Abstract: The movements of the horse's back and trunk can be deducted from the foot sequences of the horse's basic paces. This knowledge builds a solid foundation in the schooling of the rider's seat. The decisive aspects of these movements are described here.
Some basics (mostly well-known) in the schooling of the rider's seat are graded here. More recent findings from observing the horse's back and trunk movements and their consequence for the rider's seat can easily be explained in three points. These points will be enhanced by graphic explanations of the principle as a whole

Abstract: We present a review of studies on elephant social and reproductive behaviour. While the social organization of the African savannah elephant (Loxodonta africana africana) has been intensively studied,that of the African forest elephant (Loxodonta africana cyclotis) and the Asian elephant (Elephas maximus) are poorly understood. Noninvasive molecular methods are useful in combination with behavioural data in understanding social organization and dispersal strategies. The ecological determinants of social organization, and the importance of matriarchal leadership to social groups, and relative importance of different forms of communication under various ecological conditions remain interesting topics that await investigation. Reproductive behaviour also has been examined in detail only in the African savannah elephant, although rigorous chemical analyses continue to be carried out using captive elephants of both species. Improved laboratory techniques may enable future work on reproductive signalling in free-ranging elephants, allowing for comprehensive studies of male-male interactions and mate choice by females.

Abstract: previous termSocial cognition,next term in particular the derivation of previous termsocialnext term information from observation of interactions between members of a previous termsocialnext term group, has been widely investigated in primates, but it has received little attention in other previous termsocialnext term mammals, although it has been anecdotally reported in the previous termdomestic dog,next term Canis familiaris. We recorded the behaviour of previous termdogsnext term (“spectators”) that had observed controlled interactions between a human and a previous termdognext term (the “demonstrator”) competing for an object, and that were subsequently allowed to interact freely with both participants. When the competitions were playful, as indicated by signals performed by the human, the spectator was more likely to approach the winner first and/or more rapidly, suggesting that winners of games are perceived as desirable previous termsocialnext term partners. When the human did not perform play signals, changing the previous termsocialnext term context from play to contest over a resource, spectators were slower to approach either of the participants, suggesting that participants in contests were less desirable as previous termsocialnext term partners than participants in games. If the previous termdognext term was prevented from seeing the game, it still reacted differently to the winner and the loser, but its behaviour was not the same as after games that it had seen. We conclude that spectator previous termdogsnext term gain information from the players' subsequent behaviour as well as from direct observation of the game.

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.

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.