Andreas Hahn

Dr. Andreas Hahn

orcid

Research Focus & Metrics

Academic Career Length

18Years (2009-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
22 September 2009 in European Heart Journal
Verified
Journal Article
Open access
PDF file
GMGerd P. Meyer
Gerd P. Meyer
KWKai C. Wollert
Kai C. Wollert
JLJoachim Lotz
Joachim Lotz
JPJens Pirr
Jens Pirr
URUlrike Rager
Ulrike Rager
HDHelmut Drexler
Helmut Drexler
We assessed whether a single intracoronary infusion of autologous bone marrow cells (BMCs) can have a sustained impact on left ventricular ejection fraction (LVEF) in patients after ST-elevation myocardial infarction (STEMI). In the BOne marrOw transfer to enhance ST-elevation infarct regeneration (BOOST) trial, 60 patients with STEMI and successful percutaneous coronary intervention were randomized to a control and a cell therapy group. As previously reported, BMC transfer led to an improvement of LVEF by 6.0% at 6 months (P = 0.003) and 2.8% at 18 months (P = 0.27). Left ventricular ejection fraction and clinical status were re-assessed in all surviving patients after 61 ± 11 months. Major adverse cardiac events occurred with similar frequency in both groups. When compared with baseline, LVEF assessed by magnetic resonance imaging at 61 months decreased by 3.3 ± 9.5% in the control group and by 2.5 ± 11.9% in the BMC group (P = 0.30). Patients with an infarct transmurality > median appeared to benefit from BMC transfer throughout the 61-month study period (P = 0.040). A single intracoronary application of BMCs does not promote a sustained improvement of LVEF in STEMI patients with relatively preserved systolic function. It is conceivable that a subgroup of patients with more transmural infarcts may derive a sustained benefit from BMC therapy. However, this needs to be tested prospectively in a randomized trial.

1 February 2017 in Molecular and Cellular Probes
Verified
Journal Article
Open access
RHRebecca Hinz
Rebecca Hinz
NSNorbert G. Schwarz
Norbert G. Schwarz
AHAndreas Hahn
Andreas Hahn
HFHagen Frickmann
Hagen Frickmann
Schistosomiasis is a common disease in endemic areas of Sub-Saharan Africa, South America and Asia. It is rare in Europe, mainly imported from endemic countries due to travelling or human migration. Available methods for the diagnosis of schistosomiasis comprise microscopic, molecular and serological approaches, with the latter detecting antigens or antibodies associated with Schistosoma spp. infection. The serological approach is a valuable screening tool in low-endemicity settings and for travel medicine, though the interpretation of any diagnostic results requires knowledge of test characteristics and a patient's history. Specific antibody detection by most currently used assays is only possible in a relatively late stage of infection and does not allow for the differentiation of acute from previous infections for therapeutic control or the discrimination between persisting infection and re-infection. Throughout the last decades, new target antigens have been identified, and assays with improved performance and suitability for use in the field have been developed. For numerous assays, large-scale studies are still required to reliably characterise assay characteristics alone and in association with other available methods for the diagnosis of schistosomiasis. Apart from S. mansoni, S. haematobium and S. japonicum, for which most available tests were developed, other species of Schistosoma that occur less frequently need to be taken into account. This narrative review describes and critically discusses the results of published studies on the evaluation of serological assays that detect antibodies against different Schistosoma species of humans. It provides insights into the diagnostic performance and an overview of available assays and their suitability for large-scale use or individual diagnosis, and thus sets the scene for serological diagnosis of schistosomiasis and the interpretation of results.

19 May 2010 in Cerebrovascular Diseases
Verified
Journal Article
Closed access
PDF file
HWHans Worthmann
Hans Worthmann
ATA.B. Tryc
A.B. Tryc
AGA. Goldbecker
A. Goldbecker
YMY.T. Ma
Y.T. Ma
ATArgyro Tountopoulou
Argyro Tountopoulou
KWK. Weissenborn
K. Weissenborn
Background: Early inflammation has been suggested as an important factor contributing to unfavorable prognosis after acute ischemic stroke. The present study aimed to clarify the temporal dynamics of discrete inflammatory markers/mediators for future mechanism-targeting anti-inflammatory strategies in ischemic brain damage. Methods: Blood samples of 69 patients with transient ischemic attack or ischemic stroke were taken upon admission and at time points 6, 12 and 24 h, as well as 3 and 7 days after symptom onset for analysis of monocyte chemotactic protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), interleukin-6 (IL-6), C-reactive protein (CRP) and the brain damage marker S100B. Clinical scores (modified Rankin Scale, National Institute of Health Stroke Scale) were assessed on day 90. Results: MCP-1, MMP-9, TIMP-1, IL-6, CRP and S100B showed significantly different time courses depending on stroke outcome. While the levels of IL-6, MCP-1 and MMP-9 increased already a few hours after symptom onset, CRP and S100B gradually rose commencing at 12–24 h. TIMP-1 demonstrated an extended plateau. By multiple linear regression analysis IL-6, MCP-1, TIMP-1 and S100B were determined to be independently related to clinical outcome scores at specific time points. Conclusions: Our data show important differences in the early time course of several potential markers for the complex network of inflammation and brain damage after ischemic stroke depending on stroke outcome. This must be considered for any therapeutical approach using anti-inflammatory treatment.

8 December 2009 in Genes, Chromosomes and Cancer
Verified
Journal Article
Closed access
PDF file
KLKathrin Lange
Kathrin Lange
LHLisa Holm
Lisa Holm
KNKirsten Vang Nielsen
Kirsten Vang Nielsen
AHAndreas Hahn
Andreas Hahn
WHWinfried Hofmann
Winfried Hofmann
GGGudrun Göhring
Gudrun Göhring

7 September 2013 in American Journal of Epidemiology
Verified
Journal Article
Open access
PDF file
NGNan Guo
Nan Guo
CBCarola Bindt
Carola Bindt
MBMarguerite Te Bonle
Marguerite Te Bonle
JAJohn Appiah-Poku
John Appiah-Poku
RHRebecca Hinz
Rebecca Hinz
ETEgbert Tannich
Egbert Tannich
In low-income countries, perinatal depression is common, but longitudinal data on its influence on child health are rare. We examined the association between maternal depression and febrile illness in children. There were 654 mother/child dyads in Ghana and Côte d'Ivoire that were enrolled in a prospective birth cohort in 2010–2011 and underwent 2-years of follow up. Mothers were examined for depression using the Patient Health Questionnaire depression module antepartum and 3 and 12 months postpartum. The hazard of febrile illness in children of depressed and nondepressed mothers was estimated using a recurrent event Cox proportional hazards model. The prevalences of antepartum depression in mothers from Côte d'Ivoire and Ghana were 28.3% and 26.3%, respectively. The prevalences of depression at 3 and 12 months postpartum were 11.8% and 16.1% (Côte d'Ivoire) and 8.9% and 7.2% (Ghana). The crude and adjusted (for country and socioeconomic status) hazard ratios of febrile illness in children of depressed mothers compared with those in children of nondepressed mothers were 1.57 (95% confidence interval: 1.20, 2.07) and 1.32 (95% confidence interval: 1.01, 1.74) respectively. Perinatal depression was frequent and associated with febrile illness in the offspring. Our results showed that a high prevalence of depression in sub-Saharan Africa may pose a serious public health threat to women and their offspring.

1 June 2011 in Digestive and Liver Disease
Verified
Journal Article
Closed access
BBBita Boozari
Bita Boozari
BSBisharah Soudah
Bisharah Soudah
KRKinan Rifai
Kinan Rifai
SSSabine Schneidewind
Sabine Schneidewind
Arndt VogelArndt Vogel
Arndt Vogel
MGMichael Gebel
Michael Gebel