Limited research exists on pharmacy students’ training in travel medicine, and how this aligns with scope of practice. This research aimed to detail travel medicine education across pharmacy programs in Canada and map this against the scope of practice for pharmacists in each university’s jurisdiction. CP21 research buy A survey based on the International Society of Travel Medicine’s Body of Knowledge was developed and distributed to all Canadian undergraduate pharmacy schools to identify topic areas taught, teaching modalities utilized, and knowledge assessment performed. Educational data was collected and analyzed descriptively, and compared to pharmacists’ scope of practice in the province in which each university is located. Training provided to students varied significantly across universities and topic areas, with topics amenable to self-care (e.g., traveller’s diarrhea and insect bite prevention) or also encountered outside of the travel context (e.g., sexually transmitted infections) taught more regularly than travel-specific topics (e.g., dengue and altitude illness). No apparent relationship was observed between a program’s curriculum and their provincial scope of practice. For example, training in vaccine-preventable diseases did not necessarily align with scope related to vaccine administration. Alignment of education to current and future scope will best equip new practitioners to provide care to travelling patients.Bovine spongiform encephalopathy (BSE) is a prion disease characterized by spongiform degeneration and astrocytosis in the brain. Unlike classical BSE, which is caused by prion-disease-contaminated meat and bone meal, the cause of atypical BSE has not been determined. Since previous studies have reported that the somatic mutation in the human prion protein gene (PRNP) has been linked to human prion disease, the somatic mutation of the PRNP gene was presumed to be one cause of prion disease. However, to the best of our knowledge, the somatic mutation of this gene in cattle has not been investigated to date. We investigated somatic mutations in a total of 58 samples, including peripheral blood; brain tissue including the medulla oblongata, cerebellum, cortex, and thalamus; and skin tissue in 20 individuals from each breed using pyrosequencing. In addition, we estimated the deleterious effect of the K211 somatic mutation on bovine prion protein by in silico evaluation tools, including PolyPhen-2 and PANTHER. We found a high rate of K211 somatic mutations of the bovine PRNP gene in the medulla oblongata of three Holsteins (10% ± 4.4%, 28% ± 2%, and 19.55% ± 3.1%). In addition, in silico programs showed that the K211 somatic mutation was damaging. To the best of our knowledge, this study is the first to investigate K211 somatic mutations of the bovine PRNP gene that are associated with potential BSE progression.Endoscopic resection is recommended for gastric neoplasms confined to mucosa or superficial submucosa. The determination of invasion depth is based on gross morphology assessed in endoscopic images, or on endoscopic ultrasound. These methods have limited accuracy and pose an inter-observer variability. Several studies developed deep-learning (DL) algorithms classifying invasion depth of gastric cancers. Nevertheless, these algorithms are intended to be used after definite diagnosis of gastric cancers, which is not always feasible in various gastric neoplasms. This study aimed to establish a DL algorithm for accurately predicting submucosal invasion in endoscopic images of gastric neoplasms. Pre-trained convolutional neural network models were fine-tuned with 2899 white-light endoscopic images. The prediction models were subsequently validated with an external dataset of 206 images. In the internal test, the mean area under the curve discriminating submucosal invasion was 0.887 (95% confidence interval 0.849-0.924) by DenseNet-161 network. In the external test, the mean area under the curve reached 0.887 (0.863-0.910). Clinical simulation showed that 6.7% of patients who underwent gastrectomy in the external test were accurately qualified by the established algorithm for potential endoscopic resection, avoiding unnecessary operation. The established DL algorithm proves useful for the prediction of submucosal invasion in endoscopic images of gastric neoplasms.Nuptial plumage coloration is critical in the mating choice of the crested ibis. This species has a characteristic nuptial plumage that develops from the application of a black sticky substance, secreted by a patch of skin in the throat and neck region. We aimed to identify the genes regulating its coloring, by comparing skin transcriptomes between ibises during the breeding and nonbreeding seasons. In breeding season skins, key eumelanin synthesis genes, TYR, DCT, and TYRP1 were upregulated. Tyrosine metabolism, which is closely related to melanin synthesis, was also upregulated, as were transporter proteins belonging to multiple SLC families, which might act during melanosome transportation to keratinocytes. These results indicate that eumelanin is likely an important component of the black substance. In addition, we observed upregulation in lipid metabolism in breeding season skins. We suggest that the lipids contribute to an oil base, which imbues the black substance with water insolubility and enhances its adhesion to feather surfaces. In nonbreeding season skins, we observed upregulation in cell adhesion molecules, which play critical roles in cell interactions. A number of molecules involved in innervation and angiogenesis were upregulated, indicating an ongoing expansion of nerves and blood vessels in sampled skins. Feather β keratin, a basic component of avian feather filament, was also upregulated. These results are consistent with feather regeneration in the black skin of nonbreeding season ibises. Our results provide the first molecular evidence indicating that eumelanin is the key component of ibis coloration.Cellular survival is dependent on the efficient replication and transmission of genomic information. DNA damage can be introduced into the genome by several different methods, one being the act of DNA replication. Replication is a potent source of DNA damage and genomic instability, especially through the formation of DNA double strand breaks (DSBs). DNA polymerase alpha is responsible for replication initiation. One subunit of the DNA polymerase alpha replication machinery is POLA2. Given the connection between replication and genomic instability, we decided to examine the role of POLA2 in DSB repair, as little is known about this topic. We found that loss of POLA2 leads to an increase in spontaneous DSB formation. Loss of POLA2 also slows DSB repair kinetics after treatment with etoposide and inhibits both of the major double strand break repair pathways non-homologous end-joining and homologous recombination. In addition, loss of POLA2 leads to increased sensitivity to ionizing radiation and PARP1 inhibition.