PORE CONNECTIVITY, EPISODIC FLOW, AND UNSATURATED DIFFUSION IN FRACTURED TUFF

We use an integrated approach consisting of experiments and complementary pore-scale network modeling to investigate the occurrence of sparsely connected pore spaces in rock matrices at Yucca Mountain, Nevada, and their implications for matrix diffusion. Imbibition results indicate that pore spaces in devitrified tuff are not well-connected, and that this lack of connectivity is further compounded by episodic flow in fractured devitrified tuff with low matrix permeability. A rigorous methodology for investigating chemical transport in fractured rock under episodic conditions, employing a suite of both sorbing and non-sorbing tracers (including radionuclides U-235, Np-237, and Pu-242), has been developed and implemented. In addition, gas diffusion and synchrotron microtomography techniques have been under development to examine the scaling issues of diffusion and pore connectivity. Preliminary results from experiments and modeling work are presented in this paper, confirming the need to reexamine our understanding of matrix diffusion and to evaluate the impact on diffusive radionuclide retardation of episodic fracture flow and low pore connectivity

Electronic correlation in the infrared optical properties of the quasi two dimensional κ\kappa-type BEDT-TTF dimer system

The polarized optical reflectance spectra of the quasi two dimensional organic correlated electron system $\kappa$-(BEDT-TTF)$_{2}$Cu[N(CN)$_{2}$]$Y$, $Y =$ Br and Cl are measured in the infrared region. The former shows the superconductivity at $T_{\rm c} \simeq$ 11.6 K and the latter does the antiferromagnetic insulator transition at $T_{\rm N} \simeq$ 28 K. Both the specific molecular vibration mode $\nu_{3}(a_{g})$ of the BEDT-TTF molecule and the optical conductivity hump in the mid-infrared region change correlatively at $T^{*} \simeq$ 38 K of $\kappa$-(BEDT-TTF)$_{2}$Cu[N(CN)$_{2}$]Br, although no indication of $T^{*}$ but the insulating behaviour below $T_{\rm ins} \simeq$ 50-60 K are found in $\kappa$-(BEDT-TTF)$_{2}$Cu[N(CN)$_{2}$]Cl. The results suggest that the electron-molecular vibration coupling on the $\nu_{3}(a_{g})$ mode becomes weak due to the enhancement of the itinerant nature of the carriers on the dimer of the BEDT-TTF molecules below $T^{*}$, while it does strong below $T_{\rm ins}$ because of the localized carriers on the dimer. These changes are in agreement with the reduction and the enhancement of the mid-infrared conductivity hump below $T^{*}$ and $T_{\rm ins}$, respectively, which originates from the transitions between the upper and lower Mott-Hubbard bands. The present observations demonstrate that two different metallic states of $\kappa$-(BEDT-TTF)$_{2}$Cu[N(CN)$_{2}$]Br are regarded as {\it a correlated good metal} below $T^{*}$ including the superconducting state and {\it a half filling bad metal} above $T^{*}$. In contrast the insulating state of $\kappa$-(BEDT-TTF)$_{2}$Cu[N(CN)$_{2}$]Cl below $T_{\rm ins}$ is the Mott insulator.Comment: 8 pages, 7 figure

Economic crisis and the construction of a neo-liberal regulatory regime in Korea

A consistent theme of the literature on the ontology of the 1997 South Korean crisis is the key role played by regulatory failures and the growing weakness of the state. This paper seeks to briefly highlight both the insights and the limitations of this approach to understanding the crisis. Having done so, we shall set out the argument that the crisis created an opportunity for reformist Korean élites to advance their longstanding, but previously frustrated, project to create a comprehensive unambiguously neo-liberal regulatory regime. This paper will also seek to highlight the implications of our reading of the development of the Korean political economy for broader debates on economic liberalisation, crisis and the future of the developmental state

Effect of harvest time on physicochemical quality parameters, oxidation stability, and volatile compounds of extra virgin olive oil

The aim of this study was to determine the changes in some physicochemical properties of olives (fruit weight, water content and oil content) and olive oils (total chlorophyll, carotenoid, pheophytin a, peroxide value and free acidity), and in the chemical properties (fatty acids, tocopherols, phenolics, oxidation stability and volatile profiles) of oils during ripening.Ripening indices (RI) of olive samples were 1.93 (unripe), 4.28 (ripe) and 5.89 (overripe). Most of the mentioned features changed with ripening. During ripening there was a sharp decrease in total chlorophyll, carotenoid and pheophytin a contents. An increase in oleic and linoleic acids and a decrease in palmitic acid were found in the fatty acid composition. Olive oils showed strong relations among oxidation stability, tocopherol content, total phenols content, and antiradical actvity of phenol extracts and these parameters decreased with maturation. Nevertheless, higher amounts of trans-2-hexenal were found in the oil from ripe olives than from unripe and overripe olives. On the other hand, the highest concentration of hexanal was found in the oil from overripe olives.In general, significant differences were observed in fruit weight, pigments, free acidity, fatty acid, tocopherol, and total phenolics contents, radical scavenger activity, oxidation stability, phenolic profile and volatile profile between the olive oils from the Gemlik cultivar at different stages of maturation

Compound heterozygous variants in NBAS as a cause of atypical osteogenesis imperfecta

Background Osteogenesis imperfecta (OI), the commonest inherited bone fragility disorder, affects 1 in 15,000 live births resulting in frequent fractures and reduced mobility, with significant impact on quality of life. Early diagnosis is important, as therapeutic advances can lead to improved clinical outcome and patient benefit. Report Whole exome sequencing in patients with OI identified, in two patients with a multi-system phenotype, compound heterozygous variants in NBAS (neuroblastoma amplified sequence). Patient 1: NBAS c.5741G > A p.(Arg1914His); c.3010C > T p.(Arg1004*) in a 10-year old boy with significant short stature, bone fragility requiring treatment with bisphosphonates, developmental delay and immunodeficiency. Patient 2: NBAS c.5741G > A p.(Arg1914His); c.2032C > T p.(Gln678*) in a 5-year old boy with similar presenting features, bone fragility, mild developmental delay, abnormal liver function tests and immunodeficiency. Discussion Homozygous missense NBAS variants cause SOPH syndrome (short stature; optic atrophy; Pelger-Huet anomaly), the same missense variant was found in our patients on one allele and a nonsense variant in the other allele. Recent literature suggests a multi-system phenotype. In this study, patient fibroblasts have shown reduced collagen expression, compared to control cells and RNAseq studies, in bone cells show that NBAS is expressed in osteoblasts and osteocytes of rodents and primates. These findings provide proof-of-concept that NBAS mutations have mechanistic effects in bone, and that NBAS variants are a novel cause of bone fragility, which is distinguishable from ‘Classical’ OI. Conclusions Here we report on variants in NBAS, as a cause of bone fragility in humans, and expand the phenotypic spectrum associated with NBAS. We explore the mechanism underlying NBAS and the striking skeletal phenotype in our patients

Do precocial mammals develop at a faster rate? A comparison of rates of skull development in Sigmodon fulviventer and Mus musculus domesticus

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72993/1/j.1420-9101.2003.00568.x.pd

A whole-blood transcriptome meta-analysis identifies gene expression signatures of cigarette smoking

Cigarette smoking is a leading modifiable cause of death worldwide. We hypothesized that cigarette smoking induces extensive transcriptomic changes that lead to target-organ damage and smoking-related diseases. We performed a metaanalysis of transcriptome-wide gene expression using whole blood-derived RNA from 10,233 participants of European ancestry in six cohorts (including 1421 current and 3955 former smokers) to identify associations between smoking and altered gene expression levels. At a false discovery rate (FDR) < 0.1, we identified 1270 differentially expressed genes in current vs. never smokers, and 39 genes in former vs. never smokers. Expression levels of 12 genes remained elevated up to 30 years after smoking cessation, suggesting that the molecular consequence of smoking may persist for decades. Gene ontology analysis revealed enrichment of smoking-related genes for activation of platelets and lymphocytes, immune response, and apoptosis. Many of the top smoking-related differentially expressed genes, including LRRN3 and GPR15, have DNA methylation loci in promoter regions that were recently reported to be hypomethylated among smokers. By linking differential gene expression with smoking-related disease phenotypes, we demonstrated that stroke and pulmonary function show enrichment for smoking-related gene expression signatures. Mediation analysis revealed the expression of several genes (e.g. ALAS2) to be putative mediators of the associations between smoking and inflammatory biomarkers (IL6 and C-re

A meta-analysis of gene expression signatures of blood pressure and hypertension

Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%-9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension