No abstract

This review summarizes recent developments that have contributed to our understanding of how adenosine 2A receptors (A2ARs) modulate brain damage in various animal models of acute neurological injuries, including brain ischemia, traumatic brain injury, spinal cord injury and hemorrhage stroke. The main conclusions are: (1) pharmacological, neurochemical and molecular/genetic approaches to the complex actions of A2AR in different cellular elements suggest that A2AR activation exerts bidirectional effect (detrimental or protective) after brain insults; (2) modulation of glutamate excitotoxicity and neuroinflammation are involved in the protection of A2AR agonists or antagonists, but the bidirectional effect of A2AR is largely due to the bidirectional regulation of neuroinflammation (anti-inflammation or proinflammation) by A2AR on immune cells such as microglia cells and peripheral bone marrow cells; and (3) the bidirectional effect of A2AR on neuroinflammation and brain injury depends on the distinct and sometimes opposite actions of A2AR in various cellular elements and on different injury models and associated pathological conditions. The local glutamate level in the brain injury is one of the crucial factors that contribute to the direction of A2AR effect on neuroinflammation and brain injury outcome. These developments presented here clearly highlight the complexity of using A2AR agents therapeutically in acute neuronal injuries and confirm that A2AR ligands have many promising characteristics that encourage the pursuit of their full therapeutic potential.

This study investigated the roles of Rho protein in epidermal growth factor (EGF)-induced trophoblast cell migration and its mechanism. Using choriocarcinoma cell lines JEG-3 and JAR and first-trimester human chorionic villus explant cultures on matrigel, we examined EGF-mediated stimulation of trophoblast migration. EGF is shown to have a dose-dependent effect on trophoblast migration. A low concentration of EGF (1 ng/ml) has a stimulatory effect on cell migration, whereas high concentrations of EGF (100 ng/ml) shows an inhibitory effect. EGF (1 ng/ml) activates RhoA and RhoC, but not RhoB, through elevated protein levels and activity. EGF-induced migration was shown to be inhibited by either cell-permeable C3 exoenzyme transferase or selective RhoA or RhoC small interfering RNAs. The inhibition was not mitigated by the addition of EGF, suggesting that RhoA and RhoC play an important role in trophoblast migration and are obligatory for EGF action. Treatment of JEG-3 and JAR cells with RhoA small interfering RNA induced F-actin cytoskeleton disruption and cell shrinkage, which is consistent with the effect of C3 exoenzyme transferase, and this action was not mitigated by EGF treatment. RhoC small interfering RNA had no apparent effect on the F-actin arrangement, suggesting that RhoA but not RhoC takes part in the EGF-induced migration through F-actin rearrangement. These results indicate that RhoA and RhoC play more important roles than RhoB in EGF-mediated migration of trophoblast cells, and RhoA but not RhoC regulates this migration through F-actin cytoskeleton reorganization.

No abstract

It is widely accepted that glutamate is the most important excitatory neurotransmitter in the central nervous system (CNS). However, there is also a large amount of glutamate in the blood. Generally, the concentration gradient of glutamate between intraparenchymal and blood environments is stable. However, this gradient is dramatically disrupted under a variety of pathological conditions, resulting in an amplifying cascade that causes a series of pathological reactions in the CNS and peripheral organs. This eventually seriously worsens a patient’s prognosis. These two “isolated” systems are rarely considered as a whole even though they mutually influence each other. In this review, we summarize what is currently known regarding the maintenance, imbalance and regulatory mechanisms that control the intraparenchymal-blood glutamate concentration gradient, discuss the interrelationships between these systems and further explore their significance in clinical practice.

In this paper, we theoretically design a dual-band graphene-based terahertz (THz) absorber combining the magnetic resonance with a THz cold mirror without any metallic loss. The absorption spectrum of the all-dielectric THz absorber can be actively manipulated after fabrication due to the tunable conductivity of graphene. After delicate optimization, two ultra-narrow absorption peaks are achieved with respective full width at half maximum (FWHM) of 0.0272 THz and 0.0424 THz. Also, we investigate the effect of geometric parameters on the absorption performance. Coupled mode theory (CMT) is conducted on the dual-band spectrum as an analytic method to confirm the validity of numerical results. Furthermore, physical mechanism is deeply revealed with magnetic and electric field distributions, which demonstrate a totally different principle with traditional plasmonic absorber. Our research provides a significant design guide for developing tunable multi-resonant THz devices based on all-dielectric configuration.

The design of a broadband tunable absorber is proposed based on a thin vanadium dioxide metasurface, which is composed of a simple array of vanadium dioxide and a bottom gold film. When the conductivity of vanadium dioxide is equal to 2000 −1 cm −1 , simulated absorptance exceeds 90% with 71% bandwidth from 0.47 to 0.99 THz and full width at half maximum is 98% from 0.354 to 1.036 THz with center frequency of 0.695 THz. Simulated results show that absorptance peak can be tuned from 5% to 100% when the conductivity changes continually from 10 −1 cm −1 to 2000 −1 cm −1 . The designed absorber may have useful applications in terahertz spectrum such as energy harvesting, thermal emitter, and sensing.

BackgroundAcute lung injury (ALI) is a serious complication of stroke that occurs with a high incidence. Our preclinical results indicated that ALI might be related to blood glutamate levels after brain injury. The purpose of this study was to assess dynamic changes in blood glutamate levels in patients with stroke and to determine the correlation between blood glutamate levels, ALI, and long-term prognosis after stroke.MethodsVenous blood samples were collected from controls and patients with stroke at admission and on the third and seventh day after the onset of stroke. Patients were followed for 3 months. The correlations among blood glutamate levels, severities of stroke and ALI, and long-term outcomes were analyzed, and the predictive values of blood glutamate levels and severity scores for ALI were assessed.ResultsIn this study, a total of 384 patients with stroke were enrolled, with a median age of 59 years. Patients showed significantly increased blood glutamate levels within 7 days of stroke onset (p < 0.05), and patients with more severe injuries showed higher blood glutamate levels. Moreover, blood glutamate levels were closely related to the occurrence (adjusted odds ratio, 3.022, p = 0.003) and severity (p < 0.001) of ALI and the long-term prognosis after stroke (p < 0.05), and they were a more accurate predictor of ALI than the more commonly used severity scores (p < 0.01).ConclusionThese results indicated that an increased blood glutamate level was closely related to the development of ALI and a poor prognosis after stroke.Clinical Trial Registration, identifier ChiCTR-RPC-15006770.