.B. (M. B.), Sung, M. (M.), Undrus, A. (A.), Wolf, A. (A.), Zoeller, M.M. (M. M.), Nemati, B. (B.), Richichi, S.J. (S. J.), Ross, W.R. (W. R.), Severini, H. (H.), Skubic, P. (P.), Bishai, M. (M.), Fast, J. (J.), Hinson, J.W. (J. W.), Menon, N. (N.), Miller, D.H. (D. H.), Shibata, E.I. (E. I.), Shipsey, I.P.J. (I. P.J.), Yurko, M. (M.), Glenn, S. (S.), Johnson, S.D. (S. D.), Kwon, Y. (Y.), Roberts, S. (S.), Thorndike, E.H. (E. H.), Jessop, C.P. (C. P.), Lingel, K. (K.), Marsiske, H. (H.), Perl, M.L. (M. L.), Savinov, V. (V.), Ugolini, D. (D.), Wang, R. (R.), Zhou, X. (X.), Coan, T.E. (T. E.), Fadeyev, V. (V.), Korolkov, I. (I.), Maravin, Y. (Y.), Narsky, I. (I.), Shelkov, V. (V.), Staeck, J. (J.), Stroynowski, R. (R.), Volobouev, I. (I.), Ye, J. (J.), Artuso, M. (M.), Azfar, F. (F.), Efimov, A. (A.), Goldberg, M. (M.), He, D. (D.), Kopp, S. (S.), Moneti, G.C. (G. C.), Mountain, R. (R.), Schuh, S. (S.), Skwarnicki, T. (T.), Stone, S. (S.), Viehhauser, G. (G.), Xing, X. (X.), Bartelt, J. (J.), Csorna, S.E. (S. E.), Jain, V. (V.), McLean, K.W. (K. W.), Marka, S. (S.), Godang, R. (R.), Kinoshita, K. (K.), Lai, I.C. (I. C.), Pomianowski, P. (P.), Schrenk, S. (S.), Bonvicini, G. (G.), Cinabro, D. (D.), Greene, R. (R.), Perera, L.P. (L. P.), and Zhou, G.J. (G. J.)

Abstract

We present a new determination of [Formula Presented] using 5 million [Formula Presented] events obtained with the CLEO II detector. Our value is derived from our new measured ratio [Formula Presented]. Using [Formula Presented]%, we extract [Formula Presented]. We compare this result with various model calculations.

Published
1998
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9. Improved measurement of the pseudoscalar decay constantfDs

Author

Chada, M., primary, Chan, S., additional, Eigen, G., additional, Miller, J. S., additional, O’Grady, C., additional, Schmidtler, M., additional, Urheim, J., additional, Weinstein, A. J., additional, Würthwein, F., additional, Bliss, D. W., additional, Masek, G., additional, Paar, H. P., additional, Prell, S., additional, Sharma, V., additional, Asner, D. M., additional, Gronberg, J., additional, Hill, T. S., additional, Lange, D. J., additional, Morrison, R. J., additional, Nelson, H. N., additional, Nelson, T. K., additional, Roberts, D., additional, Ryd, A., additional, Balest, R., additional, Behrens, B. H., additional, Ford, W. T., additional, Park, H., additional, Roy, J., additional, Smith, J. G., additional, Alexander, J. P., additional, Baker, R., additional, Bebek, C., additional, Berger, B. E., additional, Berkelman, K., additional, Bloom, K., additional, Boisvert, V., additional, Cassel, D. G., additional, Crowcroft, D. S., additional, Dickson, M., additional, von Dombrowski, S., additional, Drell, P. S., additional, Ecklund, K. M., additional, Ehrlich, R., additional, Foland, A. D., additional, Gaidarev, P., additional, Gibbons, L., additional, Gittelman, B., additional, Gray, S. W., additional, Hartill, D. L., additional, Heltsley, B. K., additional, Hopman, P. I., additional, Kandaswamy, J., additional, Kim, P. C., additional, Kreinick, D. L., additional, Lee, T., additional, Liu, Y., additional, Mistry, N. B., additional, Ng, C. R., additional, Nordberg, E., additional, Ogg, M., additional, Patterson, J. R., additional, Peterson, D., additional, Riley, D., additional, Soffer, A., additional, Valant-Spaight, B., additional, Ward, C., additional, Athanas, M., additional, Avery, P., additional, Jones, C. D., additional, Lohner, M., additional, Patton, S., additional, Prescott, C., additional, Yelton, J., additional, Zheng, J., additional, Brandenburg, G., additional, Briere, R. A., additional, Ershov, A., additional, Gao, Y. S., additional, Kim, D. Y.-J., additional, Wilson, R., additional, Yamamoto, H., additional, Browder, T. E., additional, Li, Y., additional, Rodriguez, J. L., additional, Bergfeld, T., additional, Eisenstein, B. I., additional, Ernst, J., additional, Gladding, G. E., additional, Gollin, G. D., additional, Hans, R. M., additional, Johnson, E., additional, Karliner, I., additional, Marsh, M. A., additional, Palmer, M., additional, Selen, M., additional, Thaler, J. J., additional, Edwards, K. W., additional, Bellerive, A., additional, Janicek, R., additional, MacFarlane, D. B., additional, Patel, P. M., additional, Sadoff, A. J., additional, Ammar, R., additional, Baringer, P., additional, Bean, A., additional, Besson, D., additional, Coppage, D., additional, Darling, C., additional, Davis, R., additional, Kotov, S., additional, Kravchenko, I., additional, Kwak, N., additional, Zhou, L., additional, Anderson, S., additional, Kubota, Y., additional, Lee, S. J., additional, O’Neill, J. J., additional, Poling, R., additional, Riehle, T., additional, Smith, A., additional, Alam, M. S., additional, Athar, S. B., additional, Ling, Z., additional, Mahmood, A. H., additional, Timm, S., additional, Wappler, F., additional, Anastassov, A., additional, Duboscq, J. E., additional, Fujino, D., additional, Gan, K. K., additional, Hart, T., additional, Honscheid, K., additional, Kagan, H., additional, Kass, R., additional, Lee, J., additional, Spencer, M. B., additional, Sung, M., additional, Undrus, A., additional, Wolf, A., additional, Zoeller, M. M., additional, Nemati, B., additional, Richichi, S. J., additional, Ross, W. R., additional, Severini, H., additional, Skubic, P., additional, Bishai, M., additional, Fast, J., additional, Hinson, J. W., additional, Menon, N., additional, Miller, D. H., additional, Shibata, E. I., additional, Shipsey, I. P. J., additional, Yurko, M., additional, Glenn, S., additional, Johnson, S. D., additional, Kwon, Y., additional, Roberts, S., additional, Thorndike, E. H., additional, Jessop, C. P., additional, Lingel, K., additional, Marsiske, H., additional, Perl, M. L., additional, Savinov, V., additional, Ugolini, D., additional, Wang, R., additional, Zhou, X., additional, Coan, T. E., additional, Fadeyev, V., additional, Korolkov, I., additional, Maravin, Y., additional, Narsky, I., additional, Shelkov, V., additional, Staeck, J., additional, Stroynowski, R., additional, Volobouev, I., additional, Ye, J., additional, Artuso, M., additional, Azfar, F., additional, Efimov, A., additional, Goldberg, M., additional, He, D., additional, Kopp, S., additional, Moneti, G. C., additional, Mountain, R., additional, Schuh, S., additional, Skwarnicki, T., additional, Stone, S., additional, Viehhauser, G., additional, Xing, X., additional, Bartelt, J., additional, Csorna, S. E., additional, Jain, V., additional, McLean, K. W., additional, Marka, S., additional, Godang, R., additional, Kinoshita, K., additional, Lai, I. C., additional, Pomianowski, P., additional, Schrenk, S., additional, Bonvicini, G., additional, Cinabro, D., additional, Greene, R., additional, Perera, L. P., additional, and Zhou, G. J., additional

Published
1998
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12. Infants and Newborns with Atypical Teratoid Rhabdoid Tumors (ATRT) and Extracranial Malignant Rhabdoid Tumors (eMRT) in the EU-RHAB Registry: A Unique and Challenging Population.

Author

Nemes K, Johann PD, Steinbügl M, Gruhle M, Bens S, Kachanov D, Teleshova M, Hauser P, Simon T, Tippelt S, Eberl W, Chada M, Lopez VS, Grigull L, Hernáiz-Driever P, Eyrich M, Pears J, Milde T, Reinhard H, Leipold A, van de Wetering M, Gil-da-Costa MJ, Ebetsberger-Dachs G, Kerl K, Lemmer A, Boztug H, Furtwängler R, Kordes U, Vokuhl C, Hasselblatt M, Bison B, Kröncke T, Melchior P, Timmermann B, Gerss J, Siebert R, and Frühwald MC

Abstract

Introduction: Malignant rhabdoid tumors (MRT) predominantly affect infants and young children. Patients below six months of age represent a particularly therapeutically challenging group. Toxicity to developing organ sites limits intensity of treatment. Information on prognostic factors, genetics, toxicity of treatment and long-term outcomes is sparse. Methods: Clinical, genetic, and treatment data of 100 patients (aged below 6 months at diagnosis) from 13 European countries were analyzed (2005-2020). Tumors and matching blood samples were examined for SMARCB1 mutations using FISH, MLPA and Sanger sequencing. DNA methylation subgroups (ATRT-TYR, ATRT-SHH, and ATRT-MYC) were determined using 450 k / 850 k-profiling. Results: A total of 45 patients presented with ATRT, 29 with extracranial, extrarenal (eMRT) and 9 with renal rhabdoid tumors (RTK). Seventeen patients demonstrated synchronous tumors (SYN). Metastases (M+) were present in 27% (26/97) at diagnosis. A germline mutation (GLM) was detected in 55% (47/86). DNA methylation subgrouping was available in 50% (31 / 62) with ATRT or SYN; for eMRT, methylation-based subgrouping was not performed. The 5-year overall (OS) and event free survival (EFS) rates were 23.5 ± 4.6% and 19 ± 4.1%, respectively. Male sex (11 ± 5% vs. 35.8 ± 7.4%), M+ stage (6.1 ± 5.4% vs. 36.2 ± 7.4%), presence of SYN (7.1 ± 6.9% vs. 26.6 ± 5.3%) and GLM (7.7 ± 4.2% vs. 45.7 ± 8.6%) were significant prognostic factors for 5-year OS. Molecular subgrouping and survival analyses confirm a previously described survival advantage for ATRT-TYR. In an adjusted multivariate model, clinical factors that favorably influence the prognosis were female sex, localized stage, absence of a GLM and maintenance therapy. Conclusions: In this cohort of homogenously treated infants with MRT, significant predictors of outcome were sex, M-stage, GLM and maintenance therapy. We confirm the need to stratify which patient groups benefit from multimodal treatment, and which need novel therapeutic strategies. Biomarker-driven tailored trials may be a key option.

Published
2022
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13. Risk factors for mixed chimerism in children with hemophagocytic lymphohistiocytosis after reduced toxicity conditioning.

Author

Wustrau K, Greil J, Sykora KW, Albert MH, Burkhardt B, Lang P, Meisel R, Wössmann W, Beier R, Schulz A, Bader P, Chada M, Kühl JS, Schlegel PG, Speckmann C, Gruhn B, Seidel M, Wawer A, Ozga AK, Janka G, Ehl S, Müller I, and Lehmberg K

Subjects
Adolescent, Busulfan administration & dosage, Busulfan analogs & derivatives, Child, Child, Preschool, Female, Follow-Up Studies, Graft vs Host Disease pathology, HLA Antigens immunology, Hematopoietic Stem Cell Transplantation methods, Humans, Infant, Lymphohistiocytosis, Hemophagocytic pathology, Lymphohistiocytosis, Hemophagocytic therapy, Male, Melphalan administration & dosage, Prognosis, Retrospective Studies, Risk Factors, Survival Rate, Tissue Donors, Transplantation, Homologous, Antineoplastic Combined Chemotherapy Protocols adverse effects, Chimerism chemically induced, Graft vs Host Disease etiology, Lymphohistiocytosis, Hemophagocytic drug therapy, Transplantation Conditioning adverse effects
Abstract

Background: Reduced toxicity conditioning for hematopoietic stem cell transplantation of patients with hemophagocyticlymphohistiocytosis (HLH) results in favorable survival, however at the expense of relevant rates of mixed chimerism. Factors predisposing to mixed chimerism remain to be determined., Procedure: Patients with primary HLH transplanted 2009-2016 after treosulfan- or melphalan-based conditioning regimens were analyzed in a retrospective multicenter study for survival, engraftment, chimerism, and adverse events. Mixed chimerism was considered substantial if < 25% donor chimerism occurred and/or if secondary cell therapy was administered. Donor type, graft source, type of alkylating agent, type of serotherapy, and remission status were analyzed as potential risk factors in a multivariable logistic regression model., Results: Among 60 patients, engraftment was achieved in 95%, and the five-year estimated overall survival rate was 75%. Prevalence of any recipient chimerism was 48%. Substantial recipient chimerism was recorded in 32% of patients. Secondary post-HSCT cell therapy was administered in 30% of patients. A human leukocyte antigen (HLA)-mismatched donor (< 10/10) was the only significant risk factor for the occurrence of substantial recipient chimerism (P = 0.01; odds ratio, 5.8; CI 95%, 1.5-26.3)., Conclusion: The use of an HLA-matched donor is the most important factor to avoid substantial recipient chimerism following treosulfan -or melphalan-based conditioning in primary HLH., (© 2020 Wiley Periodicals LLC.)

Published
2020
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14. Chronic recurrent multifocal osteomyelitis in association with pyoderma gangraenosum.

Author

Wurm MC, Brecht I, Lell M, Brunner K, Mitsimponas KT, Chada M, Jahn J, Neukam FW, and von Wilmowsky C

Subjects
Adolescent, Child, Chronic Disease, Female, Germany, Humans, Recurrence, Osteomyelitis complications, Pyoderma complications
Abstract

Background: Chronic recurrent multifocal osteomyelitis (CRMO) is a rare acquired inflammatory skeletal disorder of unknown origin. CRMO was first described by Gideon in 1972 and mainly affects children and young adults of female gender. The CRMO is part of the clinical picture of non-bacterial Osteomyelitis (NBO) and typically presents a relapsing recurring course with both remission and spontaneous exacerbation. CRMO is typically encountered in the limbs and the metaphysis of long bones in particular. Usually the clinical symptoms include painful swellings of the affected regions. This case report describes the rare case of a CRMO of the mandible in association with pyoderma gangraenosum., Case Presentation: A 14-year old female caucasian patient, residing in the south of Germany, presented in the oncological outpatient clinic of our Department of Paediatrics and Adolescent Medicine in June 2014 complaining of increasing neck pain and progressive swelling at her left cheek ongoing for about 6 weeks. These symptoms had been occurring quarterly for 4 years, but had never been as pronounced. Blood biochemistry showed a moderately elevated CRP (35 mg/l) and a significantly increased blood sedimentation rate (BSR 48/120 mm). The panoramic radiograph, however, revealed a bone alteration in the left mandibular region. Further investigations confirmed the diagnosis of CRMO., Conclusion: The present case underlines the fact that rare diseases might occasionally present with even more rare symptoms. These occasions can obviously be considered to present a considerable diagnostic challenge.

Published
2016
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15. Diffuse Encephalopathy Associated with Isolated Cerebral Langerhans Cell Histiocytosis.

Author

Rompel O, Buslei R, Hammon M, Dörr HG, Chada M, Nikkhah G, Uder M, and Trollmann R

Subjects
Brain Diseases drug therapy, Child, Diagnosis, Differential, Fatal Outcome, Histiocytosis, Langerhans-Cell drug therapy, Humans, Male, Brain diagnostic imaging, Brain pathology, Brain Diseases diagnosis, Brain Diseases pathology, Histiocytosis, Langerhans-Cell diagnosis, Histiocytosis, Langerhans-Cell pathology
Abstract

Background: Langerhans cell histiocytosis is a rare disease of the monocyte-macrophage system. Abnormalities of the hypothalamic-pituitary region are common in individuals with central nervous system involvement., Patient Description: This six-year-old boy developed rapidly progressive aggressive behavior, central diabetes insipidus, and repeated complex partial seizures. Magnetic resonance imaging revealed a diffuse leukoencephalopathy-like pattern and numerous infratentorial and supratentorial granulomatous nodules in the brain parenchyma along with infundibular and hypothalamic mass lesions. Stereotactic serial biopsies enabled histopathologic and immunohistochemical diagnosis of Langerhans cell histiocytosis., Conclusions: Similar MRI findings have rarely been described in the literature. These findings represent part of the broad neuroradiological spectrum of Langerhans cell histiocytosis of the nervous system in children., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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16. Changes of orexin A plasma levels in girls with anorexia nervosa during eight weeks of realimentation.

Author

Bronsky J, Nedvidkova J, Krasnicanova H, Vesela M, Schmidtova J, Koutek J, Kellermayer R, Chada M, Kabelka Z, Hrdlicka M, Nevoral J, and Prusa R

Subjects
Adolescent, Anorexia Nervosa therapy, Eating physiology, Female, Humans, Insulin-Like Growth Factor Binding Protein 3 blood, Insulin-Like Growth Factor I metabolism, Leptin blood, Nutritional Status, Orexins, Anorexia Nervosa blood, Body Weight physiology, Intracellular Signaling Peptides and Proteins blood, Neuropeptides blood
Abstract

Objective: Orexin A (OXA) is a hypothalamic neuropeptide involved in regulation of food intake and nutritional status. There are multiple disturbances of neuropeptide signaling described in girls with anorexia nervosa (AN), but OXA levels have not been addressed in this population to date. Therefore, we analyzed OXA levels of AN girls in this study., Method: OXA (radioimmunoassay/RIA/method), leptin, insulinlike growth factor-1 (IGF-1), and insulinlike growth factor-1 binding protein-3 (IGFBP-3) levels were measured before and after 8 weeks of realimentation in 36 girls with AN and in 14 healthy controls (control group: CG)., Results: Average weight increased significantly in AN during the study (p < .0001), while plasma levels of OXA decreased (before realimentation: 56.2 ± 2.4 pg/ml; after realimentation: 47.5 ± 1.4 pg/ml; p = .0025). OXA levels before realimentation differed from levels in the CG (47.15 ± 2.6 pg/ml, p = .034), but not afterward. We did not find any correlation between OXA and age, height, weight, BMI; or IGF-1, IGFBP-3, and leptin levels., Discussion: OXA levels in untreated AN patients differ significantly from healthy subjects and decrease during realimentation. These findings indicate that OXA may be involved in the nutritional regulation of malnourished children and adolescents., (Copyright © 2010 Wiley Periodicals, Inc.)

Published
2011
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17. Parecoxib does not suppress thromboxane synthesis in newborn piglets with group B streptococcal sepsis.

Author

Nögel SC, Chada M, Schmidt AM, Bosselmann S, Kandler M, Schweer H, Watzer B, Schneider H, Gessner A, and Rascher W

Subjects
Animals, Animals, Newborn, Dinoprostone urine, Epoprostenol metabolism, Epoprostenol urine, Gene Expression Regulation drug effects, Hemodynamics drug effects, Indomethacin pharmacology, Inflammation metabolism, Inflammation pathology, Inflammation urine, Lung drug effects, Lung pathology, Platelet Count, Receptors, Prostaglandin E metabolism, Sepsis pathology, Sepsis physiopathology, Sepsis urine, Streptococcal Infections microbiology, Streptococcal Infections pathology, Streptococcal Infections urine, Swine, Thromboxanes metabolism, Thromboxanes urine, Cyclooxygenase 2 Inhibitors pharmacology, Isoxazoles pharmacology, Sepsis metabolism, Streptococcal Infections metabolism, Streptococcus agalactiae, Thromboxanes biosynthesis
Abstract

Group B streptococci (GBS) cause fatal sepsis in newborns. Strong activation of thromboxane synthesis is assumed to correlate with severe pulmonary hypertension. In this study we compared the impact of indomethacin versus parecoxib on hemodynamics and outcome and investigated the pharmacological effects on thromboxane synthesis and EP-3 receptor gene expression. Whereas both parecoxib and indometacin reduced expression of thromboxane synthase and EP-3 receptor in infected lung tissue, parecoxib did not suppress urine levels of thromboxane like indometacin. We presume that COX-2 inhibition in GBS sepsis is associated with enhanced thrombogenicity.

Published
2009
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18. Anakinra (IL-1R antagonist) lowers pulmonary artery pressure in a neonatal surfactant depleted piglet model.

Author

Chada M, Nögel S, Schmidt AM, Rückel A, Bosselmann S, Walther J, Papadopoulos T, von der Hardt K, Dötsch J, Rascher W, and Kandler MA

Subjects
Acute Lung Injury drug therapy, Animals, Animals, Newborn, Interleukin 1 Receptor Antagonist Protein therapeutic use, Male, Pulmonary Surfactants, Swine, Blood Pressure drug effects, Interleukin 1 Receptor Antagonist Protein pharmacology, Pulmonary Artery drug effects, Respiratory Mechanics drug effects
Abstract

In acute respiratory distress syndrome (ARDS) with pulmonary hypertension, interleukin-1 beta (IL-1 beta) and interleukin-8 (IL-8) are involved in the pulmonary inflammatory reaction. The purpose of this study was to determine whether systemic and aerosolized administered IL-1 receptor antagonist (IL-1Ra) Anakinra (Kineret) improves lung mechanics and pulmonary artery pressure in surfactant depleted newborn piglets. After induction of acute lung injury by lung lavage, neonatal piglets received repetitive treatment of either aerosolized IL-1Ra (IL-1Ra-Aerosol) or intravenous IL-1Ra (IL-1Ra-i.v.), or saline solution as control. IL-1Ra given as aerosol or intravenously significantly reduced mean pulmonary artery pressure (MPAP) but did not influence mean systemic arterial pressure (MAP) compared with the control group. IL-1 beta and IL-8 mRNA expressions normalized to beta-actin and hypoxanthine-guanine-phosphoribosyl transferase were significantly reduced in the IL-1Ra-Aerosol group but not in IL-1Ra-i.v. group compared to the control group. The lung injury score was not significantly different between IL-1Ra groups and the control group. Application of aerosolized IL-1Ra reduced MPAP without affecting MAP in a piglet model of surfactant depletion with pulmonary hypertension. Furthermore, there is evidence for reduction of early pro-inflammatory pulmonary reaction., ((c) 2008 Wiley-Liss, Inc.)

Published
2008
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19. Brief adrenomedullin inhalation leads to sustained reduction of pulmonary artery pressure.

Author

von der Hardt K, Kandler MA, Chada M, Cubra A, Schoof E, Amann K, Rascher W, and Dötsch J

Subjects
Administration, Inhalation, Adrenomedullin, Animals, Blood Pressure physiology, Carbon Dioxide blood, Models, Animal, Oxygen blood, Pulmonary Artery physiology, Swine, Blood Pressure drug effects, Peptides administration & dosage, Pulmonary Artery drug effects, Vasodilator Agents administration & dosage
Abstract

The effect of aerosolised adrenomedullin (ADM), a potent vasodilator peptide, on pulmonary artery pressure was studied for 24 h in a surfactant-depleted piglet model. Animals received either aerosolised ADM (50 ng.kg(-1).min(-1), ADM, n=6), or aerosolised normal saline solution (control, n=6). Aerosol therapy was performed for a 2 h treatment period followed by a 22 h observation period. Ventilator settings were adapted to keep arterial oxygen tension and carbon dioxide arterial tension between 13.3-14.6 kPa and 4.9-5.7 kPa, respectively. Aerosolised ADM reduced mean pulmonary artery pressure (MPAP) compared with the control group (end-point median 24 h after therapy start: DeltaMPAP -14.0 versus -8.0 mmHg; 23.5 h after therapy start). After therapy start, mean systemic arterial pressure (MAP) was not significantly different between the groups (end-point median: MAP ADM 70 (61/74) versus control 72 (54/81) mmHg). Endothelin-1, a potent pulmonary vasoconstrictor, is regulated by ADM via cAMP. Twenty two hours after inhalation of aerosolised ADM, endothelin-1 mRNA in lung tissue and endothelin-1 protein expression in pulmonary arteries was reduced compared with controls (median semi-quantitative immunhistochemical score: ADM 0.21, control 0.76). Aerosolised adrenomedullin significantly reduced mean pulmonary artery pressure independently of arterial oxygen tension.

Published
2004
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20. Dose response to aerosolized perflubron in a neonatal swine model of lung injury.

Author

Kandler MA, von der Hardt K, Gericke N, Chada M, Dötsch J, and Rascher W

Subjects
Animals, Animals, Newborn, Chlorofluorocarbons, Methane administration & dosage, Dose-Response Relationship, Drug, Emulsions metabolism, Humans, Hydrocarbons, Brominated, Interleukin-1 genetics, Interleukin-1 metabolism, Lung immunology, Pulmonary Surfactants metabolism, Random Allocation, Swine, Contrast Media pharmacology, Fluorocarbons pharmacology, Lung drug effects, Lung Injury
Abstract

Aerosolized perfluorocarbon (PFC) improves gas exchange, lung mechanics, and pulmonary artery pressure. The objective of this intervention was to study the dose-response effect to aerosolized perfluorooctylbromide (PFOB; perflubron, LiquiVent, Alliance Pharmaceutical Corp.) in surfactant-depleted piglets. After induction of lung injury by saline lavage, 25 newborn piglets were randomly assigned to receive 0, 1.25, 2.5, 5.0, or 7.5 mL/kg aerosolized PFOB per hour. A 2-h therapy period was followed by a 3-h observation period. In all animals, respiratory support was performed with intermittent mandatory ventilation. After aerosol treatment and 3 h of observation, arterial oxygen pressure was similarly improved in the 2.5-, 5.0-, and 7.5-mL. kg(-1). h(-1) aerosol-PFOB groups and higher compared with the 1.25-mL. kg(-1). h(-1) aerosol-PFOB (P < 0.01) and the control groups (P < 0.001). Compared with the control group, arterial carbon dioxide pressure was significantly reduced with 2.5-, 5.0-, and 7.5-mL. kg(-1). h(-1) aerosol-PFOB (P < 0.001). Treatment with 1.25 mL. kg(-1). h(-1) aerosol-PFOB did not significantly affect arterial carbon dioxide pressure. The 20% terminal dynamic compliance/dynamic compliance was significantly improved in the groups that received 2.5, 5.0, and 7.5 mL. kg(-1). h(-1) aerosol-PFOB compared with control animals. Mean pulmonary artery pressure was lower after therapy with 5.0 and 7.5 mL. kg(-1). h(-1) aerosol-PFOB (P < 0.01) than in the control group. IL-1beta gene expression in lung tissue was significantly reduced with PFOB 1.25 mL. kg(-1). h(-1). In summary, aerosolized PFOB improved terminal dynamic compliance, pulmonary gas exchange, and pulmonary artery pressure in a dose-dependent manner. In terms of oxygenation and lung mechanics, the optimum dose was between 2.5 and 5 mL. kg(-1). h(-1).

Published
2004
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21. Pilot intervention: aerosolized adrenomedullin reduces pulmonary hypertension.

Author

Kandler MA, Von Der Hardt K, Mahfoud S, Chada M, Schoof E, Papadopoulos T, Rascher W, and Dötsch J

Subjects
Adrenomedullin, Aerosols, Animals, Blood Pressure drug effects, Disease Models, Animal, Endothelin-1 metabolism, Nitric Oxide Synthase metabolism, Oxygen physiology, Swine, Antihypertensive Agents therapeutic use, Hypertension, Pulmonary drug therapy, Peptides therapeutic use
Abstract

In pulmonary hypertension, systemic infusion of adrenomedullin (ADM), a potent vasodilator peptide, leads to pulmonary vasodilatation. However, systemic blood pressure declines alike. The present study investigated the effect of aerosolized ADM on pulmonary arterial pressure in surfactant-depleted newborn piglets with pulmonary hypertension. Animals randomly received aerosolized ADM (ADM, n = 6), aerosolized ADM combined with intravenous application of NG-nitro-l-arginine methylester to inhibit nitric-oxide (NO) synthases (ADM + l-NAME, n = 5), or aerosolized normal saline solution (control, n = 6). Aerosol therapy was performed in 30-min intervals for 5 h. After a total experimental period of 8 h, mRNA expression of endothelial and inducible NO synthase and endothelin-1 (ET-1) in lung tissue was quantified using TaqMan real-time polymerase chain reaction. Aerosolized ADM reduced mean pulmonary artery pressure (MPAP) compared with control (p < 0.001; at the end of the study, Delta-MPAP -13.5 +/- 1.4 versus -6.2 +/- 2.4 mm Hg). PaO2 significantly increased in the ADM (DeltaPaO2 243.3 mm Hg) and the ADM + l-NAME group (DeltaPaO2 217.4 mm Hg) compared with the control group (DeltaPaO2 82.9 mm Hg; p < 0.001). Aerosolized ADM did not influence mean systemic arterial pressure (baseline 63.2 +/- 2.7 versus end of the study 66.3 +/- 6.5 mm Hg; not significant). NO synthases gene expressions were 20 to 30% lower with ADM compared with control. ET-1 gene expression was significantly reduced (>50%) after ADM aerosol therapy (p < 0.001). Aerosolized adrenomedullin significantly reduced MPAP without lowering the systemic arterial pressure and improved profoundly the arterial oxygen tension. This effect seems to be mediated at least in part by the reduction of ET-1.

Published
2003
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22. Inhibin B, follicle stimulating hormone, luteinizing hormone and testosterone during childhood and puberty in males: changes in serum concentrations in relation to age and stage of puberty.

Author

Chada M, Průsa R, Bronský J, Kotaska K, Sídlová K, Pechová M, and Lisá L

Subjects
Child, Child, Preschool, Humans, Infant, Infant, Newborn, Male, Puberty blood, Aging blood, Follicle Stimulating Hormone blood, Inhibins blood, Luteinizing Hormone blood, Testosterone blood
Abstract

Inhibin B is a gonadal dimeric polypeptide hormone that regulates synthesis and secretion of follicle stimulating hormone (FSH) in a negative feedback loop. The aim of the present study was to determine changes in serum inhibin B, gonadotropins and testosterone concentrations during childhood and puberty in males. We studied the relationship between circulating inhibin B, gonadotropins and testosterone in serum of healthy boys during the first two years of life and then in pubertal development. Using a recently developed two-side enzyme-linked immunosorbent assay (ELISA), inhibin B levels were measured in the serum of 78 healthy boys divided into eleven age groups from birth to the end of pubertal development. In addition, serum levels of gonadotropins and testosterone were measured. Serum inhibin B, gonadotropins and testosterone increased during the first months of postnatal life. A peak in serum inhibin B and gonadotropins concentrations was observed around 3-4 months of age. There was a significant positive correlation between serum inhibin B and gonadotropins and testosterone levels during the first 2 years of life. After this early increase, serum inhibin B, gonadotropins and testosterone levels decreased significantly and remained low until puberty followed by an increase beginning with the onset of puberty. Serum levels of inhibin B reached a peak at stage G3 of puberty. Around midpuberty, inhibin B lost its positive correlation with luteinizing hormone (LH) and testosterone from early puberty, and developed a strong negative correlation with FSH, which persisted into adulthood. We conclude that inhibin B plays a key role in the regulation of the hypothalamic-pituitary-gonadal hormonal axis during male childhood and pubertal development. Inhibin B is a direct marker of the presence and function of Sertoli cells and appears to reflect testicular function in boys.

Published
2003

23. Inhibin B, follicle stimulating hormone, luteinizing hormone, and estradiol and their relationship to the regulation of follicle development in girls during childhood and puberty.

Author

Chada M, Průsa R, Bronský J, Pechová M, Kotaska K, and Lisá L

Subjects
Adolescent, Analysis of Variance, Child, Child, Preschool, Estradiol blood, Female, Follicle Stimulating Hormone blood, Humans, Infant, Infant, Newborn, Inhibins blood, Luteinizing Hormone blood, Regression Analysis, Breast growth & development, Child Development physiology, Gonadal Hormones blood, Gonadotropins blood, Nipples growth & development, Puberty physiology
Abstract

Inhibin B, produced by granulosa cells in the ovary, is a heterodimeric glycoprotein suppressing synthesis and secretion of the follicle stimulating hormone (FSH). The aim of the present study was to determine hormone profiles of inhibin B, FSH, luteinizing hormone (LH), and estradiol in girls during childhood and puberty and to evaluate whether inhibin B is a marker of follicle development. We examined the correlation between inhibin B and gonadotropins and estradiol during the first two years and across the pubertal development. Using a specific two-side enzyme-linked immunosorbent assay (ELISA), inhibin B levels were measured in the serum of 53 healthy girls divided into 8 groups according to age. In addition, serum FSH, LH, and estradiol were measured by chemiluminescent immunoassay in all serum samples. A rise in serum levels of inhibin B (55.2+/-7.3 ng/l, mean +/- S.E.M.) and FSH (1.78+/-0.26 UI/l), concomitant with a moderate increment of serum LH (0.36+/-0.09 UI/l) and estradiol (45.8+/-12.2 pmol/l) concentrations was observed during the first three months of life and declined to prepubertal concentrations thereafter. A strong positive correlation between inhibin B and FSH (r = 0.48, p<0.05), LH (r = 0.68, p<0.001) and estradiol (r = 0.59, p<0.01) was demonstrated during the first 2 years of life. A rise in serum levels of inhibin B, FSH, LH, and estradiol was found throughout puberty. Inhibin B had a strong positive correlation with FSH (stage I of puberty: r = 0.64, p<0.05; stage II of puberty: r = 0.86, p<0.01), LH (I: r = 0.61, p<0.05; II: r = 0.67, p<0.05), and estradiol (II: r = 0.62, p<0.05) in early puberty. From pubertal stage II, inhibin B lost this relationship to gonadotropins and estradiol. Serum inhibin B and FSH levels increased significantly during pubertal development, with the highest peak found in stage III of puberty (133.5+/-14.3 ng/l), and decreased thereafter. In conclusion, inhibin B is produced in a specific pattern in response to gonadotropin stimulation and plays an important role in the regulation of the hypothalamic-pituitary-gonadal axis during childhood and puberty in girls. Inhibin B is involved in regulatory functions in developing follicles and seems to be a sensitive marker of ovarian follicle development.

Published
2003

24. Aerosolized adrenomedullin suppresses pulmonary transforming growth factor-beta1 and interleukin-1 beta gene expression in vivo.

Author

von der Hardt K, Kandler MA, Popp K, Schoof E, Chada M, Rascher W, and Dötsch J

Subjects
Adrenomedullin, Aerosols, Animals, Enzyme-Linked Immunosorbent Assay, Gene Expression, Interleukin-1 genetics, Lung metabolism, Polymerase Chain Reaction, RNA, Messenger metabolism, Swine, Transforming Growth Factor beta genetics, Transforming Growth Factor beta1, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Interleukin-1 metabolism, Lung drug effects, Peptides pharmacology, Transforming Growth Factor beta metabolism
Abstract

The effect of aerosolized adrenomedullin on interleukin-1 beta and transforming growth factor (TGF)-beta1 mRNA and protein expression was studied in surfactant depleted piglets, receiving aerosolized adrenomedullin (adrenomedullin, n=6), aerosolized adrenomedullin plus i.v. N(G)-nitro-L-arginine-methylester (adrenomedullin+L-NAME, n=5), or aerosolized saline solution (control, n=6). After 8 h of aerosol interval therapy, mRNA expression of interleukin-1 beta and TGF-beta1 in lung tissue was quantified normalized to beta-actin and hypoxanthine-guanine-phosphoribosyl-transferase by real-time polymerase chain reaction (PCR). Interleukin-1 beta and TGF-beta1 protein concentration in lung tissue was quantified by enzyme-linked immunosorbent assay (ELISA). In the adrenomedullin group, interleukin-1 beta and TGF-beta1 mRNA expression was lower than in controls. Reduction for interleukin-1 beta/beta-actin was 56% (p<0.001), for interleukin-1 beta/hypoxanthine-guanine-phosphoribosyl-transferase 60% (p<0.001), for TGF-beta1/beta-actin 65.5% (p<0.001), and for TGF-beta1/hypoxanthine-guanine-phosphoribosyl-transferase 56.2% (p<0.001). Mean interleukin-1 beta protein expression was different between the groups, p<0.05 (adrenomedullin 601+/-61, Control 836+/-88 pg/mg protein). L-NAME did not antagonize adrenomedullin effect on TGF-beta1 mRNA. In conclusion, aerosolized adrenomedullin reduced pulmonary inflammatory and pro-fibrotic response.

Published
2002
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25. [Amylin--its physiological role in humans].

Author

Bronský J, Chada M, Kotaska K, and Průsa R

Subjects
Animals, Blood Glucose metabolism, Bone and Bones metabolism, Diabetes Mellitus blood, Eating physiology, Glucagon metabolism, Humans, Islet Amyloid Polypeptide, Amyloid physiology
Abstract

Amylin is a polypeptide hormone composed of 37 aminoacids, that is produced in pancreatic beta-cells, and that was discovered in 1987. Releasing amylin into the circulation is increased postprandially, proportionally to the amount of digested food. Daily profile of amylin plasma levels corresponds to the profile of insulin. Normal plasma levels of amylin vary from 4 pmol/L (fasting) to 25 pmol/L (postprandially). Receptors for amylin are highly concentrated especially in the central nervous system--area postrema and nucleus accumbens. There is a 20% sequence homology between amylin, calcitonin and adrenomedullin and 44% homology with calcitonin gene--related peptide. Amylin contributes to the regulation of postprandial glycaemia by suppression of glucagon release and by regulation of gastric emptying. Deficit os amylin is typical for diabetes mellitus type 1 or for the late stage of diabetes type 2. Insulin resistance in obese patients is characterized by increased levels of both insulin and amylin. Amylin decreases food intake and participates in the regulation of body weight. Some biochemical forms of amylin cause proliferation of osteoblasts and inhibit bone resorption. Amylin modulates insulin sensitivity of skeletal muscle, contributes to the regulation of blood pressure and causes vasodilatation.

Published
2002

26. [Inhibin in pregnancy--a new screening marker for prenatal diagnosis?].

Author

Chada M, Lisá L, and Průsa R

Subjects
Female, Humans, Inhibins physiology, Pregnancy, Biomarkers analysis, Down Syndrome diagnosis, Inhibins analysis, Pre-Eclampsia diagnosis, Pregnancy, Ectopic diagnosis, Prenatal Diagnosis, Trophoblastic Neoplasms diagnosis, Uterine Neoplasms diagnosis
Published
2002

27. Assessment of puberty growth spurt in boys and girls--a dental radiographic method.

Author

Gupta S, Chada MK, and Sharma A

Subjects
Adolescent, Age Determination by Skeleton methods, Child, Female, Humans, Male, Odontogenesis physiology, Sesamoid Bones diagnostic imaging, Sex Characteristics, Tooth Calcification, Age Determination by Teeth methods, Puberty, Radiography, Panoramic methods
Abstract

The first radiographic appearance of adductor sesamoid bone of thumb is considered reliable and is the most commonly used indicator of puberty growth spurt. The purpose of this study was to find out whether the tooth mineralization stage/stages were as reliable an indicator of puberty growth spurt as the adductor sesamoid bone. Puberty assessment has its necessary application in diagnosis, treatment planning of various malocclusions and in medico legal cases. The results indicated that a close relationship existed between tooth mineralization Stage G and appearance of the sesamoid bone. Hence it can be used in dentistry as an indicator for onset of puberty growth spurt via periapical or panoramic radiographs. The result of this study were not applicable to boys as the apical closure of these teeth had already occurred at the time of early radiographic appearance of the adductor sesamoid bone.

Published
1995

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