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Huebener, E. (2005). Der Natur abgelauschte Erkenntnisse: Der Weg zum Balancesitz und zum Begreifen des Timers für Signale an das Pferd;. Tierärztl. Umschau, 2, 90–99.
Abstract: Zusammenfassung
Mit dem Beitrag “Die Bewegungen von Pferderumpf und -rücken aus der Sicht des Reiters” (TU 59, 327-334, 2004) wurde um universitäre Forschung zur Ermittlung gemessener Werte für diese Begleiter der Fortbewegung geworben.
Die Entdeckung des Ranges der Rumpf-Rücken-Bewegungen für pferdgerechtes und kultiviertes, feinfühliges Reiten ist mit der Entwicklung des Balancesitzes und der Technik des vom Pferd Zeitvorgaben Empfangens und ihm Signale Sendens (Reiter sagen: des Fühlens und Einwirkens) eng verbunden. Ihre Geschichte läßt sich über viereinhalb Jahrhunderte verfolgen. Ein kurzer Abriß wird hier nachgeliefert.
Er mündet erneut in ein Plädoyer für interdisziplinäres universitäres Forschen, weil auch bei Sitz und Hilfengebung, weiteren Grundlagen des Reitens – im Interesse effektiveren Unterrichts an der Basis unseres “Sports” – dringender Klärungsbedarf besteht.
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Huebener, E. (2005). Das Sitzrätsel lösen (Arbeitstitel: So kann der Reiter wirklich “sitzen”!);. Mecl. Pf.erde J., 3, 50–51.
Abstract: Zusammenfassung
Die Bewegungen des Pferderückens und des Pferderumpfes sind aus den Fußfolgen der Grundgangarten ableitbar. Damit gewinnt Sitzschulung ein solides Fundament. Die entscheidenden Merkmale dieser Bewegungen sind hier erläutert.
Einige überwiegend altbekannte Grundlagen der Sitzschulung werden bewertet. Was sich aus neueren Erkenntnissen zu den Bewegungen des Pferderückens und des Pferderumpfes für den Sitz des Reiters ergibt, ist in drei Punkten leichtverständlich erklärt. Prinzipdarstellungen unterstützten dies.
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Huebener, E. (2005). Listening to Nature: Ways to A Balanced Seat and Understanding the Correct Timing for the Rider's Aids. Tierärztl. Umschau, 2, 90–99.
Abstract: In the publication “Movements of trunk and back of the horse from a riders view” in the TU 59, 327-334, 2004 the author suggested that academic research is necessary to determine measurable parameters for these agents of the horse's movement.
The discovery of the importance of the trunk-back-movements for a sensitive and horse-oriented riding style is closely connected to the development of the balanced seat and the technique of receiving signals from and sending signals to the horse at the right time (riders would say: “the feel and the impact”). The history of this interaction between horse and rider can be traced for four and a half centuries. A short digest will be published here later. Again the studies result in a demand for interdisciplinary academic research.
There is an urgent need to clarify the impact of the riders's seat and aids (two more pillars in the art of riding) in the interest teaching riding correctly and more efficiently at the so-called 'basis' of our sport.
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Huebener, E. (2005). Hilfen für Übergänge von einer Gangart in eine andere ? Die Bewegungen von Pferderumpf und -rücken als Zeitgeber für reiterliche Einwirkung. Trakehner Hefte,, 5-11.
Abstract: Übergänge von einer Gangart in eine andere sind nach Ludwig Koch jeweils nur aus einer ganz bestimmten Phase einer Bewegungsfolge (oder Bewegungsfolgen-Hälfte) der einen in eine ganz bestimmte Bewegungsfolge (oder Bewegungsfolgen-Hälfte) der anderen Gangart möglich.
Diese Phasen dauern nur Bruchteile einer Sekunde an. In diesen Momenten muß die Hilfe nach europäischer klassischer Lehre gegeben, nur in diesen Momenten kann sie vom Pferd blitzartig-automatisch umgesetzt werden. Um die Hilfe im “passenden” Moment geben zu können, braucht der Reiter einen Zeitgeber. Den einzigen verfügbaren, zuverlässigen Timer bilden die Bewegungen des Pferderückens und des Pferderumpfes.
Die Zusammenhänge zwischen den Bewegungsphasen in den Grundgangarten, dem mit frei beweglichem Beckenring allen Bewegungen des Pferderückens folgendem Sitz des Reiters, und dem Schenkel, der von Schritt zu Schritt, von Tritt zu Tritt, von Galoppsprung zu Galoppsprung an den wegschwingenden Pferderumpf fallen möchte bis er das im rechten Augenblick – vom Reiter gesteuert – dann auch darf, sind erstmals in piktogrammartigen Miniaturbild-Folgen leicht verständlich dargestellt.
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Huebener, E. (2005). Rider's Aids for Transitions Between Different Gaits ? The Movements of the Horse's Trunk and Back as Timers for the Rider's Influence. Trakehner Hefte, 5-11.
Abstract: Abstract
According to Ludwig Koch, the horse's transition from one gait to another is only possible during a particular phase in its' movement cycle (respectively in a half of it's movement cycle) in one gait to a particular phase in its' movement cycle (respectively in a half of it's movement cycle) in the other gait.
It only takes a fraction of a second for these movements to occur. It is precisely in these moments that according to the European classical riding school principles the rider has to give the appropriate aids, because only then the horse can execute them in a flash. In order to give the aids in the “fitting” moment, the rider needs a timer. The only available and reliable indicators of the right timing are the movements of the horse's trunk and back.
The connections between the different phases of the movements during the basic gaits, the rider's seat which follows all the movements of the horse's back with a freely rotating pelvis, and the rider's leg which – from step to step, from footfall to footfall, from canter beat to canter beat – wants to follow the horse's swinging trunk (until it is finally – controlled by the rider – free to do so, at the right moment), are being shown for the first time in easy to follow miniature picture sequences.
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Deutsche Reiterliche Vereinigung e.V.(FN), Miesner, S., Putz, M., & Plewa, M. (2005). Richtlinien für Reiten und Fahren – Band 1. Warendorf: Fn-Verlag.
Abstract: Dieses Standardwerk vermittelt das Grundwissen für die Ausbildung des Reiters und des Pferdes nach den Grundsätzen der klassischen Reitkunst. Die hier beschriebene Grundausbildung dient dabei nicht ausschließlich der Vorbereitung für Turniere und Leistungsprüfungen, sie soll vielmehr die Voraussetzungen für alle pferdesportlichen Betätigungen schaffen.
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Hodgson, D., Howe, S., Jeffcott, L., Reid, S., Mellor, D., & Higgins, A. (2005). Effect of prolonged use of altrenogest on behaviour in mares (Vol. 169).
Abstract: Erratum in:
Vet J. 2005 May;169(3):321.
Corrected and republished in:
Vet J. 2005 May;169(3):322-5.
Oral administration of altrenogest for oestrus suppression in competition horses is believed to be widespread in some equestrian disciplines, and can be administered continuously for several months during a competition season. To examine whether altrenogest has any anabolic or other potential performance enhancing properties that may give a horse an unfair advantage, we examined the effect of oral altrenogest (0.044 mg/kg), given daily for a period of eight weeks, on social hierarchy, activity budget, body-mass and body condition score of 12 sedentary mares. We concluded that prolonged oral administration of altrenogest at recommended dose rates to sedentary mares resulted in no effect on dominance hierarchies, body mass or condition score.
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Wells, P. G., Bhuller, Y., Chen, C. S., Jeng, W., Kasapinovic, S., Kennedy, J. C., et al. (2005). Molecular and biochemical mechanisms in teratogenesis involving reactive oxygen species. Toxicol Appl Pharmacol, 207(2 Suppl), 354–366.
Abstract: Developmental pathologies may result from endogenous or xenobiotic-enhanced formation of reactive oxygen species (ROS), which oxidatively damage cellular macromolecules and/or alter signal transduction. This minireview focuses upon several model drugs (phenytoin, thalidomide, methamphetamine), environmental chemicals (benzo[a]pyrene) and gamma irradiation to examine this hypothesis in vivo and in embryo culture using mouse, rat and rabbit models. Embryonic prostaglandin H synthases (PHSs) and lipoxygenases bioactivate xenobiotics to free radical intermediates that initiate ROS formation, resulting in oxidation of proteins, lipids and DNA. Oxidative DNA damage and embryopathies are reduced in PHS knockout mice, and in mice treated with PHS inhibitors, antioxidative enzymes, antioxidants and free radical trapping agents. Thalidomide causes embryonic DNA oxidation in susceptible (rabbit) but not resistant (mouse) species. Embryopathies are increased in mutant mice deficient in the antioxidative enzyme glucose-6-phosphate dehydrogenase (G6PD), or by glutathione (GSH) depletion, or inhibition of GSH peroxidase or GSH reductase. Inducible nitric oxide synthase knockout mice are partially protected. Inhibition of Ras or NF-kB pathways reduces embryopathies, implicating ROS-mediated signal transduction. Atm and p53 knockout mice deficient in DNA damage response/repair are more susceptible to xenobiotic or radiation embryopathies, suggesting a teratological role for DNA damage, consistent with enhanced susceptibility to methamphetamine in ogg1 knockout mice with deficient repair of oxidative DNA damage. Even endogenous embryonic oxidative stress carries a risk, since untreated G6PD- or ATM-deficient mice have increased embryopathies. Thus, embryonic processes regulating the balance of ROS formation, oxidative DNA damage and repair, and ROS-mediated signal transduction may be important determinants of teratological risk.
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Nicol, C. J., Adachi, M., Akiyama, T. E., & Gonzalez, F. J. (2005). PPARgamma in endothelial cells influences high fat diet-induced hypertension. Am J Hypertens, 18(4 Pt 1), 549–556.
Abstract: BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful.
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Crosby, M. B., Svenson, J. L., Zhang, J., Nicol, C. J., Gonzalez, F. J., & Gilkeson, G. S. (2005). Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide. J Pharmacol Exp Ther, 312(1), 69–76.
Abstract: Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation.
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