Neutron spectral measurements in the upper atmosphere

An experiment to measure neutrons in the upper atmosphere was performed on a balloon flight from Palestine, Texas, at an altitude of about 32 km. The experimental arrangement is discussed briefly, and results of a preliminary analysis of the data for neutrons in the energy range 3 to 30 MeV are given

Wireless, in-vessel neutron monitor for initial core-loading of advanced breeder reactors

An experimental wireless, in-vessel neutron monitor was developed to measure the reactivity of an advanced breeder reactor as the core is loaded for the first time to preclude an accidental critically incident. The environment is liquid sodium at a temperature of approx. 220 C, with negligible gamma or neutron radiation. With ultrasonic transmission of neutron data, no fundamental limitation was observed after tests at 230 C for 2000 h. The neutron sensitivity was approx. 1 count/s-nv, and the potential data transmission rate was approx. 10,000 counts/s

Chronic behavioral and cognitive deficits in a rat survival model of paraoxon toxicity

Organophosphate (OP) compounds, including paraoxon (POX), are similar to nerve agents such as sarin. There is a growing concern that OP agents could be weaponized to cause mass civilian causalities. We have developed a rodent survival model of POX toxicity that is being used to evaluate chronic morbidity and to screen for medical countermeasures against severe OP exposure. It is well known that the survivors of nerve gas and chronic OP exposure exhibit neurobehavioral deficits such as mood changes, depression, and memory impairments. In this study we investigated whether animals surviving severe POX exposure exhibited long-term neurological impairments. POX exposure produced overt signs of cholinergic toxicity. Rats were rescued using an optimized atropine, 2-PAM and diazepam therapy. Surviving rats were studied using established behavioral assays for identifying symptoms of depression and memory impairment 3-months after POX exposure. In the forced swim test, POX rats exhibited increased immobility time indicative of a despair-like state. In the sucrose preference test, POX rats consumed significantly less sucrose water indicating anhedonia-like condition. POX rats also displayed increased anxiety as characterized by significantly lower performance in the open arm of the elevated plus maze. Further, when tested with a novel object recognition paradigm, POX rats exhibited a negative discrimination ratio indicative of impaired recognition memory. The results indicate that this model of survival from severe POX exposure can be employed to study some of the molecular bases for OP-induced chronic behavioral and cognitive comorbidities and develop therapies for their treatment

Pharmacological Blockade of the Calcium Plateau Provides Neuroprotection Following Organophosphate Paraoxon Induced Status Epilepticus in Rats

Organophosphate (OP) compounds which include nerve agents and pesticides are considered chemical threat agents. Currently approved antidotes are crucial in limiting OP mediated acute mortality. However, survivors of lethal OP exposure exhibit delayed neuronal injury and chronic behavioral morbidities. In this study, we investigated neuroprotective capabilities of dantrolene and carisbamate in a rat survival model of paraoxon (POX) induced status epilepticus (SE). Significant elevations in hippocampal calcium levels were observed 48-h post POX SE survival, and treatment with dantrolene (10 mg/kg, i.m.) and carisbamate (90 mg/kg, i.m.) lowered these protracted calcium elevations. POX SE induced delayed neuronal injury as characterized by Fluoro Jade C labeling was observed in critical brain areas including the dentate gyrus, parietal cortex, amygdala, and thalamus. Dantrolene and carisbamate treatment provided significant neuroprotection against delayed neuronal damage in these brain regions when administered one-hour after POX-SE. These results indicate that dantrolene or carisbamate could be effective adjuvant therapies to the existing countermeasures to reduce neuronal injury and behavioral morbidities post OP SE survival

Cardiac sarcoidosis: a comprehensive review

Sarcoidosis is a multisystem granulomatous disease of unknown etiology characterized by noncaseating granulomas in involved organs. Organs involved with sarcoidosis include lymph nodes, skin, lung, central nervous system, and eye. Only 40-50% of patients with cardiac sarcoidosis diagnosed at autopsy have the diagnosis made during their lifetime. Cardiac sarcoidosis can manifest itself as complete heart block, ventricular arrhythmias, congestive heart failure, pericardial effusion, pulmonary hypertension, and ventricular aneurysms. Diagnostic tests such as the electrocardiogram, two-dimensional echocardiography, cardiac magnetic resonance imaging, positron emission tomography scan, radionuclide scan, and endomyocardial biopsy can be helpful in the early detection of cardiac sarcoidosis. Considering the increased risk of sudden death, cardiac sarcoidosis is an indication for early treatment with corticosteroids or other immunosuppressive agents. Other treatments include placement of a pacemaker or implantable defibrillator to prevent sudden death. In refractory cases, cardiac transplantation should be considered

Pruning cuts affect wood necrosis but not the percentage of budburst or shoot development on spur pruned vines for different grapevine varieties

Two experimental studies were performed in this trial. In the first, the aim was to quantify wood necrosis generated by pruning cuts on aboveground permanent (arms and trunks) and non-permanent (spurs) woody structures of 'Cabernet Sauvignon' vines. In the second, the goal was to evaluate the effect of cutting distance from the basal end of the shoot in spur pruned vines on budburst and further shoot development for 'Grenache', 'Cabernet Franc' and 'Malbec' varieties. Based upon the first experiment, the area and depth of wood necrosis was highly influenced by the distance where the pruning cut was performed over the node. Furthermore, the diameter of the spur that was cut was not significantly related to either the area or the depth of the necrotic wood generated after the cut. Aboveground vine wood necrotic area ranged from 9 to 44 % of the total wood area measured in 'Cabernet Sauvignon' cordon trained spur pruned 25-year-old grapevines. For each vine a larger proportion of the necrotic wood (20 to 46 % of necrotic area) was present in the arms when compared to the trunks (1 to 28 % of necrotic area). As a result of the second experiment, spur budburst and further shoot development was not affected by the distance from the node where the pruning cut was performed for any of the cultivars considered in the study contrary to what is commonly believed

Development of status epilepticus, sustained calcium elevations and neuronal injury in a rat survival model of lethal paraoxon intoxication

Paraoxon (POX) is an active metabolite of organophosphate (OP) pesticide parathion that has been weaponized and used against civilian populations. Exposure to POX produces high mortality. OP poisoning is often associated with chronic neurological disorders. In this study, we optimize a rat survival model of lethal POX exposures in order to mimic both acute and long-term effects of POX intoxication. Male Sprague–Dawley rats injected with POX (4 mg/kg, ice-cold PBS, s.c.) produced a rapid cholinergic crisis that evolved into status epilepticus (SE) and death within 6–8 min. The EEG profile for POX induced SE was characterized and showed clinical and electrographic seizures with 7–10 Hz spike activity. Treatment of 100% lethal POX intoxication with an optimized three drug regimen (atropine, 2 mg/kg, i.p., 2-PAM, 25 mg/kg, i.m. and diazepam, 5 mg/kg, i.p.) promptly stopped SE and reduced acute mortality to 12% and chronic mortality to 18%. This model is ideally suited to test effective countermeasures against lethal POX exposure. Animals that survived the POX SE manifested prolonged elevations in hippocampal [Ca2+]i(Ca2+ plateau) and significant multifocal neuronal injury. POX SE induced Ca2+ plateau had its origin in Ca2+ release from intracellular Ca2+ stores since inhibition of ryanodine/IP3 receptor lowered elevated Ca2+ levels post SE. POX SE induced neuronal injury and alterations in Ca2+ dynamics may underlie some of the long term morbidity associated with OP toxicity

Characterization of spontaneous recurrent epileptiform discharges in hippocampal–entorhinal cortical slices prepared from chronic epileptic animals

AbstractEpilepsy, a common neurological disorder, is characterized by the occurrence of spontaneous recurrent epileptiform discharges (SREDs). Acquired epilepsy is associated with long-term neuronal plasticity changes in the hippocampus resulting in the expression of spontaneous recurrent seizures. The purpose of this study is to evaluate and characterize endogenous epileptiform activity in hippocampal–entorhinal cortical (HEC) slices from epileptic animals. This study employed HEC slices isolated from a large series of control and epileptic animals to evaluate and compare the presence, degree and localization of endogenous SREDs using extracellular and whole cell current clamp recordings. Animals were made epileptic using the pilocarpine model of epilepsy. Extracellular field potentials were recorded simultaneously from areas CA1, CA3, dentate gyrus, and entorhinal cortex and whole cell current clamp recordings were obtained from CA3 neurons. All regions from epileptic HEC slices (n=53) expressed SREDs, with an average frequency of 1.3Hz. In contrast, control slices (n=24) did not manifest any SREDs. Epileptic HEC slices demonstrated slow and fast firing patterns of SREDs. Whole cell current clamp recordings from epileptic HEC slices showed that CA3 neurons exhibited paroxysmal depolarizing shifts associated with these SREDs. To our knowledge this is the first significant demonstration of endogenous SREDs in a large series of HEC slices from epileptic animals in comparison to controls. Epileptiform discharges were found to propagate around hippocampal circuits. HEC slices from epileptic animals that manifest SREDs provide a novel model to study in vitro seizure activity in tissue prepared from epileptic animals

Calculating the return on investment of mobile healthcare

<p>Abstract</p> <p>Background</p> <p>Mobile health clinics provide an alternative portal into the healthcare system for the medically disenfranchised, that is, people who are underinsured, uninsured or who are otherwise outside of mainstream healthcare due to issues of trust, language, immigration status or simply location. Mobile health clinics as providers of last resort are an essential component of the healthcare safety net providing prevention, screening, and appropriate triage into mainstream services. Despite the face value of providing services to underserved populations, a focused analysis of the relative value of the mobile health clinic model has not been elucidated. The question that the return on investment algorithm has been designed to answer is: can the value of the services provided by mobile health programs be quantified in terms of quality adjusted life years saved and estimated emergency department expenditures avoided?</p> <p>Methods</p> <p>Using a sample mobile health clinic and published research that quantifies health outcomes, we developed and tested an algorithm to calculate the return on investment of a typical broad-service mobile health clinic: the relative value of mobile health clinic services = annual projected emergency department costs avoided + value of potential life years saved from the services provided. Return on investment ratio = the relative value of the mobile health clinic services/annual cost to run the mobile health clinic.</p> <p>Results</p> <p>Based on service data provided by The Family Van for 2008 we calculated the annual cost savings from preventing emergency room visits, $3,125,668 plus the relative value of providing 7 of the top 25 priority prevention services during the same period, US$17,780,000 for a total annual value of $20,339,968. Given that the annual cost to run the program was$567,700, the calculated return on investment of The Family Van was 36:1.</p> <p>Conclusion</p> <p>By using published data that quantify the value of prevention practices and the value of preventing unnecessary use of emergency departments, an empirical method was developed to determine the value of a typical mobile health clinic. The Family Van, a mobile health clinic that has been serving the medically disenfranchised of Boston for 16 years, was evaluated accordingly and found to have return on investment of $36 for every$1 invested in the program.</p