On the Elevated Temperature Thermal Stability of Nanoscale Mn-Ni-Si Precipitates Formed at Lower Temperature in Highly Irradiated Reactor Pressure Vessel Steels.

Atom probe tomography (APT) and scanning transmission electron microscopy (STEM) techniques were used to probe the long-time thermal stability of nm-scale Mn-Ni-Si precipitates (MNSPs) formed in intermediate and high Ni reactor pressure vessel steels under high fluence neutron irradiation at ≈320 °C. Post irradiation annealing (PIA) at 425 °C for up to 57 weeks was used to determine if the MNSPs are: (a) non-equilibrium solute clusters formed and sustained by radiation induced segregation (RIS); or, (b) equilibrium G or Γ2 phases, that precipitate at accelerated rates due to radiation enhanced diffusion (RED). Note the latter is consistent with both thermodynamic models and x-ray diffraction (XRD) measurements. Both the experimental and an independently calibrated cluster dynamics (CD) model results show that the stability of the MNSPs is very sensitive to the alloy Ni and, to a lesser extent, Mn content. Thus, a small fraction of the largest MNSPs in the high Ni steel persist, and begin to coarsen at long times. These results suggest that the MNSPs remain a stable phase, even at 105 °C higher than they formed at, thus are most certainly equilibrium phases at much lower service relevant temperatures of ≈290 °C

Constraints on the Local Cosmic Void from the Pantheon Supernovae Data

In principle, the local cosmic void can be simply modeled by the spherically symmetric Lemaitre-Tolman-Bondi (LTB) metric. In practice, the real local cosmic void is probably not spherically symmetric. In this paper, to reconstruct a more realistic profile of the local cosmic void, we divide it into several segments. Each segment with certain solid angle is modeled by its own LTB metric. Meanwhile, we divide the 1048 type Ia supernovae (SNIa) of the Pantheon Survey into corresponding subsets according to their distribution in the galactic coordinate system. Obviously, each SNIa subset can only be used to reconstruct the profile of one segment. Finally, we can patch together an irregular profile for the local cosmic void with the whole Pantheon sample. Note that, the paucity of each data subset lead us to focus on the inner part of each void segment and assume that the half radii of the void segments are sufficient to constrain the whole segment. We find that, despite $2\sigma$ signals of anisotropy limited to the depth of the void segments, the constraints on every void segment are consistent with $\Lambda$CDM model at $95\%$ CL. Moreover, our constraints are too weak to challenge the cosmic homogeneity and isotropy.Comment: 12 pages, 9 figure

The influence of time attitudes on alcohol-related attitudes, behaviors and subjective life expectancy in early adolescence: A longitudinal examination using mover-stayer latent transition analysis

The goal of the present study is to examine the stability of time attitudes profiles across a one-year period as well as the association between time attitudes profiles and several variables. These variables include attitudes towards alcohol, context of alcohol use, consumption of a full drink, and subjective life expectancy. We assessed the reliability and validity of time attitudes scores at baseline (mean age 12.5 years) and Wave 2 (mean age 13.5 years), the viability of time attitudes profiles at both time points, and the degree of stability in profile membership in Wave 2. A total of four latent profiles were identified (Positives, Ambivalents, Negatives, and Negative-Futures). Positives had higher scores on positive time attitude, Ambivalents did not report strong attitudes towards any of the time periods, Negatives had higher scores on negative time attitudes, and Negative-Futures were similar to Negatives, but tended to higher scores on both positive and negative time attitude for the future. Results showed that participants staying in the same time attitude profile across the first year of high school ranged from 33% to 50%. Transition to more negative profiles explained the instability, and those transitions were associated with less favorable outcomes. Having a Positive profile was associated with safer attitudes towards alcohol, lower reported uses of alcohol, and higher self-reported probability of surviving to at least the age of 35

A Whole-Body Model for Glycogen Regulation Reveals a Critical Role for Substrate Cycling in Maintaining Blood Glucose Homeostasis

Timely, and sometimes rapid, metabolic adaptation to changes in food supply is critical for survival as an organism moves from the fasted to the fed state, and vice versa. These transitions necessitate major metabolic changes to maintain energy homeostasis as the source of blood glucose moves away from ingested carbohydrates, through hepatic glycogen stores, towards gluconeogenesis. The integration of hepatic glycogen regulation with extra-hepatic energetics is a key aspect of these adaptive mechanisms. Here we use computational modeling to explore hepatic glycogen regulation under fed and fasting conditions in the context of a whole-body model. The model was validated against previous experimental results concerning glycogen phosphorylase a (active) and glycogen synthase a dynamics. The model qualitatively reproduced physiological changes that occur during transition from the fed to the fasted state. Analysis of the model reveals a critical role for the inhibition of glycogen synthase phosphatase by glycogen phosphorylase a. This negative regulation leads to high levels of glycogen synthase activity during fasting conditions, which in turn increases substrate (futile) cycling, priming the system for a rapid response once an external source of glucose is restored. This work demonstrates that a mechanistic understanding of the design principles used by metabolic control circuits to maintain homeostasis can benefit from the incorporation of mathematical descriptions of these networks into “whole-body” contextual models that mimic in vivo conditions

Cytomegalovirus Infection Causes an Increase of Arterial Blood Pressure

Cytomegalovirus (CMV) infection is a common infection in adults (seropositive 60–99% globally), and is associated with cardiovascular diseases, in line with risk factors such as hypertension and atherosclerosis. Several viral infections are linked to hypertension, including human herpes virus 8 (HHV-8) and HIV-1. The mechanisms of how viral infection contributes to hypertension or increased blood pressure are not defined. In this report, the role of CMV infection as a cause of increased blood pressure and in forming aortic atherosclerotic plaques is examined. Using in vivo mouse model and in vitro molecular biology analyses, we find that CMV infection alone caused a significant increase in arterial blood pressure (ABp) (p<0.01 $\sim$0.05), measured by microtip catheter technique. This increase in blood pressure by mouse CMV (MCMV) was independent of atherosclerotic plaque formation in the aorta, defined by histological analyses. MCMV DNA was detected in blood vessel samples of viral infected mice but not in the control mice by nested PCR assay. MCMV significantly increased expression of pro-inflammatory cytokines IL-6, TNF-$\alpha$, and MCP-1 in mouse serum by enzyme-linked immunosorbent assay (ELISA). Using quantitative real time reverse transcriptase PCR (Q-RT-PCR) and Western blot, we find that CMV stimulated expression of renin in mouse and human cells in an infectious dose-dependent manner. Co-staining and immunofluorescent microscopy analyses showed that MCMV infection stimulated renin expression at a single cell level. Further examination of angiotensin-II (Ang II) in mouse serum and arterial tissues with ELISA showed an increased expression of Ang II by MCMV infection. Consistent with the findings of the mouse trial, human CMV (HCMV) infection of blood vessel endothelial cells (EC) induced renin expression in a non-lytic infection manner. Viral replication kinetics and plaque formation assay showed that an active, CMV persistent infection in EC and expression of viral genes might underpin the molecular mechanism. These results show that CMV infection is a risk factor for increased arterial blood pressure, and is a co-factor in aortic atherosclerosis. Viral persistent infection of EC may underlie the mechanism. Control of CMV infection can be developed to restrict hypertension and atherosclerosis in the cardiovascular system