Reimagining Undergraduate Medical Education in a Post-COVID-19 Landscape

Online education due to the COVID-19 pandemic caused many medical schools to increasingly employ asynchronous and virtual learning that favored student independence and flexibility. At the same time, the COVID-19 pandemic highlighted existing shortcomings of the healthcare field in providing for marginalized and underserved communities. This perspective piece details the authors’ opinions as medical students and medical educators on how to leverage the aspects of pandemic medical education to train physicians who can better address these needs.KEY WORDS: undergraduate medical education, social determinants of health, virtual learning

“American medical education needed a revolution,” writes Professor Jon M. Barry in The Great Influenza: The Story of the Deadliest Pandemic in History¹. He described a different era of medical education, a time in the late 1800s when medical students graduated without having ever touched a patient. The revolution began at Johns Hopkins Hospital with William Osler’s teaching hospital model for postgraduate training, a model that spread across the nation and has formed the foundation for modern medical education². A few decades later, the Flexner Report commissioned by the American Medical Association codified recommendations for standardized curriculum based on Osler’s program at Hopkins, giving rise to the biomedical model of medical education^{3, 4}. In the same decade, the 1918 influenza pandemic, one of the deadliest pandemics in the history of humankind, infected approximately one-third of the world’s population, causing an estimated 50 million deaths⁵. Clearly, as Barry describes, it was a time of great crisis, ripe for great change.The Flexner Report and 1918 pandemic thus led to many medical schools adopting the biomedical model and overhauling their curricula. Since then, shortcomings of the Flexner Report, such as limiting the opportunities of Black physicians and excluding social determinants of health from the medical model^{4, 6}, have been acknowledged and medical education has increasingly prioritized diversity and inclusion and public health education to better serve the diverse health needs of society^7–9. The biopsychosocial model of medicine has largely supplanted the biomedical model^{7, 8}, and many medical schools have modified their biomedical curricula to incorporate systems-based learning and social determinants of health.Yet healthcare is far from perfect today, with issues of cost, access, and systemic inequality still plaguing patients. As medical students and medical educators, we strive for a medical education that will better prepare the next generation of physicians to address these failures of the profession. We also have experienced how the current COVID-19 pandemic, similar to the 1918 influenza pandemic, has caused great crises in healthcare and changes in medical education^10–12. As vaccines have made a post-COVID era more tangible, we believe the medical field is once again ripe for revolution. In this perspective piece, we detail how we can leverage the current flux in medical education, capitalizing on asynchronous and virtual learning with a focus on social determinants and disparities, to better train physicians who will be prepared to serve the public health in a post-COVID era.     

ATP7B mutations in families in a predominantly Southern Indian cohort of Wilson's disease patients.

OBJECTIVE: To analyze ATP7B mutations in Wilson's disease (WD) patients from the Indian subcontinent and to correlate these with WD phenotype. METHODS: We studied 27 WD patients from 25 unrelated families. Twenty-two families were from three southern Indian states - Tamil Nadu andhra Pradesh and Kerala. We applied conformation- sensitive gel electrophoresis (CSGE) to screen for the mutations in patients and their families. PCR products exhibiting aberrant patterns in CSGE were subjected to direct DNA sequencing. As siblings affected by WD within a family share identical ATP7B genotype, we compared WD phenotype among affected siblings within families. RESULTS: ATP7B mutations were detected in 22 of the 25 probands -13 were homozygotes and 9 were compound heterozygotes. Eleven novel mutations were detected. Only two common mutations were found: G3182A in 4 (16%) and C813A in 3 (12%) probands. 'Hot spots' for ATP7B mutations were exons 18 and 13. Lack of common dominant mutations prevented correlation of individual ATP7B mutations with WD phenotype. Symptomatic WD in a live sibling was not found in any family. In 8 families, a sibling died of presumed WD - in 6 of these, WD phenotype was identical to that in the proband. CONCLUSIONS: We describe the spectrum of ATP7B mutations including 11 novel mutations in Indian WD patients and document lack of a single dominant mutation. Identical WD phenotype among siblings in only 6 of 8 families with >1 child affected by WD suggests that factors other than ATP7B mutations influence WD phenotype.     

Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN

Severe GN involves local neutrophil extracellular trap (NET) formation. We hypothesized a local cytotoxic effect of NET-related histone release in necrotizing GN. In vitro, histones from calf thymus or histones released by neutrophils undergoing NETosis killed glomerular endothelial cells, podocytes, and parietal epithelial cells in a dose-dependent manner. Histone-neutralizing agents such as antihistone IgG, activated protein C, or heparin prevented this effect. Histone toxicity on glomeruli ex vivo was Toll-like receptor 2/4 dependent, and lack of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice. Anti–glomerular basement membrane GN involved NET formation and vascular necrosis, whereas blocking NET formation by peptidylarginine inhibition or preemptive anti-histone IgG injection significantly reduced all aspects of GN (i.e., vascular necrosis, podocyte loss, albuminuria, cytokine induction, recruitment or activation of glomerular leukocytes, and glomerular crescent formation). To evaluate histones as a therapeutic target, mice with established GN were treated with three different histone-neutralizing agents. Anti-histone IgG, recombinant activated protein C, and heparin were equally effective in abrogating severe GN, whereas combination therapy had no additive effects. Together, these results indicate that NET-related histone release during GN elicits cytotoxic and immunostimulatory effects. Furthermore, neutralizing extracellular histones is still therapeutic when initiated in established GN.     

Use of Mono Cortical Screws as an Aid to Zygomatic Complex Fracture Reduction

Introduction

Zygomatic complex fractures by virtue of its anatomic area poses a great challenge in reduction of the fracture. Uses of various methods have been mentioned in English literature.

Method

A new technique describing the use of reduction screw with a self-holding screwdriver in reduction of the zygomatic complex fracture.

Conclusion

We found the method to be simple and effective and recommend its application in daily practice.     

The Effect of Alloplastic Bone Graft and Absorbable Gelatin Sponge in Prevention of Periodontal Defects on the Distal Aspect of Mandibular Second Molars,After Surgical Removal of Impacted Mandibular Third Molar: A Comparative Prospective Study

Aim

Recent studies claim that haemostatic agents can be used as bone graft substitutes. The aim of this study was to compare the efficacy of alloplastic bone graft with absorbable gelatin sponge in prevention of periodontal defects distal to mandibular second molar after the surgical removal of impacted mandibular third molars.

Materials and methods

A prospective, randomized, single-blind split-mouth study was designed. The study consisted of 25 patients requiring surgical removal of bilateral impacted mandibular 3rd molars. The surgical sites were randomly divided into 2 groups: group I: G-graft (hydroxyapatite + collagen, study group) and group II: Abgel (absorbable gelatin sponge, control group). Patients were recalled on lst and 7th postoperative days and 3rd and 6th postoperative months. Probing depth, alveolar bone levels and soft tissue wound healing were evaluated. Paired t test was used to compare pre and post-operative alveolar bone levels and probing depth (PD). Wilcoxon signed ranks test was used to compare the wound healing.

Results

The soft tissue wound healing, PD and the distance between the cemento–enamel junction on the distal aspect of mandibular second molar (point A) and the alveolar crest on the distal aspect of the same tooth (point B) were significantly higher in group I as compared to group II.

Conclusion

This study reveals an increase in the alveolar bone level, improvement of PD and better wound healing in group I. Group II subjects required longer healing time than the normal. The authors disagree the claim that the haemostatic agents can be used as bone graft substitutes. However, long-term, multicenter, randomized controlled clinical trials are required.     

Rare copy number variation in cerebral palsy

Recent studies have established the role of rare copy number variants (CNVs) in several neurological disorders but the contribution of rare CNVs to cerebral palsy (CP) is not known. Fifty Caucasian families having children with CP were studied using two microarray designs. Potentially pathogenic, rare (<1% population frequency) CNVs were identified, and their frequency determined, by comparing the CNVs found in cases with 8329 adult controls with no known neurological disorders. Ten of the 50 cases (20%) had rare CNVs of potential relevance to CP; there were a total of 14 CNVs, which were observed in <0.1% (<8/8329) of the control population. Eight inherited from an unaffected mother: a 751-kb deletion including FSCB, a 1.5-Mb duplication of 7q21.13, a 534-kb duplication of 15q11.2, a 446-kb duplication including CTNND2, a 219-kb duplication including MCPH1, a 169-kb duplication of 22q13.33, a 64-kb duplication of MC2R, and a 135-bp exonic deletion of SLC06A1. Three inherited from an unaffected father: a 386-kb deletion of 12p12.2-p12.1, a 234-kb duplication of 10q26.13, and a 4-kb exonic deletion of COPS3. The inheritance was unknown for three CNVs: a 157-bp exonic deletion of ACOX1, a 693-kb duplication of 17q25.3, and a 265-kb duplication of DAAM1. This is the first systematic study of CNVs in CP, and although it did not identify de novo mutations, has shown inherited, rare CNVs involving potentially pathogenic genes and pathways requiring further investigation.