Chronic pain in childhood and adolescence has been shown to heighten risk for depressive and anxiety disorders in specific samples in adulthood; however, less is known about the association between a wider variety of chronic pains and internalizing mental health disorders. Using nationally representative data, the objectives of this study were to establish prevalence rates of internalizing mental health disorders (anxiety and depressive disorders) among cohorts with or without adolescent chronic pain, and to examine whether chronic pain in adolescence is associated with lifetime history of internalizing mental health disorders reported in adulthood. Data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) was used (N = 14,790). Individuals who had chronic pain in adolescence subsequently reported higher rates of lifetime anxiety disorders (21.1% vs. 12.4%) and depressive disorders (24.5% vs. 14.1%) in adulthood as compared to individuals without a history of adolescent chronic pain. Multivariate logistic regression confirmed that chronic pain in adolescence was associated with an increased likelihood of lifetime history of anxiety (odds ratio (OR): 1.33; 95% confidence interval (CI): 1.09-1.63, p=0.005) and depressive disorders (OR: 1.38; CI: 1.16-1.64, p<0.001) reported in adulthood. Future research is needed to examine neurobiological and psychological mechanisms underlying these co-morbidities.

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Rotavirus causes severe diarrheal disease in children by broadly dysregulating intestinal homeostasis. However, the underlying mechanism(s) of rotavirus-induced dysregulation remains unclear. We found that rotavirus-infected cells produce paracrine signals that manifested as intercellular calcium waves (ICWs), observed in cell lines and human intestinal enteroids. Rotavirus ICWs were caused by the release of extracellular adenosine 5′-diphosphate (ADP) that activated P2Y1 purinergic receptors on neighboring cells. ICWs were blocked by P2Y1 antagonists or CRISPR-Cas9 knockout of the P2Y1 receptor. Blocking the ADP signal reduced rotavirus replication, inhibited rotavirus-induced serotonin release and fluid secretion, and reduced diarrhea severity in neonatal mice. Thus, rotavirus exploited paracrine purinergic signaling to generate ICWs that amplified the dysregulation of host cells and altered gastrointestinal physiology to cause diarrhea.

Introduction: Cadaver dissection has long been hailed as a vital component of medical education. Although most physicians acknowledge positive impacts of cadaver dissection on their learning, they are less likely to will their bodies for anatomical dissection than the general public. This study aims to determine whether the proportion of medical students open to willed body donation changes after completing cadaver dissection. Methods:We conducted a longitudinal study surveying 323 medical students across three cohorts before and after anatomical dissection of human cadavers. Through the survey, students indicated whether they would will their body for anatomical dissection. Additionally, students responded to items regarding the rationale underlying their decision, demographics and perceived effects of anatomical dissection on medical education. Results:The proportion of students who expressed openness to willed body donation decreased by 25% after cadaver dissection. Of the 171 students who initially stated they would will their body, 61 (35%) changed their response after completing cadaver dissection. Those who cited religion as a motivating factor were less likely to show openness to body donation, whereas those who cited ethical factors were more likely.Conclusions: This study documents a substantial decrease in the proportion of students open to willed body donation after completion of cadaver dissection. Despite this, students almost universally report educational benefits of cadaver dissection. This raises interesting questions regarding the emotional impact of cadaver dissection and the ethical implications of willed body donation. | INTRODUCTIONAnatomical dissection of human cadavers has long been considered a rite of passage in medical education. 1 Prior to the SARS-CoV-2 pandemic, around 90% of US medical schools still incorporated cadaver labs into their anatomy curriculum. 2 Although the pandemic spurred a shift toward virtual learning, the majority of medical schools still offer in-person labs for first-year students. 2 Many studies have documented a positive impact of cadaver dissection on student learning. [3][4][5] Likewise, the majority of physicians, particularly those in surgical specialties, look favourably on their experiences with cadaver dissection. 5,6 Despite this, a disproportionately small number of physicians donate their bodies to medical school Willed Body Programs. [7][8][9] The discordance between the proportion of physicians who claim to have benefited from cadaver dissection and the proportion willing to donate their own body for medical education remains poorly explained. It is reasonable to posit that physicians, having directly experienced the positive impact of cadaver dissection on their

Viruses are among the most prevalent enteric pathogens. While virologists historically relied on cell lines and animal models, human intestinal organoids (HIOs) continue to grow in popularity. HIOs are non-transformed, stem cell derived, ex vivo cell cultures that maintain the cell type diversity of the intestinal epithelium. They offer higher throughput than standard animal models while more accurately mimicking the native tissue of infection than transformed cell lines. Here, we review recent literature that highlights virological advances facilitated by HIOs. We discuss the variations and limitations of HIOs, but also how HIOs have allowed for the cultivation of previously uncultivatable viruses and how they have offered insight into tropism, entry, replication kinetics, and host-pathogen interactions. In each case, we discuss exemplary viruses and archetypal studies. We discuss how the speed and flexibility of HIO-based studies contributed to our knowledge of SARS-CoV-2 and anti-viral therapeutics. Finally, we discuss current limitations of HIOs and future directions to overcome these.