Background1471-2229-9-51: American chestnut (Castanea dentata) was devastated by an exotic pathogen in the beginning of the twentieth century. This chestnut blight is caused by Cryphonectria parasitica, a fungus that infects stem tissues and kills the trees by girdling them. Because of the great economic and ecological value of this species, significant efforts have been made over the century to combat this disease, but it wasn't until recently that a focused genomics approach was initiated. Prior to the Genomic Tool Development for the Fagaceae project, genomic resources available in public databases for this species were limited to a few hundred ESTs. To identify genes involved in resistance to C. parasitica, we have sequenced the transcriptome from fungal infected and healthy stem tissues collected from blight-sensitive American chestnut and blight-resistant Chinese chestnut (Castanea mollissima) trees using ultra high throughput pyrosequencing.

Silicon (Si) can improve drought tolerance in plants, but the mechanism is still not fully understood. Previous research has been concentrating on Si’s role in leaf water maintenance in Si accumulators, while little information is available on its role in water uptake and in less Si-accumulating plants. Here, we investigated the effects of Si on root water uptake and its role in decreasing oxidative damage in relation to root hydraulic conductance in tomato (Solanum lycopersicum ‘Zhongza No.9’) under water stress. Tomato seedlings were subjected to water stress induced by 10% (w/v) polyethylene glycol-6000 in the absence or presence of 2.5 mM added silicate. The results showed that Si addition ameliorated the inhibition in tomato growth and photosynthesis, and improved water status under water stress. The root hydraulic conductance of tomato plants was decreased under water stress, and it was significantly increased by added Si. There was no significant contribution of osmotic adjustment in Si-enhanced root water uptake under water stress. The transcriptions of plasma membrane aquaporin genes were not obviously changed by Si under water stress. Water stress increased the production of reactive oxygen species and induced oxidative damage, while added Si reversed these. In addition, Si addition increased the activities of superoxide dismutase and catalase and the levels of ascorbic acid and glutathione in the roots under stress. It is concluded that Si enhances the water stress tolerance via enhancing root hydraulic conductance and water uptake in tomato plants. Si-mediated decrease in membrane oxidative damage may have contributed to the enhanced root hydraulic conductance.

Pain after nerve injury, a phenomenon referred to as neuropathic pain, is a debilitating clinical condition, but the underlying mechanisms remain unclear. As leptin, an adipocytokine produced mainly by nonneuronal tissue, has been implicated in the regulation of neuronal functions, we examined the role of leptin in neuropathic pain using a rat model of the condition chronic constriction sciatic nerve injury (CCI). We report that leptin critically contributed to pain behaviors following CCI. Specifically, spinal administration of a leptin antagonist prevented and reversed neuropathic pain behaviors in rats. Further examination revealed that levels of both leptin and the long form of the leptin receptor (Ob-Rb) were substantially increased within the ipsilateral spinal cord dorsal horn after peripheral nerve injury. Mechanistic studies showed that leptin upregulated the expression of both the spinal NMDA receptor and IL-1β through the JAK/STAT pathway. Furthermore, these CCI-induced behavioral and cellular responses were diminished in leptin-deficient mice and mimicked by spinal administration of exogenous leptin in naive rats. Our findings reveal a critical role for spinal leptin in the pathogenesis of neuropathic pain and suggest what we believe to be a novel form of nonneuronal and neuronal interactions in the mechanisms of pathological pain. IntroductionPain resulting from injury to the nervous system (neuropathic pain) has several salient clinical features, including hyperalgesia and allodynia beyond the dermatome distribution. Both peripheral and central mechanisms, including glial activation and release of proinflammatory cytokines, have been proposed for the pathogenesis of neuropathic pain (1-3). Despite recent progress, the mechanisms underlying clinical features of neuropathic pain remain unclear. Leptin is an adipocytokine produced mainly by white adipose tissue and well known for its role in metabolic regulation and obesity (4-8). A growing body of evidence indicates that leptin has broad roles in the regulation of neuronal functions (3, 9-11). Furthermore, leptin's signal transduction pathways have much in common with those of proinflammatory cytokines (6,8,12).Recent clinical reports suggest that there might be a link between the plasma leptin level and tissue injury. For example, patients with spinal cord injury, chronic angina pectoris, or acute myocardial infarction display a higher than normal plasma leptin level (13-15). In laboratory animals, intraperitoneal injection of exogenous leptin lowers the hot plate withdrawal latency in mice, although intracerebroventricular injection of leptin does not alter the hot plate test in rats (16). Moreover, mice with the leptin receptor null mutation (db/db) demonstrate a decreased sensitivity to mechanical stimulation and a decreased nociceptive response in the affected hind paw during the second phase of a formalin test (17). These data suggest that leptin may have an important and yet unknown role in the mechanisms of pain.We explored the possibilities ...

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Background-Induced hypothermia is recommended to improve neurological outcomes in unconscious survivors of out-of-hospital ventricular fibrillation (VF) cardiac arrest. Patients resuscitated from a VF arrest are at risk of refibrillation, but there are few data on the effects of already existing hypothermia on defibrillation and resuscitation. Methods and Results-Thirty-two swine (meanϮSE weight, 23.0Ϯ0.6 kg) were divided into 4 groups: normothermia (nϭ8), mild hypothermia (35°C) (nϭ8), moderate hypothermia (33°C) (nϭ8), and severe hypothermia (30°C) (nϭ8). Hypothermia was induced by surrounding the animal with ice, and VF was electrically induced. After 8 minutes of unsupported VF (no CPR), the swine were defibrillated (biphasic waveform) with successive shocks as needed and underwent CPR until resumption of spontaneous circulation or no response (Ն10 minutes). First-shock defibrillation success was higher in the moderate hypothermia group (6 of 8 hypothermia versus 1 of 8 normothermia; Pϭ0.04). The number of shocks needed for late defibrillation (Ն1 minute after initial shock) was less in all 3 hypothermia groups compared with normothermia (all PϽ0.05). None of the 8 animals in the normothermia group achieved resumption of spontaneous circulation compared with 3 of 8 mild hypothermia (PϭNS), 7 of 8 moderate hypothermia (Pϭ0.001), and 5 of 8 severe hypothermia (Pϭ0.03) animals. Coronary perfusion pressure during CPR was not different between the groups. Conclusions-When VF was induced in the setting of moderate or severe hypothermia, resuscitative measures were facilitated with significantly improved defibrillation success and resuscitation outcome. The beneficial effect of hypothermia was not due to alteration of coronary perfusion pressure, which suggests that changes in the mechanical, metabolic, or electrophysiological properties of the myocardium may be responsible.