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The interaction between resonant magnetic perturbations (RMP) and plasma is an active topic in fusion energy research. RMP involves the use of radial magnetic fields generated by external coils installed on a tokamak device. The resonant interaction between the plasma and the RMP field has many favorable effects such as suppression of instabilities and, under certain conditions, improvement of discharge parameters in tokamaks. The RMP technique has been successfully implemented in the STOR-M tokamak. A set of ( m = 2, n = 1) helical coils carrying a current pulse was used to study the effects of RMP on magnetic islands, plasma rotation, and other edge plasma parameters. A new RMP system is being developed for the STOR-M tokamak. The system consists of a number of external saddle coils distributed in the poloidal and toroidal directions and powered by AC power supplies to generate a rotating RMP field. Numerical simulations have been carried out to calculate several parameters for the new RMP system such as the magnetic field and the dominant modes generated by the coils. The dominant mode generated by the new RMP coil system may be tuned to (2, 1) with significant contributions from (2, 3) and (2, 5) modes.

There is a lack of knowledge regarding in-vehicle concentrations of nitrogen dioxide (NO2) during transit through road tunnels in urban environments. Furthermore, previous studies have tended to involve a single vehicle and the range of in-vehicle NO2 concentrations that vehicle occupants may be exposed to is not well defined. This study describes simultaneous measurements of in-vehicle and outside-vehicle NO2 concentrations on a route through Sydney, Australia that included several major tunnels, minor tunnels and busy surface roads. Tests were conducted on nine passenger vehicles to assess how vehicle characteristics and ventilation settings affected in-vehicle NO2 concentrations and the in-vehicle-to-outside vehicle (I/O) concentration ratio. NO2 was measured directly using a cavity attenuated phase shift (CAPS) technique that gave a high temporal and spatial resolution. In the major tunnels, transit-average in-vehicle NO2 concentrations were lower than outside-vehicle concentrations for all vehicles with cabin air recirculation either on or off. However, markedly lower I/O ratios were obtained with recirculation on (0.08–0.36), suggesting that vehicle occupants can significantly lower their exposure to NO2 in tunnels by switching recirculation on. The highest mean I/O ratios for NO2 were measured in older vehicles (0.35–0.36), which is attributed to older vehicles having higher air exchange rates. The results from this study can be used to inform the design and operation of future road tunnels and modelling of personal exposure to NO2.

An approach that combines weight loss with additional health benefits is very desirable. Glucomannan is a dietary fibre that expands in the stomach, creating the feeling of fullness, while chromium can regulate insulin response. Oligofructose is a non-digestible prebiotic fibre with well-established bifidogenic properties that may also have a role in regulating satiety and systemic inflammation. The aim of this 4-week pilot human intervention was to investigate the effect of agglomerated glucomannan, oligofructose and chromium, as part of a calorie restricted diet plan, on weight loss, satiety, satiation, mood and gut microbiota in 12 females (18–65 years, BMI 25–35 kg/m2). Significant reductions were observed in the anthropometric parameters and systolic blood pressure at the end of trial along with a positive impact on gut microbiota and food cravings. This pilot study suggests that this dietary combination, within an energy restricted, diet may be beneficial in managing obesity related health outcomes.

Chronic stress leads to changes in energy status and is a major risk factor for depression, with common symptoms of reductions in body weight and effortful motivation for reward. Indeed, stress-induced disturbed energy status could be a major aetio-pathogenic factor for depression. Improved understanding of these putative inter-relationships requires animal model studies of effects of stress on both peripheral and central energy-status measures and determinants. Here we conducted a study in mice fed on a standard low-fat diet and exposed to either 15-day chronic social stress (CSS) or control handling (CON). Relative to CON mice, CSS mice had attenuated body weight maintenance/gain despite consuming the same amount of food and expending the same amount of energy at any given body weight. The low weight of CSS mice was associated with less white and brown adipose tissues, and with a high respiratory exchange ratio consistent with increased dependence on glucose as energy substrate. Basal plasma insulin was low in CSS mice and exogenous glucose challenge resulted in a relatively prolonged elevation of blood glucose. With regard to hunger and satiety hormones, respectively, CSS mice had higher levels of acylated ghrelin in plasma and of ghrelin receptor gene expression in ventromedial hypothalamus and lower levels of plasma leptin, relative to CON mice. However, whilst CSS mice displayed this constellation of peripheral changes consistent with increases in energy need and glucose utilization relative to CON mice, they also displayed attenuated uptake of [18F]FDG in brain tissue specifically. Reduced brain glucose utilization in CSS mice could contribute to the reduced effortful motivation for reward in the form of sweet-tasting food that we have reported previously for CSS mice. It will now be important to utilize this model to further understanding of the mechanisms via which chronic stress can increase energy need but decrease brain glucose utilization and how this relates to regional and cellular changes in neural circuits for reward processing relevant to depression.

Uroguanylin is a peptide gut hormone proposed to have a role in signalling post meal satiety. Uroguanylin circulates as its pro-hormone, prouroguanylin. There has been limited investigation of the regulation of prouroguanylin by food; therefore we investigated prouroguanylin regulation following meals. In separate experiments we investigated the effects of high calorie (1451 kcal) and medium calorie (725 kcal), high fat meals, on plasma prouroguanylin concentrations. We then examined the effect of a 722.5 kcal high carbohydrate breakfast on prouroguanylin concentrations, comparing the response in healthy weight adults versus those who are overweight/ with obesity. The 1451 kcal meal increased prouroguanylin concentrations, versus fasting at 60 (P

The etiologic agent of Bolivian hemorrhagic fever (BHF), Machupo virus (MACV) is reported to have a mortality rate of 25 to 35%. First identified in 1959, BHF was the cause of a localized outbreak in San Joaquin until rodent population controls were implemented in 1964. The rodent Calomys collosus was identified as the primary vector and reservoir for the virus. Multiple animal models were considered during the 1970’s with the most human-like disease identified in Rhesus macaques but minimal characterization of the pathogenesis has been published since. A reemergence of reported BHF cases has been reported in recent years, which necessitates the further study and development of a vaccine to prevent future outbreaks.

Prevention of weight gain in adults is a major public health target. Animal experiments have consistently demonstrated a relationship between fermentable carbohydrate intake, such as oligofructose, anorectic gut hormones, and appetite suppression and body weight control. This study was designed to determine the dose of oligofructose which would augment the release of anorectic gut hormones and reduce appetite consistently in non-obese humans. Twelve non-obese participants were recruited for a 5-week dose-escalation study. Following a 9-14-day run-in, participants increased their daily oligofructose intake every week from 15, 25, 35, 45, to 55 g daily. Subjective appetite and side effects were monitored daily. Three-day food diaries were completed every week. Appetite study sessions explored the acute effects of 0, 15, 35, and 55 g oligofructose on appetite-related hormones, glycaemia, subjective appetite, and energy intake. In the home environment, oligofructose suppressed hunger, but did not affect energy intake. Oligofructose dose-dependently increased peptide YY, decreased pancreatic polypeptide and tended to decrease ghrelin, but did not significantly affect appetite profile, energy intake, glucose, insulin, or glucagon-like peptide 1 concentrations during appetite study sessions. In conclusion, oligofructose supplementation at ≥ 35 g/day increased peptide YY and suppressed pancreatic polypeptide and hunger; however, energy intake did not change significantly.

TC83 is a human vaccine with investigational new drug status and is used as a prototype Venezuelan equine encephalitis virus for pathogenesis and antiviral research. Differing from other experimental models, the virus causes high titer infection in the brain and 90–100% mortality in the C3H/HeN murine model. To better characterize the susceptibility to disease development in C3H/HeN mice, we have analyzed the gene transcriptomes and cytokine production in the brains of infected mice. Our analysis indicated the potential importance of natural killer cells in the encephalitic disease development. This paper describes for the first time a pathogenic role for natural killer cells in VEEV encephalitis.

Rapid and accurate identification of disease progression are key factors in testing novel vaccines and antivirals against encephalitic alphaviruses. Typical efficacy studies utilize a large number of animals and severe morbidity or mortality as an endpoint. New technologies provide a means to reduce and refine the animal use as proposed in Hume’s 3Rs (replacement, reduction, refinement) described by Russel and Burch. In vivo imaging systems (IVIS) and bioluminescent enzyme technologies accomplish the reduction of animal requirements while shortening the experimental time and improving the accuracy in localizing active virus replication. In the case of murine models of viral encephalitis in which central nervous system (CNS) viral invasion occurs rapidly but the disease development is relatively slow, we visualized the initial brain infection and enhance the data collection process required for efficacy studies on antivirals or vaccines that are aimed at preventing brain infection. Accordingly, we infected mice through intranasal inoculation with the genetically modified pathogen, Venezuelan equine encephalitis, which expresses a luciferase gene. In this study, we were able to identify the invasion of the CNS at least 3 days before any clinical signs of disease, allowing for reduction of animal morbidity providing a humane means of disease and vaccine research while obtaining scientific data accurately and more rapidly. Based on our data from the imaging model, we confirmed the usefulness of this technology in preclinical research by demonstrating the efficacy of Ampligen, a TLR-3 agonist, in preventing CNS invasion.

Summary Objectives To develop and test the feasibility and acceptability of a structured design for a massage therapy clinical trial that included a treatment arm designed to control for the non-specific effects of a massage therapy intervention. Design Pilot randomized controlled clinical trial. Setting University-integrated medicine research clinic. Interventions Participants were randomized to a structured Swedish-style massage therapy intervention, a light-touch bodywork control intervention, or usual medical care. Details of the interventions are provided. Main outcome measures The primary outcome measures were the adherence of the participants to the study protocol and the perception of the intervention experience. Results Forty-four participants were randomized. Participants often found adherence to the twice-weekly outpatient bodywork interventions to be somewhat difficult; while, overall, 84% of participants completed the study, only 76% of those in an intervention arm successfully completed the trial. Participants randomized to the massage arm expressed uniformly positive attitudes both before and after the intervention. While some participants randomized to the light-touch bodywork arm initially expressed some reservations about their randomization assignment, all participants available for interview were pleased with their experience after the intervention period. Conclusions The proposed design was found to be relatively straightforward to implement and acceptable to participants. Early disappointment with not receiving massage therapy expressed by the light-touch intervention participants dissipated quickly. Twice-weekly outpatient intervention appointments were found to be highly burdensome for many patients actively undergoing chemotherapy, thus reducing adherence.

Insomnia affects approximately one-third of the adult population and contributes to increased rates of absenteeism, health care use, and social disability. Extracts of the roots of valerian (Valeriana officinalis) are widely used for inducing sleep and improving sleep quality. A systematic review of randomized, placebo-controlled trials of valerian for improving sleep quality is presented. An extensive literature search identified 16 eligible studies examining a total of 1093 patients. Most studies had significant methodologic problems, and the valerian doses, preparations, and length of treatment varied considerably. A dichotomous outcome of sleep quality (improved or not) was reported by 6 studies and showed a statistically significant benefit (relative risk of improved sleep = 1.8, 95% confidence interval, 1.2-2.9), but there was evidence of publication bias in this summary measure. The available evidence suggests that valerian might improve sleep quality without producing side effects. Future studies should assess a range of doses of standardized preparations of valerian and include standard measures of sleep quality and safety.

We have evaluated the effects of fatty acid chain length on ghrelin, peptide YY (PYY), glucagon-like peptide-2 (GLP-2) and pancreatic polypeptide (PP) secretion and hypothesized that intraduodenal administration of dodecanoic ("C12"), but not decanoic ("C10"), acid would decrease plasma ghrelin and increase PYY, GLP-2 and PP concentrations. Plasma hormone concentrations were measured in seven healthy men during 90-min intraduodenal infusions of: (i) C12, (ii) C10 or (iii) control (rate: 2 ml/min, 0.375 kcal/min for C12/C10) and after a buffet-meal consumed following the infusion. C12 markedly suppressed plasma ghrelin and increased both PYY and GLP-2 (all P < 0.05) compared with control and C10, while C10 had no effect. Both C10 and C12 increased PP concentrations slightly (P < 0.05). We conclude that the effects of intraduodenal fatty acids on ghrelin, PYY and GLP-2 secretion are dependent on their chain length.

Breakfast is commonly described as being beneficial for health and people who eat breakfast have frequently been reported as having a lower body mass index compared to people who skip breakfast; however reasons for this potential association are still not clear. The aim of this study was to focus particularly on pre-prandial hunger and serum ghrelin levels in lean and overweight breakfast eaters and breakfast skippers (n ¼ 37) when asked to consume breakfast for 7 days and skip breakfast for 7 days. Measurements were taken at the start and the end of each breakfast condition. Habitual breakfast eaters reported greater levels of hunger in each breakfast condition compared with breakfast skippers (p

Gene transfer as a therapeutic modality for the treatment of myocardial ischemia and/or infarction has been proposed as a revolutionary approach to improve collateral circulation, enhance myocardial viability and amplify healing. Our study was undertaken to assess the feasibility, efficiency, anatomic distribution, timing and localization of adenovirus-mediated gene transfer into the vicinity of infarcted myocardium in the adult mammalian heart. We induced myocardial infarction by subjecting rats to 60 min of coronary artery occlusion followed by sustained reperfusion. Gene transfer into the infarction area was performed using direct injection of a replication-defective adenovirus vector encoding the bacterial reporter gene, beta-galactosidase. A total of 5.0 x 10(9) plaque-forming units of virus was delivered into the left ventricular myocardium either immediately (n = 7) or at 7 (n = 6), 22 (n = 5) or 30 days (n = 5) after reperfusion of rat hearts. Control rats received either 50 microliters of saline 13 days after myocardial infarction (n = 2) or were not subjected to infarction and received Adenovirus carrying the beta-galactosidase gene as described above (n = 4). All rats were killed at 7 days after cardiac injection. Hearts were harvested, frozen and sectioned and stained for beta-galactosidase activity and with hematoxylin and eosin. Sections were evaluated by light microscopy. Relative beta-galactosidase activity was measured by digital planimetry and expressed as the ratio of the maximal area of beta-galactosidase staining relative to the total area of the section examined (% +/- S.E.M.). beta-galactosidase gene expression was limited mainly to viable myocytes at the border of the myocardial infarction. The area of transgene expression in the non-infarcted hearts (28 +/- 7%) was significantly higher (P = 0.02) than at any time point studied in infarcted tissues (3.4 +/- 1.2%, 1.4 +/- 1.0%, 2.8 +/- 0.8% and 3.4 +/- 0.9% at reperfusion and at 7, 22 and 30 days after myocardial infarction, respectively). Hearts injected 7 days after infarction had significantly less transgene activity (P = 0.03) with three of five samples displaying no macroscopically visible beta-gal activity. Following viral injection, an inflammatory response consisting of mononuclear cell infiltration was much less intense seven days following injection in non-infarcted control rat hearts than at any of the time points examined for infarcted hearts. Gene transfer into infarcted myocardium, while feasible, was limited by low transfection efficiency when compared to non-infarcted normal myocardium. Transgene expression in the infarcted myocardium appears restricted to residual cardiomyocytes in the periphery. Nevertheless, the ability to introduce genes into these viable peripheral cells might be a useful therapeutic strategy for enhancing neovascularization, collateral flow and healing.

Time and time again, the Department of Defense, the Executive Branch, and other government officials have claimed publicly that Guantanamo Bay detainees who have been released have “returned to the battlefield” where they have then been re-captured or killed. On January 13, 2009, during a press conference the Department of Defense provided its 43rd attempt to report on the number of detainees released from Guantanamo who returned to the battlefield. This latest report alleges that 61 detainees have returned to the battlefield. This report seeks to examine the last numbers.

The Seton Hall School of Law Center for Policy and Research Report, Death in Camp Delta, analyzed the official investigation into the June 9-10, 2006 deaths of three detainees at Guantanamo Bay Naval Base Detention Facility. The Center found a deeply flawed investigation, which failed to resolve serious questions about what really happened that night that resulted in the deaths of three men in U.S. military custody. In response to an article in Harper’s Magazine which built on the Seton Hall study and independently investigated the events at Camp Delta, the Department of Defense (DOD) provided further information. Unfortunately, this response, like the initial investigation itself, is disturbingly flawed. While the response confirms at least some of Seton Hall’s criticisms of the earlier investigation in the course of providing new information, it also contradicts factual claims in its own investigation, raising new questions as to whether the DOD can be trusted to investigate its own conduct. In analyzing the DODs response, the Center finds that

A review of the Department of Defense’s own data reveals that there is not a consistent practice of releasing Guantanamo Bay detainees based on their alleged association to al Qaeda and/or the Taliban. In addition, the number of charges against any given detainee does not seem to affect his release date. Instead, the only constant correlation to detainees who are released earlier than others is the nationality of those released. A finding that the only causal relation to release date is nationality shows that either the Department of Defense never believed their own allegations for the basis of detention, or that they knowingly released individuals they believed to be dangerous.

The latest "Fact Sheet" drafted by the Department of Defense ("DOD"), dated April 7, 2009, claims that 74 out of more than 530 former Guantanamo detainees have "reengaged in terrorist activities." Undermining that claim is the further assertion that, out of the 74, only 27 are considered "confirmed" recidivists. The total shrinks further since only 15 of the alleged 27 are named in the document, and only 13 of these 15 can be shown to have actually been detained at Guantanamo. Even assuming that the DOD's number of 13 "Confirmed" recidivist former Guantanamo detainees is accurate, this number represents virtually no change over the past year, and remains a far cry from the alleged 74. The April 2009 report marks the fourth list of names issued by the government since 2007, and, in an ongoing trend, each of these "partial" lists has proven rife with errors, inconsistencies, and inflated statistics. In this report as well as in previous reports, all relying on the Government's own data and official statements, the Seton Hall Center for Law and Policy concludes the following: 1. While the Government has stated a number of detainee recidivists on at least 45 occasions, on 41 of those occasions it provided no names to corroborate the number. No list of names released equals the contemporaneously reported number of total purported recidivists. 2. The DOD's previous statements about post-release conduct of former detainees were produced in July 2007, May 2008, and June 2008. The DOD has not asserted a change in policy in the time since. 3. The April 7, 2009 report announces 74 alleged recidivists, but lacks 45 names. Of the 29 names given, only half are labeled "confirmed" recidivists. This number is representative of previous claims by the DOD and makes the "74" figure appear inflated. 4. Many of the names provided in the latest report raise the same problems of identity and consistency posed by earlier DOD reports. 5. The scope of "reengaged in terrorism" extends far beyond the battlefield, and raises questions as to the ends the Department of Defense takes the term "recidivism." 6. With each new DOD report, the difference between the asserted total number of recidivists and the number of named and confirmed recidivists grows greater.

On the night of June 9, 2006, three detainees died in maximum security section of the Guantanamo Bay Detention facility. The military’s initial press releases reported not only that the detainees were found hanging in their cells but also that their actions were a conspiracy as part of “asymmetrical warfare” against the United States. At the same time, the military ordered all media off the island and prevented all lawyers from visiting their clients. Questions immediately arose about how three detainees, under constant supervision, were able to conspire effectively to commit coordinated suicides in non -adjacent cells. In August 2008 a heavily redacted report of the investigation concluded that the detainees had hanged themselves in their cells and that one detainee, while walking the corridors that night, had announced, “tonight’s the night.” The investigation, however, leaves many unanswered questions. Three years later it is still unclear how such coordinated conduct would have occurred, much less how heavily supervised detainees could have been dead for more than two hours before they were discovered. Further, the exact manner of the deaths remain uncertain, and the presence of rags stuffed in the detainees’ throats is unexplained. Negligence of the guards seems to have been ruled out by the absence of any disciplinary action by any military personnel. The guards were formally advised of their right to remain silent, their right to counsel and the fact that anything that they said could be used against them because their original statements were suspected to be false. No such original statement appears in the record and no guard was ultimately charged with either making a false statement or being derelict in his duty. This paper examines the investigation, not to determine what happened that night, but rather to assess why an investigation into three deaths could have could have failed to address significant issues. Further, the report raises serious questions that must be addressed if the government is to dispel rumors that the deaths were the result of something was more sinister than “asymmetrical warfare.” This report reveals the following facts: The original military press releases did not report that the detainees had been dead for more than two hours when they were discovered, nor that rigor mortis had set in by the time of discovery. There is no explanation of how three bodies could have hung in cells for at least two hours while the cells were under constant supervision, both by video camera and by guards continually walking the corridors and responsible for only 28 detainees. There is no explanation of how each of the detainees, much less all three, could have done the following: braided a noose by tearing up his sheets and/or clothing; made a mannequin of himself so it would appear to the guards he was asleep in his cell; hung sheets to block vision into the cell - a violation of Standard Operating Procedures; tied his feet together; tied his hands together; hung the noose from the metal mesh of the cell and wall and/or ceiling; climbed up on the sink; put the noose around his neck and released his weight to result in death by strangulation; and then hung undetected for at least two hours.

Introduction Heavy exercise results in gut symptoms and in extreme cases “heat stroke” due, in part, to increased intestinal permeability of luminal toxins. We examined if bovine colostrum a rich source of growth factors and immune modulators could prevent these permeability changes. Methods Twelve healthy volunteers completed a double-blind, placebo-controlled, crossover protocol (14 days colostrum or placebo) prior to standardised exercise. Gut permeability utilised 5 h urinary lactulose: rhamnose ratios. In vitro studies (T84 cells) examined effects of colostrum on temperature-induced apoptosis (active caspase-3) and epithelial resistance. Results For both arms of study, exercise increased the blood lactate, heart rate, core temperature (mean 2°C rise) and plasma VIP by similar amounts. However, GLP-1 plasma levels results were discordant; rising by 88.7 pmol/l in placebo arm but falling by 4.2 pmol/l in colostrum arm (p=0.026). Intestinal permeability in placebo arm increased 2.5-fold following exercise (0.38±0.012 baseline value, to 0.92±0.014, p Conclusion Bovine colostrum reduced exercise-induced increase in gut permeability, possibly through mechanisms including reducing temperature-induced apoptosis. This may have value in enhancing athletic performance and preventing heat stroke.