Al2O3-based nanofluids: a review

Ultrahigh performance cooling is one of the important needs of many industries. However, low thermal conductivity is a primary limitation in developing energy-efficient heat transfer fluids that are required for cooling purposes. Nanofluids are engineered by suspending nanoparticles with average sizes below 100 nm in heat transfer fluids such as water, oil, diesel, ethylene glycol, etc. Innovative heat transfer fluids are produced by suspending metallic or nonmetallic nanometer-sized solid particles. Experiments have shown that nanofluids have substantial higher thermal conductivities compared to the base fluids. These suspended nanoparticles can change the transport and thermal properties of the base fluid. As can be seen from the literature, extensive research has been carried out in alumina-water and CuO-water systems besides few reports in Cu-water-, TiO2-, zirconia-, diamond-, SiC-, Fe3O4-, Ag-, Au-, and CNT-based systems. The aim of this review is to summarize recent developments in research on the stability of nanofluids, enhancement of thermal conductivities, viscosity, and heat transfer characteristics of alumina (Al2O3)-based nanofluids. The Al2O3 nanoparticles varied in the range of 13 to 302 nm to prepare nanofluids, and the observed enhancement in the thermal conductivity is 2% to 36%

Studies of the Decay B+- -> D_CP K+-

We report studies of the decay B+- -> D_CP K+-, where D_CP denotes neutral D mesons that decay to CP eigenstates. The analysis is based on a 29.1/fb data sample of collected at the \Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e+ e- storage ring. Ratios of branching fractions of Cabibbo-suppressed to Cabibbo-favored processes involving D_CP are determined to be B(B- -> D_1 K-)/B(B- -> D_1 pi-)=0.125 +- 0.036 +- 0.010 and B(B- -> D_2 K-)/B(B- -> D_2 pi-)=0.119 +- 0.028 +- 0.006, where indices 1 and 2 represent the CP=+1 and CP=-1 eigenstates of the D0 - anti D0 system, respectively. We also extract the partial rate asymmetries for B+- -> D_CP K+-, finding A_1 = 0.29 +- 0.26 +- 0.05 and A_2 = -0.22 +- 0.24 +- 0.04.Comment: 10 pages, 2 figures, submitted to Physical Review Letter

The impact of IL28B genotype on the gene expression profile of patients with chronic hepatitis C treated with pegylated interferon alpha and ribavirin

<p>Abstract</p> <p>Background</p> <p>Recent studies of CH-C patients have demonstrated a strong association between IL28B CC genotype and sustained virologic response (SVR) after PEG-IFN/RBV treatment. We aimed to assess whether IL28B alleles rs12979860 genotype influences gene expression in response to PEG-IFN/RBV in CH-C patients.</p> <p>Methods</p> <p>Clinical data and gene expression data were available for 56 patients treated with PEG-IFN/RBV. Whole blood was used to determine IL28B genotypes. Differential expression of 153 human genes was assessed for each treatment time point (Days: 0, 1, 7, 28, 56) and was correlated with IL28B genotype (IL28B C/C or non-C/C) over the course of the PEG-IFN/RBV treatment. Genes with statistically significant changes in their expression at each time point were used as an input for pathway analysis using KEGG Pathway Painter (KPP). Pathways were ranked based on number of gene involved separately per each study cohort.</p> <p>Results</p> <p>The most striking difference between the response patterns of patients with IL28B C/C and T* genotypes during treatment, across all pathways, is a sustained pattern of treatment-induced gene expression in patients carrying IL28B C/C. In the case of IL28B T* genotype, pre-activation of genes, the lack of sustained pattern of gene expression or a combination of both were observed. This observation could potentially provide an explanation for the lower rate of SVR observed in these patients. Additionally, when the lists of IL28B genotype-specific genes which were differentially expressed in patients without SVR were compared at their baseline, IRF2 and SOCS1 genes were down-regulated regardless of patients' IL28B genotype. Furthermore, our data suggest that CH-C patients who do not have the SOCS1 gene silenced have a better chance of achieving SVR. Our observations suggest that the action of SOCS1 is independent of IL28B genotype.</p> <p>Conclusions</p> <p>IL28B CC genotype patients with CH-C show a sustained treatment-induced gene expression profile which is not seen in non-CC genotype patients. Silencing of SOCS1 is a negative and independent predictor of SVR. These data may provide some mechanistic explanation for higher rate of SVR in IL28B CC patients who are treated with PEG-IFN/RBV.</p

Fibroblast growth factor 21 reflects liver fat accumulation and dysregulation of signalling pathways in the liver of C57BL/6J mice

Fibroblast growth factor 21 (Fgf21) has emerged as a potential plasma marker to diagnose non-alcoholic fatty liver disease (NAFLD). To study the molecular processes underlying the association of plasma Fgf21 with NAFLD, we explored the liver transcriptome data of a mild NAFLD model of aging C57BL/6J mice at 12, 24, and 28 months of age. The plasma Fgf21 level significantly correlated with intrahepatic triglyceride content. At the molecular level, elevated plasma Fgf21 levels were associated with dysregulated metabolic and cancerrelated pathways. The up-regulated Fgf21 levels in NAFLD were implied to be a protective response against the NAFLD-induced adverse effects, e.g. lipotoxicity, oxidative stress and endoplasmic reticulum stress. An in vivo PPARα challenge demonstrated the dysregulation of PPARα signalling in the presence of NAFLD, which resulted in a stochastically increasing hepatic expression of Fgf21. Notably, elevated plasma Fgf21 was associated with declining expression of Klb, Fgf21’s crucial co-receptor, which suggests a resistance to Fgf21. Therefore, although liver fat accumulation is a benign stage of NAFLD, the elevated plasma Fgf21 likely indicated vulnerability to metabolic stressors that may contribute towards progression to end-stage NAFLD. In conclusion, plasma levels of Fgf21 reflect liver fat accumulation and dysregulation of metabolic pathways in the liver

Role of Sphingosine Kinase 1 and Sphingosine-1-Phosphate Axis in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is primarily diagnosed in the latter stages of disease progression and is the third leading cause of cancer deaths worldwide. Thus, there is a need to find biomarkers of early HCC as well as the development of more effective treatments for the disease. Sphingosine-1-phosphate (S1P) is a pleiotropic lipid signaling molecule produced by two isoforms of sphingosine kinase (SphK1 and SphK2) that is involved in regulation of many aspects of mammalian physiology and pathophysiology, including inflammation, epithelial and endothelial barrier function, cancer, and metastasis, among many others. Abundant evidence indicates that SphK1 and S1P promote cancer progression and metastasis in multiple types of cancers. However, the role of SphK/S1P in HCC is less well studied. Here, we review the current state of knowledge of SphKs and S1P in HCC, including evidence for the correlation of SphK1 expression and S1P levels with progression of HCC and negative outcomes, and discuss how this information could lead to the design of more effective diagnostic and treatment modalities for HCC

Observation of Ds+K- and evidence for D-s(+)pi(-) final states in neutral B decays

We report the first observation of a B meson decay that is not accessible by a direct spectator process. The channel (B) over bar (0)-->Ds+K- is found in a sample of 85x10(6) B (B) over bar events, collected with the Belle detector at KEKB, with a branching fraction B((B) over bar (0)-->Ds+K-)=(4.6(-1.1)(+1.2)+/-1.3)x10(-5). We also obtain evidence for the B-0-->D(s)(+)pi(-) decay with branching fraction B(B-0-->D(s)(+)pi(-))=(2.4(-0.8)(+1.0)+/-0.7)x10(-5). This value may be used to extract a model-dependent value of \V-ub\

Evidence for direct CP violation in B-0 -> K+pi(-) decays

We report evidence for direct CP violation in the decay B-0-->K(+)pi(-) with 253 fb(-1) of data collected with the Belle detector at the KEKB e(+)e(-) collider. Using 275x10(6) B(B) over bar pairs we observe a B-->K(+/-)pi(-/+) signal with 2140+/-53 events. The measured CP violating asymmetry is A(CP)(K(+)pi(-))=-0.101+/-0.025(stat)+/-0.005(syst), corresponding to a significance of 3.9sigma including systematics. We also search for CP violation in the decays B+-->K(+)pi(0) and B+-->pi(+)pi(0). The measured CP violating asymmetries are A(CP)(K(+)pi(0))=0.04+/-0.05(stat)+/-0.02(syst) and A(CP)(pi(+)pi(0))=-0.02+/-0.10(stat)+/-0.01(syst), corresponding to the intervals -0.05< A(CP)(K(+)pi(0))<0.13 and -0.18< A(CP)(pi(+)pi(0))<0.14 at 90% confidence level

Study of CP violating effects in time dependent B-0((B)over-bar(0))-> D-(*)-/+pi(+/-) decays

We report measurements of time dependent decay rates for B-0((B) over bar (0))-->D((*)-/+)pi(+/-) decays and extraction of CP violation parameters containing phi(3). Using fully reconstructed D((*))pi events from a 140 fb(-1) data sample collected at the Y(4S) resonance, we obtain the CP violation parameters for D(*)pi and Dpi decays, 2R(D)((*))pisin(2phi(1)+phi(3)+/-delta(D)((*))pi), where R(D)((*))pi is the ratio of the magnitudes of the doubly Cabibbo-suppressed and Cabibbo-favored amplitudes, and delta(D)((*))pi is the strong phase difference between them. Under the assumption of delta(D)((*))pi being close to either 0degrees or 180degrees, we obtain \2R(D)(*)pisin(2phi(1)+phi(3))\=0.060+/-0.040(stat)+/-0.019(syst) and \2R(Dpi)sin(2phi(1)+phi(3))\=0.061+/-0.037(stat)+/-0.018(syst)