Technology in the Pharmacy Learning Environment: Surveys of Use and Misuse

The use of technology in the classroom may have positive and negative effects on learning. The purpose of this investigation was twofold: to identify the effect technology is having on the pharmacy learning environment; and, to assess students’ use of technology during class time for non-academic purposes. This study included a national cross-sectional survey as well as a single, college-specific survey. The national survey had a faculty response rate of 71.2%. Of the responders, approximately 61% identified significant problems related to students’ use of technology in the pharmacy learning environment. Cell phones were a recognized concern and more than 90% of programs have chosen to restrict cell phone use in the classroom. The single college survey examining technology use during class for non-academic purposes had a student response rate of 87% and faculty response rate of 100%. Students and faculty members disagreed regarding the negative effects of technology use during class for non-academic purposes. Notably, 16% of students acknowledged their in-class use of technology for non-academic purposes had been disruptive to their learning, as compared to 95.7% of faculty. According to students, common reasons for off-task technology use included checking e-mail/text messages (75.1%), lack of engagement (58.1%), multitasking (56.2%), and accessing social media sites (33%). Faculty and students were asked about enforcement of technology policy. More faculty than students supported policy enforcement by faculty (65.2% versus 22.8%, respectively; p<0.001) as well as policy enforcement by students (78.3% versus 31.9%, respectively; p<0.001). Overall, technology use during class for non-academic purposes was common. Many schools and colleges of pharmacy are developing approaches to address these evolving issues by revising their technology use policies

Convolutional Neural Networks with Data Augmentation against Jitter-Based Countermeasures.

International audienceIn the context of the security evaluation of cryptographic implementations, profiling attacks (aka Template Attacks) play a fundamental role. Nowadays the most popular Template Attack strategy consists in approximating the information leakages by Gaussian distributions. Nevertheless this approach suffers from the difficulty to deal with both the traces misalignment and the high dimensionality of the data. This forces the attacker to perform critical preprocessing phases, such as the selection of the points of interest and the realignment of measurements. Some software and hardware countermeasures have been conceived exactly to create such a misalignment. In this paper we propose an end-to-end profiling attack strategy based on the Convolutional Neural Networks: this strategy greatly facilitates the attack roadmap, since it does not require a previous trace realignment nor a precise selection of points of interest. To significantly increase the performances of the CNN, we moreover propose to equip it with the data augmentation technique that is classical in other applications of Machine Learning. As a validation, we present several experiments against traces misaligned by different kinds of countermeasures, including the augmentation of the clock jitter effect in a secure hardware implementation over a modern chip. The excellent results achieved in these experiments prove that Convolutional Neural Networks approach combined with data augmentation gives a very efficient alternative to the state-of-the-art profiling attacks

Catalytic living ring-opening metathesis polymerization

In living ring-opening metathesis polymerization (ROMP), a transition-metal–carbene complex polymerizes ring-strained olefins with very good control of the molecular weight of the resulting polymers. Because one molecule of the initiator is required for each polymer chain, however, this type of polymerization is expensive for widespread use. We have now designed a chain-transfer agent (CTA) capable of reducing the required amount of metal complex while still maintaining full control over the living polymerization process. This new method introduces a degenerative transfer process to ROMP. We demonstrate that substituted cyclohexene rings are good CTAs, and thereby preserve the ‘living’ character of the polymerization using catalytic quantities of the metal complex. The resulting polymers show characteristics of a living polymerization, namely narrow molecular-weight distribution, controlled molecular weights and block copolymer formation. This new technique provides access to well- defined polymers for industrial, biomedical and academic use at a fraction of the current costs and significantly reduced levels of residual ruthenium catalyst

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Human malarial disease: a consequence of inflammatory cytokine release

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease