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BACKGROUND: Mammalian target of rapamycin (mTOR) signaling regulates cell energy metabolism and cell proliferation. Recent studies have demonstrated that mTOR activation is associated with increased cardiac infarct volume and necroptosis. The role of mTOR in cerebral ischemia has not been studied. The aim of this study is to explore how mTOR pathway behavior after cerebral ischemia and whether inhibition of mTOR reduces or increases ischemic brain damage. METHODS: Ten minutes of global ischemia was induced in Wistar rats (2-3 months old). Animals were either treatment with mTOR inhibitor rapamycin (6 mg/kg) or its vehicle. Animal brains were harvested after 3 hrs, 16 hrs and 7 days for histopathology and protein analyses. Sham-operated non-ischemic rats were used as control. Rapamycin was i.p. injected 1 hr after reperfusion in 7-day subgroups and injected 7 days prior to ischemia in 3 and 16 hrs subgroups. RESULTS: 10 minutes of global ischemia caused neuronal damage to the striatum, hippocampal CA1, and neocortical regions at 7 days of reperfusion. Levels of p-mTOR, p-S6K were increased significantly after 3 and 16 hrs in both the hippocampus and cortex. In addition, p-Akt and cytochrome c were elevated in the hippocampi after 3 hrs, peaked at 16 hrs and remained elevated after 7 days of reperfusion. Post-ischemic treatment with rapamycin 1 hrs after reperfusion significantly reduced brain damage in the CA1 and cortical areas at 7 days of reperfusion. Levels of p-mTOR, p-S6K, p-Akt and cytochrome c were significantly suppressed by rapamycin in non-ischemic and ischemic animals. CONCLUSION: Cerebral ischemia activates mTOR signaling pathway and inhibition of mTOR activativity reduces ischemic brain damage.

A synthetic approach has recently been developed which results in Cu(x)In(y)S2 quantum dots (QDs) possessing localized surface plasmon resonance (LSPR) modes in the near-infrared (NIR) frequencies.1 In this study, we investigate the potential benefits of near-field plasmonic effects centered upon light absorbing nanoparticles in a photovoltaic system by developing and verifying nonplasmonic counterparts as an experimental control. Simple QD-sensitized solar cells (QD-SSCs) were assembled which show an 11.5% relative increase in incident photon conversion efficiency (IPCE) achieved in the plasmon-enhanced devices. We attribute this increase in IPCE to augmented charge excitation stemming from near-field "antenna" effects in the plasmonic Cu(x)In(y)S2 QD-SSCs. This study represents the first of its kind; direct interrogation of the influence of plasmon-on-semiconductor architectures with respect to excitonic absorption in photovoltaic systems.

Psychological reactions to privacy invasions are important to information sharing in online dyadic exchange. Although previous studies have enriched understanding on cognitive reaction to privacy invasions, rarely have researchers examined the emotional component. This study aims to fill the gap in the literature by examining the effects of cognitive and emotional reactions on information sharing. To develop the research model, we drew on the relational dialectic perspective and social exchange theories to explain the effects of dialectic tensions on information sharing through privacy threats and negative affect. The research model was tested on survey data gathered from 89 actual chat room users. We found that anonymity status, interaction intrusiveness, and disclosure by counterparts affect privacy threats. Interaction intrusiveness and disclosure by counterparts influence negative affect. Additionally, privacy threats and negative affect were found to be important in shaping information sharing.