Wilhelm Bloch

Publications (191)686.45 Total impact

• Article: Influence of a six month endurance exercise program on the immune function of prostate cancer patients undergoing Antiandrogen- or Chemotherapy: design and rationale of the ProImmun study.

  Philipp Zimmer, Elke Jäger, Wilhelm Bloch, Eva Maria Zopf, Freerk T Baumann
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  ABSTRACT: BACKGROUND: Exercise seems to minimize prostate cancer specific mortality risk and treatment related side effects like fatigue and incontinence. However the influence of physical activity on the immunological level remains uncertain. Even prostate cancer patients undergoing palliative treatment often have a relatively long life span compared to other cancer entities. To optimize exercise programs and their outcomes it is essential to investigate the underlying mechanisms. Further, it is important to discriminate between different exercise protocols and therapy regimes. METHODS: The ProImmun study is a prospective multicenter patient preference randomized controlled trial investigating the influence of a 24 week endurance exercise program in 80--100 prostate cancer patients by comparing patients undergoing Antiandrogen therapy combined with exercise (AE), Antiandrogen therapy without exercise (A), Chemotherapy with exercise(CE) or Chemotherapy without exercise (C). The primary outcome of the study is a change in prostate cancer relevant cytokines and hormones (IL-6, MIF, IGF-1, Testosterone). Secondary endpoints are immune cell ratios, oxidative stress and antioxidative capacity levels, VO2 peak, fatigue and quality of life. Patients of the intervention group exercise five times per week, while two sessions are supervised. During the supervised sessions patients (AE and CE) exercise for 33 minutes on a bicycle ergometer at 70-75% of their VO2 peak. To assess long term effects and sustainability of the intervention two follow-up assessments are arranged 12 and 18 month after the intervention. DISCUSSION: The ProImmun study is the first trial which primarily investigates immunological effects of a six month endurance exercise program in prostate cancer patients during palliative care. Separating patients treated with Antiandrogen therapy from those who are additionally treated with Chemotherapy might allow a more specific view on the influence of endurance training interventions and the impact of different therapy protocols on the immune function.Trial registrationGerman Clinical Trials Register: DRKS00004739.
  BMC Cancer 06/2013; 13(1):272. · 3.01 Impact Factor
• Article: Specific Deficit Analyses in Motor Performance and Quality of Life of Pediatric Cancer Patients-A Cross-Sectional Pilot Study.

  Julia Beulertz, Wilhelm Bloch, Aram Prokop, Freerk T Baumann
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  ABSTRACT: Although survival rates in childhood cancer have distinctly improved, pediatric cancer patients often experience various disease- and treatment-related side effects with long-term consequences. Despite current studies investigating inactivity and limitations in physical functioning and quality of life in pediatric cancer patients, only little information regarding specific deficits in physical functioning and quality of life has been available until now. No study has yet analyzed these parameters from a global perspective and then identified specific deficits in a mixed childhood cancer population. Within this cross-sectional pilot study, motor performance and quality of life of 26 pediatric cancer patients were assessed after inpatient medical treatment, using standardized motor test batteries (MOT 4-6; DMT 6-18) and a quality of life questionnaire (KINDL®). Reference data have been mainly provided by the German "Children and Young People Health Survey" (KiGGS). Patients achieved lower motor performance scores (p = .000) (more than 27% below the average of healthy peers). Specific deficits were identified in motor speed and motor control (4-6 years), as well as in endurance, strength and coordination under time pressure (6-17 years). In terms of quality of life, no significant differences were examined compared to healthy children of the same age. The results of this study confirm that children with oncological diseases frequently have specific motor problems. Future research in pediatric oncology must investigate the impact of targeted, individualized exercise interventions addressing these specific deficits.
  Pediatric Hematology and Oncology 03/2013; · 0.89 Impact Factor
• Article: Aldara activates TLR7-independent immune defence.

  Anne Walter, Matthias Schäfer, Virginia Cecconi, Claudia Matter, Mirjana Urosevic-Maiwald, Benedetta Belloni, Nicola Schönewolf, Reinhard Dummer, Wilhelm Bloch, Sabine Werner, Hans-Dietmar Beer, Alexander Knuth, Maries van den Broek
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  ABSTRACT: Aldara is a cream used for topical treatment of non-melanoma skin cancer, and is thought to act through stimulation of anti-tumour immunity. The active ingredient, imiquimod, has been shown to stimulate toll-like receptor 7. Aldara also induces psoriasis-like lesions when applied to naive murine skin, and as such is used as a mouse model for psoriasis. Here we find that in naive murine skin, Aldara induces inflammation largely independently of toll-like receptor 7. Surprisingly, inflammasome activation, keratinocyte death and interleukin 1 release also occur in response to the vehicle cream in the absence of imiquimod. We show that isostearic acid, a major component of the vehicle, promotes inflammasome activation in cultured keratinocytes, and so may contribute to the observed effects of Aldara on murine skin. Aldara therefore stimulates at least two immune pathways independently, and both imiquimod and vehicle are required for a full inflammatory response. Although it remains to be tested, it is possible that imiquimod-independent effects also contribute to the therapeutic efficacy of Aldara.
  Nature Communications 03/2013; 4:1560. · 7.40 Impact Factor
• Article: Deletion of integrin linked kinase in endothelial cells results in defective RTK signaling caused by caveolin 1 mislocalization.

  Daniela Malan, Andrea Elischer, Michael Hesse, Sara A Wickström, Bernd K Fleischmann, Wilhelm Bloch
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  ABSTRACT: Integrin linked kinase (ILK) connects the ILK-Pinch-Parvin complex with integrin adhesion sites. Because of the functional relevance of integrin-linked signaling for endothelial cell (EC) biology, we have explored this pathway in Ilk(-/-) embryonic stem (ES) cells differentiated into ECs and vessel-like structures. We have focused in particular on the mechanistic relevance of ILK-Pinch-Parvin complex-related signaling for EC development and tube formation. Our analysis revealed that the formation of vessel-like structures was strongly reduced in Ilk(-/-) ES cells and that this phenotype could be rescued by re-expression of ILK in ES cells. ECs were MACS sorted from wild-type (WT) and Ilk(-/-) ES cells and functional analysis using intracellular calcium imaging as the read-out yielded a complete lack of vascular endothelial growth factor- and epidermal growth factor-dependent responses. The possibility of a caveolin 1-related defect was investigated by transfecting WT and Ilk(-/-) ECs with a caveolin 1-EGFP fusion protein. Time-lapse microscopy showed that the prominent phenotype is due to altered dynamics of caveolin 1 and to a lack of positioning of caveolin 1 in the vicinity of the plasma membrane and that it is rescued by re-expressing ILK in the Ilk(-/-) ES cells. We also found that the defect is caused by the perturbed organization of microtubules and cortical actin filaments. Thus, ILK is required as a scaffold to allow actin-microtubule interactions and correct positioning of caveolin 1 close to the plasma membrane. This is crucial for signaling compartmentalization in ECs and explains the key role of ILK for EC development and function.
  Development 03/2013; 140(5):987-95. · 6.60 Impact Factor
• Article: Influence of a moderate physical activity intervention on red cell deformability in patients suffering from chronic obstructive pulmonary disease (COPD).

  Basit Ahmad, Nina Ferrari, Georgina Montiel, Wilhelm Bloch, Anke Raabe-Oetker, Nina Skrobala, Klara Brixius
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  ABSTRACT: The present study investigates whether a moderate physical activity intervention may alter red cell deformability (RCD) of patients suffering from chronic obstructive pulmonary disease (COPD). Subjects (n = 10; age: 62 ± 4; body-mass index (BMI): 25.8 ± 7.5) performed a training regimen for 10 weeks. In the beginning of the study and after the training period, COPD patients underwent a WHO cycle ergometry test. Venous blood samples were taken before (T0), immediately after (T1) and 30 min after (T2) the intervention. RCD was measured with the laser-assisted optical rotational cell analyzer (LORCA). Significant improvements of the RCD were detected. The semi-maximal shear stress increased significantly. Acute exhaustion had no effect on RCD. Thus, the training period of 10 weeks influenced RCD.
  Wiener Medizinische Wochenschrift 02/2013;
• Source

  Available from: Haymo Kurz

  Dataset: DevDyn2004.HagedornMetal

  Martin Hagedorn, Maurice Balke, Annette Schmidt, Wilhelm Bloch, Haymo Kurz, Sophie Javerzat, Benoît Rousseau, Joerg Wilting, Andreas Bikfalvi
• Article: The L-type Ca(2+) Channels Blocker Nifedipine Represses Mesodermal Fate Determination in Murine Embryonic Stem Cells.

  Filomain Nguemo, Bernd K Fleischmann, Manoj K Gupta, Tomo Sarić, Daniela Malan, Huamin Liang, Kurt Pfannkuche, Wilhelm Bloch, Heribert Schunkert, Jürgen Hescheler, Michael Reppel
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  ABSTRACT: Dihydropyridines (DHP), which nifedipine is a member of, preferentially block Ca(2+) channels of different cell types. Moreover, influx of Ca(2+) through L-type Ca(2+) channels (LTCCs) activates Ca(2+) signaling pathways, which in turn contribute to numerous cellular processes. Although LTCCs are expressed in undifferentiated cells, very little is known about its contributions to the transcriptional regulation of mesodermal and cardiac genes. This study aimed to examine the contribution of LTCCs and the effect of nifedipine on the commitment of pluripotent stem cells toward the cardiac lineage in vitro. The murine embryonic stem (ES, cell line D3) and induced pluripotent stem (iPS, cell clone 09) cells were differentiated into enhanced green fluorescence protein (EGFP) expressing spontaneously beating cardiomyocytes (CMs). Early treatment of differentiating cells with 10 µM nifedipine led to a significant inhibition of the cardiac mesoderm formation and cardiac lineage commitment as revealed by gene regulation analysis. This was accompanied by the inhibition of spontaneously occurring Ca(2+) transient and reduction of LTCCs current density (I(CaL)) of differentiated CMs. In addition, nifedipine treatment instigated a pronounced delay of the spontaneous beating embryoid body (EB) and led to a poor surface localization of L-type Ca(2+) channel α(1C) (Ca(V)1.2) subunits. Contrary late incubation of pluripotent stem cells with nifedipine was without any impact on the differentiation process and did not affect the derived CMs function. Our data indicate that nifedipine blocks the determined path of pluripotent stem cells to cardiomyogenesis by inhibition of mesodermal commitment at early stages of differentiation, thus the proper upkeep Ca(2+) concentration and pathways are essentially required for cardiac gene expression, differentiation and function.
  PLoS ONE 01/2013; 8(1):e53407. · 4.09 Impact Factor
• Source

  Available from: dx.plos.org

  Article: Perlecan maintains microvessel integrity in vivo and modulates their formation in vitro.

  Erika Gustafsson, Maylin Almonte-Becerril, Wilhelm Bloch, Mercedes Costell
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  ABSTRACT: Perlecan is a heparan sulfate proteoglycan assembled into the vascular basement membranes (BMs) during vasculogenesis. In the present study we have investigated vessel formation in mice, teratomas and embryoid bodies (EBs) in the absence of perlecan. We found that perlecan was dispensable for blood vessel formation and maturation until embryonic day (E) 12.5. At later stages of development 40% of mutant embryos showed dilated microvessels in brain and skin, which ruptured and led to severe bleedings. Surprisingly, teratomas derived from perlecan-null ES cells showed efficient contribution of perlecan-deficient endothelial cells to an apparently normal tumor vasculature. However, in perlecan-deficient EBs the area occupied by an endothelial network and the number of vessel branches were significantly diminished. Addition of FGF-2 but not VEGF(165) rescued the in vitro deficiency of the mutant ES cells. Furthermore, in the absence of perlecan in the EB matrix lower levels of FGFs are bound, stored and available for cell surface presentation. Altogether these findings suggest that perlecan supports the maintenance of brain and skin subendothelial BMs and promotes vasculo- and angiogenesis by modulating FGF-2 function.
  PLoS ONE 01/2013; 8(1):e53715. · 4.09 Impact Factor
• Article: Skeletal Muscle Function during Exercise-Fine-Tuning of Diverse Subsystems by Nitric Oxide.

  Frank Suhr, Sebastian Gehlert, Marijke Grau, Wilhelm Bloch
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  ABSTRACT: Skeletal muscle is responsible for altered acute and chronic workload as induced by exercise. Skeletal muscle adaptations range from immediate change of contractility to structural adaptation to adjust the demanded performance capacities. These processes are regulated by mechanically and metabolically induced signaling pathways, which are more or less involved in all of these regulations. Nitric oxide is one of the central signaling molecules involved in functional and structural adaption in different cell types. It is mainly produced by nitric oxide synthases (NOS) and by non-enzymatic pathways also in skeletal muscle. The relevance of a NOS-dependent NO signaling in skeletal muscle is underlined by the differential subcellular expression of NOS1, NOS2, and NOS3, and the alteration of NO production provoked by changes of workload. In skeletal muscle, a variety of highly relevant tasks to maintain skeletal muscle integrity and proper signaling mechanisms during adaptation processes towards mechanical and metabolic stimulations are taken over by NO signaling. The NO signaling can be mediated by cGMP-dependent and -independent signaling, such as S-nitrosylation-dependent modulation of effector molecules involved in contractile and metabolic adaptation to exercise. In this review, we describe the most recent findings of NO signaling in skeletal muscle with a special emphasis on exercise conditions. However, to gain a more detailed understanding of the complex role of NO signaling for functional adaptation of skeletal muscle (during exercise), additional sophisticated studies are needed to provide deeper insights into NO-mediated signaling and the role of non-enzymatic-derived NO in skeletal muscle physiology.
  International Journal of Molecular Sciences 01/2013; 14(4):7109-39. · 2.60 Impact Factor
• Article: Phosphorylation of myocardial eNOS is altered in patients suffering from type 2 diabetes.

  Ulrike Streit, Hannes Reuter, Wilhelm Bloch, Thorsten Wahlers, Robert H G Schwinger, Klara Brixius
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  ABSTRACT: Aim: The present study investigated whether eNOS-activation may be dysregulated in cardiac tissue of patients suffering from type 2 diabetes (T2D). Main methods: We performed immunohistochemical measurements of translocated eNOS-activation as well as eNOS-phosphorylation at Ser1177, Thr495, Ser 635, Ser114 and of the protein kinase B (Akt) in isolated right atrial trabeculae of patients undergoing cardiac bypass or valve surgery with (n=12, 68.1 ± 2.5 years) and without T2D (n=12, 64.7 ± 2.7 years). In addition, we investigated oxidative (8-isoprostane) and nitrosative stress markers (nitrotyrosine) as well as the effect of pharmacological stimulation of angiotensin (AT)-receptors on eNOS-phosphorylation. Key findings: Translocation-dependent eNOS-activation was similar in both groups. The same holds true for eNOS-phosphorylation at Ser114. eNOS-phosphorylation at Ser635 was significantly increased, whereas eNOS-phosphorylation of Ser1177 was significantly decreased in the diabetic group paralleled by a decrease in phosphorylation of Akt and Thr495. These alterations were accompanied by a significant decrease in nitrotyrosine. After application of angiotensin II (10 µM, 2 min.) for investigation of the AT-receptor-dependent eNOS-stimulation, we did not find differences between the increases in eNOS-Ser1177-phosphorylation in the non-diabetic (+39.7% ± 23.5%) and in the diabetic group (32.22% ± 11.45%). A simultaneous increase in Akt-phosphorylation could not be observed. Significance: The present study indicates that T2D goes along with a decrease in eNOS-phosphorylation at Ser1177 under basal conditions in cardiac tissue. Whether this may be attributed to the insulin resistance of cardiac muscle has to be further investigated. Receptor-stimulated eNOS-activation still works at least for angiotensin II-dependent eNOS-activation.
  Journal of Applied Physiology 12/2012; · 3.75 Impact Factor
• Article: Endothelial cell apoptosis: a new focal adhesion assembly makes the difference.

  Frank Suhr, Wilhelm Bloch
  Circulation Research 12/2012; 111(12):1488-90. · 9.49 Impact Factor
• Article: Influence of intermittent hypoxia interval training on exercise-dependent erythrocyte NOS activation and blood pressure in diabetic patients.

  Dennis Ladage, Christian Braunroth, Edward Lenzen, Sandra Berghöfer, Christine Graf, Wilhelm Bloch, Klara Brixius
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  ABSTRACT: NOS-activation in erythrocytes (eryNOS) is impaired in patients suffering from type 2 diabetes. We investigated the effect of physical exercise on eryNOS activation and whether 6 week hypoxia interval training may alter this process. Male patients with diabetes mellitus type 2 (NIDDM, n = 12; age, 61.3 ± 8.4 years; BMI, 29.8 ± 3.7 kg/m(2)) underwent physical exercise training before and after 6 week hypoxia interval training. Training was conducted 4 times per week for 90 min at 15.4-12.7 Vol% of inspired oxygen. Vital parameters were recorded. Before hypoxia intervention, eryNOS phosphorylation at serine(1177) decreased significantly during exercise (basal 17.4 ± 12.0 compared with exercise 8.4 ± 9.2 arbitrary grey values (arGV); P < 0.05). After 6 weeks of hypoxia intervention, eryNOS-pSer(1177) (2.2 ± 2.5 arGV) was significantly lower at baseline. Ergometry showed an increase (7.6 ± 3.0 arGV; P < 0.05) followed by a decrease to almost baseline levels after 30 min (3.8 ± 1.5 arGV). Maximal exercise capacity and O(2)-uptake ([Formula: see text]  max) increased significantly. The effects were independent from exercise-induced elevation of blood pressure. Exercise-dependent eryNOS phosphorylation at serine(1177) was increased similar to that described for the endothelium in diabetic patients. EryNOS dysregulation was partially restored after intermittent hypoxia training.
  Canadian Journal of Physiology and Pharmacology 12/2012; 90(12):1591-8. · 1.95 Impact Factor
• Article: Training-induced alterations of skeletal muscle mitochondrial biogenesis proteins in non-insulin-dependent type 2 diabetic men.

  Nana Chung, Thorsten Kreutz, Thorsten Schiffer, David Opitz, Robin Hermann, Sebastian Gehlert, Wilhelm Bloch, Klara Brixius, Christian Brinkmann
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  ABSTRACT: This study investigates whether regular physical activity (moderate endurance or resistance training twice a week for 3 months) influences the key regulatory molecules of mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α), nuclear respiratory factor-1 (NRF1), and mitochondrial transcription factor A (TFAM)) in patients suffering from non-insulin-dependent type 2 diabetes mellitus (T2DM) (n = 16, years = 62 ± 7, body mass index (BMI) = 30 ± 4 kg/m(2)). Seven T2DM men took part in endurance training, and 9 men participated in resistance training. BMI-matched non-diabetic male control subjects (CON) (n = 7, years = 53 ± 6, BMI = 30 ± 4 kg/m(2)) were studied for comparison. The protein contents of PGC1α, NRF1, and TFAM were determined using immunohistochemical staining methods on biopsies taken from the musculus vastus lateralis. At baseline, no differences were observed in NRF1-density between the T2DM men and the CON, while the contents of PGC1α and TFAM were decreased in the T2DM men. PGC1α and TFAM contents were not changed in the T2DM patients after the training period, but NRF1 was decreased. The down-regulation of mitochondrial signaling molecules might explain the patho-physiological reduction in mitochondrial biogenesis found in T2DM. Physical training, as performed in our study, did not reverse the down-regulation of mitochondrial signaling molecules - at least not at 3 months after the training.
  Canadian Journal of Physiology and Pharmacology 12/2012; 90(12):1634-41. · 1.95 Impact Factor
• Article: Histone methylation and acetylation indicates epigenetic change in the aged cochlea of mice.

  Ken-Ichi Watanabe, Wilhelm Bloch
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  ABSTRACT: It is currently accepted that epigenetics plays an important role in normal genetics and differentiation, and its failure triggers various diseases such as cancer, aging, metabolic diseases, and abnormal differentiations. The typical mechanism involves the modification of histones and the methylation of DNA. In this study, we investigated the modification of histones in the aged cochlea of mice using immunohistochemistry. Eight mice [C57BL/6(B6)] at the age of 8 weeks (young group) and 132 weeks (aged group) were used. Cochleas were fixed with paraformaldehyde and then decalcified. Hematoxylin-eosin staining was performed for the morphological study using a light microscope. After removing paraffin, the sections were incubated with the primary antibody to acetyl-histone H3 Lys9 or dimethyl-histone H3 Lys9. Confocal scanning microscopy was performed for observation. The degeneration was severest in the spiral ganglion cells and the organ of Corti of the basal turn as determined by light microscopy. Acetylated histone H3 was detected in the spiral ganglion cells and the organ of Corti of the young group, but not in those of the aged group. Dimethylated histone H3 was detected in the spiral ganglion cells and the organ of Corti of the aged group, but not in those of the young group. Acetylation was switched to methylation during ageing. Histone modification is known to have a critical role in neuro-degeneration. Our findings suggest that epigenetic change participates in the process of presbycusis.
  Archives of Oto-Rhino-Laryngology 10/2012; · 1.29 Impact Factor
• Source

  Available from: PubMed Central

  Article: Implementation and scientific evaluation of rehabilitative sports groups for prostate cancer patients: study protocol of the ProRehab Study.

  Eva M Zopf, Moritz Braun, Stefan Machtens, Jürgen Zumbé, Wilhelm Bloch, Freerk T Baumann
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  ABSTRACT: Although treatment regimen have improved in the last few years, prostate cancer patients following a radical prostatectomy still experience severe disease- and treatment-related side effects, including urinary incontinence, erectile dysfunction and psychological issues. Despite high incidence rates and the common adverse effects there is a lack of supportive measures for male patients and specific physical exercise recommendations for prostate cancer patients during rehabilitation or in the aftercare are still missing. The ProRehab Project aims to establish rehabilitative sports groups particularly for prostate cancer patients and to evaluate the effects of the offered exercise program. Starting 8-12 weeks after prostatectomy or combination therapy, prostate cancer patients will exercise for 15 months within a patient preference randomized controlled trial. One exercise session will be conducted within a pre-established rehabilitative sports group, while the other will be completed independently. Patients in the control group will not participate in the intervention. The main outcomes of the study include aerobic fitness, quality of life, incontinence and erectile dysfunction. By combining science, practice, and public relations the first rehabilitative sports groups for prostate cancer patients in Germany have been set up and thus contribute to the care structure for prostate cancer patients. By offering a 15-month physical exercise intervention that is conducted in supervised group sessions, long-term lifestyle changes and therefore improvements in quality of life in prostate cancer patients can be expected. German Clinical Trials Register DRKS00004184.
  BMC Cancer 07/2012; 12:312. · 3.01 Impact Factor
• Conference Proceeding: THE INFLUENCE OF WHOLE-BODY VIBRATION AND IGF-I ON MUSCLE PARALYSIS-INDUCED BONE DEGRADATION

  Anja Niehoff, Nina Hamann, Oana Ratiu, Philipp Lechner, Sven Reuter, Gert-Peter Brüggemann, Eckhard Schönau, Wilhelm Bloch, Ralf Beccard
  European Society of Biomechanics; 07/2012
• Article: Passive recovery is superior to active recovery during a high intensity shock microcycle.

  Patrick Wahl, Christoph Zinner, Christoph Grosskopf, Roman Rossmann, Wilhelm Bloch, Joachim Mester
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  ABSTRACT: The purpose was to examine the effects of a two week high intensity shock microcycle on maximal oxygen consumption and parameters of exercise performance in junior triathletes on the one hand, and to evaluate the long term effects of active (A) vs. passive (P) recovery on the other hand. 16 healthy junior triathletes participated in the study. For the assignment to the A- or P-group subjects were matched according to age and performance. Within two weeks, a total of 15 high-intensity interval sessions within three 3-day training blocks were performed. Before and one week after the last training session, athletes performed a ramp test to determine VO2max, a time trial (TT) and a Wingate-test. Furthermore total Hb-mass was determined. The results of the whole group, independent of the arrangement of recovery were analyzed at first; second the A- and P-groups were analyzed separately. Peak power output (PPO) during ramp test and TT performance significantly increased in the whole group. The comparison of the two groups revealed increases for the mentioned parameters and for VO2 and power output at VT2 only for the P-group. VO2max did not change. Wingate performance increased in the A-group only. tHb-mass slightly decreased. The main finding of the present study was that a 14-day shock microcycle is able to improve TT performance and PPO in junior triathletes in a short period of time. Furthermore, not only the intensity, but also the arrangement of interval training seems to be important as well, since only the P-group showed improvements in endurance performance, despite a slightly lower training volume. These findings might be relevant for future arrangements of high intensity interval training.
  The Journal of Strength and Conditioning Research 06/2012; · 1.83 Impact Factor
• Article: Different domains in nidogen-1 and nidogen-2 drive basement membrane formation in skin organotypic cocultures.

  Manuela Bechtel, Manuel V Keller, Wilhelm Bloch, Takako Sasaki, Petra Boukamp, Frank Zaucke, Mats Paulsson, Roswitha Nischt
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  ABSTRACT: Nidogen-1 and nidogen-2 are homologous proteins found in all basement membranes (BMs). They show comparable binding activities in vitro and partially redundant functions in vivo. Previously, we showed that in skin organotypic cocultures, BM formation was prevented in the absence of nidogens and that either nidogen was able to rescue this failure. We now dissected the two nidogens to identify the domains required for BM deposition. For that purpose, HaCaT cells were grown on collagen matrices containing nidogen-deficient, murine fibroblasts. After addition of nidogen-1 or nidogen-2 protein fragments comprising different binding domains, BM deposition was analyzed by immunofluorescence and electron microscopy. We could demonstrate that the rod-G3 domain of nidogen-2 was sufficient to achieve deposition of BM components at the epidermal-collagen interface. In contrast, for nidogen-1, both the G2 and G3 domains were required. Immunoblot analysis confirmed that all BM components were present in comparable amounts under all culture conditions. This finding demonstrates that nidogens, although homologous proteins, exert their effect on BM assembly through different binding domains, which may in turn result in alterations of BM structure and functions, thus providing an explanation for the phenotypical differences observed between nidogen-1 and -2 deficient mice.
  The FASEB Journal 05/2012; 26(9):3637-48. · 5.71 Impact Factor
• Article: Zur Funktion des β3-Adrenozeptors am Herzen: Signaltransduktion, inotroper Effekt und therapeutischer Ausblick

  Christian Pott, Dirk Steinritz, Andreas Napp, Wilhelm Bloch, Robert H.G. Schwinger, Klara Brixius
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  ABSTRACT: Die β-adrenerge Stimulation ist einer der wichtigsten Regulationsmechanismen kardialer Funktion. Neben β1- und β2-Adrenorezeptoren wurde eine dritte β-Adrenozeptorpopulation im menschlichen Herzen nachgewiesen, der β3-Adrenozeptor. Die Stimulation kardialer β3-Adrenozeptoren führt über eine Ausschüttung von Stickoxid (NO) zu einer Herabsetzung der kardialen Kontraktilität. Dabei wurden verschiedene molekulare Mechanismen β3-adrenerger Aktivierung der endothelialen Stickoxidsynthase (eNOS) in Kardiomyozyten identifiziert. Im gesunden aber auch im insuffizienten Herzen könnte die β3-adrenerge Stimulation einen Schutzmechanismus gegen exzessive catecholaminerge Stimulation, wie sie bei körperlichem und psychischem Stress, sowie bei der Herzinsuffizienz auftritt, darstellen. Aus diesem Grund wird der β3-Adrenozeptor als Zielprotein für die Pharmakotherapie der Herzinsuffizienz diskutiert. β-adrenergic stimulation is an important regulatory mechanism of cardiac function. Next to β1- and β2-adrenoceptors, the expression of a third β-adrenoceptor population, the β3-adrenoceptor, has recently been evidenced in the human heart. Stimulation of cardiac β3-adrenoceptors leads to a decrease in contractility via a release of nitric oxide (NO). In this context, different molecular mechanisms of endothelial nitric oxide synthase (eNOS) activation have been uncovered to occur as a consequence of β3-adrenergic stimulation. In both nonfailing and failing myocardium, β3-adrenergic stimulation may have a protective effect against excessive chatecolaminergic stimulation as it occurs during somatic and mental stress and during heart failure. For this reason, the β3-adrenoceptor is discussed as a possible target for the pharmacological therapy of heart failure.
  Wiener Medizinische Wochenschrift 04/2012; 156(15):451-458.
• Article: The Ca2+-binding protein calretinin is selectively enriched in a subpopulation of the epithelial rests of Malassez

  Yüksel Korkmaz, Franz-Josef Klinz, Thomas Beikler, Thorsten Blauhut, Kurt Schneider, Klaus Addicks, Wilhelm Bloch, Wolfgang H-M Raab
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  ABSTRACT: During tooth development, the inner and outer enamel epithelia fuse by mitotic activity to produce a bilayered epithelial sheath termed Hertwig’s epithelial root sheath (HERS). The epithelial rests of Malassez (ERM) are the developmental residues of HERS and remain in the adult periodontal ligament (PDL). Although the cellular regulation of the Ca2+-binding proteins parvalbumin, calbindin-D28k, and calretinin has been reported in the inner and outer enamel epithelia during tooth development, an involvement of Ca2+-binding proteins in the ERM has not so far been characterized. Among the three Ca2+-binding proteins tested (calbindin D28k, parvalbumin, calretinin), we have only been able to detect calretinin in a subpopulation of adult rat molar ERM, by using quantitative immunohistochemical and confocal immunofluorescence techniques. TrkA (a marker for ERM) is present in numerous epithelial cell clusters, whereas calretinin has been localized in the cytosol and perinuclear region of a subpopulation of TrkA-positive cells. We conclude that, in inner and outer enamel epithelial cells, Ca2+ is regulated by calbindin, parvalbumin, and calretinin during tooth development, whereas in the ERM of adult PDL, Ca2+ is regulated only by calretinin. The expression of Ca2+-binding proteins is restricted in a developmental manner in the ERM. KeywordsEpithelial rests of Malassez-Ca2+-binding proteins-Calretinin-Calbindin-D28k-Parvalbumin-Rat (Wistar)
  Cell and Tissue Research 04/2012; 342(3):391-400. · 3.11 Impact Factor