Pre-doctoral dental students' knowledge, training, perceptions, and attitudes regarding obesity and treatments: A survey study.

OBJECTIVE: The aims of this study were to assess first-year predoctoral dental students' knowledge, training, perceptions, and attitudes on obesity and to compare knowledge, perceptions, and attitudes before and after attending an educational presentation. METHODS: A presentation explaining the impact of obesity and its treatments on oral health was developed and presented to first-year predoctoral dental students (D1's) in the Doctor of Dental Medicine program. Before ("pre") and after ("post") the presentation, attending students were given the opportunity to take an anonymous and voluntary survey. Questions on the survey covered topics on knowledge, training, perceptions, and attitudes about obesity. RESULTS: Thirty-four of the 213 students in the course (response rate = 16.0%) attended the presentation and completed both the pre- and post-surveys. Most participating students reported receiving 0-5 h of education on obesity since starting their dental education. Regarding pre-survey answers to knowledge-based items, the percentage of students answering, "strongly agree" (representing the greatest knowledge level) ranged from 5.9% to 61.8% across items. Significant improvements from pre- to post-survey were observed for all knowledge-based items except a statement that obesity is associated with serious medical conditions. Significant improvements were also found for perception-based items asking about accommodations for patients and the importance of assessing dietary habits. Additionally, at post-survey, students reported significantly less discomfort asking about dietary habits and weight loss medications. CONCLUSION: Dental curricula policy makers and developers should consider the incorporation of obesity and its treatments, with nutrition experts teaching the content.

Exploring dental faculty perceptions of current strategies and barriers to retention.

PURPOSE: The aims of the study were to identify perceived strategies for and barriers to faculty retention and examine differences regarding age, gender, and race. METHODS: Cross-sectional data was captured from the eight author-affiliated dental schools. A Qualtrics survey was emailed to all faculty members at these institutions (1467 possible participants) between November 2021 and February 2022. The survey was formulated from best practices listed in the American Dental Education Association Faculty Diversity Toolkit. It consisted of 18 questions, including demographic information and faculty perceptions of their respective workplaces. These responses were then evaluated with descriptive statistics, Chi-squared analysis, Pearson Correlation, and Fleiss' kappa. RESULTS: The survey's response rate was 19.2%. There was no significant difference in perceived retention strategies across race, age, gender, practice tenure, practice type, or clinical versus tenure track. The top four barriers identified were inadequate financial compensation, workload, poor work environment, and burnout. There was a significant difference between racial groups and their perceived barrier of support for promotion (p = 0.048). This was more prevalent among clinical faculty (47.7%) than tenure track faculty (16.2%). The work environment was listed as a leading factor for both promoting retention and encouraging the exodus of faculty members. CONCLUSION: Strategies aimed at improving financial compensation, career recognition, and transparency of the promotion process, along with those aimed at improving the work environment were shown to be vital to retaining faculty. Though the low response rate is a study limitation, these findings provide valuable information and a framework for future studies regarding dental faculty recruitment and retention.

Zinc deficiency impairs neuronal precursor cell proliferation and induces apoptosis via p53-mediated mechanisms.

The potential importance of stem cells in the adult central nervous system (CNS) that cannot only divide, but also participate in neurogenesis, is now widely appreciated. While we know that the trace element zinc is needed for brain development, the role of this essential nutrient in adult stem cell proliferation and neurogenesis has not been investigated. Adult male rats fed a zinc-restricted diet had approximately 50% fewer Ki67-positive stem cells in the subgranular zone (SGZ) and granular cell layer of the dentate gyrus compared to both zinc-adequate and pair-fed controls (p<0.05). Zinc-deficient rats also had a significant increase the number of TUNEL-labeled cells in the SGZ compared to pair-fed rats (p<0.05). To explore the mechanisms responsible for the effects of zinc deficiency, cultured human Ntera-2 (NT2) neuronal precursor cells were deprived of zinc using the chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). Consistent with the effects of deficiency in vivo, TPEN treatment resulted in a significant decrease in cellular proliferation, as measured by bromodeoxyuridine (BrdU) uptake, and an increase in caspase3/7-dependent apoptosis. These changes were accompanied by increases in nuclear p53. Oligonucleotide arrays, coupled with use of a dominant-negative p53 construct in NT2 cells, identified 14 differentially regulated p53 target genes. In the early phases zinc deficiency, p53 targets responsible for cell cycle arrest were induced. Continuation of deficiency resulted in the induction of a variety of pro-apoptotic genes such as transforming growth factor-beta (TGF-beta) and retinoblastoma-1 (Rb-1), as well as cellular protection genes such as glutathione peroxidase (GPx). These data suggest that zinc plays a role in neurogenesis by regulating p53-dependent molecular mechanisms that control neuronal precursor cell proliferation and survival.

Zinc deficiency induces depression-like symptoms in adult rats.

There is mounting evidence suggesting a link between serum zinc levels and clinical depression. Not only is serum zinc negatively correlated with the severity of symptoms, but zinc levels appear to be lowest in patients who do not respond to antidepressant drug therapy. It is not known if reduced zinc levels are contributing to depression, or the result of dietary or other factors associated with major depression. Thus, we designed this study to test the hypothesis that dietary zinc deficiency would induce depression-like behaviors in rats. Two-month-old male rats were fed zinc adequate (ZA, 30 ppm), deficient (ZD, 1 ppm), or supplemented (ZS, 180 ppm) diets for 3 weeks. Consistent with the development of depression, ZD rats displayed anorexia (p<0.001), anhedonia (reduced saccharin:water intake, p< 0.001), and increased anxiety-like behaviors in a light-dark box test (p<0.05). Furthermore, the antidepressant drug fluoxetine (10 mg/kg body wt) reduced behavioral despair, as measured by the forced swim test, in rats fed the ZA and ZS rats (p<0.05), but was ineffective in ZD rats. Together these studies suggest that zinc deficiency leads to the development of depression-like behaviors that may be refractory to antidepressant treatment.

Copper alters the conformation and transcriptional activity of the tumor suppressor protein p53 in human Hep G2 cells.

The tumor suppressor protein p53 plays a role in the molecular response to DNA damage by acting as a DNA-binding transcription factor that regulates specific target genes to arrest the cell cycle, induce repair mechanisms, and initiate apoptotic cell death. To test the effect of copper on the transcriptional activity of p53, Hep G2 cells were transiently transfected with a luciferase reporter gene downstream from multiple p53 response elements. Co-transfection with the p53 gene resulted in a 6-fold increase in luciferase activity, showing that p53 acts as a transcription factor in this system. However, in the presence of copper, luciferase activity was significantly reduced. Oligonucleotide arrays representing 145 known p53-associated genes were hybridized with biotinylated cDNAs from mRNA extracted from control and copper-treated Hep G2 cells. Among the genes that were differentially regulated were fos, RB1, glutathione peroxidase, TGF-beta, and 15-lipoxygenase, a gene known to be activated by mutant p53. Although control Hep G2 cells synthesize wild-type p53, immunocytochemistry identified not only wild type, but also mutant p53 in the presence of copper and other agents that induce oxidative damage. Thus, this report not only identifies genes that may play a role in copper-mediated apoptosis, but also suggests that copper-induced oxidative processes result in the synthesis of mutant p53 with altered transcriptional properties.

Expression profiling of p53-target genes in copper-mediated neuronal apoptosis.

Copper toxicity associated with Wilson's disease is known to cause neuronal damage and death in the basal ganglia and frontal cortex leading to Parkinson-like symptoms and cognitive deficits. Our previous work in cultured human NTERA-2-N neurons showed that copper-induced neuronal apoptosis is dependent on the induction and nuclear translocation of the tumor suppressor protein, p53. Because p53 acts as a DNA-binding transcription factor, this work used an oligonucleotide array to identify p53 target genes that are differentially regulated in copper-loaded neurons. Arrays representing 145 human genes expressed downstream of p53 were hybridized with labeled mRNA from control and copper-treated neurons. Differentially regulated mRNAs included those involved in the regulation of the cell cycle, cytoprotective mechanisms, and apoptotic mechanisms. Transfection of cells with a dominant-negative p53 construct enabled us to determine which molecular events were dependent on p53 expression. Copper treatment resulted in the upregulation of p21, reprimo, stathmin, and Tp53INP1, all known to participate in cell cycle arrest. Protective mechanisms included the upregulation of stat-3, and the heat-shock proteins, heat-shock protein (Hsp) 70 and Hsp 27. Both p53-dependent and -independent mechanisms leading to apoptosis were identified including insulin-like growth factor binding protein-6, glutathione peroxidase, bcl-2, RB-1, PUMA, and several members of the redox active PIG family of proteins. Thus it appears that following copper-mediated neuronal DNA damage, the regulation of a variety of pro- and antiapoptotic genes are responsible for determining neuronal fate.

Iron and ageing: an introduction to iron regulatory mechanisms.

While there have been significant advances made in our understanding of the cellular and molecular mechanisms that regulate iron absorption, transport, storage, and utilization, the effect of ageing on these mechanisms and the role of iron in the ageing process is not fully understood. Thus, this review will provide an overview of the iron regulatory mechanisms that may be a factor in the ageing process. Additional reviews in this volume represent an attempt to explore the very latest information on the regulation of iron with a particular emphasis on age-related pathology including mitochondrial function, Parkinson's disease, Alzheimer's disease, stroke, and cardiovascular disease.