Mechanics of Fracture in Adhesive Joints

Interdependence of continuum mechanics and physical chemistry in failure analysis of adhesive

Factors associated with pregnancy and STI among Aboriginal students in British Columbia.

BACKGROUND: Aboriginal adolescents are more likely to become pregnant and contract an STI than other Canadian adolescents. This study provides some of the first data on factors associated with these outcomes among Aboriginal adolescents. METHODS: A secondary analysis was conducted using 2003 data from a large cross-sectional survey of British Columbia secondary school students. 445 young women and 360 young men who identified as Aboriginal and reported ever having sex were included in analyses. Associations between self-reported pregnancy and STI and 11 exposure variables were examined using logistic regression. RESULTS: Of young women, 10.6% reported a pregnancy; 10.5% of young men reported causing a pregnancy. An STI diagnosis was reported by 4.2% of young women and 3.9% of young men. In multivariate analyses for young men, ever having been sexually abused was the strongest consistent risk factor for causing a pregnancy (AOR = 4.30, 95% CI 1.64-11.25) and STI diagnosis (AOR = 5.58, 95% CI 1.61-19.37). For young women, abuse was associated with increased odds of pregnancy (AOR = 10.37, 95% CI 4.04-26.60) but not STI. Among young women, substance use was the strongest consistent risk factor for both pregnancy (AOR = 3.36, 95% CI 1.25-9.08) and STI (AOR = 5.27, 95% CI 1.50-18.42); for young men, substance use was associated with higher odds of STI (AOR = 4.60, 95% CI 1.11-19.14). Factors associated with decreased risk included community, school and family involvement. CONCLUSIONS: Health care professionals, communities and policy-makers must urgently address sexual abuse and substance use. Exploring promotion of school and community involvement and family cohesion may be useful for sexual health interventions with Aboriginal students

Acute neuroinflammation induces AIS structural plasticity in a NOX2-dependent manner

Background Chronic microglia-mediated inflammation and oxidative stress are well-characterized underlying factors in neurodegenerative disease, whereby reactive inflammatory microglia enhance ROS production and impact neuronal integrity. Recently, it has been shown that during chronic inflammation, neuronal integrity is compromised through targeted disruption of the axon initial segment (AIS), the axonal domain critical for action potential initiation. AIS disruption was associated with contact by reactive inflammatory microglia which wrap around the AIS, increasing association with disease progression. While it is clear that chronic microglial inflammation and enhanced ROS production impact neuronal integrity, little is known about how acute microglial inflammation influences AIS stability. Here, we demonstrate that acute neuroinflammation induces AIS structural plasticity in a ROS-mediated and calpain-dependent manner. Methods C57BL/6J and NOX2−/− mice were given a single injection of lipopolysaccharide (LPS; 5 mg/kg) or vehicle (0.9% saline, 10 mL/kg) and analyzed at 6 h–2 weeks post-injection. Anti-inflammatory Didox (250 mg/kg) or vehicle (0.9% saline, 10 mL/kg) was administered beginning 24 h post-LPS injection and continued for 5 days; animals were analyzed 1 week post-injection. Microglial inflammation was assessed using immunohistochemistry (IHC) and RT-qPCR, and AIS integrity was quantitatively analyzed using ankyrinG immunolabeling. Data were statistically compared by one-way or two-way ANOVA where mean differences were significant as assessed using Tukey’s post hoc analysis. Results LPS-induced neuroinflammation, characterized by enhanced microglial inflammation and increased expression of ROS-producing enzymes, altered AIS protein clustering. Importantly, inflammation-induced AIS changes were reversed following resolution of microglial inflammation. Modulation of the inflammatory response using anti-inflammatory Didox, even after significant AIS disruption occurred, increased the rate of AIS recovery. qPCR and IHC analysis revealed that expression of microglial NOX2, a ROS-producing enzyme, was significantly increased correlating with AIS disruption. Furthermore, ablation of NOX2 prevented inflammation-induced AIS plasticity, suggesting that ROS drive AIS structural plasticity. Conclusions In the presence of acute microglial inflammation, the AIS undergoes an adaptive change that is capable of spontaneous recovery. Moreover, recovery can be therapeutically accelerated. Together, these findings underscore the dynamic capabilities of this domain in the presence of a pathological insult and provide evidence that the AIS is a viable therapeutic target

Trading interactions for topology in scale-free networks

Scale-free networks with topology-dependent interactions are studied. It is shown that the universality classes of critical behavior, which conventionally depend only on topology, can also be explored by tuning the interactions. A mapping, $\gamma' = (\gamma - \mu)/(1-\mu)$, describes how a shift of the standard exponent $\gamma$ of the degree distribution $P(q)$ can absorb the effect of degree-dependent pair interactions $J_{ij} \propto (q_iq_j)^{-\mu}$. Replica technique, cavity method and Monte Carlo simulation support the physical picture suggested by Landau theory for the critical exponents and by the Bethe-Peierls approximation for the critical temperature. The equivalence of topology and interaction holds for equilibrium and non-equilibrium systems, and is illustrated with interdisciplinary applications.Comment: 4 pages, 5 figure

Earthquake Cycle Deformation in the Tibetan Plateau with a Weak Mid-Crustal Layer

Geodetic observations of interseismic deformation across the Tibetan plateau contain information about both tectonic and earthquake cycle processes. Time-variations in surface velocities between large earthquakes are sensitive to the rheological structure of the subseismogenic crust, and, in particular, the viscosity of the middle and lower crust. Here we develop a semianalytic solution for time-dependent interseismic velocities resulting from viscoelastic stress relaxation in a localized midcrustal layer in response to forcing by a sequence of periodic earthquakes. Earthquake cycle models with a weak midcrustal layer exhibit substantially more near-fault preseismic strain localization than do classic two-layer models at short (50 mm/yr) postseismic velocities in the years following the coseismic ruptures. We suggest that earthquake cycle models with a localized midcrustal layer can simultaneously explain both preseismic and postseismic geodetic observations with a single Maxwell viscosity, while the classic two-layer model requires a rheology with multiple relaxation time scales.Earth and Planetary Science