25 research outputs found
Standard of disocclusion in complete dentures supported by implants without free distal ends: analysis by the finite elements method
Autogenous shrinkage of fly ash and ground granulated blast furnace slag concrete
Supplementary cementitious materials (SCMs) are widely used to reduce the cement content to achieve economic and environmental objectives. As a result, understanding the shrinkage of blended cement-based concrete is essential. In total, 21 concrete mixes were produced with type general purpose cement and with cement replacements of 30% by fly ash, 40% and 60% by ground granulated blast furnace slag (GGBFS). The concrete compressive strength ranged from 25 MPa to 100 MPa. Experimental results were also compared with the predictions by models. Additional tests on pastes with the same SCM content were conducted to investigate both autogenous and chemical shrinkage in relation to their time-dependent pore structure refinement. For concretes with strength below 50 MPa, no significant difference in autogenous shrinkage could be observed between the different blends up to 28 days. However, the autogenous shrinkage of GGBFS concrete increased significantly after 28 days, being about 50% higher than all other concretes at 100 days. This late increase in autogenous shrinkage between 28 and 100 days can be attributed to pore refinement processes. No clear difference was observed for GGBFS concretes with strength greater than 50 MPa. Autogenous shrinkage of fly ash concretes was overall equivalent to that of reference concretes. </jats:p
Gene Expression in Brain and Liver Produced by Three Different Regimens of Alcohol Consumption in Mice: Comparison with Immune Activation
Chronically available alcohol escalates drinking in mice and a single injection of the immune activator lipopolysaccharide can mimic this effect and result in a persistent increase in alcohol consumption. We hypothesized that chronic alcohol drinking and lipopolysaccharide injections will produce some similar molecular changes that play a role in regulation of alcohol intake. We investigated the molecular mechanisms of chronic alcohol consumption or lipopolysaccharide insult by gene expression profiling in prefrontal cortex and liver of C57BL/6J mice. We identified similar patterns of transcriptional changes among four groups of animals, three consuming alcohol (vs water) in different consumption tests and one injected with lipopolysaccharide (vs. vehicle). The three tests of alcohol consumption are the continuous chronic two bottle choice (Chronic), two bottle choice available every other day (Chronic Intermittent) and limited access to one bottle of ethanol (Drinking in the Dark). Gene expression changes were more numerous and marked in liver than in prefrontal cortex for the alcohol treatments and similar in the two tissues for lipopolysaccharide. Many of the changes were unique to each treatment, but there was significant overlap in prefrontal cortex for Chronic-Chronic Intermittent and for Chronic Intermittent-lipopolysaccharide and in liver all pairs showed overlap. In silico cell-type analysis indicated that lipopolysaccharide had strongest effects on brain microglia and liver Kupffer cells. Pathway analysis detected a prefrontal cortex-based dopamine-related (PPP1R1B, DRD1, DRD2, FOSB, PDNY) network that was highly over-represented in the Chronic Intermittent group, with several genes from the network being also regulated in the Chronic and lipopolysaccharide (but not Drinking in the Dark) groups. Liver showed a CYP and GST centered metabolic network shared in part by all four treatments. We demonstrate common consequences of chronic alcohol consumption and immune activation in both liver and brain and show distinct genomic consequences of different types of alcohol consumption.This work was supported by grants from the National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism (NIH/NIAAA) Integrated Neuroscience Initiative on Alcoholism (INIA-West, http://www.scripps.edu/california/resear​ch/inia/; AA13520), NIH K award to IP (AA017234), and NIH grant AA013518 to RAH (NIH, http://www.nih.gov/). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No additional external funding was received for this study.Pharmac