The effects of the geosynchronous energetic particle radiation environment on spacecraft charging phenomena

The energetic electron environment at the geosynchronous orbit is responsible for a variety of adverse charging effects on spacecraft components. The most serious of these is the degradation and failure of a complementary-metal-oxide-semiconductor (CMOS) electronic components as a result of internal charge-buildup induced by the energetic electrons. Efforts to accurately determine the expected lifetime of these components in this orbit are hampered by the lack of detailed knowledge of the electron spectrum and intensity, particularly of the more penetrating energies greater than 1.5 MeV. This problem is illustrated through the calculation of the dose received by a CMOS device from the energetic electrons and associated bremsstrahlung as a function of aluminum shielding thickness using the NASA AE-6 and the Aerospace measured electron environments. Two computational codes which were found to be in good agreement were used to perform the calculations. For a given shielding thickness the dose received with the two radiation environments differ by as much as a factor of seven with a corresponding variation in lifetime of the CMOS

Muscogiana Vol. 18(1), Spring 2007

https://csuepress.columbusstate.edu/muscogiana/1038/thumbnail.jp

Muscogiana Vol. 17(2), Fall 2006

https://csuepress.columbusstate.edu/muscogiana/1037/thumbnail.jp

When Ferae Naturae Attack: Public Policy Implications and Concerns for the Public and State Regarding the Classification of Indigenous Wildlife as Interpreted Under State Immunity Statutes

Generally, most states have Immunity Statutes that grant municipal entities, and the government, immunity from particular tort-suit liabilities. Every state has a varied list of elements and factors that fall under particular municipality protection. One such protection is for when injuries arise from a “natural condition”, which has been interpreted to include many natural elements like: a rushing river; an avalanche, falling rocks, heavy rain, etc. But what about wildlife—especially indigenous wildlife? This article examines a case recently decided by the Utah Supreme Court, which involved the horrific story of an 11-year-old boy who was stolen from his tent by a wild black bear, and mauled to death. The court refused to include the indigenous black bear within the “natural condition” exception within Utah’s Immunity Act, which opened the State to liability. Specifically, this article examines and proposes that the Utah Supreme Court came to the wrong decision in the case by excluding a black bear from the “natural condition” exception under Utah’s Immunity Act, and that the State should have been immune from the incident. Further, the article displays that indigenous wildlife is a condition of the natural land generally, and examines statutes from other jurisdictions that include such wildlife. The article suggests that for strong public policy reasons, Immunity Acts generally should be broadly interpreted to include indigenous wildlife within the “natural condition” exceptions, and alternatively should be drafted include indigenous wildlife. State costs, wildlife preservation, tourist funding, local economy, taxes, and other public and private interests are examined to display that wildlife should be considered within Immunity Statutes. Lastly, the article expressly recommends a change to Utah’s Immunity Act to include wildlife within the “natural condition exception”—in order to better reflect the aforementioned interests, and to save the State from future liabilities from injuries resulting from wildlife

Differential desensitization of pre- and postsynaptic mu opioid receptors regulating proopiomelanocortin neurons of the arcuate nucleus

2017 Spring.Includes bibliographical references.The mu opioid receptor (MOR) is the primary target of powerful opiate analgesics such as morphine and codeine. Repeated use of opiates, as may occur in patients with chronic pain, leads to the development of tolerance to the drugs' analgesic effects and may result in the development of dependence. This reduces the effectiveness of opiate-based treatments over extended periods of time, and can result in withdrawal when such a treatment is terminated. Many years of study have been dedicated to understanding the processes that lead to the development of tolerance, as an understanding of the mechanisms underlying tolerance could lead the development of novel therapeutic strategies that prolong the efficacy of opioid-based pain treatments. One particular area of focus has been on acute desensitization of the MOR. Studies of acute desensitization, defined as the loss of receptor function that occurs in the seconds to minutes following activation with an agonist, largely focus on the attenuation of desensitization of desensitization-susceptible MORs found on the somato-dendritic region of neurons in various parts of the nervous system. In these studies, we will focus on characterizing desensitization-resistant MORs located on the axon terminal region of GABAergic neurons that form synapses with hypothalamic proopiomelanocortin (POMC) neurons. Activation of presynaptic MORs, as well as other Gαi/o-coupled GPCRs located on presynaptic terminals, results in an inhibition of GABA release, which causes a subsequent inhibition of the amplitude or frequency of inhibitory postsynaptic currents (IPSCs). Our findings demonstrate that apparent resistance to desensitization by presynaptic MORs, measured as a sustained inhibition of IPSC amplitude or frequency, cannot be explained by a large receptor reserve, nor can desensitization become detectable after chronic treatment with the opiate morphine. It was also found that resistance to desensitization is a common, but not universal, property of Gαi/o-coupled G-protein coupled receptors located on presynaptic terminals. Comparison of desensitization-resistant MORs with desensitization-susceptible GABAB receptors revealed that both populations of receptors have similar receptor-effector coupling, and that resistance or susceptibility to desensitization is unaffected by experimental conditions that isolate either Ca2+-independent spontaneous release or Ca2+-dependent synchronous release. These findings provide evidence that resistance or susceptibility to desensitization is not dependent on particular receptor-effector coupling, and is likely receptor delimited. The previous findings suggest that resistance to desensitization by the MOR may be conferred by altered physical properties of presynaptic receptors relative to their postsynaptic counterparts. A likely way that these physical differences could manifest would be through differential mobility of pre- and postsynaptic receptors. To provide proof of principle that such measurements can be made, single-particle tracking of MORs containing an N-terminal FLAG tag was performed the AtT20 cell line. MOR diffusion was measured before and after activation with a maximal, desensitizing concentration of the full MOR agonist DAMGO. In the absence of DAMGO, FLAG-MORs could be found in either a mobile or immobile state. After ten minutes in the presence of DAMGO the fraction of immobile FLAG-MORs was increased, but both mobile and immobile receptors were still present. Because ten minutes in a maximal concentration of DAMGO is sufficient to cause MOR desensitization to reach a maximum and for the internalization of most desensitized receptors to occur, the findings demonstrate that steady-state signaling of the MOR may be maintained by both mobile and immobile receptors. These findings provide a basis for future studies comparing the mobility of pre- and postsynaptic MORs in neurons, as well as determining the role of mobile and immobile MORs in signaling pathways recruited by the receptor

Muscogiana Vol. 19(1), Spring 2008

https://csuepress.columbusstate.edu/muscogiana/1040/thumbnail.jp