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Hepatitis C virus (HCV) is estimated to affect up to 150 million people worldwide. Despite worldwide prevalence, treatment modalities prior to 2011 remained suboptimal, with low virologic response rates and intolerable side effect profiles. Fortunately, the landscape of treatment for chronic hepatitis C has rapidly evolved since the introduction of HCV NS3/4 protease inhibitors in 2011. Elbasvir, a NS5A inhibitor, combined with grazoprevir, a NS3/4A protease inhibitor, is the latest FDA-approved therapy for patients with genotype 1 or 4 chronic hepatitis C, with or without compensated cirrhosis. This review will focus on the current literature and clinical evidence supporting elbasvir/grazoprevir as first-line therapy in patients with genotypes 1 and 4 chronic hepatitis C.

The Gerstein Science Information Centre is the Science and Health Sciences library serving the University of Toronto community. As the second largest library on campus, Gerstein is a mecca for studying and can accommodate 1100 students. Research has shown that high levels of stress, anxiety, depression, and other mental health disorders are prevalent among both medical students and the student population as a whole. In recent years, Gerstein staff members have seen evidence of the rising levels of student stress in their dealings with the public while providing reference and research help. Animal-assisted therapy (AAT) is often used in hospital and rehabilitation settings and, most recently, to help young children learn to read by providing a stress-free learning environment in public libraries and schools. Studies on animal-assisted therapy have shown that AAT decreases blood pressure, cortisol, and reduces anxiety overall. In response to these findings, staff at Gerstein decided to implement an AAT program, "Paws for a Study Break," comprised of several sessions when a therapy dog and her handler would visit the library to hold 'office hours' and give students a break from their studying during the Winter 2012 exam period. Through a total of six visits of ninety minutes each, 417 visitors were received. Best practices and lessons learned are discussed, including steps involved in coordination of the event, working with volunteers, publicity avenues, dealing with media requests, costs involved, and evaluation techniques. Based on the completed evaluation forms, the response to the therapy dog program at Gerstein was overwhelmingly positive; students were very appreciative, and there are plans underway to repeat this program on an ongoing basis.

Human lung neoplasms frequently express mutations that down-regulate expression of various tumor suppressor molecules, including mitogen-activated protein kinases such as p38 MAPK. Conversely, activation of p38 MAPK in tumor cells results in cancer cell cycle inhibition or apoptosis initiated by chemotherapeutic agents such as retinoids or cisplatin, and is therefore an attractive approach for experimental anti-tumor therapies. We now report that 4-phenyl-3-butenoic acid (PBA), an experimental compound that reverses the transformed phenotype at non-cytotoxic concentrations, activates p38 MAPK in tumorigenic cells at concentrations and treatment times that correlate with decreased cell growth and increased cell-cell communication. H2009 human lung carcinoma cells and ras-transformed liver epithelial cells treated with PBA showed increased activation of p38 MAPK and its downstream effectors which occurred after 4 h and lasted beyond 48 h. Untransformed plasmid control cells showed low activation of p38 MAPK compared to ras-transformed and H2009 carcinoma cells, which correlates with the reduced effect of PBA on untransformed cell growth. The p38 MAPK inhibitor, SB203580, negated PBA’s activation of p38 MAPK downstream effectors. PBA also increased cell-cell communication and connexin 43 phosphorylation in ras-transformed cells, which were prevented by SB203580. In addition, PBA decreased activation of JNK, which is upregulated in many cancers. Taken together, these results suggest that PBA exerts its growth regulatory effect in tumorigenic cells by concomitant up-regulation of p38 MAPK activity, altered connexin 43 expression, and down-regulation of JNK activity. PBA may therefore be an effective therapeutic agent in human cancers that exhibit down-regulated p38 MAPK activity and/or activated JNK and altered cell-cell communication.