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    ABSTRACT: The gelada baboon is a graminivorous primate whose ecology is unusually sensitive to ambient temperature. A systems model of the socio-ecology of the gelada is used to predict the impact of global warming on the species’ altitudinal distribution. The species’ lower altitudinal limit will rise by ≈ 500 m for every 2 °C increase in global mean temperature. A 7 °C rise in temperature would be sufficient to result in the species being confined to a small number of isolated mountain peaks, where its chances of survival will be greatly reduced. Changes in local climate are also likely to have significant effects on agricultural practice on the Ethiopian highlands, and this in turn is likely to have repercussions for the distribution patterns of the gelada by further constraining the habitat available to them.
    Global Change Biology 02/1998; 4(3):293 - 304.
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    ABSTRACT: Social group size has been shown to correlate with neocortex size in primates. Here we use comparative analyses to show that social group size is independently correlated with the size of non-V1 neocortical areas, but not with other more proximate components of the visual system or with brain systems associated with emotional cueing (e.g. the amygdala). We argue that visual brain components serve as a social information 'input device' for socio-visual stimuli such as facial expressions, bodily gestures and visual status markers, while the non-visual neocortex serves as a 'processing device' whereby these social cues are encoded, interpreted and associated with stored information. However, the second appears to have greater overall importance because the size of the V1 visual area appears to reach an asymptotic size beyond which visual acuity and pattern recognition may not improve significantly. This is especially true of the great ape clade (including humans), that is known to use more sophisticated social cognitive strategies.
    Proceedings of the Royal Society B: Biological Sciences 10/1997; 264(1386):1303-7.
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    ABSTRACT: Lactate dehydrogenase (LDH) leaks from the perfused rat kidney under the artificial conditions of a Ca(2+)-paradox protocol, namely Ca(2+)-repletion following a 20 minute period of Ca(2+)-depletion. LDH leakage was markedly suppressed by perfusion at 25 degrees C or with 0.1 mM dibucaine or 2 mM lidocaine. Lidocaine inhibited leakage only during Ca(2+)-depletion. Lowering the perfusion rate significantly reduced LDH escape. No LDH loss occurred if the osmotic pressure of the perfusion fluid was raised by 420 mOsm during either Ca(2+)-depletion or Ca(2+)-repletion. Amiloride (2 mM) significantly reduced LDH leakage to 43%. Reduction of the pH of the perfusion fluid to 6.8 significantly inhibited LDH loss, and at pH 6.4 this leakage was almost completely suppressed. LDH loss was equally suppressed at pH 6.4 only during Ca(2+)-depletion, whereas pH 6.4 was markedly less effective when perfused only during Ca(2+)-repletion. Ouabain (5 x 10(-6) M) had only a limited effect in exacerbating LDH leakage. Raising [K+]o significantly protected against LDH leakage, which fell to 36% at 16 mM [K+]. These features correspond with the Ca(2+)-paradox of the perfused rat heart an it is suggested that: (i) a Ca(2+)-paradox can be produced in the rat kidney; (ii) a similar mechanism governs the release of cytosolic proteins in these two preparations; and (iii) the damage mechanism of the plasmalemma is a transmembrane oxidoreductase-diaphorase molecular complex which generates H+ when activated by Ca(2+)-depletion.
    Kidney International 04/1996; 49(3):639-46.
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    ABSTRACT: Exposure of the isolated mouse soleus preparation to 1.0 mM phenazine methosulphate (PMS) caused (i) a slow and modest release of creatine kinase (CK) that was exacerbated by removal of extracellular Ca2+, (ii) a specific type of ultrastructural damage, namely a characteristic spacing of the myofibrils, (iii) swelling of the mitochondria, indicating a modest rise in [Ca2+]i, and (iv) swelling of the sarcoplasmic reticulum (SR). It is suggested that PMS (i) activates a sarcolemma oxidoreductase which synergistically interacts with raised [Ca2+]i to cause modest CK efflux and (ii) activates an oxidoreductase on the SR, thereby generating electrons which directly modify the integrity and organisation of the contractile apparatus.
    Pathobiology 02/1995; 63(5):278-82.
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    ABSTRACT: The 1993 British Photobiology Society DNA Repair meeting was held at City University, London, on December 20th. The well supported meeting heard presentations covering diverse aspects of repair, mutation and recombination in both prokaryotes and eukaryotes. The meeting particularly aims to provide a forum for presentations from postgraduate and postdoctoral workers, and contributions were received from many of the British laboratories engaged in these fields.
    Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 08/1994; 315(1):75-84.
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    ABSTRACT: No reduction in creatine kinase (CK) release during standard Ca2+ paradox in the Langendorff-perfused rat heart was afforded by anoxic perfusion, nor by addition of the radical scavengers superoxide dismutase (150,000 U/L), catalase (150,000 U/L), mannitol (15 or 50 mM), dimethylthiourea (DMTU, 10 mM), the antioxidant vitamin E (0.25 or 0.75 mM), or the iron chelator desferrioxamine (0.8 mM). Even under mild Ca(2+)-paradox conditions, achieved by (a) reducing the duration of the Ca(2+)-free period, (b) increasing [Ca2+]0 during the "Ca(2+)-free" period, or (c) reperfusing with 0.1 mM Ca2+, no protection was achieved by mannitol, DMTU, or desferrioxamine. Perfusion with N2 did not cause a reduction in CK release caused by caffeine or dinitrophenol or Ca2+ paradox. We conclude that no evidence supports the hypothesis that oxygen radicals are implicated in release of CK in Ca2+ paradox.
    Journal of Cardiovascular Pharmacology 02/1994; 23(1):51-6.
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    ABSTRACT: The Langendorff-perfused rat heart has been used to test the hypothesis that Ca2+-activation of the phospholipase A2 (PLA2) is implicated in the damage of the sarcolemma. Creatine kinase (CK) efflux was monitored following a standard Ca2+-paradox or treatment with 10 mM caffeine or 1 mM 2,4-dinitrophenol. Mepacrine (PLA2 inhibitor) or nordihydroguaretic acid (NDGA, lipoxygenase inhibitor) did not protect against CK release in the standard Ca2+-paradox. Mepacrine, NDGA or phenidone (lipoxygenase and cycloxygenase inhibitor) did not protect against mild conditions of the Ca2+-paradox. No reduction in caffeine- or DNP-induced CK release was afforded by mepacrine. It is concluded that the PLA2 cascade is stimulated by a rise in [Ca2+]i but has no major role in CK release.
    Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology. 01/1994;
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    ABSTRACT: 1. The standard O2-paradox has been studied in the Langendorff-perfused rat heart. 2. Perfusion of glucose-free saline under anoxia did not cause release of creatine kinase (CK) although, it is suggested, there was a progressive rise in [Ca2+]i. 3. Ca(2+)-depletion after anoxia caused CK release. 4. Prolonged anoxic perfusion (55 min) produced a markedly reduced release of CK on Ca(2+)-depletion because, it is suggested, of the reduction in substrates for the release mechanism. 5. No protection against the O2-paradox was found with oxygen radical scavengers and inhibitors. 6. Lowering [Ca2+]o during reoxygenation to 0.1 mM did not reduce CK release. 7. Neither 1 mM amiloride (Na+/H+ antiporter inhibitor) nor 2 x 10(-6) M 1-(5-isoquinolinesulphonyl) piperazine (protein kinase C inhibitor) reduced CK release, unlike their effects in the Ca(2+)-paradox. 8. An hypothesis for events in the O2-paradox in presented: anoxia causes a loss of Ca(2+)-homeostasis and a rise in [Ca2+]i thereby activating a transmembrane NAD(P) oxido-reductase/diaphorase (stage 1); the return of O2 synergistically activates this molecular complex and causes CK release (stage 2).
    Comparative biochemistry and physiology. Comparative physiology. 09/1993; 105(4):659-65.
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    ABSTRACT: 1. Langendorff-perfusion of rat hearts with either 10 mM caffeine or 1 mM 2,4-dinitrophenol (DNP) caused severe ultrastructural damage to the myofilaments and mitochondria that was similar to that found in a standard Ca(2+)-paradox. 2. This damage occurred in the presence and absence of extracellular Ca2+. 3. Creatine kinase (CK) release (indicative of sarcolemma breakdown) was not recorded unless the caffeine- or DNP-perfusion was preceded by Ca(2+)0-depletion. 4. It is concluded that: (i) the pathways leading to damage to the myofilaments and sarcolemma are independent; (ii) the CK release mechanism requires dual activation of Ca(2+)0-depletion plus a rise in [Ca2+]i; and (iii) current theories concerning the mechanisms underlying the genesis of the Ca(2+)-paradox are incorrect or incomplete.
    Comparative Biochemistry and Physiology Part C Comparative Pharmacology and Toxicology 07/1993; 105(2):225-9.
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    ABSTRACT: 1. The release of creatine kinase (CK) in the Langendorff-perfused rat heart during the Ca(2+)-paradox, was critically dependent on the duration and [Ca2+]o of the initial Ca(2+)-depletion phase. 2. When [Ca2+]i was raised by perfusion with caffeine or under N2, activation of the protein kinase C pathway (PKC) produced a small but significant release of CK. PKC stimulation is therefore able to substitute for the Cao(2+)-depletion of the Ca(2+)-paradox. 3. The PKC inhibitor, 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine, (2 x 10(-6) M) inhibited both the Ca(2+)-paradox and caffeine-induced release of CK. 4. It is concluded that the PKC pathway has a regulatory role for the damage system of the sarcolemma that is responsible for the release of cytosolic proteins.
    Comparative biochemistry and physiology. Comparative physiology. 07/1993; 105(2):329-32.
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