Leipzig University , located in Leipzig in the Free State of Saxony, Germany, is one of the oldest universities in the world and the second-oldest university in Germany. Famous alumni include Leibniz, Goethe, Ranke, Nietzsche, Wagner, Angela Merkel, Raila Odinga, Tycho Brahe and nine Nobel laureates are associated with this university.The university was founded on December 2, 1409 by Frederick I, Elector of Saxony and his brother William II, Margrave of Meissen, and originally comprised the four scholastic faculties. Since its inception the university has engaged in teaching and research for over 600 years without interruption. Wikipedia.
Bluher M.,University of Leipzig
Current Opinion in Endocrinology, Diabetes and Obesity | Year: 2012
Purpose of review: Obesity is associated with an increased risk of premature death and represents a fast growing worldwide health problem that is reaching epidemic proportions. Obesity significantly increases the risk of developing metabolic disorders, hypertension, coronary heart disease, stroke, and several types of cancer. However, a subgroup of 'healthy' obese patients seems to be protected against metabolic and cardiovascular obesity comorbidities. This review focuses on potential mechanisms underlying the healthy obese subphenotype. Recent findings: Individuals with obesity typically develop type 2 diabetes, dyslipidemia, fatty liver disease, gout, hypertension, and cardiovascular disease. In the past years it became clear that up to 30% of obese patients are metabolically healthy with insulin sensitivity similar to healthy lean individuals, lower liver fat content, and lower intima media thickness of the carotid artery than the majority of metabolically 'unhealthy' obese patients. Recent studies suggest that protection against development of hepatic steatosis, ectopic fat deposition, inflammation of visceral adipose tissue, and adipose tissue dysfunction contributes to healthy obesity. Summary: For the stratification of obesity treatment, definition of metabolically healthy or high-risk phenotypes will facilitate the identification of the obese person who will benefit the most from early lifestyle, bariatric surgery, or pharmacological interventions. © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Age-related effects of exercise training on diastolic function in heart failure with reduced ejection fraction: the Leipzig Exercise Intervention in Chronic Heart Failure and Aging (LEICA) Diastolic Dysfunction Study.
Sandri M.,University of Leipzig
European heart journal | Year: 2012
Diastolic dysfunction (DD) was identified as a predictor of adverse prognosis in heart failure with reduced ejection fraction (HFREF). It is, however, unknown if DD is improved by exercise training, which is known to induce reverse remodelling, and if the training effect is attenuated in elderly HFREF patients. We therefore assessed DD in a cohort of referent controls (RCs) and HFREF patients and studied the response of DD to endurance exercise in two age groups (≤55 years and ≥65 years). Sixty RC (30 ≤ 55 years, mean age 50 ± 5 years; 30 ≥ 65 years, 72 ± 4 years) and 60 HFREF patients (30 ≤ 55 years, 46 ± 5 years; 30 ≥ 65 years, 72 ± 5 years, EF 28 ± 5%) were randomized to 4 weeks of supervised endurance training or to a control group. Exercise training was effective in reducing LV isovolumetric relaxation time by 29% in young and by 26% in old HFREF patients (P< 0.05 for both). As assessed by tissue Doppler, septal E' increased by 37% in young and by 39% among old HFREF patients (P< 0.005 for both) resulting in a significant decrease in the E/E' ratio from 13 ± 1 to 10 ± 1 in young and 14 ± 1 to 11 ± 1 in old HFREF patients (P< 0.05 for both). Serum levels of N-terminal pro brain natriuretic peptide were significantly reduced after endurance training in HFREF patients of all ages. In HFREF, diastolic function is significantly impaired in all age groups. Endurance training is highly effective in improving left ventricular diastolic function in HFREF patients regardless of age. This study is registered at ClinicalTrials.gov (number: NCT00176319).
Mierke C.T.,University of Leipzig
Reports on Progress in Physics | Year: 2014
The role of mechanical properties in cancer disease and inflammation is still underinvestigated and even ignored in many oncological and immunological reviews. In particular, eight classical hallmarks of cancer have been proposed, but they still ignore the mechanics behind the processes that facilitate cancer progression. To define the malignant transformation of neoplasms and finally reveal the functional pathway that enables cancer cells to promote cancer progression, these classical hallmarks of cancer require the inclusion of specific mechanical properties of cancer cells and their microenvironment such as the extracellular matrix as well as embedded cells such as fibroblasts, macrophages or endothelial cells. Thus, this review will present current cancer research from a biophysical point of view and will therefore focus on novel physical aspects and biophysical methods to investigate the aggressiveness of cancer cells and the process of inflammation. As cancer or immune cells are embedded in a certain microenvironment such as the extracellular matrix, the mechanical properties of this microenvironment cannot be neglected, and alterations of the microenvironment may have an impact on the mechanical properties of the cancer or immune cells. Here, it is highlighted how biophysical approaches, both experimental and theoretical, have an impact on the classical hallmarks of cancer and inflammation. It is even pointed out how these biophysical approaches contribute to the understanding of the regulation of cancer disease and inflammatory responses after tissue injury through physical microenvironmental property sensing mechanisms. The recognized physical signals are transduced into biochemical signaling events that guide cellular responses, such as malignant tumor progression, after the transition of cancer cells from an epithelial to a mesenchymal phenotype or an inflammatory response due to tissue injury. Moreover, cell adaptation to mechanical alterations, in particular the understanding of mechano-coupling and mechano-regulating functions in cell invasion, appears as an important step in cancer progression and inflammatory response to injuries. This may lead to novel insights into cancer disease and inflammatory diseases and will overcome classical views on cancer and inflammation. In addition, this review will discuss how the physics of cancer and inflammation can help to reveal whether cancer cells will invade connective tissue and metastasize or how leukocytes extravasate and migrate through the tissue. In this review, the physical concepts of cancer progression, including the tissue basement membrane a cancer cell is crossing, its invasion and transendothelial migration as well as the basic physical concepts of inflammatory processes and the cellular responses to the mechanical stress of the microenvironment such as external forces and matrix stiffness, are presented and discussed. In conclusion, this review will finally show how physical measurements can improve classical approaches that investigate cancer and inflammatory diseases, and how these physical insights can be integrated into classical tumor biological approaches. © 2014 IOP Publishing Ltd.
Bluher M.,University of Leipzig
Current Opinion in Lipidology | Year: 2010
Purpose of review: The prevalence and severity of obesity are dramatically increasing throughout the world. Obesity causes a decline in life expectancy due to its associated metabolic and cardiovascular comorbid disorders. Therefore, it will become more important to distinguish obese individuals at high risk for obesity-related metabolic diseases from those who are metabolically 'healthy'. This review focuses on recent evidence suggesting that normal adipose tissue function contributes to the healthy obese phenotype. Recent findings: The majority of individuals with obesity develop insulin resistance, type 2 diabetes, dyslipidemia, gout, hypertension and cardiovascular disease. However, approximately 10-25% of obese individuals are metabolically healthy most likely due to preserved insulin sensitivity. Recent studies suggest that inflammation of visceral adipose tissue, ectopic fat deposition and adipose tissue dysfunction mediate insulin resistance in human obesity independently of total body fat mass. This suggests that mechanisms beyond a positive caloric balance such as inflammation and adipokine release determine the pathological metabolic consequences in patients with obesity. Summary: Recommendations for obesity treatment should distinguish the metabolically 'healthy' from 'unhealthy' obese phenotype to identify early the obese person who will benefit the most from losing weight. In addition, novel antiobesity treatment strategies targeting adipose tissue dysfunction are needed. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Katzerke C.,University of Leipzig
Blood | Year: 2013
The transcription factor CCAAT enhancer binding protein α (C/EBPα) is a master regulator in granulopoiesis and is frequently disrupted in acute myeloid leukemia (AML). We have previously shown that C/EBPα exerts its effects by regulating microRNAs (miRs) such as miR-223 and miR-34a. Here, we confirm miR-30c as a novel important target of C/EBPα during granulopoiesis. Thus, wild-type C/EBPα-p42 directly upregulates miR-30c expression, whereas C/EBPα-p30, found in AML, does not. miR-30c is downregulated in AML, especially in normal karyotype AML patients with CEBPA mutations. An induced C/EBPα knockout in mice leads to a significant downregulation of miR-30c expression in bone marrow cells. We identified NOTCH1 as a direct target of miR-30c. Finally, a block of miR-30c prevents C/EBPα-induced downregulation of Notch1 protein and leads to a reduced CD11b expression in myeloid differentiation. Our study presents the first evidence that C/EBPα, miR-30c, and Notch1 together play a critical role in granulocytic differentiation and AML, and particularly in AML with CEBPA mutations. These data reveal the importance of deregulated miRNA expression in leukemia and may provide novel biomarkers and therapeutic targets in AML.