The Ethics of Using a Live Patient for Dental Board Exams

Objective: This study will discuss the various viewpoints regarding the ethics of using a live patient for board examination in dentistry. It will expand upon the inconsistency of the exam to include the compromised patient care, dishonorable delay in care needed so students can perform care during boards, the dignity of both the student and the patient that is paid to agree to be subject to such procedures, and the potential and irreversible harm caused to these patients. The research in this paper will explore various options for obtaining a license for clinical boards in dentistry and dental hygiene in place of using a live patient. Methods: Throughout the project we plan to review literature from various sources to collect research within the last five years supporting the elimination of using a live patient for dentistry board exams. Research will be from primary and secondary sources. After successfully collecting research that supports our objective, we will devise a lesson plan that outlines a provision to care regarding dentistry’s clinical boards examinations. Results: The results of this study will highlight the current compromised patient care in dentistry’s clinical boards setting and identify an alternative method to the current clinical boards exam that holds participants to the same level of competency, while sustaining ethical patient care. Conclusion: Despite the current ADHA and ADA guidelines, dentistry’s clinical board exam is not ethically beneficial to a patient’s well being and ongoing health. Through research we aim to identify sources that establish facts which support the elimination of live patient use in a clinical board exam.https://scholarscompass.vcu.edu/denh_student/1022/thumbnail.jp

Extracellular Matrix as a Key Mediator of Mammary Tumor Cell Normalization

Some epithelial cancers can be induced to revert to quiescent differentiated tissues when combined with embryonic mesenchyme; however, the mechanism of this induction is unknown. This dissertation is based on the hypothesis that because extracellular matrix (ECM) plays a critical role during organ development in the embryo, it also may mediate the differentiation-inducing effects of embryonic mesenchyme on cancer cells. To test this hypothesis, I first optimized methods to isolate ECMs from whole tissues or cultured cells, and to repopulate them with cultured cells, using embryonic tooth as a model system. In Chapter 2, I describe these studies and use them to demonstrate that embryonic ECM is sufficient to regulate odontogenic signaling, cell fate decisions and histodifferentiation during normal tooth development. In Chapter 3, I adapt these methods to show that culture of breast cancer cells with ECM derived from embryonic mammary mesenchyme decreases tumor cell proliferation, and stimulates differentiation, including formation of hollow acini and ducts as well as enhanced expression of estrogen receptor-alpha and decreased migration. Further, when the inductive ECMs were injected into fast-growing breast tumors in mice, they significantly inhibited cancer expansion. Critically, the differentiation observed with ECM was the same as that observed in co-culture with mammary mesenchyme cells, showing that ECM is playing a dominant role in tumor cell normalization. In Chapter 4, I then set out to determine the mechanism by which embryonic ECM normalizes tumor cells, I analyzed the contributions of bound cytokines, ECM composition and mechanics. Western blot analysis revealed several bound growth factors, which remained following decellularization; however, removal of these growth factors using high salt washes had no effect on ECM-mediated normalization of tumors. Further, using proteomics analysis I identified eleven ECM proteins present only within inductive ECMs and by testing these proteins in 3D culture, I found three proteins -- collagen III, biglycan and SPARC -- that increased lumen formation to a similar extent as embryonic ECM. These data confirm that mesenchyme-induced tumor cell normalization is mediated by the insoluble ECM, and reveal the identity of some of the inductive molecules responsible for these effects

Designing a solution to enable agency-academic scientific collaboration for disasters

© The Author(s), 2017. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Ecology and Society 22 (2017): 18, doi:10.5751/ES-09246-220218.As large-scale environmental disasters become increasingly frequent and more severe globally, people and organizations that prepare for and respond to these crises need efficient and effective ways to integrate sound science into their decision making. Experience has shown that integrating nongovernmental scientific expertise into disaster decision making can improve the quality of the response, and is most effective if the integration occurs before, during, and after a crisis, not just during a crisis. However, collaboration between academic, government, and industry scientists, decision makers, and responders is frequently difficult because of cultural differences, misaligned incentives, time pressures, and legal constraints. Our study addressed this challenge by using the Deep Change Method, a design methodology developed by Stanford ChangeLabs, which combines human-centered design, systems analysis, and behavioral psychology. We investigated underlying needs and motivations of government agency staff and academic scientists, mapped the root causes underlying the relationship failures between these two communities based on their experiences, and identified leverage points for shifting deeply rooted perceptions that impede collaboration. We found that building trust and creating mutual value between multiple stakeholders before crises occur is likely to increase the effectiveness of problem solving. We propose a solution, the Science Action Network, which is designed to address barriers to scientific collaboration by providing new mechanisms to build and improve trust and communication between government administrators and scientists, industry representatives, and academic scientists. The Science Action Network has the potential to ensure cross-disaster preparedness and science-based decision making through novel partnerships and scientific coordination.The authors thank the David and Lucile Packard Foundation for a grant to undertake this project and enable participation of a wide range of participants and interviewees. We thank the Center for Ocean Solutions and ChangeLabs for their oversight and support

Varied Length Stokes Shift BODIPY-Based Fluorophores for Multicolor Microscopy

Multicolor microscopy tools necessary to localize and visualize the complexity of subcellular systems are limited by current fluorophore technology. While commercial fluorophores cover spectral space from the ultraviolet to the near infrared region and are optimized for conventional bandpass based fluorescence microscopy, they are not ideal for highly multiplexed fluorescence microscopy as they tend to have short Stokes shifts, restricting the number of fluorophores that can be detected in a single sample to four to five. Herein, we synthesized a library of 95 novel boron-dipyrromethene (BODIPY)- based fluorophores and screened their photophysical, optical and spectral properties for their utility in multicolor microscopy. A subset of our BODIPY-based fluorophores yielded varied length Stokes shifts probes, which were used to create a five-color image using a single excitation with confocal laser scanning microscopy for the first time. Combining these novel fluorophores with conventional fluorophores could facilitate imaging in up to nine to ten colors using linear unmixing based microscopy approaches

c-erbB-2 expression in benign and malignant breast disease.

An antibody, 21N, raised against a synthetic peptide from the predicted sequence of the c-erbB-2 protein has been used immunocytochemically in a retrospective study of formalin fixed paraffin embedded breast biopsies. Fourteen out of 103 infiltrating ductal carcinomas exhibited positive membrane staining. Fifty-four of these tumours had lymph node involvement of which nine contained stained cells. These were all cases where the primary tumour was positive. In this series there was no correlation between c-erbB-2 overexpression and lymph node status. In five of the positive cases studied there was an associated in situ component which was also positively stained. Ten out of 24 pure intraduct carcinomas showed membrane staining, but none of the 149 benign conditions studied, which included 22 radial scars and 13 cases of atypical ductal proliferation, demonstrated the pattern of staining associated with overexpression. It is concluded that the c-erbB-2 protein is overexpressed in a minority (approximately 14%) of infiltrating ductal carcinomas and only in cells that are cytologically malignant. Overexpression of c-erbB-2 is considered in relation to pathogenesis

Changing hearts and minds: Results from a multi-country gender and sexual diversity training

Engaging key populations, including gender and sexual minorities, is essential to meeting global targets for reducing new HIV infections and improving the HIV continuum of care. Negative attitudes toward gender and sexual minorities serve as a barrier to political will and effective programming for HIV health services. The President’s Emergency Plan for AIDS Relief (PEPFAR), established in 2003, provided Gender and Sexual Diversity Trainings for 2,825 participants including PEPFAR staff and program implementers, U.S. government staff, and local stakeholders in 38 countries. The outcomes of these one-day trainings were evaluated among a subset of participants using a mixed methods pre- and post-training study design. Findings suggest that sustainable decreases in negative attitudes toward gender and sexual minorities are achievable with a one-day training

Gender essentialism and occupational segregation in insolvency practice

Advances towards egalitarianism in professional recruitment may be offset by processes of occupational re-segregation. Drawing on gender theory this paper investigates horizontal segregation in the UK insolvency profession, as revealed through the lived experiences of female and male practitioners. It is shown that horizontal segregation pervades at different levels of practice and is undergirded by various elements of gender essentialism. Physical essentialism explains why insolvency practice has been traditionally gendered male. Interactional essentialism combines with the management of work-life balance to define the subfields of corporate and personal insolvency as masculine and feminine respectively. Gender essentialist assumptions also pervade the distribution of roles and the allocation of work tasks. Networks are identified as arenas for the reproduction and perpetuation of occupational segregation. The findings indicate the continuing potency of gender in everyday professional life, the limitations of diversity-orientated policies and the complexities of formulating transformative agendas

A density functional theory study of uranium-doped thoria and uranium adatoms on the major surfaces of thorium dioxide

Thorium dioxide is of significant research interest for its use as a nuclear fuel, particularly as part of mixed oxide fuels. We present the results of a density functional theory (DFT) study of uranium-substituted thorium dioxide, where we found that increasing levels of uranium substitution increases the covalent nature of the bonding in the bulk ThO2 crystal. Three low Miller index surfaces have been simulated and we propose the Wulff morphology for a ThO2 particle and STM images for the (100), (110), and (111) surfaces studied in this work. We have also calculated the adsorption of a uranium atom and the U adatom is found to absorb strongly on all three surfaces, with particular preference for the less stable (100) and (110) surfaces, thus providing a route to the incorporation of uranium into a growing thoria particle

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN