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        <title>Editor's picks</title>
        <link>http://www.biomedcentral.com/bmcphysiol/</link>
        <description>The editor's pick of recent articles published by BMC Physiology</description>
        <dc:date>2012-05-02T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1472-6793/12/5" />
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        <title>Contractile Properties and Movement Behaviour in Neonatal Rats with Axotomy, treated with the NMDA Antagonist DAP5</title>
        <description>Background:
It is well known that axotomy in the neonatal period causes massive loss of motoneurons, which is reflected in the reduction of the number of motor units and the alteration in muscle properties. This type of neuronal death is attributed to the excessive activation of the ionotropic glutamate receptors (glutamate excitotoxicity). In the present study we investigated the effect of the NMDA antagonist DAP5 [D-2-amino-5-phosphonopentanoic acid] in systemic administration, on muscle properties and on behavioural aspects following peripheral nerve injury.
Methods:
Wistar rats were subjected to sciatic nerve crush on the second postnatal day. Four experimental groups were included in this study: a) controls (normal saline injection), b) crush c) DAP5 treated and d) crush and DAP5 treated. Animals were examined with isometric tension recordings of the fast extensor digitorum longus and the slow soleus muscles, as well as with locomotor tests at four time points, at P14, P21, P28 and adulthood (2 months).
Results:
1. Administration of DAP5 alone did not provoke any side-effects. 2. In all age groups, animals with crush developed significantly less tension than the controls in both muscles and had a worse performance in locomotor tests (p&lt;0.01). Crush animals injected with DAP5 were definitely improved as their tension recordings and their kinetic behaviour were significantly improved compared to axotomized ones (p&lt;0.01). 3. The time course of soleus contraction was not altered by axotomy and the muscle remained slow-contracting in all developmental stages in all experimental groups. EDL, on the other hand, became slower after the crush (p&lt;0.05). DAP5 administration restored the contraction velocity, even up to the level of control animals 4. Following crush, EDL becomes fatigue resistant after P21 (p&lt;0.01). Soleus, on the other hand, becomes less fatigue resistant. DAP5 restored the profile in both muscles.
Conclusions:
Our results confirm that contractile properties and kinetic behaviour of animals are severely affected by axotomy, with a differential impact on fast contracting muscles. Administration of DAP5 reverses these devastating effects, without any observable side-effects. This agent could possibly show a therapeutic potential in other models of excitotoxic injury as well.</description>
        <link>http://www.biomedcentral.com/1472-6793/12/5</link>
                <dc:creator>Konstantinos Petsanis</dc:creator>
                <dc:creator>Athanasios Chatzisotiriou</dc:creator>
                <dc:creator>Dorothea Kapoukranidou</dc:creator>
                <dc:creator>Constantina Simeonidou</dc:creator>
                <dc:creator>Dimitrios Kouvelas</dc:creator>
                <dc:creator>Maria Albani</dc:creator>
                <dc:source>BMC Physiology 2012, 12:5</dc:source>
        <dc:date>2012-05-02T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1472-6793-12-5</dc:identifier>
                            <dc:title>Motor behavior improved by DAP5</dc:title>
                            <dc:description>Systemic administration of the NMDA antagonist DAP5 has positive effects on recovery of muscle contractile properties and motor behavior after sciatic nerve crush in neonatal rats and may have therapeutic potential in other models of excitotoxic injury.</dc:description>
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                <prism:publicationName>BMC Physiology</prism:publicationName>
        <prism:issn>1472-6793</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2012-05-02T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1472-6793/12/3">
        <title>Small molecule screening platform for assessment of cardiovascular toxicity on adult zebrafish heart</title>
        <description>Background:
Cardiovascular toxicity is a major limiting factor in drug development and requires multiple cost-effective models to perform toxicological evaluation. Zebrafish is an excellent model for many developmental, toxicological and regenerative studies. Using approaches like morpholino knockdown and electrocardiogram, researchers have demonstrated physiological and functional similarities between zebrafish heart and human heart. The close resemblance of the genetic cascade governing heart development in zebrafish to that of humans has propelled the zebrafish system as a cost-effective model to conduct various genetic and pharmacological screens on developing embryos and larvae. The current report describes a methodology for rapid isolation of adult zebrafish heart, maintenance ex vivo, and a setup to perform quick small molecule throughput screening, including an in-house implemented analysis script.
Results:
Adult zebrafish were anesthetized and after rapid decapitation the hearts were isolated. The short time required for isolation of hearts allows dissection of multiple fishes, thereby obtaining a large sample size. The simple protocol for ex vivo culture allowed maintaining the beating heart for several days. The in-house developed script and spectral analyses allowed the readouts to be presented either in time domain or in frequency domain. Taken together, the current report offers an efficient platform for performing cardiac drug testing and pharmacological screens.
Conclusion:
The new methodology presents a fast, cost-effective, sensitive and reliable method for performing small molecule screening. The variety of readouts that can be obtained along with the in-house developed analyses script offers a powerful setup for performing cardiac toxicity evaluation by researchers from both academics and industry.</description>
        <link>http://www.biomedcentral.com/1472-6793/12/3</link>
                <dc:creator>Satish Kitambi</dc:creator>
                <dc:creator>Erik S Nilsson</dc:creator>
                <dc:creator>Petra Sekyrova</dc:creator>
                <dc:creator>Cristian Ibarra</dc:creator>
                <dc:creator>Gilbert Tekeoh</dc:creator>
                <dc:creator>Michael Andäng</dc:creator>
                <dc:creator>Patrik Ernfors</dc:creator>
                <dc:creator>Per Uhlén</dc:creator>
                <dc:source>BMC Physiology 2012, 12:3</dc:source>
        <dc:date>2012-03-26T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1472-6793-12-3</dc:identifier>
                            <dc:title>Cardiovascular toxicity evaluated</dc:title>
                            <dc:description>Zebrafish hearts can be used for screening the cardiovascular toxicity of small molecules in a new sensitive and reliable method that allows a variety of readouts, such as expression of biomarkers.</dc:description>
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                <prism:publicationName>BMC Physiology</prism:publicationName>
        <prism:issn>1472-6793</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2012-03-26T00:00:00Z</prism:publicationDate>
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