25 research outputs found

    Myristate and the ecology of AM fungi : significance, opportunities, applications and challenges

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    A recent study by Sugiura and coworkers reported the nonsymbiotic growth and spore production of an arbuscular mycorrhizal (AM) fungus, Rhizophagus irregularis, when the fungus received an external supply of certain fatty acids, myristates (C:14). This discovery follows the insight that AM fungi receive fatty acids from their hosts when in symbiosis. If this result holds up and can be repeated under nonsterile conditions and with a broader range of fungi, it has numerous consequences for our understanding of AM fungal ecology, from the level of the fungus, at the plant community level, and to functional consequences in ecosystems. In addition, myristate may open up several avenues from a more applied perspective, including improved fungal culture and supplementation of AM fungi or inoculum in the field. We here map these potential opportunities, and additionally offer thoughts on potential risks of this potentially new technology. Lastly, we discuss the specific research challenges that need to be overcome to come to an understanding of the potential role of myristate in AM ecology

    Mechanisms of microthrombi formation after experimental subarachnoid hemorrhage

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    Microcirculatory dysfunction may contribute to delayed cerebral ischemia after subarachnoid hemorrhage (SAH). Using a prechiasmatic injection model, this study investigated ultrastructural changes in microvessels in brain parenchyma to determine the nature of the microthromboemboli, the involvement of nitric oxide (NO) and P-selectin in their formation, and relationship to brain injury after SAH. Brains were examined by electron microscopy (EM) and immunohistochemistry. EM demonstrated that mice with SAH had significantly more arterioles filled with lesions consistent with microthrombi (in cortex, 20±5 for SAH, 8±4 saline-injected and 2.4±0.2 for sham). SAH animals also had more constriction of arterioles. The concentration of NO was lower in mice with SAH (44±9 for sham, 46±20 for saline-injected and 24±11 for SAH). The number of microthrombi correlated with the number of apoptotic neuronal cells (R =0.80 in cortex). Cell membrane P-selectin increased in the endothelium of arterioles in mice with SAH (11.4±0.7 for SAH, 6.8±0.9 for sham and 6.1±0.9 for saline-injected controls). This correlated with decreased NO in the brain. In conclusion, SAH causes microthrombosis and constriction of arterioles, which correlates with neuronal cell death. Increased P-selectin and decreased NO suggest a mechanism for microthrombosis and arteriolar constriction. © 2012 IBRO.

    Mechanisms of microthrombi formation after experimental subarachnoid hemorrhage

    No full text
    Microcirculatory dysfunction may contribute to delayed cerebral ischemia after subarachnoid hemorrhage (SAH). Using a prechiasmatic injection model, this study investigated ultrastructural changes in microvessels in brain parenchyma to determine the nature of the microthromboemboli, the involvement of nitric oxide (NO) and P-selectin in their formation, and relationship to brain injury after SAH. Brains were examined by electron microscopy (EM) and immunohistochemistry. EM demonstrated that mice with SAH had significantly more arterioles filled with lesions consistent with microthrombi (in cortex, 20±5 for SAH, 8±4 saline-injected and 2.4±0.2 for sham). SAH animals also had more constriction of arterioles. The concentration of NO was lower in mice with SAH (44±9 for sham, 46±20 for saline-injected and 24±11 for SAH). The number of microthrombi correlated with the number of apoptotic neuronal cells (R =0.80 in cortex). Cell membrane P-selectin increased in the endothelium of arterioles in mice with SAH (11.4±0.7 for SAH, 6.8±0.9 for sham and 6.1±0.9 for saline-injected controls). This correlated with decreased NO in the brain. In conclusion, SAH causes microthrombosis and constriction of arterioles, which correlates with neuronal cell death. Increased P-selectin and decreased NO suggest a mechanism for microthrombosis and arteriolar constriction. © 2012 IBRO.
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