Increasing Undergraduate Exposure to Oncology: the Role of Oncology Interest Groups.

This study describes a medical school oncology interest group (OIG) and assesses its influence on student perceptions of oncology, interest in pursuing oncology as a career, and comfort levels with oncology topics such as breaking bad news. From 2015 to 2017, the OIG annual event took place at a satellite campus of a larger Canadian undergraduate medical school. The event provided a question and answer period with a panel of physicians from multiple oncology specialties-discussions focused around lifestyle, training, clinical work, lifestyle, and career focus. Small physician-led groups taught breaking bad news using the SPIKES framework. The interest group also provided a mentoring and networking opportunity to interested students. Pre- and post-event surveys were distributed to students and physicians. For three consecutive years, the student-run, and physician-mentored OIG successfully recruited student and physician participants, providing a clinical skill teaching session as well as mentorship opportunities to students. Pre-event surveys found that only 20% of students believed their current curriculum was adequate as it relates to oncology education. In pre-session, 13% (6/45) of students indicated comfort with the skill of breaking bad news, compared with that in post-session with 81% (34/42) of students feeling comfortable. When asked "How likely are you to pursue a future elective opportunity in oncology?" 49% (20/41) of students indicated "likely" as their response in the pre-session. This response increased post-session to 70% (28/40). The event highlighted the potential for OIGs to increase student interest in pursuing oncology electives and student-perceived comfort with breaking bad news. OIGs are important in promoting interest in the field of oncology and in improving confidence in breaking bad news. This medical student-created, run and maintained oncology interest group supplemented standard curriculum by providing relevant educational and mentorship opportunities to students. This study highlights the feasibility of implementing a self-sustaining medical school oncology interest group and its potential to positively impact student learning and interest in oncology.

Mechanisms and Mediators That Drive Arthritis Pain.

There are over 100 different types of arthritis and each can differ greatly in their aetiology and pathophysiology; however, one characteristic that is common to all arthritic conditions is joint pain. Musculoskeletal pain is the leading cause of disability in the world, and the number one reason arthritis patients visit their primary care physician. Despite the prevalence and burden of arthritis pain, current analgesics lack sufficient efficacy and are plagued by multiple adverse side effects. In this review, we outline the current landscape of research concerning joint pain, drawing from both preclinical and clinical studies. Specifically, this review is a discussion of the different neurophysiological processes that occur during joint disease and how inflammatory and neuropathic aspects contribute to the development of arthritis pain.

A novel ß-adrenergic response element regulates both basal and agonist-induced expression of cyclin-dependent kinase 1 gene in cardiac fibroblasts.

Cardiac fibrosis, a known risk factor for heart disease, is typically caused by uncontrolled proliferation of fibroblasts and excessive deposition of extracellular matrix proteins in the myocardium. Cyclin-dependent kinase 1 (CDK1) is involved in the control of G2/M transit phase of the cell cycle. Here, we showed that isoproterenol (ISO)-induced cardiac fibrosis is associated with increased levels of CDK1 exclusively in fibroblasts in the adult mouse heart. Treatment of primary embryonic ventricular cell cultures with ISO (a nonselective ß-adrenergic receptor agonist) increased CDK1 protein expression in fibroblasts and promoted their cell cycle activity. Quantitative PCR analysis confirmed that ISO increases CDK1 transcription in a transient manner. Further, the ISO-responsive element was mapped to the proximal -100-bp sequence of the CDK1 promoter region using various 5'-flanking sequence deletion constructs. Sequence analysis of the -100-bp CDK1 minimal promoter region revealed two putative nuclear factor-Y (NF-Y) binding elements. Overexpression of the NF-YA subunit in primary ventricular cultures significantly increased the basal activation of the -100-bp CDK1 promoter construct but not the ISO-induced transcription of the minimal promoter construct. In contrast, dominant negative NF-YA expression decreased the basal activity of the minimal promoter construct and ISO treatment fully rescued the dominant negative effects. Furthermore, site-directed mutagenesis of the distal NF-Y binding site in the -100-bp CDK1 promoter region completely abolished both basal and ISO-induced promoter activation of the CDK1 gene. Collectively, our results raise an exciting possibility that targeting CDK1 or NF-Y in the diseased heart may inhibit fibrosis and subsequently confer cardioprotection.