Innovative Strategies For Teaching Principles Of Accounting And Federal Taxation Classes

By integrating meaningful group learning experiences into my Principles of Accounting and Tax classes, Accounting was effectively promoted as an undergraduate major or minor, as supported by student satisfaction surveys. Many accounting programs are facing unprecedented challenges raised by declining enrollments and dynamic changes in profession. Using Baker, Simon, and Bazelli’s (1985) Instructional Design for Accounting based on Kolb’s Experiential Group Learning Model, multiple teaching strategies were incorporated into my classes appealing to multiple student learning styles and, as a result, student’s attitude towards Accounting were significantly effected. The following is a brief list of group or solo activities used in my classes: ·                   Played Financial Accounting and Tax Jeopardy Games that are published on my website (www.geocities.com/docseda) ·                     Accounting students developed Excel-based Accounting Information System for service and merchandising businesses.·                     Accounting students presented an analysis of an annual report.·                     Accounting students played Stock Market Simulation Game (www. ncarolinasms.org).·                     Accounting students played Monopoly.·                     Accounting students played business simulation game at AICPA website (www. startheregoplaces.com). ·                     Tax students worked on three comprehensive tax returns prepared with TaxCut software.·                     Selected Tax students took IRS exam to qualify for VITA program in spring of 2004.·                     Accounting and Tax students prepared posters summarizing various concepts.  This article will provide a detailed summary of learning experiences used in the Fall Semester of 2003 at Shaw University and an analysis of student surveys.&nbsp

An Examination of Computer Forensics and Related Certifications In The Accounting Curriculum

Forensic accounting has been a fast-growing niche area within the accounting field for many years. While there has been dramatic growth in the number of courses and degrees in forensic accounting offered by universities, certain relevant topics receive little coverage, such as computer forensics. The purpose of this paper is to examine the views of accounting academics and practitioners pertaining to integrating computer forensics in the accounting curriculum, as well as to determine which forensic accounting certifications the respondents hold. Differences in opinions between the two groups are discussed, along with recommendations on how to improve the forensic accounting curriculum pertaining to computer forensics education

Slip distribution of the 2017 M(w)6.6 Bodrum-Kos earthquake: resolving the ambiguity of fault geometry

SUMMARY The 2017 July 20, Mw6.6 Bodrum–Kos earthquake occurred in the Gulf of Gökova in the SE Aegean, a region characterized by N–S extension in the backarc of the easternmost Hellenic Trench. The dip direction of the fault that ruptured during the earthquake has been a matter of controversy where both north- and south-dipping fault planes were used to model the coseismic slip in previous studies. Here, we use seismic (seismicity, main shock modelling, aftershock relocations and aftershock mechanisms using regional body and surface waves), geodetic (GPS, InSAR) and structural observations to estimate the location, and the dip direction of the fault that ruptured during the 2017 earthquake, and the relationship of this event to regional tectonics. We consider both dip directions and systematically search for the best-fitting locations for the north- and south-dipping fault planes. Comparing the best-fitting planes for both dip directions in terms of their misfit to the geodetic data, proximity to the hypocenter location and Coulomb stress changes at the aftershock locations, we conclude that the 2017 earthquake ruptured a north-dipping fault. We find that the earthquake occurred on a 20–25 km long, ∼E–W striking, 40° north-dipping, pure normal fault with slip primarily confined between 3 and 15 km depth, and the largest slip exceeding 2 m between depths of 4 and 10 km. The coseismic fault, not mapped previously, projects to the surface within the western Gulf, and partly serves both to widen the Gulf and separate Kos Island from the Bodrum Peninsula of SW Anatolia. The coseismic fault may be an extension of a mapped, north-dipping normal fault along the south side of the Gulf of Gökova. While all of the larger aftershocks are consistent with N–S extension, their spatially dispersed pattern attests to the high degree of crustal fracturing within the basin, due to rapid trenchward extension and anticlockwise rotation within the southeastern Aegean

JIP1-Mediated JNK Activation Negatively Regulates Synaptic Plasticity and Spatial Memory

The c-Jun N-terminal kinase (JNK) signal transduction pathway is implicated in learning and memory. Here, we examined the role of JNK activation mediated by the JIP1 scaffold protein. We compared male wild-type mice with a mouse model harboring a point mutation in the Jip1 gene that selectively blocks JIP1-mediated JNK activation. These male mutant mice exhibited increased NMDA receptor currents, increased NMDA receptor-mediated gene expression, and a lower threshold for induction of hippocampal long-term potentiation. The JIP1 mutant mice also displayed improved hippocampus-dependent spatial memory and enhanced associative fear conditioning. These results were confirmed using a second JIP1 mutant mouse model that suppresses JNK activity. Together, these observations establish that JIP1-mediated JNK activation contributes to the regulation of hippocampus-dependent, NMDA receptor-mediated synaptic plasticity and learning. SIGNIFICANCE STATEMENT: The results of this study demonstrate that JNK activation induced by the JIP1 scaffold protein negatively regulates the threshold for induction of long-term synaptic plasticity through the NMDA-type glutamate receptor. This change in plasticity threshold influences learning. Indeed, mice with defects in JIP1-mediated JNK activation display enhanced memory in hippocampus-dependent tasks, such as contextual fear conditioning and Morris water maze, indicating that JIP1-JNK constrains spatial memory. This study reports the identification of JIP1-mediated JNK activation as a novel molecular pathway that negatively regulates NMDA receptor-dependent synaptic plasticity and memory

POTs: Protective Optimization Technologies

Algorithmic fairness aims to address the economic, moral, social, and political impact that digital systems have on populations through solutions that can be applied by service providers. Fairness frameworks do so, in part, by mapping these problems to a narrow definition and assuming the service providers can be trusted to deploy countermeasures. Not surprisingly, these decisions limit fairness frameworks' ability to capture a variety of harms caused by systems. We characterize fairness limitations using concepts from requirements engineering and from social sciences. We show that the focus on algorithms' inputs and outputs misses harms that arise from systems interacting with the world; that the focus on bias and discrimination omits broader harms on populations and their environments; and that relying on service providers excludes scenarios where they are not cooperative or intentionally adversarial. We propose Protective Optimization Technologies (POTs). POTs provide means for affected parties to address the negative impacts of systems in the environment, expanding avenues for political contestation. POTs intervene from outside the system, do not require service providers to cooperate, and can serve to correct, shift, or expose harms that systems impose on populations and their environments. We illustrate the potential and limitations of POTs in two case studies: countering road congestion caused by traffic-beating applications, and recalibrating credit scoring for loan applicants.Comment: Appears in Conference on Fairness, Accountability, and Transparency (FAT* 2020). Bogdan Kulynych and Rebekah Overdorf contributed equally to this work. Version v1/v2 by Seda G\"urses, Rebekah Overdorf, and Ero Balsa was presented at HotPETS 2018 and at PiMLAI 201

Translational development of ABCB5+ dermal mesenchymal stem cells for therapeutic induction of angiogenesis in non-healing diabetic foot ulcers

Background While rapid healing of diabetic foot ulcers (DFUs) is highly desirable to avoid infections, amputations and life-threatening complications, DFUs often respond poorly to standard treatment. GMP-manufactured skin-derived ABCB5+ mesenchymal stem cells (MSCs) might provide a new adjunctive DFU treatment, based on their remarkable skin wound homing and engraftment potential, their ability to adaptively respond to inflammatory signals, and their wound healing-promoting efficacy in mouse wound models and human chronic venous ulcers. Methods The angiogenic potential of ABCB5+ MSCs was characterized with respect to angiogenic factor expression at the mRNA and protein level, in vitro endothelial trans-differentiation and tube formation potential, and perfusion-restoring capacity in a mouse hindlimb ischemia model. Finally, the efficacy and safety of ABCB5+ MSCs for topical adjunctive treatment of chronic, standard therapy-refractory, neuropathic plantar DFUs were assessed in an open-label single-arm clinical trial. Results Hypoxic incubation of ABCB5+ MSCs led to posttranslational stabilization of the hypoxia-inducible transcription factor 1α (HIF-1α) and upregulation of HIF-1α mRNA levels. HIF-1α pathway activation was accompanied by upregulation of vascular endothelial growth factor (VEGF) transcription and increase in VEGF protein secretion. Upon culture in growth factor-supplemented medium, ABCB5+ MSCs expressed the endothelial-lineage marker CD31, and after seeding on gel matrix, ABCB5+ MSCs demonstrated formation of capillary-like structures comparable with human umbilical vein endothelial cells. Intramuscularly injected ABCB5+ MSCs to mice with surgically induced hindlimb ischemia accelerated perfusion recovery as measured by laser Doppler blood perfusion imaging and enhanced capillary proliferation and vascularization in the ischemic muscles. Adjunctive topical application of ABCB5+ MSCs onto therapy-refractory DFUs elicited median wound surface area reductions from baseline of 59 % (full analysis set, n = 23), 64 % (per-protocol set, n = 20) and 67 % (subgroup of responders, n = 17) at week 12, while no treatment-related adverse events were observed. Conclusions The present observations identify GMP-manufactured ABCB5+ dermal MSCs as a potential, safe candidate for adjunctive therapy of otherwise incurable DFUs and justify the conduct of a larger, randomized controlled trial to validate the clinical efficacy. Trial registration ClinicalTrials.gov, NCT03267784, Registered 30 August 2017, https://clinicaltrials.gov/ct2/show/NCT0326778

A Nuclear Poly(ADP-Ribose)-Dependent Signalosome Confers DNA Damage-Induced IκB Kinase Activation

Upon genotoxic stresses, cells activate I{kappa}B kinases (IKKs) and the transcription factor NF-{kappa}B to modulate apoptotic responses. The SUMO-1 ligase PIASy and the kinase ataxia talengiectasia mutated (ATM) have been implicated to SUMOylate and phosphorylate nuclear IKK{gamma} (NEMO) in a consecutive mode of action, which in turn results in activation of cytoplasmic IKK holocomplexes. However, the nuclear signals and scaffold structures that initiate IKK{gamma} recruitment and activation are unknown. Here, we show that poly(ADP-ribose)-polymerase-1 (PARP-1) is the DNA proximal regulator, which senses DNA strand breaks and, through poly(ADP-ribose) (PAR) synthesis, assembles IKK{gamma}, PIASy, and ATM in a dynamic manner. Signalosome formation involves direct protein-protein interactions and binding to ADP-ribose polymers through PAR binding motifs (PARBM). Activated PARP-1 and a PARBM in PIASy are required to trigger IKK{gamma} SUMOylation, which in turn permits IKK and NF-{kappa}B activation, as well as NF-{kappa}B-regulated resistance to apoptosis

Low-dose carbon monoxide inhibits progressive chronic allograft nephropathy and restores renal allograft function

Chronic allograft nephropathy (CAN) represents progressive deterioration of renal allograft function with fibroinflammatory changes. CAN, recently reclassified as interstitial fibrosis (IF) and tubular atrophy (TA) with no known specific etiology, is a major cause of late renal allograft loss and remains a significant deleterious factor of successful renal transplantation. Carbon monoxide (CO), an effector byproduct of heme oxygenase pathway, is known to have potent anti-inflammatory and antifibrotic functions. We hypothesized that inhaled CO would inhibit fibroinflammatory process of CAN and restore renal allograft function, even when the treatment was initiated after CAN was established. Lewis rat kidney grafts were orthotopically transplanted into binephrectomized allogenic Brown Norway rats under brief tacrolimus (0.5 mg/kg im, days 0–6). At day 60, CO (20 ppm) inhalation was initiated to recipients and continued until day 150 or animal death. Development of CAN was confirmed at day 60 with decreased creatinine clearance (CCr), significant proteinuria, and histopathological findings of TA, IF, and intimal arteritis. Air-treated control recipients continued to deteriorate with further declines of CCr and increases of urinary protein excretion and died with a median survival of 82 days. In contrast, progression of CAN was decelerated when recipients received CO on days 60–150, showing markedly improved graft histopathology, restored renal function, and improved recipient survival to a median of >150 days. CO significantly reduced intragraft mRNA levels for IFN-γ and TNF-α at day 90. Expression of profibrotic TGF-β/Smad was significantly suppressed with CO, together with downregulation of ERK-MAPK pathways. Continuous CO (20 ppm) treatment for days 0–30, days 30–60, or days 0–90, or daily 1-h CO (250 ppm) treatment for days 0–90, also showed efficacy in inhibiting CAN. The study demonstrates that CO is able to inhibit progression of fibroinflammatory process of CAN, restore renal allograft function, and improve survival even when the treatment is started after CAN is diagnosed

Slip distribution of the 2017 M(w)6.6 Bodrum-Kos earthquake: resolving the ambiguity of fault geometry

SUMMARYThe 2017 July 20, Mw6.6 Bodrum–Kos earthquake occurred in the Gulf of Gökova in the SE Aegean, a region characterized by N–S extension in the backarc of the easternmost Hellenic Trench. The dip direction of the fault that ruptured during the earthquake has been a matter of controversy where both north- and south-dipping fault planes were used to model the coseismic slip in previous studies. Here, we use seismic (seismicity, main shock modelling, aftershock relocations and aftershock mechanisms using regional body and surface waves), geodetic (GPS, InSAR) and structural observations to estimate the location, and the dip direction of the fault that ruptured during the 2017 earthquake, and the relationship of this event to regional tectonics. We consider both dip directions and systematically search for the best-fitting locations for the north- and south-dipping fault planes. Comparing the best-fitting planes for both dip directions in terms of their misfit to the geodetic data, proximity to the hypocenter location and Coulomb stress changes at the aftershock locations, we conclude that the 2017 earthquake ruptured a north-dipping fault. We find that the earthquake occurred on a 20–25 km long, ∼E–W striking, 40° north-dipping, pure normal fault with slip primarily confined between 3 and 15 km depth, and the largest slip exceeding 2 m between depths of 4 and 10 km. The coseismic fault, not mapped previously, projects to the surface within the western Gulf, and partly serves both to widen the Gulf and separate Kos Island from the Bodrum Peninsula of SW Anatolia. The coseismic fault may be an extension of a mapped, north-dipping normal fault along the south side of the Gulf of Gökova. While all of the larger aftershocks are consistent with N–S extension, their spatially dispersed pattern attests to the high degree of crustal fracturing within the basin, due to rapid trenchward extension and anticlockwise rotation within the southeastern Aegean