The Possibility of Discharging Student Loan Debt and Assessing the Differing Standards Applied by the Courts

(Excerpt) Discharging student loan debt under the United States Bankruptcy Code (the “Bankruptcy Code”) is more difficult than attempting to discharge other types of debt. Although discharging student loan debt is not a simple hurdle to surpass, it is possible in certain circumstances. Under the Bankruptcy Code, student loan debt may not be discharged “unless excepting such debt from discharge . . . would impose an undue hardship on the debtor and the debtor\u27s dependents . . . .” The Bankruptcy Code does not define undue hardship. Congress “left it up to the various Bankruptcy Courts to utilize their discretion in defining what that term means after an analysis of the statute and a review of applicable legislative history.” This created an imbalance between the circuits, and courts have implemented a variety of tests throughout the years to decide undue hardship cases. Presently, all student loans are subject to the undue hardship standard, and the two main tests applied by the courts are the Brunner test and the totality of the circumstances test. Because the undue hardship standard was enacted without guidance on how to evaluate it, two questions arise: (1) whether it is possible to discharge student loan debt, and (2) how have courts applied the differing standards in determining whether to discharge student loan debt? This memorandum will examine the two undue hardship standards. Part I discusses both the Brunner test and totality of the circumstances test. Part II assesses how the standards compare to each other

The Effectiveness of Active and Passive Teaching Methods on the Retention of Material Taught to the Naval Intelligence Officer\u27s Basic Course (NIOC) Students for the Period of One Week

Based on the problem statement, the research hypothesis for this study is as follows: 1. Student Intelligence Officers taught using active teaching methods will attain higher academic scores and retain more information over the duration of the Naval Intelligence Officer Basic Course (NIOBC) than student Intelligence Officers taught using passive teaching methods

SLIDES: Forest and Rangeland Planning, NEPA Analysis and Decisions

Presenter: Glenn Casamassa, Forest Supervisor, Arapahoe-Roosevelt National Forest 17 slide

SLIDES: Forest and Rangeland Planning, NEPA Analysis and Decisions

Presenter: Glenn Casamassa, Forest Supervisor, Arapahoe-Roosevelt National Forest 17 slide

Knocking out the Na+/Ca2+ exchanger NCX3 impairs oligodendrocyte lineage responses and worsens clinical symptoms in experimental autoimmune encephalomyelitis-induced multiple sclerosis in mice

Abstract The dysregulation of [Ca2+]i and [Na+]i homeostasis is involved in neuronal and glial response occurring in several neurodegenerative diseases, including Multiple Sclerosis. The Na+/Ca2+ exchanger can be considered a key player in modulating the [Ca2+]i and [Na+]i homeostasis following the injury. Recent evidence point out to the isoform NCX3 of the Na+/Ca2+ exchanger as a new potential therapeutic target for neuroprotection. The aim of the present study was to establish the role played by NCX3 in a murine model of Multiple Sclerosis. The experimental model used in these studies was the Experimental Autoimmune Encephalomyelitis (EAE). Biochemical analysis performed on spinal cord tissue homogenates revealed that NCX3 protein levels were progressively up-regulated during EAE progression; this effect was more significant at EAE chronic stage. In addition, quantitative confocal double immunofluorescence experiments showed that the co-expression of NCX3 with both the myelin marker myelin basic protein (MBP) and the axonal marker neurofilament 200 (NF200) was significantly down-regulated at peak and chronic stages of EAE disease. By contrast, quantification of co-localization studies revealed that the co-expression of NCX3 with the oligodendrocyte lineage markers, the membrane chondroitin sulfate proteoglycan NG2, the Galactocebroside (GalC), and the 2’-3’-cyclic nucleotide-3’-phosphodiesterase (CNPase) was up-regulated during EAE progression. Interestingly, this up-regulation was more significant at EAE chronic stage. These early results suggested that NCX3 isoform might be involved in neuroprotective responses mediated by oligodendrocytes during the EAE recovery phase. The importance of the NCX3 isoform in oligodendroglial responses following EAE insult was supported by several findings: 1) at chronic stage of EAE disease, NCX3 knockout (ncx3-/-) mice displayed a reduced number of NG2 and CNPase positive cells when compared to NCX3 congenic wild type (ncx3+/+) mice; 2) NCX3 knockout (ncx3-/-) mice showed an earlier onset of symptoms and an increased susceptibility to the EAE disease when compared to NCX3 congenic wild type (ncx3+/+) mice. In conclusion, our findings suggested that NCX3 exchanger, by modulating [Na+]i and [Ca2+]i homeostasis might play an important role in controlling oligodendrocyte response after a demyelinating insult

Geopolymer based brake pads

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K+-Dependent Na+/Ca2+ Exchanger Isoform 2, Nckx2, Takes Part in the Neuroprotection Elicited by Ischemic Preconditioning in Brain Ischemia

Sodium/Calcium exchangers are neuronal plasma membrane antiporters which, by coupling Ca2+ and Na+ fluxes across neuronal membranes, play a relevant role in brain ischemia. The most brain-expressed isoform among the members of the K+-dependent Na+/Ca2+ exchanger family, NCKX2, is involved in the progression of the ischemic lesion, since both its knocking-down and its knocking-out worsens ischemic damage. The aim of this study was to elucidate whether NCKX2 functions as an effector in the neuroprotection evoked by ischemic preconditioning. For this purpose, we investigated: (1) brain NCKX2 expression after preconditioning and preconditioning + ischemia; (2) the contribution of AKT and calpain to modulating NCKX2 expression during preconditioning; and (3) the effect of NCKX2 knocking-out on the neuroprotection mediated by ischemic preconditioning. Our results showed that NCKX2 expression increased in those brain regions protected by ischemic preconditioning. These changes were p-AKT-mediated since its inhibition prevented NCKX2 up-regulation. More interestingly, NCKX2 knocking-out significantly prevented the protection exerted by ischemic preconditioning. Overall, our results suggest that NCKX2 plays a fundamental role in the neuroprotective effect mediated by ischemic preconditioning and support the idea that the enhancement of its expression and activity might represent a reasonable strategy to reduce infarct extension after stroke

The Anemonia sulcata Toxin BDS-I Protects Astrocytes Exposed to Aβ1–42 Oligomers by Restoring [Ca2+]i Transients and ER Ca2+ Signaling

Intracellular calcium concentration ([Ca2+]i) transients in astrocytes represent a highly plastic signaling pathway underlying the communication between neurons and glial cells. However, how this important phenomenon may be compromised in Alzheimer’s disease (AD) remains unexplored. Moreover, the involvement of several K+ channels, including KV3.4 underlying the fast-inactivating currents, has been demonstrated in several AD models. Here, the effect of KV3.4 modulation by the marine toxin blood depressing substance-I (BDS-I) extracted from Anemonia sulcata has been studied on [Ca2+]i transients in rat primary cortical astrocytes exposed to Aβ1–42 oligomers. We showed that: (1) primary cortical astrocytes expressing KV3.4 channels displayed [Ca2+]i transients depending on the occurrence of membrane potential spikes, (2) BDS-I restored, in a dose-dependent way, [Ca2+]i transients in astrocytes exposed to Aβ1–42 oligomers (5 µM/48 h) by inhibiting hyperfunctional KV3.4 channels, (3) BDS-I counteracted Ca2+ overload into the endoplasmic reticulum (ER) induced by Aβ1–42 oligomers, (4) BDS-I prevented the expression of the ER stress markers including active caspase 12 and GRP78/BiP in astrocytes treated with Aβ1–42 oligomers, and (5) BDS-I prevented Aβ1–42-induced reactive oxygen species (ROS) production and cell suffering measured as mitochondrial activity and lactate dehydrogenase (LDH) release. Collectively, we proposed that the marine toxin BDS-I, by inhibiting the hyperfunctional KV3.4 channels and restoring [Ca2+]i oscillation frequency, prevented Aβ1–42-induced ER stress and cell suffering in astrocytes