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BackgroundDepression is a common and important cause of morbidity, and results in a significant economic burden. Recent human studies have demonstrated that that depression is contagious, and depression in family and friends might cumulatively increase the likelihood that a person will exhibit depressive behaviors. The mechanisms underlying contagion depression are poorly understood, and there are currently no animal models for this condition.MethodsRats were divided into 3 groups: depression group, contagion group, and control group. After induction of depression by 5 weeks of chronic unpredictable stress, rats from the contagion group were housed with the depressed rats (1 naïve rat with 2 depressed rats) for 5 weeks. Rats were then subjected to sucrose preference, open field, and forced swim tests.ResultsThe sucrose preference was significantly reduced in the depressed rats (p

BACKGROUND Previous study has demonstrated the efficacy of hemodialysis in reducing blood glutamate levels. The purpose of the present study is to investigate whether peritoneal dialysis (PD) may be effective in lowering blood glutamate levels, which may serve as a potential tool for improving neurological function after brain injury. METHODS Two liters of dialysis solution were infused over 10 minutes into 18 patients with stage V chronic kidney disease. Blood samples were collected immediately before initiation of PD, and hourly for a total of 5 blood samples. Blood samples were sent for determination of glutamate, creatinine, urea, glucose, glutamate oxaloacetate transaminase, and glutamate pyruvate transaminase. PD samples were collected and analyzed for glutamate, creatinine, urea, and glucose at the same time points as the blood samples. RESULTS Blood glutamate concentrations were significantly reduced by 60 minutes after the infusion of dialysis solution (P

BACKGROUND The exact mechanism of hypothermia-induced neuroprotection has not been determined yet; however, we hypothesized that it may be mediated by a blood glutamate-scavenging effect. Here, we examine the effect of hypothermic conditions (mild, moderate, and deep) on blood glutamate levels in naive rats. To identify the mechanism of hypothermia-induced glutamate reduction, we also measured concentrations of glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT), the primary regulators of glutamate concentration in blood. METHODS Rats were anesthetized with isoflurane, and their rectal temperature was maintained for 6 hours at 36 to 37°C, 33 to 36°C, 30 to 32°C, 18 to 22°C, or was not maintained artificially. At 6 hours, active cooling was discontinued and rats were allowed to rewarm. There were 12 rats in each group for a total of 60 rats. Blood samples were drawn at 0, 3, 6, 12, 24, and 48 hours for the determination of blood glutamate, GOT, and GPT levels. RESULTS A strong correlation between body temperature and blood glutamate levels was observed (P

The method of ionisation potential (dopant contrast) microscopy in the HRSEM is applied to the study of the electric field distribution in p-i-n structures used as quantum well solar cells. Our results show a secondary electron signal which varies between the different layers, being greatest in the p-type and smallest in the n-type regions respectively. The stacks of 8 nm wide quantum wells and their corresponding barriers are clearly distinguished in the intrinsic region of the devices. In-situ observation of reverse biased structures has been performed to determine the effect of bias on the potential distribution within the devices.

Finding an optimal biomarker for the noninvasive evaluation of acute liver injury (ALI) may be of great value in predicting clinical outcomes and investigating potential treatments. We investigated cell-free DNA (CFD) as a potential biomarker to predict carbon tetrachloride-induced ALI in rats.Forty-five Sprague-Dawley rats were randomly assigned to three groups. ALI was induced by carbon tetrachloride via a nasogastric tube at 1, 2.5, or 5 ml/kg of a 50 % solution. Fifteen additional rats underwent a sham procedure. Blood samples were drawn at time t which was 0 (baseline), 3, 6, 12, 24, 48, 72, 96, and 120 h for the measurements of CFD, glutamate-pyruvate transaminase (GPT), glutamate-oxaloacetate transaminase (GOT), and total bilirubin. Prothrombin time and histology were examined at 24 and 120 h following injection of 5 ml/kg carbon tetrachloride in 18 additional rats and in 10 control rats.CFD levels in rats subjected to carbon tetrachloride-induced ALI were significantly increased in all blood samples starting at 12 h after the induction of ALI (p 0.001), reaching peak levels at 24 h. Blood GOT, GPT, and total bilirubin were elevated in all blood samples starting at 3 h after the induction of ALI (p 0.0001), reaching peak levels by 48 h. A positive correlation was demonstrated between CFD levels and GOT (R (2) = 0.92), GPT (R (2) = 0.92), and total bilirubin (R (2) = 0.76). CFD levels correlated with liver damage seen on histological examination, as well as predicted liver damage, at 24 h after ALI.CFD may be a useful biomarker for the prediction and measurement of ALI. There is no evidence to suggest that CFD is superior to other available noninvasive biomarkers.

Excess glutamate in the brain is thought to be implicated in the pathophysiology of fetal anoxic brain injury, yet little is known about the mechanisms by which glutamate is regulated in the fetal brain. This study examines whether there are differences between maternal and fetal glutamate concentrations, and whether a correlation between them exists.10 ml of venous blood was extracted from 87 full-term (37 weeks gestation) pregnant women in active labor. Immediately after delivery of the neonate, 10 ml of blood from the umbilical artery and vein was extracted. Samples were analyzed for levels of glutamate, glutamate-oxaloacetate transaminase (GOT), and glutamate pyruvate transaminase (GPT).Fetal blood glutamate concentrations in both the umbilical artery and vein were found to be significantly higher than maternal blood (p0.001). Similarly, fetal serum GOT levels in the umbilical artery and vein were found to be significantly higher than maternal GOT levels (p0.001). The difference in GPT levels between maternal and fetal serum was not statistically significant. There was no difference in fetal glutamate, GOT or GPT between the umbilical artery and vein. There was an association observed between glutamate levels in maternal blood and glutamate levels in both venous (R=0.32, p0.01) and arterial (R=0.33, p0.05) fetal blood.This study demonstrated that higher baseline concentrations of blood glutamate are present in fetal blood compared with maternal blood, and this was associated with elevated GOT, but not GPT levels. An association was observed between maternal and fetal blood glutamate levels.

Brain insults are characterized by a multitude of complex processes, of which glutamate release plays a major role. Deleterious excess of glutamate in the brain’s extracellular fluids stimulates glutamate receptors, which in turn lead to cell swelling, apoptosis, and neuronal death. These exacerbate neurological outcome. Approaches aimed at antagonizing the astrocytic and glial glutamate receptors have failed to demonstrate clinical benefit. Alternatively, eliminating excess glutamate from brain interstitial fluids by making use of the naturally occurring brain-to-blood glutamate efflux has been shown to be effective in various animal studies. This is facilitated by gradient driven transport across brain capillary endothelial glutamate transporters. Blood glutamate scavengers enhance this naturally occurring mechanism by reducing the blood glutamate concentration, thus increasing the rate at which excess glutamate is cleared. Blood glutamate scavenging is achieved by several mechanisms including: catalyzation of the enzymatic process involved in glutamate metabolism, redistribution of glutamate into tissue, and acute stress response. Regardless of the mechanism involved, decreased blood glutamate concentration is associated with improved neurological outcome. This review focuses on the physiological, mechanistic and clinical roles of blood glutamate scavenging, particularly in the context of acute and chronic CNS injury. We discuss the details of brain-to-blood glutamate efflux, auto-regulation mechanisms of blood glutamate, natural and exogenous blood glutamate scavenging systems, and redistribution of glutamate. We then propose different applied methodologies to reduce blood and brain glutamate concentrations and discuss the neuroprotective role of blood glutamate scavenging.

Traumatic brain injury (TBI) and stroke lead to elevated levels of glutamate in the brain that negatively affect the neurological outcomes in both animals and humans. Intravenous administration of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) enzymes can be used to lower the blood glutamate levels and to improve the neurological outcome following TBI and stroke. The objective of this study was to analyze the pharmacokinetics and to determine the glutamate-lowering effects of GOT and GPT enzymes in naïve rats. We determined the time course of serum GOT, GPT, and glutamate levels following a single intravenous administration of two different doses of each one of the studied enzymes. Forty-six male rats were randomly assigned into one of 5 treatment groups: saline (control), human GOT at dose 0.03 and 0.06 mg/kg and porcine GPT at dose 0.6 and 1.2 mg/kg. Blood samples were collected at baseline, 5 min, and 2, 4, 8, 12, and 24 h after the drug injection and GOT, GPT and glutamate levels were determined. The pharmacokinetics of both GOT and GPT followed one-compartment model, and both enzymes exhibited substantial glutamate-lowering effects following intravenous administration. Analysis of the pharmacokinetic data indicated that both enzymes were distributed predominantly in the blood (central circulation) and did not permeate to the peripheral organs and tissues. Several-hour delay was present between the time course of the enzyme levels and the glutamate-lowering effects (leading to clock-wise hysteresis on concentration-effect curves), apparently due to the time that is required to affect the pool of serum glutamate. We conclude that the interaction between the systemically-administered enzymes (GOT and GPT) and the glutamate takes place in the central circulation. Thus, glutamate-lowering effects of GOT and GPT apparently lead to redistribution of the excess glutamate from the brain's extracellular fluid into the blood and can reduce secondary brain injury due to glutamate neurotoxicity. The outcomes of this study regarding the pharmacokinetic and pharmacodynamic properties of the GOT and GPT enzymes will be subsequently verified in clinical studies that can lead to design of effective neuroprotective treatment strategies in patients with traumatic brain diseases and stroke.

Blood glutamate scavengers have been shown to effectively reduce blood glutamate concentrations and improve neurological outcome after traumatic brain injury and stroke in rats. This study investigates the efficacy of blood glutamate scavengers oxaloacetate and pyruvate in the treatment of subarachnoid hemorrhage (SAH) in rats. Isotonic saline, 250 mg/kg oxaloacetate, or 125 mg/kg pyruvate was injected intravenously in 60 rats, 60 minutes after induction of SAH at a rate of 0.1 ml/100 g/min for 30 minutes. There were 20 additional rats that were used as a sham-operated group. Blood samples were collected at baseline and 90 minutes after SAH. Neurological performance was assessed at 24 h after SAH. In half of the rats, glutamate concentrations in the cerebrospinal fluid were measured 24 h after SAH. For the remaining half, the blood brain barrier permeability in the frontal and parieto-occipital lobes was measured 48 h after SAH. Blood glutamate levels were reduced in rats treated with oxaloacetate or pyruvate at 90 minutes after SAH (p

Several motor-function scales have been developed to assess neurological function in animal models of stroke, subarachnoid hemorrhage and closed head injury. We hypothesize that the location of arterial and venous catheters, even in the absence of brain injury, may impact rats' motor performance. Our study examined the effect of catheter location, rate of infection and the time required for catheter placement. We further describe an original technique of tail artery cannulation without exposure of the artery. Sixty-one rats were anesthetized and randomly assigned to one of seven groups, including no catheter, tail artery or artery + vein catheters, or femoral artery or artery + vein catheters. A neurological severity score (NSS) was determined at 1 h, 24 h and 48 h after surgical preparation or catheter placement. NSS at 1 h after placement of unilateral and bilateral femoral catheters was higher than the NSS observed at 1 h after placement of tail arterial and venous catheters (P < 0.01). The NSS also was higher at 24 h in the bilateral femoral catheter groups as compared with the tail catheter groups (P < 0.05). There were no differences in the NSS observed between the groups that had tail catheters and the sham group at 1 h, 24 h or 48 h. Infection rate at the site of catheter placement and the time required for catheter placement was also higher in the femoral catheter groups (P < 0.001). Thus, we propose that the line location may bias a study's results and lead to deceptive interpretations of neurological assessment following rat head injury. Compared to femoral vessels, tail blood vessels are preferable locations for lines placement.

Isoflurane-anesthetized rats subjected to traumatic brain injury (TBI) show a transient reduction in blood L-glutamate levels. Having previously observed that isoproterenol produces a sustained decrease in blood glutamate levels in naive rats, we investigated the possible effects of nonselective and selective β1 and β2 adrenergic agonists and antagonists both on blood glutamate levels and on the neurological outcomes of rats subjected to TBI.Rats received either 10 mL/kg of isotonic saline 1 hour after TBI, 50 µg/kg of isoproterenol pretreatment 30 minutes before TBI, 10 mg/kg of propranolol pretreatment 60 minutes before TBI, 10 mg/kg of metoprolol pretreatment 60 minutes before TBI, or 10 mg/kg of butaxamine pretreatment 40 minutes before TBI and 10 minutes before pretreatment with 50 µg/kg isoproterenol or 10 mg/kg of propranolol 60 minutes after TBI. A neurological severity score (NSS) was measured at 1, 24, and 48 hours after TBI. Blood glutamate, blood glucose, mean arterial blood pressure, and heart rate were measured at the time of drug injection, at the time of TBI, 60 minutes after TBI, and 90 minutes after TBI.Blood glutamate levels decreased spontaneously by 60 minutes after TBI in the control group (P0.05), reverting to baseline levels by 90 minutes after TBI. A pretreatment with either 10 mg/kg of metoprolol 60 minutes before TBI or with 50 µg/kg of isoproterenol 30 minutes before TBI also reduced blood glutamate levels (P0.05) both at 90 minutes after TBI and improved the NSS measured 24 and 48 hours after TBI in comparison with the control saline-treated group. However, a 10-mg/kg butoxamine pretreatment 40 minutes before TBI and 10 minutes before pretreatment with 50 µg/kg of isoproterenol or 10 mg/kg of propranolol 60 minutes before TBI neither affected blood glutamate levels across time after TBI nor caused any significant change in the NSS measured 24 and 48 hours after TBI in comparison with the control saline-treated group. A strong correlation (r(2)=0.73) was demonstrated between the percent decrease in blood glutamate levels at 90 minutes after TBI and the percent improvement of NSS measured 24 hours after TBI.The results suggest that the transient blood glutamate reduction seen after TBI is the result of a stress response and of the activation of the sympathetic nervous system through the β2 adrenergic receptors, causing an increase of the brain-to-blood efflux of glutamate observed with excess brain glutamate levels after a brain insult. This strongly correlates with the neurological improvement observed 24 hours after TBI.

BACKGROUND Elevated levels of glutamate in brain fluids, in the context of several neurodegenerative conditions, are associated with a worsened neurological outcome. Because there is a clear relationship between brain glutamate levels and glutamate levels in the blood, and an association of the latter with stress, the purpose of this study was to investigate the effects of glucose, insulin, and glucagon on rat blood glutamate levels. METHODS Rats received either 1 mL/100 g of rat body weight (BW) intravenous isotonic saline (control), 150 mg/1 mL/100 g BW intravenous glucose, 75 mg/1 mL/100 g BW intravenous glutamate, 50 g/100 g BW intraparitoneal glucagon, or 0.2 UI/100 g BW intraparitoneal insulin. Blood samples were subsequently drawn at 0, 30, 60, 90, and 120 minutes for determination of blood glutamate and glucose levels. RESULTS We observed a significant decrease in blood glutamate levels at 30 minutes after injection of glucose (P

In previous studies, we have shown that by increasing the brain-to-blood glutamate efflux upon scavenging blood glutamate with either oxaloacetate or pyruvate, one achieves highly significant neuroprotection particularly in the context of traumatic brain injury. The current study examines, for the first time, how the blood glutamate scavenging properties of glutamate-pyruvate transaminase (GPT), alone or in combination with pyruvate, may contribute to the spectrum of its neuroprotective mechanisms and improve the outcome of rats exposed to brain ischemia, as they do after head trauma. Rats that were exposed to permanent middle cerebral artery occlusion (MCAO) and treated with intravenous 250 mg/kg pyruvate had a smaller volume of infarction and reduced brain edema, resulting in an improved neurological outcome and reduced mortality compared to control rats treated with saline. Intravenous pyruvate at the low dose of 31.3 mg/kg did not demonstrate any neuroprotection. However, when combined with 0.6 mg/kg of GPT there was a similar neuroprotection observed as seen with pyruvate at 250 mg/kg. Animals treated with 1.69 g/kg glutamate had a worse neurological outcome and a larger extent of brain edema. The decrease in mortality, infarcted brain volume and edema, as well as the improved neurological outcome following MCAO, was correlated with a decrease in blood glutamate levels. We therefore suggest that the blood glutamate scavenging activity of GPT and pyruvate contributes to the spectrum of their neuroprotective mechanisms and may serve as a new neuroprotective strategy for the treatment of ischemic stroke.

Middle cerebral artery occlusion (MCAO) is widely used as a rat model of focal brain ischemia. Evaluation of brain damage often includes the morphological analysis of the injury area, MRI, and various scales which depend on functional tests, commonly known as neurological severity score (NSS). We determined the optimal number of NSS tests and assessed their capacity for non-invasive evaluation of brain ischemic injury in the rat MCAO model. 275 male Sprague-Dawley rats were randomly divided into five groups, given either permanent (p) MCAO or transient (t) MCAO using an uncoated 4-0 monofilament catheter or a silicone-coated monofilament. The rats' neurological status was examined before and at 1 and 24h following MCAO. The size of brain injury was then measured histologically and the extent of right cerebral hemisphere edema was calculated. We established a correlation between these tests and morphological data for brain injury. Adjusted R(2) of the prediction of total histology score was 0.7. The Hosmer-Lemeshow p-value of this model was 0.812 for total brain histology. For the brain edema the adjusted R(2) of the prediction model was 0.48. The Hosmer-Lemeshow p-value of this model was 0.558 for brain edema. Our methods of estimating infarct size produces reliable and well correlated results at 24h and demonstrates to be an easy and quick way to assess infarct size soon after ischemic injury has occurred. The described method for neurological assessment could ultimately aid in assessing various treatment modalities in the early hours following stroke.

This study examines the effects of the activation of β1 and β2-adrenergic receptors on glutamate homeostasis in the blood of naive rats. Forty five male Sprague–Dawley rats were randomly assigned into one of seven treatment groups that were treated with various β-adrenergic receptor agonist and antagonist drugs. Blood glutamate levels were determined at t = 0, 30, 60, 90, and 120 min. The activation of β1 and β2-adrenergic receptors via isoproterenol hydrochloride administration produced a marked sustained decrease in blood glutamate levels by 60 min after treatment (ANOVA, t = 60, 90 min: P < 0.05, t = 120 min: P < 0.01). Pretreatment with propranolol hydrochloride (a non-selective β-adrenergic receptor blocker) or butaxamine hydrochloride (a selective β2-adrenergic receptor blocker) occluded the isoproterenol-mediated decrease in blood glutamate levels. Propranolol alone had no effect on blood glutamate levels. Selective β1-adrenergic receptor blockade with metoprolol resulted in decreased blood glutamate levels (ANOVA, t = 90 min: P < 0.05, t = 120 min: P < 0.01). Butaxamine hydrochloride alone resulted in a delayed-onset increase in glutamate levels (ANOVA, t = 120 min: P < 0.05). The results suggest that the activation of β2 receptors plays an important role in the homeostasis of glutamate in rat blood.

The local voltage fluctuations in the supply and ground grids triggered by on-die logic cell switching in VLSI devices have been experimentally studied. The results show that these fluctuations have a resonant-like form i.e., the on-die power grid should be described as an RLC circuit. The studies reveal that the active element (i.e., CMOS logic cell) affects the frequency properties of power supply and ground grids during its switching (as opposed to before or after switching). It is demonstrated that the frequency properties of the both grids are inter-related via the interconnecting active elements.

Isoflurane-anesthetized rats submitted to a closed head injury (CHI) display a significant decrease of their blood glutamate levels. Having demonstrated that a decrease of blood L-glutamate (glutamate) causes an increase of the driving force for a spontaneous brain-to-blood glutamate efflux, and consequently affords brain neuroprotection, we investigated here the possible mechanisms which can affect blood glutamate levels. Reasoning that the spontaneous decrease of blood glutamate levels post CHI could be part of a stress response, we observed that the stress involved in tail artery catheterization under isoflurane anesthesia does not affect blood glutamate levels. Investigating in naïve rats the stress effectors, we found that corticotropin-releasing factor (CRF) significantly decreased blood glutamate levels. Pretreatment with antalarmine (a selective type-1 CRF receptor antagonist) occludes the CRF-mediated decrease in blood glutamate levels. In contrast, the adrenocorticotrophic hormone (ACTH) did not affect blood glutamate levels. Investigating the effectors of the sympathetic/adrenomedullary system, we observed that in naïve rats, adrenaline but not noradrenaline decreased blood glutamate levels. Confirming the role of adrenaline, propranolol pretreatment (a non-selective beta-antagonist) prevented the spontaneous decrease of blood glutamate observed post CHI. On the strength of these results, we further observed that isoproterenol (a beta(1/2)-selective adrenoreceptor agonist) produced a marked sustained decrease in blood glutamate levels. These results suggest that stress induces a decrease of blood glutamate levels partly via the activation of peripheral CRF receptors and the activation of the beta-adrenoreceptors. We propose that this newly identified component of the stress response could be a peripherally mediated defense mechanism of the injured brain against the deleterious effects of excess glutamate.

Anesthetized rats were assigned to sham; brain injury (BI); controlled hemorrhagic shock (CHS); BI combined with CHS (combined injury [CI]); and CI groups resuscitated with 2.5 mL/kg Ringer's lactate solution (RL-2.5), 10 mL/kg RL (RL-10), or 40 mL/kg RL (RL-40). Brain injury was induced by applying 400 millibar negative pressure for 10 s through a hollow screw inserted into a 4.5-mm burr hole drilled into the left parietal region of the skull. Five minutes after BI, 30% of circulating blood volume was withdrawn for 10 min to induce CHS. One hour of fluid resuscitation commenced 20 min posthemorrhage. MAP, lactate, and base excess levels were significantly improved in the RL-40 group compared with all other hemorrhaged groups. The hematocrit level 1 h after resuscitation began was significantly lower in the RL-40 group (27.6% +/- 0.57%) than in all other groups. The RL-40 group had the worst neurological severity score 24 h postsurgery. MAP, lactate, and base excess levels were not significantly improved in the RL-2.5 group, however, the number of surviving neuronal cells in the perilesional brain region was significantly higher than in the CI or RL-40 groups. MAP, lactate, and base excess levels were significantly improved in the RL-10 group (P < 0.05). Mobility and the number of surviving neurons in the perilesional region of the brain were significantly better in the RL-10 group than in the CI or RL-40 groups (P < 0.05). Although massive fluid resuscitation yields preferable hemodynamic and metabolic outcomes, neurological outcomes are better after moderate fluid resuscitation for BI combined with controlled hemorrhagic shock.

On-die measurements of V DD and V SS voltages inside a 90-nm VLSI technology chip are presented. The results show local fluctuations in the V DD and V SS voltages with amplitudes that can reach, in severe cases, more than 10% of V DD. These fluctuations can distort analog signals, cause immediate logic faults, and also aggravate other reliability wear-out mechanisms. Both measurements and simulations predict the aggravation of this phenomenon for future technologies.

Time-dependent dielectric breakdown (TDDB) is one of the major issues concerning long-range reliability of dielectric layers in SiC-based high-power devices. Despite the extensive research on TDDB of SiO2 layers on Si, there is a lack of high-quality statistical TDDB data of SiO2 layers on SiC. This paper presents comprehensive TDDB data of 4H-SiC capacitors with a SiO2 gate insulator collected over a wide range of electric fields and temperatures. The results show that at low fields, the electric field acceleration parameter is between 2.07 and 3.22 cm/MV. At fields higher than 8.5 MV/cm, the electric field acceleration parameter is about 4.6 cm/MV, indicating a different failure mechanism under high electric field stress. Thus, lifetime extrapolation must be based on failure data collected below 8.5 MV/cm. Temperature acceleration follows the Arrhenius model with activation energy of about 1 eV, similar to thick SiO2 layers on Si. Based on these experimental data, we propose an accurate model for lifetime assessment of 4H-SiC MOS devices considering electric field and temperature acceleration, area, and failure rate percentile scaling. It is also demonstrated that temperatures as high as 365degC can be used to accelerate TDDB of SiC devices at the wafer level.

The power performance of GaAs/AlGaAs pseudomorphic high electron mobility transistors (PHEMTs) has been modeled by using the statistical Design of Experiment approach. Empirical models for the small signal gain, output power and power added efficiency have been developed. The ''walk-out/in'' phenomenon has been observed in the devices as a result of power measurements. The evolution of surface photovoltage spectra after RF power stress indicates accumulation of positive electrical charge in the buffer and the surface layer of the devices.

Threshold voltage and drain current instabilities in state-of-the-art 4H-SiC MOSFETs with thermal as-grown SiO2 and NO-annealed gate oxides have been studied using fast I-V measurements. These measurements reveal the full extent of the instability underestimated by dc measurements. Furthermore, fast measurements allow the separation of negative and positive bias stress effects. Postoxidation annealing in NO was found to passivate the oxide traps and dramatically reduce the instability. A physical model involving fast transient charge trapping and detrapping at and near the SiC/SiO2 interface is proposed.

In non-obese patients ketamine decreases inflammatory responses and prevents overexpression of immune re- sponses. Its effect in obese patients is unknown. This prospective, blinded, randomized controlled trial was designed to determine the effect of ketamine on cytokines and immune cell responses after short-duration surgery in obese patients. Thirty-six patients received either ketamine 0.15 mg/kg IV prior to induction of general anesthesia, or an equal volume of normal saline. Cytokine concentrations and immune cell responses were determined pre-operatively and at 4, 24, and 48 h after operation. Interleukin (IL)-6 production was significantly greater in the control group (126.0 ± 18.8 ng/ml, mean ± SEM, n = 19) than in the ketamine group (57.9 ± 8.4 ng/ml) at 4 h. At other time periods IL-6 and tumor necrosis factor � increased and IL-2, lymphocyte proliferation, and natural killer cell cytotoxity decreased compared to pre-operative values in the control group but not in the ketamine group. We conclude that effects of ketamine on inflammatory and immune re- sponses after short-duration surgery in obese patients are similar to those previously reported in non-obese patients.

Nonuniform light emission from power transistors at 2-3-dB compression levels has been imaged using a microscope- mounted camera. The nonuniformity depends on the device lateral geometry, load impedance, dc and radio frequency (RF) conditions, and the negative gate current, which is a result of the RF-induced impact ionization in the transistors. Numerical simulations demonstrated a nonuniform distribution of the RF overstress in the transistors under the same conditions. The simulations indicate that the nonuniformity in the light intensity may be attributed to the RF-induced voltage overstress. Therefore, the observed light emission may be used as a direct and contactless monitor of the RF-induced overstress in transistors and power amplifiers.

Summary Background Gastrointestinal (GI) tract dysfunction is well documented following head injury. Our study sought to determine whether head injury causes an immediate impairment of the splanchnic circulation which may contribute to later GI sequelae. Methods Three groups of eight rats each received either no closed head trauma (CHT) (group 1) or CHT (groups 2 and 3) immediately following baseline measurements at time 0. The primary measures of interest – individual organ blood flows and cardiac output (radioactive microspheres), and individual organ and systemic vascular resistances – were determined in the control group, at 5min after CHT in group 2, and at 15min after CHT in group 3. Results CHT caused no significant change in portal venous inflow (flows were 2.40±0.36, 2.38±0.54, and 2.33±0.62mlmin −1 100g −1 bw, mean±S.D., in groups 1, 2, and 3, respectively). Individual organ and total hepatic blood flow, cardiac index, splanchnic, portal, and total peripheral resistance, and mean arterial or portal venous pressure also did not differ significantly among groups. Conclusion We found no significant changes in splanchnic circulation immediately after CHT in this rat model. Our results do not support the hypothesis that the splanchnic circulation is impaired immediately after head injury and that splanchnic blood flow impairment immediately after head injury may contribute to post-head injury GI dysfunction.

Illumination induced charge separation processes at tetraphenyl-porphyrin (H2TPP)/InP interfaces are characterized. The results indicate that upon illumination an electronic transition takes place between the organic highest occupied molecular orbital (HOMO) and the InP conduction band. A 70 meV blue shift in the characteristic modulated surface photovoltage spectrum of a 50 nm H2TPP film was observed when n-InP substrate was used. Such blue shift was not observed when Au, SnO2:F or p-InP substrates were used. The shift may suggest a presence of an ordered interfacial sub-layer in an almost lying orientation, due to chemical or physical interactions at the interface. The results indicate that the Fermi level is unpinned at the interface. An exciton diffusion barrier in close proximity to the H2TPP/n-InP interface has been demonstrated.

The electronic properties of anatase and rutile TiO2 polycrystalline particle films have been studied using surface photovoltage (SPV) and infrared (IR) spectroscopies. The films were prepared from...

The electrically active defects in high-k/SiO"2 dielectric stacks are examined using a combination of low frequency noise (LFN) and charge pumping (CP) methods. The volume trap profile in the stacks is obtained by modeling the drain current noise spectra and charge pumping currents, with each technique covering a different depth range. The LFN is dependent on both the high-k and interfacial (IL) SiO"2 thicknesses while the CP current is mainly dependent on the IL thickness.

Ketamine was reported to decrease cytokine production and improve survival after Escherichia coli-induced sepsis. We examined whether ketamine decreased interleukin (IL)-6 production and improved survival after 1) burn injury or 2) burn injury combined with sepsis (E. coli) at 24 h. Ketamine (10 mg/kg) or saline was given at 1 h after burn injury (G 1, 2, 5, 6), 24 h after burn injury (G 3, 4), or at E. coli inoculation (G 7, 8). Mortality was recorded for 7 days and IL-6 was measured in serum at 6 h after burn (G 1-2), 30 h after burn (G 3-4), or 6 h after sepsis (30 h after burn) (G 5-8). Burn injury only: Ketamine given immediately (1 h) after burn injury but not 24 h after, decreased the burn-induced increase of IL-6 but did not improve survival. Burn injury + sepsis: Ketamine given immediately after burn injury did not significantly decrease the sepsis-induced increase of IL-6 or improve survival. In contrast, ketamine given immediately after sepsis significantly improved survival (46.1% versus 13.3%, P = 0.008) and decreased IL-6 production (72,640 +/- 40,990 vs 332,300 +/- 32,300 pg/mL, P = 0.008). We conclude that ketamine therapy improves survival in burn injury followed by sepsis. This beneficial effect is probably achieved through interference with the inflammatory cascade, as evidenced by attenuation of the proinflammatory marker IL-6.

We discuss methodological aspects of first principles calculations of surface dipoles and potentials in general, and surface-adsorbed self-assembled monolayers in particular, using density functional theory with a slab/super-cell approach. We show that calculations involving asymmetric slabs may yield highly erroneous results for the surface dipole and demonstrated the efficacy of a simple dipole correction scheme. We explain the importance of the electrostatic dipole distribution, show how to compute it, and establish conditions for the equivalence of calculations for the dipole distribution and the electrostatic potential distribution.

The properties of Si(111) surfaces grafted with benzene derivatives were investigated using ultraviolet photoemission spectroscopy (UPS) and X-ray photoelectron spectroscopy (XPS). The investigated materials were nitro-, bromo-, and methoxybenzene layers (-C(6)H(4)-X, with X = NO(2), Br, O-CH(3)) deposited from diazonium salt solutions in a potentiostatic electrochemical process. The UPS spectra of the valence band region are governed by the molecular orbital density of states of the adsorbates, which is modified from the isolated state in the gas phase due to molecule-molecule and molecule-substrate interaction. Depending on the adsorbate, clearly different emission features are observed. The analysis of XPS intensities clearly proves multilayer formation for bromo- and nitrobenzene in agreement with the amount of charge transferred during the grafting process. Methoxybenzene forms only a sub-monolayer coverage. The detailed analysis of binding energy shifts of the XPS emissions for determining the band bending and the secondary electron onset in UPS spectra for determining the work function allow one to discriminate between surface dipole layers--changing the electron affinity--and band bending, affecting only the work function. Thus, complete energy band diagrams of the grafted Si(111) surfaces can be constructed. It was found that silicon surface engineering can be accomplished by the electrochemical grafting process using nitrobenzene and bromobenzene: silicon-derived interface gap states are chemically passivated, and the adsorbate-related surface dipole effects an increase of the electron affinity.

The electrochemical grafting process of 4-nitrobenzene and 4-methoxybenzene (anisole) from diazonium salt solutions has been investigated in situ by monitoring the current density, the band bending, and the nonradiative surface recombination during grafting at different potentials and different concentrations of the diazonium salt in the solution. Ex situ infrared spectroscopic ellipsometry has been used to inspect the Si surface species before and after the grafting process. The band bending decreases with either increasing concentration of diazonium salt or when the redox potential of the diazonium compound (anisole) is nearer to the competing H+/H2 couple. The surface recombination increases at more cathodic potentials if an electron donor group is present at the phenyl ring (nitrobenzene) and vice versa for the electron acceptor group (anisole). The influence of side reactions can be reduced by use of moderate concentration and moderate or strong cathodic potential, depending on the redox potential of the diazonium compound.

Measurements of photon emission and substrate current in metal-oxide-semiconductor field effect transistors at various temperatures have been carried out using electrical and NIR microscopy. The results received at room temperature have extended the correlation between the substrate current and the photon emission, which was previously found in the visible, to the NIR range. On the basis of this correlation, an empirical model based on the substrate current was used to describe the static emission intensity dependence on the transistor bias. Temperature resolved measurements show that the correlation between emission intensity and the substrate current appears to be coincidental.

Objective: In a previous study, ketamine suppressed Escherichia coli-induced production of the cytokines interleukin (IL)-6 and tumor necrosis factor alpha (TNFα). In other previous studies ketamine improved survival after E. coli inoculation. However, the relationship between cytokines and survival following ketamine treatment is uncertain because no study has examined both cytokines and survival after E. coli inoculation. Methods: Rats were given E. coli (0.4×109 colony forming unit (CFU)) at time 0, followed by ketamine (50 mg/kg, n=30) or saline (n=30) at 5 min or 2 h. IL-6 and TNFα were measured in serum at 6 h, and mortality was recorded for 7 days. Results: Survival rate with ketamine was 57% (17/30) and was significantly increased compared to saline (27%, 8/30, P=0.01). IL-6 and TNFα were lower with ketamine than saline (15,197±3444 versus 30,725±4623 pg/ml [mean±S.E.M.], P=0.013 and 38.5±9.5 versus 122.5±14.0 pg/ml, P=0.001, respectively). With ketamine, IL-6 (but not TNFα) concentrations were lower in the survivors (10,900±776 pg/ml) as compared to the non-survivors (P=0.01). IL-6 in ketamine-treated survivors was not different from that in saline-treated survivors. Conclusion: We conclude that ketamine given 5 min or 2 h after induction of E. coli sepsis significantly improves survival, possibly by interfering with the inflammatory cascade (as evidenced by attenuation of cytokine production).

The electronic properties of C60 thin films have been studied using surface photovoltage (SPV) spectroscopy at 120–300 K. Temperature variations of the SPV spectra are correlated with temperature-dependent x-ray diffraction patterns of the same samples, which indicate the first-order phase transition at Tc=250 K. Absolute values of both the band-to-band and band (or band tail) -to-band tail SPV signals are shown to exhibit a clear minimum at Tc=250 K in contrast with the well-known increasing background of the SPV intensity with decreasing temperature. The energy positions of the thresholds of the band-to-band and band (or band tail) -to-band tail regions in the SPV spectra also exhibit nonmonotonic behavior with a mirror symmetry and distinct extrema near Tc. On the basis of the presented results, we discuss possible reasons behind the effect of rotational and orientational states of C60 molecules on the electronic structure of the C60 fullerite and charge carrier transport in C60 thin films.

Light-emitting devices based on ruthenium(II)(4,7-diphenyl-1,10-phenanthroline)3 ([Ru(dphphen)3]2+) as emitter have been fabricated. The effect of an electron transport layer of tris-(8-hydroxyquinoline) aluminum (Alq3) on device performance has been investigated. The emission, peaking at 630 nm, for the indium–tin–oxide (ITO)glass/[Ru(dphphen)3]2+/Ag device reaches maximum luminance after about 15 min at a turn on voltage of 2.5 V. The use of an ITO/[Ru(dphphen)3]2+/Alq3/Ag device reduces this response time to about 120 s at a turn on voltage of 7 V. A maximum brightness of 1300 cd/m2 can be obtained at 15 V within 2 s, with a luminous efficiency of 0.27 cd/A. Based on the charge transporting characteristics of [Ru(dphphen)3]2+ and Alq3 films determined by surface photovoltage spectroscopy, the improved device response time and efficiency are attributed to the enhanced electron injection at [Ru(dphphen)3]2+/Alq3 interface.

Silicon nitride thin films are widely used in GaAs device fabrication. Plasma enhanced chemical vapor deposition is the most commonly used technique by which silicon nitride is deposited. Changing the process conditions may significantly change the layer physical properties and chemical composition. The device definition includes both deposition of the dielectric layer and its patterning, by etching the exposed SiN via a photoresist mask with sub-microns resolution. The current study examines the influence of the deposition and etching process conditions on the layer characteristics and the devices critical dimension (CD) control. Empirical formulae that correlate process parameters (temperature, gas flow ratio, pressure and RF power) with layer properties have been found and with very high precision yield the deposition rate, wet and dry etching rates and refractive index of the layer. Better understanding of the deposition and etching processes led to significant improvement in controlling the device CD.

A systematic study of impact ionization in pseudomorphic high electron mobility transistors (PHEMTs) has been carried out using temperature-dependent electrical measurements as well as modeling for optimizing the power performance of the devices through the best layout parameters. A measurement procedure makes it possible to define a safe transistor operation region is proposed. Impact ionization in the channel is parameterized by specific gate current and voltage values. Temperature-dependent measurements are shown to provide distinction between the impact ionization current and the thermionic field emission current. A methodology for defining an optimum vertical structure and a lateral layout for a given application and operational conditions is developed. Empirical models for optimum lateral layout for a power application were developed based on a statistical "Device Zoo" approach. The results point to an optimal gate-to-drain distance for minimum impact ionization current.

SummaryThe present study aimed to determine different peripheral blood neutrophil functions in 18 morbidly obese subjects with body mass index (BMI) ranging between 35 and 69 kg/m2 in parallel with age- and gender-matched lean controls. Peripheral blood neutrophil functions of obese subjects and matched lean controls were determined. Neutrophils of obese subjects showed significant elevation of the release of basal superoxides (P < 0·0001), formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated superoxides (P < 0·0001) and opsonized zymosan (OZ)-stimulated superoxides (P < 0·045) compared with lean controls. Interestingly, there were no differences in phorbol myristate acetate (PMA)-stimulated superoxide production by neutrophils of the obese subjects and controls. There was also a significant elevation of chemotactic (P < 0·0003) and random (P < 0·0001) migration of neutrophils from obese subjects compared with lean controls. Phagocytosis, CD11b surface expression and adherence of neutrophils from obese subjects were not significantly different from those of the lean controls. The elevated superoxide production and chemotactic activity, together with the normal phagocytosis and adherence, suggest that neutrophils from obese subjects are primed and have the capability to combat infections. However, neutrophils in the priming state may participate in the pathogenesis of obesity-related diseases.

UNLABELLED Surgery is associated with activation of neutrophils and their influx into affected tissue. The pathogenic role of superoxide production generated by activated neutrophils has been documented repeatedly. Ketamine suppresses neutrophil oxygen radical production in vitro. In the present study, we compared the effect of adding small-dose ketamine to opioids during the induction of general anesthesia on superoxide production by neutrophils after coronary artery bypass grafting (CABG). Thirty-five patients undergoing elective CABG were randomized to one of two groups and prospectively studied in a double-blinded manner. The patients received either ketamine 0.25 mg/kg or a similar volume of saline in addition to large-dose fentanyl anesthesia. Blood samples were drawn before the operation, immediately after cardiopulmonary bypass, 24 and 48 postoperative h, and on postoperative Days 3-6. Functional capacity of neutrophils was assessed by superoxide generation after stimulation with phorbol 12-myristate 13-acetate, opsonized zymosan, or formyl-methionyl-leucyl-phenylalanine. The addition of small-dose ketamine to general anesthesia attenuates increased production of the superoxide anion (O2-) by neutrophils without chemical stimulation and after stimulation with phorbol 12-myristate 13-acetate, formyl-methionyl-leucyl-phenylalanine, and opsonized zymosan for 4-6 days after CABG. In addition, ketamine attenuated the percentage of neutrophils on postoperative Days 2-6. In the Control group, superoxide production significantly increased compared with the baseline value. By contrast, in the Ketamine group, this difference was not significant. IMPLICATIONS In a randomized, double-blinded, prospective clinical study, we compared the effect of adding small-dose ketamine to opioids during general anesthesia on superoxide production and showed that ketamine suppressed the increase of superoxide anion production by neutrophils after coronary artery bypass grafting.

The alloy composition of a Cd1−xZnxTe(111) sample and its spatial homogeneity have been determined by surface photovoltage spectroscopy (SPS) and compared to conventional energy dispersive x-ray spectroscopy measurements. Experimental improvements of the former technique yield a contactless, surface sensitive, and highly accurate spectral resolution of the band gap (error

It is well known that abnormally elevated glutamate levels in the brain are associated with secondary brain injury following acute and chronic brain insults. As such, a tight regulation of brain glutamate concentrations is of utmost importance in preventing the neurodegenerative effects of excess glutamate. There has been much effort in recent years to better understand the mechanisms by which glutamate is reduced in the brain to non-toxic concentrations, and in how to safely accelerate these mechanisms. Blood glutamate scavengers such as oxaloacetate, pyruvate, glutamate–oxaloacetate transaminase, and glutamate-pyruvate transaminase have been shown to reduce blood glutamate concentrations, thereby increasing the driving force of the brain to blood glutamate efflux and subsequently reducing brain glutamate levels. In the past decade, blood glutamate scavengers have gained increasing international interest, and its uses have been applied to a wide range of experimental contexts in animal models of traumatic brain injury, ischemic stroke, subarachnoid hemorrhage, epilepsy, migraine, and malignant gliomas. Although glutamate scavengers have not yet been used in humans, there is increasing evidence that their use may provide effective and exciting new therapeutic modalities. Here, we review the laboratory evidence for the use of blood glutamate scavengers. Other experimental neuro-protective treatments thought to scavenge blood glutamate, including estrogen and progesterone, beta-adrenergic activation, hypothermia, insulin and glucagon, and hemodialysis and peritoneal dialysis are also discussed. The evidence reviewed here will hopefully pave the way for future clinical trials.