563 research outputs found
Recommendations for the standardization of clinical outcomes used in allergen immunotherapy trials for allergic rhinoconjunctivitis: an EAACI Position Paper.
No full textAnwendung von Biologika bei allergischen und Typ-2- entzündlichen Erkrankungen in der aktuellen COVID-19-Pandemie – ein Positionspapier von AeDA, DGAKI, GPA, ÖGAI, LGAI, ÖGP, ARIA und EAACI
No full textAllergen-Immuntherapie in der aktuellen COVID-19-Pandemie – ein Positionspapier von ARIA, EAACI, AeDA und DGAKI
No full textDifferential effects of neurotensin and cholecystokinin on intestinal microcirculation after ischemia-reperfusion
No full textBackground. We investigated the effect of neurotensin and cholecystokinin (CCK) on intestinal microcirculation after ischemia-reperfusion. Method: Ischemia was induced in Wistar rats by occlusion of the superior mesenteric artery for 40 min. Ten minutes before reperfusion, infusion of either neurotensin or CCK was started. Afterwards. the microhemodynamics of the jejunum were examined by means of intravital microscopy. Results. Ischemia-reperfusion decreased functional capillary density from 873.4+/-18.1 to 362.5+/-8.3 cm(-1) and red blood cell velocity from 0.49+/-0.03 to 0.34+/-0.02 mm/s. Furthermore, leukocyte-endothelium interaction was increased. Neurotensin infusion significantly increased functional capillary density to 483.2+/-9.0 cm(-1) and red blood cell velocity to 0.69+/-0.01 mm/s in the mucosal capillaries compared with ischemic controls. Despite the amelioration of villus perfusion, the number of nonperfused villi significantly increased (11.8+/-3.6%) compared with ischemic controls. CCK infusion also resulted in a significant increase of functional capillary density (535.2+/-7.4 cm(-1)) and red blood cell velocity (0.67+/-0.01 mm/s). In contrast to neurotensin, the number of non-perfused villi was not increased (5.8+/-2.2%). Conclusion: We conclude that neurotensin further aggravates perfusion inhomogeneity and stasis when administered during the ischemic period. In contrast, CCK has no negative influence on perfusion homogeneity after ischemia-reperfusion. It may be superior to neurotensin in the reconstitution of normal microvascular perfusion patterns after ischemia-reperfusion
Differential effects of neurotensin and cholecystokinin on intestinal microcirculation after ischemia-reperfusion
No full textBackground. We investigated the effect of neurotensin and cholecystokinin (CCK) on intestinal microcirculation after ischemia-reperfusion. Method: Ischemia was induced in Wistar rats by occlusion of the superior mesenteric artery for 40 min. Ten minutes before reperfusion, infusion of either neurotensin or CCK was started. Afterwards. the microhemodynamics of the jejunum were examined by means of intravital microscopy. Results. Ischemia-reperfusion decreased functional capillary density from 873.4+/-18.1 to 362.5+/-8.3 cm(-1) and red blood cell velocity from 0.49+/-0.03 to 0.34+/-0.02 mm/s. Furthermore, leukocyte-endothelium interaction was increased. Neurotensin infusion significantly increased functional capillary density to 483.2+/-9.0 cm(-1) and red blood cell velocity to 0.69+/-0.01 mm/s in the mucosal capillaries compared with ischemic controls. Despite the amelioration of villus perfusion, the number of nonperfused villi significantly increased (11.8+/-3.6%) compared with ischemic controls. CCK infusion also resulted in a significant increase of functional capillary density (535.2+/-7.4 cm(-1)) and red blood cell velocity (0.67+/-0.01 mm/s). In contrast to neurotensin, the number of non-perfused villi was not increased (5.8+/-2.2%). Conclusion: We conclude that neurotensin further aggravates perfusion inhomogeneity and stasis when administered during the ischemic period. In contrast, CCK has no negative influence on perfusion homogeneity after ischemia-reperfusion. It may be superior to neurotensin in the reconstitution of normal microvascular perfusion patterns after ischemia-reperfusion
Impact of gastrin-releasing peptide on intestinal microcirculation after ischemia-reperfusion in rats
No full textWe investigated the effect of gastrin-releasing peptide (GRP) and its antagonist RC-3095 on intestinal microcirculation after ischemia-reperfusion. Intestinal ischemia was induced in female Wistar rats by occlusion of the superior mesenteric artery for 40 min. Ten minutes prior to reperfusion, infusion of GRP or RC-3095 was started. A jejunal segment was exteriorized and the microhemodynamics of the mucosa and submucosa were examined by intravital microscopy and compared both with normal and ischemic controls (without application of the regulatory peptide). Ischemia-reperfusion significantly decreased functional capillary density from 891.2 +/- 14.1 to 398.3 +/- 11.4 cm(-1). Capillary red blood cell velocity was reduced from 0.46 +/- 0.01 to 0.37 +/- 0.01 mm/s (p < 0.05). Furthermore, both sticking and rolling of leukocytes were enhanced. 3.4 +/- 1.1% of the villi were not perfused at all. GRP infusion reversed the microcirculatory ischemia-reperfusion injury by increasing functional capillary density to 669.8 +/- 8.3 cm(-1) and red blood cell velocity to 0.62 +/- 0.01 mm/s (p < 0.05). In addition, application of GRP resulted in a complete absence of stasis (0%) in the villi. Leukocyte-endothelium adherence remained unchanged when compared to the ischemic controls. In contrast, application of RC-3095 caused an aggravation of microcirculatory disturbances demonstrated by a markedly increased number of non-perfused villi (42.5 +/- 4.2%; p < 0.05 vs. ischemic controls) and a significantly reduced functional capillary density (346.2 +/- 8.4 cm(-1), p < 0.05 vs. ischemic controls). In addition, RC-3095 led to an increased permanent leukocyte adherence in postcapillary venules whereas rolling was significantly reduced when compared to normal controls. We conclude that GRP in pharmacological doses has a protective effect on intestinal microcirculation during reperfusion. Furthermore, these data suggest that endogenous GRP may play a decisive role in the maintenance of microvascular integrity during reperfusion. Copyright (C) 2000 S. Karger AG, Basel
Correction to “ARIA guideline 2019: Treatment of allergic rhinitis in the German health system” (Allergo Journal International, (2019), 28, 7, (255-276), 10.1007/s40629-019-00110-9).
No full textAffiliation and disclaimer have been misrepresented and are hereby corrected: Vera Mahler: Affiliation: Med. Faculty, Friedrich-Alexander-University (FAU) Erlangen-Nürnberg, Germany. Disclaimer: The views expressed in this review are the personal views of the author and may not be understood or quoted as being made on behalf of or reflecting the position of the respective national competent authorities, the EuropeanMedicines Agency, or one of its committees or working parties.One conflict of interest has been misrepresented and is hereby corrected: Oliver Pfaar
Wirksamkeit von sublingualen Gräserpollentabletten bei saisonaler allergischer Rhinitis - Eine systematische "bersicht und Metaanalyse
No full textimmunolog
DGAKI and PEI in dialogue 2023: Diagnostics and allergen immunotherapy
No full textPfaar O, Hamelmann E, Taube C, et al. DGAKI and PEI in dialogue 2023: Diagnostics and allergen immunotherapy. Allergologie Select. 2023;7(1):229-235.A roundtable discussion on February 10, 2023 between the German Society for Allergology and Clinical Immunology (DGAKI) and the Paul-Ehrlich-Institut (PEI) aimed to discuss in detail current aspects of allergen immunotherapy (AIT), its regulatory framework under the transitional provision of the Therapy Allergen Ordinance (TAO), and the consequences for the planned guideline work of the DGAKI, regulatory challenges in the approval of AIT products for children and adolescents as well as allergy diagnostics. The content and discussion points of this dialogue are summarized and are set in context with the current literature. © Dustri-Verlag Dr. K. Feistle
Allergen-Immuntherapie in der aktuellen COVID-19-Pandemie – ein Positionspapier von ARIA, EAACI, AeDA, GPA und DGAKI (Kurzversion) – Positionspapier der deutschen ARIA-GruppeA in Kooperation mit der österreichischen ARIA-GruppeB, der schweizerischen ARIA-GruppeC, dem Ärzteverband Deutscher Allergologen (AeDA)D, der Deutschen Gesellschaft für Allergologie und Klinische Immunologie (DGAKI)E und der Gesellschaft für Pädiatrische Allergologie (GPA)F in Kooperation mit der AG Klinische Immunologie, Allergologie und Umweltmedizin der DGHNO-KHCG und der Europäischen Akademie für Allergologie und Klinische Immunologie (EAACI)H
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