Wilhelm Bloch

Deutsche Sporthochschule Köln, Köln, North Rhine-Westphalia, Germany

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Publications (383)1329.85 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Benzo[a]pyrene (BaP) is a known carcinogenic and cell damaging agent. The underlying cell damaging pathomechanisms have not been totally revealed. Especially BaP-related induction of oxidative and nitrosative stress has not been previously investigated in detail. The presented study investigated these effects in order to elucidate the pathomechanism and as well to identify potential biological markers that may indicate a BaP exposure. Human immortalized keratinocytes (HaCaT cells) were exposed to BaP (1 μM) for either 5 minutes or 6 hours, respectively. BaP-induced cellular damage was evaluated by immunocytochemistry analysis of multiple signaling cascades (e.g. apoptosis, Akt, MAPK, NOS, nitrotyrosine and 8-isoprostane formation), detection of nitrosative stress using diaminofluorescein (DAF-FM) and oxidative stress using 3'-(p aminophenyl)fluorescein (APF). Our results show that BaP exposure significantly enhanced NO and ROS productions in HaCaT cells. BaP led to eNOS-phosphorylation at Ser(1177), Thr(495) and Ser(116) residues. Using specific inhibitors, we found that the Erk1/2 pathways seemed to have strong impact on eNOS phosphorylation. In addition, BaP-induced apoptosis was observed by caspase-3 activation and PARP cleavage. Our results suggest that BaP mediates its toxic effect in keratinocytes through oxidative and nitrosative stress which is accompanied by complex changes of eNOS phosphorylation and changes of Akt and MAPK pathways.
    Toxicology in Vitro 03/2014; · 2.65 Impact Factor
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    ABSTRACT: We investigated the cellular distribution of lactate transporter (MCT1) and its chaperone CD147 (using immunohistochemistry and fluorescence-activated cell sorting) in the erythrocytes of men with non-insulin-dependent type-2 diabetes (NIDDM, n = 11, 61 ± 8 years of age) under acute exercise (ergometer cycling test, World Health Organisation scheme) performed before and after a 3-month strength training program. Cytosolic MCT1 distribution and membraneous CD147 density did not change after acute exercise (ergometer). After the 3-month strength training, MCT1-density was increased and the reaction of MCT1 (but not that of CD147) towards acute exercise (ergometer) was altered. MCT1 localisation was shifted from the centre to the cellular membrane. This resulted in a decrease in the immunohistochemically measured cytosolic MCT1-density. We conclude that strength training alters the acute exercise reaction of MCT1 but not that of CD147 in erythrocytes in patients with NIDDM. This reaction may contribute to long-term normalisation and stabilisation of the regulation of lactate plasma concentration in NIDDM.
    Canadian Journal of Physiology and Pharmacology 03/2014; 92(3):259-62. · 1.56 Impact Factor
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    ABSTRACT: Intermittent intense ultraviolet (UV) exposure represents an important aetiological factor in the development of malignant melanoma. The ability of UV radiation to cause tumour-initiating DNA mutations in melanocytes is now firmly established, but how the microenvironmental effects of UV radiation influence melanoma pathogenesis is not fully understood. Here we report that repetitive UV exposure of primary cutaneous melanomas in a genetically engineered mouse model promotes metastatic progression, independent of its tumour-initiating effects. UV irradiation enhanced the expansion of tumour cells along abluminal blood vessel surfaces and increased the number of lung metastases. This effect depended on the recruitment and activation of neutrophils, initiated by the release of high mobility group box 1 (HMGB1) from UV-damaged epidermal keratinocytes and driven by Toll-like receptor 4 (TLR4). The UV-induced neutrophilic inflammatory response stimulated angiogenesis and promoted the ability of melanoma cells to migrate towards endothelial cells and use selective motility cues on their surfaces. Our results not only reveal how UV irradiation of epidermal keratinocytes is sensed by the innate immune system, but also show that the resulting inflammatory response catalyses reciprocal melanoma-endothelial cell interactions leading to perivascular invasion, a phenomenon originally described as angiotropism in human melanomas by histopathologists. Angiotropism represents a hitherto underappreciated mechanism of metastasis that also increases the likelihood of intravasation and haematogenous dissemination. Consistent with our findings, ulcerated primary human melanomas with abundant neutrophils and reactive angiogenesis frequently show angiotropism and a high risk for metastases. Our work indicates that targeting the inflammation-induced phenotypic plasticity of melanoma cells and their association with endothelial cells represent rational strategies to specifically interfere with metastatic progression.
    Nature 02/2014; · 38.60 Impact Factor
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    ABSTRACT: This pilot study aimed to investigate the feasibility of two different training programs in patients with advanced gastrointestinal cancer undergoing palliative chemotherapy. Potential effects of training programs on the patients' quality of life, physical performance, physical activity in daily living, and biological parameters were exploratorily evaluated. Patients were randomly assigned to a resistance (RET) and aerobic exercise training group (AET). Both underwent supervised training sessions twice a week for 12 weeks. RET was performed at 60-80 % of the one-repetition maximum and consisted of 2-3 sets of 15-25 repetitions. The AET group performed endurance training at 60-80 % of their predetermined pulse rate (for 10 to 30 min). A total of 26 gastrointestinal cancer patients could be randomized. Twenty-one patients completed the 12 weeks of intervention. The median adherence rate to exercise training of all 26 patients was 65 %, while in patients who were able to complete 12 weeks, adherence was 75 %. The fatigue score of all patients decreased from 66 to 43 post-intervention. Sleeping duration increased in both groups and muscular strength increased in the RET group. A higher number of steps in daily living was associated with higher levels of physical and social functioning as well as lower scores for pain and fatigue. RET and AET are feasible in gastrointestinal cancer patients undergoing palliative chemotherapy. Both training programs seem to improve cancer-related symptoms as well as the patient's physical activities of daily living.
    Supportive Care in Cancer 02/2014; · 2.09 Impact Factor
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    ABSTRACT: The transcription factor Nrf2 is a key regulator of the cellular stress response, and pharmacological Nrf2 activation is a promising strategy for skin protection and cancer prevention. We show here that prolonged Nrf2 activation in keratinocytes causes sebaceous gland enlargement and seborrhea in mice due to upregulation of the growth factor epigen, which we identified as a novel Nrf2 target. This was accompanied by thickening and hyperkeratosis of hair follicle infundibula. These abnormalities caused dilatation of infundibula, hair loss, and cyst development upon aging. Upregulation of epigen, secretory leukocyte peptidase inhibitor (Slpi), and small proline-rich protein 2d (Sprr2d) in hair follicles was identified as the likely cause of infundibular acanthosis, hyperkeratosis, and cyst formation. These alterations were highly reminiscent to the phenotype of chloracne/"metabolizing acquired dioxin-induced skin hamartomas" (MADISH) patients. Indeed, SLPI, SPRR2, and epigen were strongly expressed in cysts of MADISH patients and upregulated by dioxin in human keratinocytes in an NRF2-dependent manner. These results identify novel Nrf2 activities in the pilosebaceous unit and point to a role of NRF2 in MADISH pathogenesis.
    EMBO Molecular Medicine 02/2014; · 7.80 Impact Factor
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    ABSTRACT: p63 is a multi-isoform member of the p53 family of transcription factors. There is compelling genetic evidence that ΔNp63 isoforms are needed for keratinocyte proliferation and stemness in the developing vertebrate epidermis. However, the role of TAp63 isoforms is not fully understood, and TAp63 knockout mice display normal epidermal development. Here, we show that zebrafish mutants specifically lacking TAp63 isoforms, or p53, display compromised development of breeding tubercles, epidermal appendages which according to our analyses display more advanced stratification and keratinization than regular epidermis, including continuous desquamation and renewal of superficial cells by derivatives of basal keratinocytes. Defects are further enhanced in TAp63/p53 double mutants, pointing to partially redundant roles of the two related factors. Molecular analyses, treatments with chemical inhibitors and epistasis studies further reveal the existence of a linear TAp63/p53->Notch->caspase 3 pathway required both for enhanced proliferation of keratinocytes at the base of the tubercles and their subsequent differentiation in upper layers. Together, these studies identify the zebrafish breeding tubercles as specific epidermal structures sharing crucial features with the cornified mammalian epidermis. In addition, they unravel essential roles of TAp63 and p53 to promote both keratinocyte proliferation and their terminal differentiation by promoting Notch signalling and caspase 3 activity, ensuring formation and proper homeostasis of this self-renewing stratified epithelium.
    PLoS Genetics 01/2014; 10(1):e1004048. · 8.52 Impact Factor
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    ABSTRACT: Acute ischemic injury is a strong inductor of cardiac remodelling, resulting in structural changes of the extracellular matrix (ECM) and basement membrane (BM). In a large animal model of ischemia-reperfusion (I/R) we investigated the post-ischemic liberation of the collagen-IV-fragments Tumstatin (TUM; 28 kDa-fragment of collagen-IV-alpha-3), Arresten (ARR; 26 kDa-fragment of collagen-IV-alpha-1) and Endorepellin (LG3, 85 kDa-fragment of perlecan) which are biologically active in angiogenesis and vascularization in the post-ischemic myocardium. In this blinded study, 30 pigs were randomized to 60 min of global I/R at either 4°C or 32°C or served as control. Three transmyocardial tissue samples were collected prior to ischemia and within 30 min and 150 min of reperfusion. Tissue content of TUM, ARR and LG3 was analyzed by western blotting and immunostaining. Within 150 min of mild hypothermic I/R a significantly increased tissue content of ARR (0.17±0.14 vs. 0.56±0.56; p = 0.001) and LG3 (1.13±0.34 vs. 2.51±1.71, p<0.001) was observed. In contrast, deep hypothermic I/R was not associated with a significant release of cleavage products. Cleavage of TUM remained unchanged irrespective of temperature. Increased matrix processing following mild hypothermia I/R is further supported by a >11fold elevation of creatine kinase (2075±2595 U/l vs. 23248±6551 U/l; p<0.001) in the coronary sinus plasma samples. Immunostaining demonstrated no changes for ARR and LG3 presentation irrespective of temperature. In contrast, TUM significantly decreased in the BM surrounding cardiomyocytes and capillaries after mild and deep hypothermic I/R, thus representing structural alterations of the BM in these groups. The study demonstrates an early temperature-dependent processing of Col-IV as major component of the BM of cardiomyocytes and vascular endothelium. These observations support the protective effects of deep hypothermia during I/R. Furthermore, the results suggest an increased structural remodelling of the myocardial basement membrane with potential functional impairment during mild hypothermic I/R which may contribute to the progression to post-ischemic heart failure.
    PLoS ONE 01/2014; 9(3):e92833. · 3.73 Impact Factor
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    ABSTRACT: Type 2 diabetes mellitus associated with obesity, or "diabesity", coincides with an altered nitric oxide (NO) metabolism in skeletal muscle. Three isoforms of nitric oxide synthase (NOS) exist in human skeletal muscle tissue. Both neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) are constitutively expressed under physiological conditions, producing low levels of NO, while the inducible nitric oxide synthase (iNOS) is strongly up-regulated only under pathophysiological conditions, excessively increasing NO concentrations. Due to chronic inflammation, overweight/obese type 2 diabetic patients exhibit up-regulated protein contents of iNOS and concomitant elevated amounts of NO in skeletal muscle. Low muscular NO levels are important for attaining an adequate cellular redox state - thereby maintaining metabolic integrity - while high NO levels are believed to destroy cellular components and to disturb metabolic processes, e.g., through strongly augmented posttranslational protein S-nitrosylation. Physical training with submaximal intensity has been shown to attenuate inflammatory profiles and iNOS protein contents in the long term. The present review summarizes signaling pathways which induce iNOS up-regulation under pathophysiological conditions and describes molecular mechanisms by which high NO concentrations are likely to contribute to triggering skeletal muscle insulin resistance and to reducing mitochondrial capacity during the development and progression of type 2 diabetes. Based on this information, it discusses the beneficial effects of regular physical exercise on the altered NO metabolism in the skeletal muscle of overweight/obese type 2 diabetic subjects, thus unearthing new perspectives on training strategies for this particular patient group.
    Nitric Oxide 12/2013; · 3.27 Impact Factor
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    ABSTRACT: The main problems of autogenous bone transplants are their unpredictable atrophy and their loss of structure. One key factor lies in the poor revascularization of simple onlay grafts. The the aim of this study was to evaluate the revascularization processes in autogenous bone grafts from the iliac crest to the alveolar ridge. In a sheep model, autogenous bone grafts were harvested from the iliac crest. A combination of a resorbable collagen membrane (CM) and deproteinized bovine bone material (DBBM) was used to modify the bone graft (experiment 2). This was compared with a simple onlay bone graft (control group, experiment 1). The amount of vessels in bone and connective tissue (CT), and the amount of CT were analyzed. The expression of von Willebrand factor (vWF) was compared between the two experimental groups using immunohistochemical analysis. The ratio of the amount of vessels in bone and CT changed over time, and more vessels could be detected in bone at 12-16 weeks of graft healing. The number of vessels were significantly higher in experiment 2 than in experiment 1. More CT was found in experiment 1, whereas the amount of CT in both experiments decreased over time. This study shows a more intensive and extensive revascularization in experiment 2, as significantly more vessels were detected. The decreased amount of CT in experiment 2 clarifies its clinical superiority.
    Head & Face Medicine 12/2013; 9(1):40. · 0.98 Impact Factor
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    ABSTRACT: The aim of the study protocol is to investigate different adapted physical training programs in patients with advanced lung cancer undergoing palliative chemo- or radiotherapy and to evaluate their effects on physical performance, quality of life, symptom burden, and efficacy of oncologic treatment. Patients will be randomised into three study arms: interventional group 1 performing aerobic exercise, interventional group 2 performing resistance training, and a control group without specific physical training. Interventional training will be performed for 12weeks consisting of two supervised and one self-instructed training sessions per week each. Respiratory therapy over 12weeks is provided in all three study arms as an established supportive therapy in lung cancer patients. Primary efficacy endpoint is physical performance measured by peak oxygen consumption (VO2peak). Secondary efficacy endpoints include additional parameters of physical performance (resistance, lung function, perceived exertion, level of physical activity and IPAQ-questionnaire), health-related quality of life (EORTC QLQ C30-questionnaire), disease and treatment related symptoms (Memorial Symptom Assessment Scale), biologic parameter (e.g. body composition, blood values of immune system, chronic inflammation, glucose and lipid metabolism), and parameter of efficacy of oncologic treatment. The results of this study will offer an overview over possible effects of specific training interventions on health related quality of life, physical and psychological symptoms, and on the efficacy of oncologic treatment. The primary aim of this study is to detect adapted intervention programs for metastatic lung cancer undergoing palliative chemotherapy.
    Contemporary clinical trials 12/2013; · 1.51 Impact Factor
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    ABSTRACT: The present manuscript seeks to discuss methodological aspects regarding the application of the novel unloading orthosis 'HEPHAISTOS' that has been specifically developed to study physiological effects of muscular unloading without altering the impact of gravitational loading. The 'HEPHAISTOS' has been applied in an ambulatory clinical interventional study. During gait, the 'HEPHAISTOS' significantly reduces activation and force production of calf muscles while it completely retains body mass-related force on the tibia. Eleven healthy male subjects participated in the study and followed their normal everyday lives while wearing the orthosis. Several measurement sessions have been performed to investigate the time course of structural and functional adaptations during intervention and recovery. Follow-up measurements were performed for one year after the intervention. In consideration of the experiences of a unique ambulant unloading study, organizational and methodological recommendations are discussed in this manuscript. Activity monitoring data obtained with portable accelerometers reveal unchanged gait activities and good subject compliance throughout the intervention. Moreover, electromyography (EMG) and motion data investigating gait properties on reambulation day are illustrated. These data show that during the initial steps following removal of 'HEPHAISTOS', gait was significantly asynchronous indicating an acutely altered motor control in the unloaded lower leg muscles.
    Journal of musculoskeletal & neuronal interactions 12/2013; 13(4):487-95. · 2.45 Impact Factor
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    ABSTRACT: Botulinum toxin A (BTX)-induced muscle paralysis results in pronounced bone degradation with substantial bone loss. We hypothesized that whole-body vibration (WBV) and insulin-like growth factor-I (IGF-I) treatment can counteract paralysis-induced bone degradation following BTX injections by activation of the protein kinase B (Akt) signaling pathway. Female C57BL/6 mice (n = 60, 16 weeks) were assigned into six groups (n = 10 each): SHAM, BTX, BTX+WBV, BTX+IGF-I, BTX+WBV+IGF-I, and a baseline group, which was killed at the beginning of the study. Mice received a BTX (1.0 U/0.1 mL) or saline (SHAM) injection in the right hind limb. The BTX+IGF-I and BTX+WBV+IGF-I groups obtained daily subcutaneous injections of human IGF-I (1 μg/day). The BTX+WBV and BTX+WBV+IGF-I groups underwent WBV (25 Hz, 2.1 g, 0.83 mm) for 30 min/day, 5 days/week for 4 weeks. Femora were scanned by pQCT, and mechanical properties were determined. On tibial sections TRAP staining, static histomorphometry, and immunohistochemical staining against Akt, phospho-Akt, IGF-IR (IGF-I receptor), and phospho-IGF-IR were conducted. BTX injection decreased trabecular and cortical bone mineral density. The WBV and WBV+IGF-I groups showed no difference in trabecular bone mineral density compared to the SHAM group. The phospho-IGF-IR and phospho-Akt stainings were not differentially altered in the injected hind limbs between groups. We found that high-frequency, low-magnitude WBV can counteract paralysis-induced bone loss following BTX injections, while we could not detect any effect of treatment with IGF-I.
    Calcified Tissue International 11/2013; · 2.50 Impact Factor
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    ABSTRACT: The aim of the present study was to compare the effects of active (A) vs. passive (P) recovery during high-intensity interval training on the acute hormonal and metabolic response. Twelve triathletes/cyclists performed four 4 min intervals on a cycle ergometer, either with A- or P-recovery between each bout. Testosterone, hGH, cortisol, VEGF, HGF and MIF were determined pre, 0', 30', 60' and 180' after both interventions. Metabolic perturbations were characterized by lactate, blood gas and spirometric analysis. A-recovery caused significant increases in circulating levels of cortisol, testosterone, T/C ratio, hGH, VEGF and HGF. Transient higher levels were found for cortisol, testosterone, hGH, VEGF, HGF and MIF after A-recovery compared to P-recovery, despite no differences in metabolic perturbations. A-recovery was more demanding from an athlete's point of view. Based on the data of testosterone, hGH and the T/C-ratio, as well as on the data of VEGF and HGF it appears that this kind of exercise protocol with A-recovery phases between the intervals may promote anabolic processes and may lead to pro-angiogenic conditions more than with P-recovery. These data support the findings that also the long term effects of both recovery modes seem to differ, and that both can induce specific adaptations.
    International Journal of Sports Medicine 11/2013; · 2.27 Impact Factor
  • 10/2013;
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    ABSTRACT: In the light of the dynamic nature of habitual plantar flexor activity, we utilized an incremental isokinetic exercise test (IIET) to assess the work-related power deficit (WoRPD) as a measure for exercise-induced muscle fatigue before and after prolonged calf muscle unloading and in relation to arterial blood flow and muscle perfusion. Eleven male subjects (31 ± 6 years) wore the HEPHAISTOS unloading orthosis unilaterally for 56 days. It allows habitual ambulation while greatly reducing plantar flexor activity and torque production. Endpoint measurements encompassed arterial blood flow, measured in the femoral artery using Doppler ultrasound, oxygenation of the soleus muscle assessed by near-infrared spectroscopy, lactate concentrations determined in capillary blood and muscle activity using soleus muscle surface electromyography. Furthermore, soleus muscle biopsies were taken to investigate morphological muscle changes. After the intervention, maximal isokinetic torque was reduced by 23·4 ± 8·2% (P<0·001) and soleus fibre size was reduced by 8·5 ± 13% (P = 0·016). However, WoRPD remained unaffected as indicated by an unchanged loss of relative plantar flexor power between pre- and postexperiments (P = 0·88). Blood flow, tissue oxygenation, lactate concentrations and EMG median frequency kinematics during the exercise test were comparable before and after the intervention, whereas the increase of RMS in response to IIET was less following the intervention (P = 0·03). In conclusion, following submaximal isokinetic muscle work exercise-induced muscle fatigue is unaffected after prolonged local muscle unloading. The observation that arterial blood flow was maintained may underlie the unchanged fatigability.
    Clinical Physiology and Functional Imaging 10/2013; · 1.33 Impact Factor
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    ABSTRACT: Most scientific studies regarding physical activity in cancer patients involve breast cancer patients. It is apparent that physical activity during medical treatment and aftercare is not only feasible and safe but also effective. Current studies clearly show that regular and specific endurance and/or resistance training can reduce a number of side effects caused by medical treatment. Among others, improvements in physical performance, body composition, and quality of life as well as a reduction in fatigue, have been observed. Since inactivity appears to exacerbate lymphedema, patients with lymphedema are also encouraged to exercise. Few studies have been carried out regarding physical exercise in metastatic patients. However, experts in the field also recommend regular physical activity for patients with advanced-stage breast cancer.
    Breast Care 10/2013; 8(5):330-334. · 0.68 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate the role of oxidative and nitrosative stress in autogenous bone grafts to the mandible based on immunohistochemical analysis. Using a well-established sheep model autogenous bone grafts were harvested form the iliac bone. A combination of a Collagen Membrane (CM) and Deproteinized Bovine Bone Material (DBBM) was used to cover the bone graft (Experiment 2). This modification was compared with simple onlay bone grafts (Experiment 1). Immunohistochemically, the expression of specific stable degradation products of oxidative and nitrosative stress was compared between the two experimental groups. Specific markers for oxidative and nitrosative stress showed statistically significant differences in expression in the different experimental groups. The influence of oxidative and nitrosative stress on osteoblasts (OB), osteoclasts (OC), and osteocytes (OCy) was analysed. Experiment 2 showed increased expression of markers in OB and decreased expression in OC. Taking the result of this study and reports from the literature into consideration grafts in Experiment 2 showed less resorption and atrophy, higher activity of OB and inhibition of OC, and less expression of Reactive Oxygen and Nitrogen Species (RONS) as markers of oxidative stress within the graft. These data illustrate the improved remodelling processes in grafts using CM and DBBM.
    Journal of cranio-maxillo-facial surgery: official publication of the European Association for Cranio-Maxillo-Facial Surgery 09/2013; · 1.25 Impact Factor
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    ABSTRACT: Purpose: This investigation assessed whether endurance training altered the red cell deformability (RCD) of male HIV patients. Methods: Eight subjects (38 ± 9 years, BMI 23 ± 3.6 kg/m2, highly active antiretroviral therapy) trained for a marathon run for the duration of one year. Each subject underwent an acute exercise test on a treadmill at the beginning of this study (baseline) and after four months of training. Blood samples were taken at rest (T0) and at the end (T1) of each exercise test, as well as before (T0) and after the marathon run (T1). RCD was measured using the Laser Assisted Optical Rotational Cell Analyzer (LORCA), the maximal elongation index (EImax) and shear stress at half maximal deformation (SS 1/2 were determined using the Lineweaver Burke model. Results: No changes were observed in RCD and SS 1/2 between T0 and T1 in all measurements. EImax significantly increased between T0 baseline and T0 after four months of training (P < 0.05). Measurements prior to the marathon run revealed significantly decreased EImax and SS 1/2 values (P < 0.05). Conclusions: The intensity of training in pathophysiological diseases like HIV is dependent for the alterations in RCD and possible improvements in microcirculation.
    Clinical hemorheology and microcirculation 09/2013; · 3.40 Impact Factor
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    ABSTRACT: It has been demonstrated that alterations of adipocytokines can alter immune status in type 2 diabetes. The present study investigated changes of adipocytokine plasma concentrations and cellular immune status in overweight men, suffering from non-insulin dependent type 2 diabetes (n=14, age 61.0±8.7 years, BMI 31.1±3.5 kg/cm2). Subjects underwent a 3 months endurance exercise intervention (twice per week for up to 45 min) cycling at a heart rate corresponding to a 2 mmol/l lactate threshold. Before and after the intervention testing for adipocytokines (leptin, adiponectin, resistin) and cellular immune status (including T memory-cells and regulative T-cells) was performed by RIA and FACS accordingly.The exercise intervention improved anthropometric and metabolic parameters of all subjects. We observed a significant decline for resistin and for the CD19+ B-cells. The CD4+CD25+CD127low Treg-cells decreased, however not statistically significant. All other parameters remained unchanged.In conclusion, even though only training twice a week, the exercise affected parts of the cellular immune system as well as resistin levels in men suffering from non-insulin dependent type 2 diabetes.
    Experimental and Clinical Endocrinology & Diabetes 08/2013; 121(8):475-82. · 1.56 Impact Factor
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    ABSTRACT: Fatigue is a serious problem for the majority of patients with cancer. In this context, several studies have shown benefits of physical activity during and following treatment. However, uncertainties remain regarding the optimal type and duration of physical activity. Therefore, this study examined the relationship between cancer-related fatigue and physical activity in the course of inpatient rehabilitation. Fatigue (Multidimensional Fatigue Inventory) and physical activity (Freiburg Questionnaire of Physical Activity) were assessed in a consecutive series of 35 patients with cancer attending oncological inpatient rehabilitation during a six-month study period. The three-week rehabilitation program included daily exercise therapy consisting of aerobic endurance training, moderate resistance training, coordination exercises, relaxation training and individual physiotherapy. At discharge, a significant improvement in each dimension of cancer-related fatigue (p=0.001-0.003) and a significant increase of physical activity levels (p=0.001) were observed. A small, but significant negative correlation was found between cancer-related fatigue and the level of physical activity (R=-0.438, p=0.004). The largest effects were associated with a weekly energy expenditure of 3000 kcal through physical activity. The results support a non-linear dose-response relationship between cancer-related fatigue and physical activity. Since this is the first study providing specific exercise recommendations for an effective treatment of cancer-related fatigue in the context of inpatient rehabilitation, further research is required to validate the observed trends.
    Anticancer research 08/2013; 33(8):3415-22. · 1.71 Impact Factor

Publication Stats

6k Citations
1,329.85 Total Impact Points

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  • 2004–2014
    • Deutsche Sporthochschule Köln
      • • Institut für Trainingswissenschaft und Sportinformatik
      • • Institut für Kreislaufforschung und Sportmedizin
      Köln, North Rhine-Westphalia, Germany
    • Università degli Studi di Torino
      Torino, Piedmont, Italy
  • 2006–2013
    • University Medical Center Hamburg - Eppendorf
      • Department of Urology
      Hamburg, Hamburg, Germany
    • Universitätsklinikum Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2002–2013
    • University of Bonn
      • Institut für Physiologie I
      Bonn, North Rhine-Westphalia, Germany
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2012
    • German Aerospace Center (DLR)
      Köln, North Rhine-Westphalia, Germany
  • 2005–2012
    • Universität Ulm
      • Clinic of Dermatology and Allergology
      Ulm, Baden-Württemberg, Germany
  • 2004–2012
    • Heinrich-Heine-Universität Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2002–2012
    • ETH Zurich
      • Department of Biology
      Zürich, ZH, Switzerland
  • 2000–2012
    • Nippon Medical School
      • Department of Otolaryngology
      Tokyo, Tokyo-to, Japan
  • 2007–2010
    • Max Planck Institute of Biochemistry
      • Department of Molecular Medicine
      München, Bavaria, Germany
  • 2009
    • University of Texas Medical School
      Houston, Texas, United States
    • Friedrich-Schiller-University Jena
      Jena, Thuringia, Germany
    • RWTH Aachen University
      Aachen, North Rhine-Westphalia, Germany
  • 1995–2009
    • University of Cologne
      • • Institute of Neurophysiology
      • • Department of Cardiothoracic Surgery
      • • Institute of Anatomy I
      • • Department of Internal Medicine
      • • Department of Neurology
      Köln, North Rhine-Westphalia, Germany
    • Institut für Diabetes Gerhardt Katsch
      Karlsburg, Mecklenburg-Vorpommern, Germany
  • 2008
    • Texas A&M University
      College Station, Texas, United States
  • 2005–2006
    • Axiogenesis AG
      Köln, North Rhine-Westphalia, Germany
  • 1999–2001
    • Lund University
      Lund, Skåne, Sweden
  • 1997
    • MediaPark Klinik Köln
      Köln, North Rhine-Westphalia, Germany