Accommodations for disabilities in dental education: A focus on technical standards and clinical skills.

Providing disability-based accommodations is a multifaceted process that must balance the needs of dental students and their institutions. Reasonable accommodations must not compromise patient safety or cause an undue burden on the student or institution. Therefore, more creative approaches must be considered as the number of individuals and the types of learning disabilities have increased in recent years. In the clinical setting, providing accommodations also requires detailed advanced planning and collaboration to maintain program quality. However, current technical standards (TS) may serve as a barrier to entry into the health professions for people with disabilities. These individuals remain substantially underrepresented in dentistry despite bringing unique perspectives and experiences that can contribute to a diverse workforce of culturally proficient practitioners. In response, many schools have adopted a "functional" approach to TS that emphasizes a student's abilities rather than their limitations. In addition, innovative assistive technologies coupled with the application of critical pedagogy and universal design learning practices that engage people with the widest possible range of capabilities allows equitable approaches for learning and assessment while maintaining professional standards.

Affirming and Inclusive Care Training for Medical Students and Residents to Reduce Health Disparities Experienced by Sexual and Gender Minorities: A Systematic Review.

Purpose: Providing inclusive and comprehensive gender-affirming care is critical to reducing health disparities (gaps in care) experienced by sexual and gender minorities (SGM). Currently, little is known about how medical students and residents are being trained to address the health needs of SGM persons or of the most effective methods. Methods: We conducted a systematic review of the research literature from 2000 to 2020 on the effectiveness of teaching medical students and residents on knowledge, attitudes, and skills in addressing the health of SGM persons and the strength of the research sample, design, and methods used. Results: We identified a total of 36 articles that assessed the impact of medical student and resident education on knowledge, comfort, attitudes, confidence, and skills in working with SGM patients. All studies utilized quasi-experimental designs, and found efficacious results. No study examined the impact of training on patient outcomes. Conclusion: Future studies will need to be powered and designed to assess the impact of training on patient outcomes.

Transforming Medical Education to Provide Gender-Affirming Care for Transgender and Gender-Diverse Patients: A Policy Brief.

Transgender and gender-diverse (TGD) patients experience a greater burden of health disparities compared with their heterosexual/cisgender counterparts. Some of the poorer health outcomes observed in these populations are known to be associated with the prevalence of implicit bias, bullying, emotional distress, alcoholism, drug abuse, intimate partner violence, sexually transmitted infections (eg, human immunodeficiency virus and human papilloma virus), and cancer. The TGD populations face unique barriers to receiving both routine and gender-affirming health care (acquiring hormones and gender-affirming surgeries). Additional barriers to implementing affirming care training for TGD patients are lack of expertise among medical education faculty and preceptors both in undergraduate and in graduate medical education programs. Drawing on a systematic review of the literature, we propose a policy brief aimed at raising awareness about gender-affirming care among education planners and policy makers in government and advisory bodies.

Correction to: IAMSE Meeting Report: Student Plenary at the 24th Annual Conference of the International Association of Medical Science Educators.

[This corrects the article DOI: 10.1007/s40670-020-01087-9.].

A Dental Student's Perspective of Mid-level Providers in the Oral Healthcare Team.

The idea of mid-level providers in dentistry grew from the increasing lack of access to oral care in rural and other underserved communities. To meet this need, dental therapists emerged. However, from an educational standpoint, the topic is hardly mentioned or discussed. This commentary discusses the role that dental therapists play in addressing oral health disparities and the reason more information about them should be included in dental and medical curricula. As the field of dentistry evolves and the lack of access to oral care persists, educating dental students and students in other healthcare professions about dental therapists should be an equally important task.

Impact and educational outcomes of a small group self-directed teaching strategy in a clinical neuroscience curriculum.

The complexity of the material being taught in clinical neuroscience within the medical school curriculum requires creative pedagogies to teach medical students effectively. Many clinical teaching strategies have been developed and are well described to address these challenges. However, only a few have been evaluated to determine their impact on the performance of students studying clinical neuroscience. Interactive, 2-hour, self-directed small-group interactive clinical case-based learning sessions were conducted weekly for 4 weeks to integrate concepts learned in the corresponding didactic lectures. Students in the small groups analyzed cases of patients suffering from neurological disease that were based on eight learning objectives that allowed them to evaluate neuroanatomical data and clinical findings before presenting their case analysis to the larger group. Students' performances on the formative quizzes and summative tests were compared to those of first-year medical students in the previous year for whom the self-directed, small-group interactive clinical sessions were not available. There was a significant improvement in the summative performance of first-year medical students with self-directed clinical case learning in the second year (Y2) of teaching clinical neuroscience (P < 0.05) when compared with first-year students in the first year (Y1) for whom the self-directed learning approach was not available. Student performance in the formative assessments between Y1 and Y2 was not significantly different (P = 0.803). A target of ≥70% student scoring above 80% in the final summative examination was met. The current study revealed evidence for the impact and educational outcomes of a self-directed, clinical teaching strategy in a clinical neuroscience curriculum for first-year medical students. Anat Sci Educ 11: 478-487. © 2017 American Association of Anatomists.

The attenuation of early benzo(a)pyrene-induced carcinogenic insults by diallyl disulfide (DADS) in MCF-10A cells.

Diallyl disulfide (DADS), a garlic organosulfur compound, has been researched as a cancer prevention agent; however, the role of DADS in the suppression of cancer initiation in nonneoplastic cells has not been elucidated. To evaluate DADS inhibition of early carcinogenic events, MCF-10A cells were pretreated (PreTx) with DADS followed by the ubiquitous carcinogen benzo(a)pyrene (BaP), or cotreated (CoTx) with DADS and BaP for up to 24 h. The cells were evaluated for changes in cell viability/proliferation, cell cycle, induction of peroxide formation, and DNA damage. BaP induced a statistically significant increase in cell proliferation at 6 h, which was attenuated with DADS CoTx. PreTx with 6 and 60 µM of DADS inhibited BaP-induced G2/M arrest by 68% and 78%, respectively. DADS, regardless of concentration or method, inhibited BaP-induced extracellular aqueous peroxide formation within 24 h. DADS attenuated BaP-induced DNA single-strand breaks at all time points through both DADS Pre- and CoTx, with significant inhibition for all treatments sustained after 6 h. DADS was effective in inhibiting BaP-induced cell proliferation, cell cycle transitions, reactive oxygen species, and DNA damage in a normal cell line, and thus may inhibit environmentally induced breast cancer initiation.

Achieving student diversity in dental schools: a model that works.

It is well known that there is a large disparity between the proportions of African Americans, Hispanics, and American Indians in the general U.S. population and in the nation's dental profession. While these underrepresented minorities (URMs) together make up almost 30 percent of the population, they comprise only about 6 percent of U.S. dentists. For years, the American Dental Education Association has been diligently working with U.S. dental schools to reduce this disparity by increasing the diversity of their student bodies. However, with approximately 13 percent of first-year dental students coming from URM groups, the proportion of URM students entering dental school continues to remain significantly below that of the general population. Diversifying the dental profession is important for improving access to care for underrepresented groups, and student diversity provides better educational experiences for all students. Texas A&M Health Science Center Baylor College of Dentistry's strategy for increasing the number of URM dentists was to create a series of initiatives that together form a successful comprehensive program addressing students' awareness of and attraction to a dental career, academic enrichment, admissions, and graduation. The cumulative impact of this program is that the college enrolled greater numbers and proportions of URM students than any other non-minority U.S. dental school from 2006 to 2009. This article describes the program that led to these successes.

Diallyl trisulfide as an inhibitor of benzo(a)pyrene-induced precancerous carcinogenesis in MCF-10A cells.

Diallyl trisulfide (DATS) is a garlic organosulfide that is toxic to cancer cells, however, little is known about its effect in the initiation phase of carcinogenesis. We sought to determine whether DATS could inhibit the carcinogen, benzo(a)pyrene (BaP), from inducing precancerous activity, in vitro. MCF-10A cells were either pre-treated (PreTx) or concurrently treated (CoTx) with 1 µM BaP, and 6 or 60 µM DATS for up to 24h. The DATS 6 and 60 µM CoTx inhibited BaP-induced cell proliferation by an average of 71.1% and 120.8%, respectively, at 6h. The 60 µM DATS pretreatment decreased BaP-induced G2/M cell cycle transition by 127%, and reduced the increase in cells in the S-phase by 42%; whereas 60 µM DATS CoTx induced a 177% increase in cells in G1. DATS effectively inhibited (P<0.001) BaP-induced peroxide formation by at least 54%, which may have prevented the formation of BaP-induced DNA strand breaks. In this study, we reveal mechanisms involved in DATS inhibition of BaP-induced carcinogenesis, including inhibition of cell proliferation, regulation of cell cycle, attenuation of ROS formation, and inhibition of DNA damage. At the doses evaluated, DATS appears to be an effective attenuator of BaP-induced breast carcinogenesis, in vitro.

Zoledronic acid inhibits macrophage SOCS3 expression and enhances cytokine production.

Suppressor of cytokine signaling-3 (SOCS3) has multiple functions including inhibition of Janus kinase (Jak) activity, regulation of protein degradation, and suppression of cytokine signaling. SOCS3 modulates macrophage response to cytokines such as IL-6 and leptin that are systemically induced in obesity. Obesity is a suspected risk factor for SOCS3-related pathology such as rheumatoid arthritis and Crohn's disease as well as zoledronic acid (ZA)-induced osteonecrosis of the jaw (ONJ). Thus, understanding the ability of bisphosphonates to modulate SOCS3 is necessary to qualify their contribution to these disorders. ONJ occurs in up to 10% of patients using intravenous bisphosphonates and has an unknown pathogenesis that may be linked to decreased bone turnover, altered vascularity, bacterial invasion, and compromised wound healing. Given the increased risk of ONJ with obesity and importance of macrophages in wound healing, we hypothesized that amino-bisphosphonates could contribute to the pathogenesis of ONJ by regulating macrophage responses to cytokines such as leptin and IL-6. We report that ZA is a novel inhibitor of SOCS3 in primary macrophages and human ONJ biopsy specimens. Inhibition of SOCS3 by ZA resulted in significant increases in IL-6 production. SOCS3 transcription is regulated by nuclear accumulation of phosphorylated-Stat3 (P-Stat3). We found that ZA decreased phosphorylation of Stat3 in a mevalonate-pathway dependent manner. However, restoration of P-Stat3 was not sufficient to correct SOCS3 inhibition. We propose that disruption of macrophage SOCS3 expression by amino-bisphosphonates such as ZA may be a novel contributor to inflammatory phenotypes in obesity and the pathogenesis of ONJ.

Bisphosphonates inhibit phosphorylation of signal transducer and activator of transcription 3 and expression of suppressor of cytokine signaling 3: implications for their effects on innate immune function and osteoclastogenesis.

OBJECTIVE: This study tested the effects of bisphosphonates (BPs) on the suppressor of cytokine signaling 3 (SOCS3) protein in macrophages. SOCS3 has been shown to regulate cell differentiation and survival; however, its potential role in mediating the effects of BPs has not been explored. STUDY DESIGN: The cell viability of murine RAW 267.4 macrophages was assessed after culturing with control medium or media containing increasing concentrations of 2 BPs (ibandronate or clodronate) for 24, 48, and 72 hours. The phosphorylation status of signal transducer and activator of transcription 3 (STAT3) and the expression of SOCS3 protein levels were determined by Western blot analysis. RESULTS: In control cultures, STAT3 phosphorylation and STAT3 and SOCS3 protein levels increased within 5 minutes after the addition of fresh medium. This increase was inhibited in cultures treated with both BPs. Macrophage cell viability also decreased after BP treatment. CONCLUSIONS: These data demonstrate that, in addition to their effects on macrophage viability, BPs can decrease STAT3 and SOCS3 expression, which are important modulators of immune responses and bone homeostasis.

Retention of underrepresented minority students in dental school: one dental schools story.

There is a large disparity between the proportions of African-Americans, Hispanics, and Native Americans in the general population and in the dental profession. While these underrepresented minorities (URMs) as a group make up almost 30% of the United States population, they constitute only about 6% of the nation's dentists. Eliminating this disparity is important in addressing access to care for underrepresented groups. Texas A&M Health Science Center Baylor College of Dentistry (TAMHSC-BCD) enrolled greater numbers and proportions of URM students than any other non-minority school from 2006-2010. Strategies used to achieve this level of diversity include a Whole File Review process; career awareness activities for elementary, junior high and high school students; and academic enrichment programs for college students and college graduates. Retaining and graduating URM students is just as important as enrolling them. TAMHSC-BCD's retention rate over the last five years is 95.7% for all students and 92.5% for URM students. A wide range of services aids in the retention process. These services are available to all students and include monitoring of students' academic performance followed up with academic advisement as appropriate, peer tutoring, an alternative five-year curriculum, professional psychological counseling, professional learning assessments, social support; and mentoring through student organizations. The retention program at TAMHSC-BCD can serve as a model for other dental and other health professions schools seeking ways to ensure the academic success of their URM students. The more of these students we enroll and graduate, the more the problem of access to dental care is addressed.

Acute lung injury:apoptosis and signaling mechanisms.

Acute lung injury (ALI) has been documented clinically following several pathological states such as trauma, septic shock and pneumonia. The histopathological characteristics, paired with the production of a number of cellular pro-inflammatory mediators, play a crucial role in the progression of ALI. During ALI, polymorphonuclear neutrophil (PMN)-mediated apoptosis is delayed by macrophages, possibly via effects on the Fas/FasL mediated pathway, leading to the accumulation of these cells at the site of injury and inflammation. The transcriptional regulation of NFkappaB, CREB, and AP-1 also regulates the pathogenesis of ALI. During sepsis and septic shock, we found evidence of infiltrating leukocytes in the alveolar spaces along with an increased number of TUNEL-positive cells in the lung sections. We also observed an increased expression of TRADD and Bax/Bcl(2) ratio at 7 days post-sepsis. In contrast, the NFkappaB/IkappaB ratio increased at 1 day post-sepsis. Together, these data provide evidence illustrating the induction of apoptosis in lung tissues subsequent to the onset of polymicrobial sepsis. The results support the concept that the upregulation of apoptosis following lung inflammation plays a crucial role in the development of acute lung injury and related disorders such as ARDS.

Ability of antioxidant liposomes to prevent acute and progressive pulmonary injury.

We recently showed that acute oxidant-related lung injury (ALI) in rats after application of 2-chloroethyl ethyl sulfide (CEES) is attenuated by the airway instillation of antioxidants. We investigated whether intratracheal administration of antioxidant-containing liposomes immediately after instillation of CEES would attenuate short-term as well as long-term (fibrotic) effects of CEES-induced lung injury. In the acute injury model (4 h after injury), N-acetylcysteine (NAC)-containing liposomes were protective and reduced to baseline levels both the lung permeability index and the appearance of proinflammatory mediators in bronchoalveolar lavage fluids from CEES-exposed lungs. Similar results were obtained when rat alveolar macrophages were incubated in vitro with either CEES or lipopolysaccharide in the presence of NAC-liposomes. When lung fibrosis 3 weeks after CEES was quantitated by using hydroxyproline content, liposomes containing NAC or NAC + glutathione had no effects, but liposomes containing alpha/gamma-tocopherol alone or with NAC significantly suppressed the increase in lung hydroxyproline. The data demonstrate that delivery of antioxidants via liposomes to CEES-injured lungs is, depending on liposomal content, protective against ALI, prevents the appearance of proinflammatory mediators in bronchoalveolar fluids, and suppresses progressive fibrosis. Accordingly, the liposomal strategy may be therapeutically useful in CEES-induced lung injury in humans.

Divergent signaling pathways in phagocytic cells during sepsis.

Neutrophil accumulation in the lung plays a pivotal role in the pathogenesis of acute lung injury during sepsis. Directed movement of neutrophils is mediated by a group of chemoattractants, especially CXC chemokines. Local lung production of CXC chemokines is intensified during experimental sepsis induced by cecal ligation and puncture (CLP), as reflected by rising levels of MIP-2 and cytokine-induced neutrophil chemoattractant-1 in bronchoalveolar lavage fluids. Alveolar macrophages are primed and blood neutrophils are down-regulated for production of MIP-2 and cytokine-induced neutrophil chemoattractant production in response to LPS and C5a. Under these conditions of stimulation, activation of MAPKs (p38, p42/p44) occurs in sham neutrophils but not in CLP neutrophils, while under the same conditions phosphorylation of p38 and p42/p44 occurs in both sham and CLP alveolar macrophages. These data indicate that, under septic conditions, there is impaired signaling in neutrophils and enhanced signaling in alveolar macrophages, resulting in CXC chemokine production, and C5a appears to play a pivotal role in this process. As a result, CXC chemokines increase in lung, setting the stage for neutrophil accumulation in lung during sepsis.

Regulatory role of C5a in LPS-induced IL-6 production by neutrophils during sepsis.

Experimental sepsis in rodents occurring after cecal ligation/puncture (CLP) is associated with excessive complement activation and a systemic inflammatory response. The proinflammatory mediator IL-6 has recently been shown to be an important inducer of the C5a receptor (C5aR) during sepsis. We now provide evidence that serum IL-6 production during sepsis in rats was reduced in neutrophil-depleted animals and that absence of C5aR in mice as well as antibody-blockade of C5a in rats significantly reduced serum levels of IL-6 during sepsis. Lipopolysaccharide (LPS)-induced production in vitro of IL-6 by neutrophils was significantly enhanced in the co-presence of C5a, likely due to transcriptional up-regulation of IL-6. Production of IL-6 in neutrophils by LPS was NF-kappaB dependent (but not on the presence of p50) and dependent on phosphorylation of p38-mitogen activated protein kinase (MAPK) as well as p44/p42 MAPK (ERK1/2) but not on phosphorylation of c-Jun N-terminal kinases (JNK1/2). C5a stimulation of neutrophils elicited a rapid phosphorylation of ERK1/2 and p38 MAPK. Accordingly, we suggest that induction of IL-6 after CLP is neutrophil and C5a/C5aR dependent, likely due to the ability of C5a to cause activation of ERK1/2 and p38 MAPK signaling pathways.

Selectin inhibition modulates Akt/MAPK signaling and chemokine expression after liver ischemia-reperfusion.

Tissue damage after ischemia and reperfusion (I/R) is largely caused by the sequelae of neutrophil infiltration. This inflammatory process can be initiated as the result of stroke, coronary ischemia, trauma, and other related conditions. The infiltration of neutrophils is facilitated by the expression of adhesion molecules on the surface of endothelial cells. Particularly important are the selectin family of adhesion molecules at the onset of neutrophil-mediated injury. The aim of this study was to determine the role of selectin inhibition in the modulation of chemokine expression and Akt/MAPK signaling after liver I/R. In addition, we evaluated the optimal dose and time of administration of a small molecule selectin inhibitor, TBC-1269. Mice subjected to 90 min of partial (70-80%) hepatic ischemia followed by 3 h of reperfusion were divided into 15 groups (n = 4/group); sham, ischemic control, and 10, 20, and 40 mg/kg dose groups for the antiselectin molecule were studied at 3 times of drug administration: 1 h before reperfusion (but after ischemia), at the time of reperfusion, and at 15 min after reperfusion. The parameters measured after 3 h of reperfusion included liver function tests (ALT and AST), histopathology, and tissue myeloperoxidase (MPO). Chemokine expression (MIP-1alpha, MIP-1beta, MIP-2 and KC), Akt, MAPK (p44/p42), and RSK expressions were also measured in liver tissue by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis, respectively. It was demonstrated that the small molecule multi-selectin inhibitor (TBC-1269) offered the most significant protection for the ischemic liver when given at 40 mg/kg at the time ofreperfusion. AST significantly differed between the control group and the group receiving 40 mg/kg at the time of reperfusion (p = .01). MPO levels in the liver tissue of the ischemic controls were significantly increased when compared to the levels of this enzyme in the TBC-1269 group at 40 mg/kg. Histological examination reflected the same results, with a significant difference (p = .02) between these same two groups. The chemokine profile also showed that the same treatment group had a downregulation of MIP-lalpha, MIP-1beta, MIP-2, and KC, as well as a lower expression of Akt, MAPK(p44/42), and RSK when compared to the control group. Thus, we demonstrated that the small molecule selectin inhibitor, TBC-1269, offered significant functional and structural protection of the ischemic liver when given at 40 mg/kg at the time of reperfusion. Lower doses and different times of administration did not show as prominent a drug effect. This selectin inhibition modulated the expression of Akt, MAPK (p44/42), and RSK, as well as MIP-1alpha, MIP-1beta, MIP-2, and KC chemokines. These alterations in cellular signaling and chemokine expression represent potential mechanisms or pathways of inflammatory response in I/R.

Neutrophil C5a receptor and the outcome in a rat model of sepsis.

Complement fragment 5a (C5a)-C5a receptor (C5aR) signaling plays an essential role in neutrophil innate immunity. Blockade of either the ligand or the receptor improves survival rates in experimental sepsis. In the current study, sepsis was induced in rats by cecal ligation/puncture. Early in sepsis C5aR content on neutrophils significantly dropped, reached the nadir at 24 h after onset of sepsis, and progressively elevated thereafter. Western-blot, RT-PCR, and confocal microscopy analyses revealed that the loss and re-expression of C5aR during sepsis might be due, at least in part, to the receptor internalization and reconstitution. The reduction and reconstitution of C5aR correlate with the loss and restoration of innate immune functions of blood neutrophils (chemotaxis and reactive oxygen species production), respectively. Quantitative measurements of C5aR on blood neutrophils are highly predictive of survival or death during sepsis. These data suggest that neutrophil C5aR content represents an essential component of an efficient defense system in sepsis and may serve as a prognostic marker for the outcome.

Regulation by C5a of neutrophil activation during sepsis.

In sepsis, there is evidence that excessive C5a generation leads to compromised innate immune functions, being associated with poor outcome. We now report that in vitro exposure of neutrophils to C5a causes increased levels of IkappaBalpha, decreased NF-kappaB-dependent gene transcription of TNFalpha, and decreased lipopolysaccharide (LPS)-induced TNFalpha production. Similar findings were obtained with neutrophils from cecal ligation/puncture (CLP)-induced septic rats. Such changes were reversed by antibody-induced in vivo blockade of C5a. In contrast, in vitro exposure of alveolar macrophages to C5a and LPS resulted in enhanced production of TNFalpha and no increase in IkappaBalpha. These data suggest that CLP-induced sepsis causes a C5a-dependent dysfunction of neutrophils, which is characterized by altered signaling associated with NF-kappaB activation.