Stability of Solid State Reaction Fronts

We analyze the stability of a planar solid-solid interface at which a chemical reaction occurs. Examples include oxidation, nitridation, or silicide formation. Using a continuum model, including a general formula for the stress-dependence of the reaction rate, we show that stress effects can render a planar interface dynamically unstable with respect to perturbations of intermediate wavelength

Normal-state magnetic susceptibility in a bilayer cuprate

The magnetic susceptibility of high-T_c superconductors is investigated in the normal state using a coupled bilayer model. While this model describes in a natural way the normal-state pseudogaps seen in c-axis optical conductivity on underdoped samples, it predicts a weakly increasing susceptibility with decreasing temperature and cannot explain the magnetic pseudogaps exhibited in NMR measurements. Our result, together with some experimental evidence suggest that the mechanism governing the c-axis optical pseudogap is different from that for the $a-b$ plane magnetic pseudogap.Comment: 5 pages, 2 figure

The pseudogap in high-temperature superconductors: an experimental survey

We present an experimental review of the nature of the pseudogap in the cuprate superconductors. Evidence from various experimental techniques points to a common phenomenology. The pseudogap is seen in all high temperature superconductors and there is general agreement on the temperature and doping range where it exists. It is also becoming clear that the superconducting gap emerges from the normal state pseudogap. The d-wave nature of the order parameter holds for both the superconducting gap and the pseudogap. Although an extensive body of evidence is reviewed, a consensus on the origin of the pseudogap is as lacking as it is for the mechanism underlying high temperature superconductivity.Comment: review article, 54 pages, 50 figure

A cut-off of daily sedentary time and all-cause mortality in adults: a meta-regression analysis involving more than 1 million participants

Background The appropriate limit to the amount of daily sedentary time (ST) required to minimize mortality is uncertain. This meta-analysis aimed to quantify the dose-response association between daily ST and all-cause mortality and to explore the cut-off point above which health is impaired in adults aged 18–64 years old. We also examined whether there are differences between studies using self-report ST and those with device-based ST. Methods Prospective cohort studies providing effect estimates of daily ST (exposure) on all-cause mortality (outcome) were identified via MEDLINE, PubMed, Scopus, Web of Science, and Google Scholar databases until January 2018. Dose-response relationships between daily ST and all-cause mortality were examined using random-effects meta-regression models. Results Based on the pooled data for more than 1 million participants from 19 studies, the results showed a log-linear dose-response association between daily ST and all-cause mortality. Overall, more time spent in sedentary behaviors is associated with increased mortality risks. However, the method of measuring ST moderated the association between daily ST and mortality risk (p < 0.05). The cut-off of daily ST in studies with self-report ST was 7 h/day in comparison with 9 h/day for those with device-based ST. Conclusions Higher amounts of daily ST are log-linearly associated with increased risk of all-cause mortality in adults. On the basis of a limited number of studies using device-based measures, the findings suggest that it may be appropriate to encourage adults to engage in less sedentary behaviors, with fewer than 9 h a day being relevant for all-cause mortality

A Threshold of Objectively-Assessed Daily Sedentary Time for All-Cause Mortality in Older Adults: A Meta-Regression of Prospective Cohort Studies

BACKGROUND: This meta-analysis aimed to estimate the shape of the dose-response association between objectively-assessed daily sedentary time (ST) and all-cause mortality, and to explore whether there is a threshold of ST above which there is an increase in mortality risk in older adults. METHODS: Searches for prospective cohort studies providing effect estimates of daily ST (exposure) on all-cause mortality (outcome) were undertaken in five databases up to 31 March 2019. A random-effects meta-regression model was conducted to quantify the dose-response relationship between daily ST and all-cause mortality. Sensitivity analyses were also performed to test the stability of the results. RESULTS: Our analysis of pooled data from 11 eligible studies did not reveal a consistent shape of association between ST and mortality. After excluding three studies with potential confounding bias, there was a log-linear dose-response relationship between daily ST and all-cause mortality. Overall, higher amounts of time spent in sedentary behaviors were associated with elevated mortality risks in older adults. Visual assessments of dose-response relationships based on meta-regression analyses indicated that increased mortality risks became significant when total ST exceeded approximately 9 h/day. CONCLUSIONS: Based on a limited number of studies, this meta-analysis provides a starting point for considering a cut-off of daily sedentary time, suggesting older adults spend less time in daily sitting

Control of Grain-Boundary Pinning in Al 2 O 3 /ZrO 2 Composites with Ce 3+ /Ce 4+ Doping

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65897/1/j.1151-2916.1992.tb04147.x.pd

Rosiglitazone Inhibits Acyl-CoA Synthetase Activity and Fatty Acid Partitioning to Diacylglycerol and Triacylglycerol via a Peroxisome Proliferator-Activated Receptor- -Independent Mechanism in Human Arterial Smooth Muscle Cells and Macrophages

Rosiglitazone is an insulin-sensitizing agent that has recently been shown to exert beneficial effects on atherosclerosis. In addition to peroxisome proliferator–activated receptor (PPAR)-γ, rosiglitazone can affect other targets, such as directly inhibiting recombinant long-chain acyl-CoA synthetase (ACSL)-4 activity. Because it is unknown if ACSL4 is expressed in vascular cells involved in atherosclerosis, we investigated the ability of rosiglitazone to inhibit ACSL activity and fatty acid partitioning in human and murine arterial smooth muscle cells (SMCs) and macrophages. Human and murine SMCs and human macrophages expressed Acsl4, and rosiglitazone inhibited Acsl activity in these cells. Furthermore, rosiglitazone acutely inhibited partitioning of fatty acids into phospholipids in human SMCs and inhibited fatty acid partitioning into diacylglycerol and triacylglycerol in human SMCs and macrophages through a PPAR-γ–independent mechanism. Conversely, murine macrophages did not express ACSL4, and rosiglitazone did not inhibit ACSL activity in these cells, nor did it affect acute fatty acid partitioning into cellular lipids. Thus, rosiglitazone inhibits ACSL activity and fatty acid partitioning in human and murine SMCs and in human macrophages through a PPAR-γ–independent mechanism likely to be mediated by ACSL4 inhibition. Therefore, rosiglitazone might alter the biological effects of fatty acids in these cells and in atherosclerosis

On the Nucleon Distribution Amplitude: The Heterotic Solution

We present a new nucleon distribution amplitude which amalgamates features of the Chernyak-Ogloblin-Zhitnitsky model with those of the Gari-Stefanis model. This "heterotic" solution provides the possibility to have asymptotically a small ratio \hbox{$\vert G_{M}^{n}\vert/G_{M}^{p}\le 0.1$}, while fulfilling most of the sum-rule requirements up to the third order. Using this nucleon distribution amplitude we calculate the electromagnetic and weak nucleon form factors, the transition form factor $\gamma p \Delta^{+}$ and the decay widths of the charmonium levels $^3S_{1}$, $^3P_{1}$, and $^3P_{2}$ into $p\bar p$. The agreement with the available data is remarkable in all cases.Comment: 15 pages, RUB-TPII-21/92 Preprin

Computer Simulation of Final-Stage Sintering: I, Model Kinetics, and Microstructure

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65565/1/j.1151-2916.1990.tb06686.x.pd