511 keV γ\gamma-ray emission from the galactic bulge by MeV millicharged dark matter

We propose a possible explanation for the recently observed anomalous 511 keV line with a new "millicharged" fermion. This new fermion is light [${\cal O}({\rm MeV})$]. Nevertheless, it has never been observed by any collider experiments by virtue of its tiny electromagnetic charge $\epsilon e$. In particular, we constrain parameters of this millicharged particle if the 511 keV cosmic $\gamma$-ray emission from the galactic bulge is due to positron production from this new particle.Comment: 3 pages, 1 figure, A talk given by J.C.Park at the 16th International Conference on Supersymmetry and the Unification of Fundamental Interactions (SUSY08), Seoul, Korea, June 16-21, 200

Use of microwave remote sensors for determination of water in sub-soils

Student supported: 1 Graduate AssistantThe development of instruments for rapidly measuring the water content of subsoils is important in many areas of water resources research. For example, knowing the excess or lack of subsoil water can improve crops. The marked dielectric contrast, which exists between water and other common soil constituents (Fig. 1 and Table I) at microwave frequencies, provides a valuable means of sensing water content in soil.Project # A-070-MO Agreement # 14-31-0001-402

Sequences of acetyl CoA carboxylase promoter for tumour necrosis factor action

Tumour necrosis factor (TNF) inhibits the accumulation of acetyl CoA carboxylase (ACC) mRNA by decreasing the rate of ACC gene transcription. The ACC mRNA species found in 30A5 cells are generated from promoter II and TNF inhibits the accumulation of class 2 type mRNAs. By using 5' deletion mutants of promoter II fused to the bacterial chloramphenicol acetyltransferase (CAT) gene, the DNA mobility shift assay and the DNase I footprinting assay, the authors have identified the 30 bp from −389 to −359 as the TNF responsive element in promoter II. TNF treatment causes a decrease in the binding activity of nuclear protein(s) specific to the TNF responsive element. When the fragment containing the TNF responsive element was incorporated into the thymidine kinase promoter, the chimeric gene exhibited TNF induced inhibition of expression

High-Density Lipoprotein Metabolism in Human Apolipoprotein B\u3csub\u3e100\u3c/sub\u3e Transgenic/Brown Adipose Tissue Deficient Mice: A Model of Obesity-Induced Hyperinsulinemia

Obese and diabetic humans display decreased plasma high-density lipoprotein cholesterol (HDL-C) concentrations and an increased risk for coronary heart disease. However, investigation on HDL metabolism in obesity with a particular emphasis on hepatic ATP-binding cassette transporter A1 (ABCA1), the primary factor for HDL formation, has not been well studied. Human apolipoprotein B100 transgenic (hApoBtg) and brown adipose tissue deficient (BATless) mice were crossed to generate hApoBtg/BATless mice. Male and female hApoBtg and hApoBtg/BATless mice were maintained on either a regular rodent chow diet or a diet high in fat and cholesterol until 24 weeks of age. The hApoBtg/BATless mice that were fed a HF/HC diet became obese, developed hepatic steatosis, and had significantly elevated plasma insulin levels compared with their hApoBtg counterparts, but plasma concentrations of total cholesterol, HDL-C, triglycerides, and free fatty acids and lipoprotein distribution between genotypes were not significantly different. Hepatic expression of genes encoding HDL-modifying factors (e.g., scavenger receptor, class B, type I, hepatic lipase, lecithin:cholesterol acyltransferase, and phospholipid transfer protein) was either altered significantly or showed a trend of difference between 2 genotypes of mice. Importantly, hepatic protein levels of ABCA1 were significantly lowered by ∼35% in male obese hApoBtg/BATless mice with no difference in mRNA levels compared with hApoBtg counterparts. Despite reduced hepatic ABCA1 protein levels, plasma HDL-C concentrations were not altered in male obese hApoBtg/BATless mice. The result suggests that hepatic ABCA1 may not be a primary contributing factor for perturbations in HDL metabolism in obesity-induced hyperinsulinemia

Unsaturated Fatty Acids Repress the Expression of ATP-Binding Cassette Transporter A1 in HepG2 and FHs 74 Int Cells

Adenosine triphosphate–binding cassette transporter A1 (ABCA1) plays a critical role in the formation and metabolism of high-density lipoproteins (HDLs). Adenosine triphosphate–binding cassette transporter A1 in the liver and small intestine, in particular, accounts for approximately 90% of plasma HDL cholesterol. Therefore, any alterations in the hepatic and intestinal expression of ABCA1 could have a large impact on HDL biogenesis. We tested the hypothesis that ABCA1 expression is regulated differentially by different types of fatty acids in the liver and small intestine. Human hepatoma HepG2 and human small intestine epithelial FHs 74 Int cells were used as an in vitro model. Cells were incubated with saturated and unsaturated fatty acids in the presence or absence of T0901317, a synthetic agonist of liver X receptor. Unsaturated fatty acids decreased ABCA1 protein levels at 100 μmol/L of concentration regardless of the agonist with a minimal effect on messenger RNA abundance. Incubation of HepG2 and FHs 74 Int cells with rottlerin, a protein kinase C δ (PKCδ) inhibitor, increased ABCA1 protein but did not abolish linoleic acid–induced decrease in ABCA1 protein levels. Depletion of PKCδ using small interfering RNA showed decreased ABCA1 protein levels in control, palmitic acid–, and linoleic acid–treated cells, but the repressive effect of linoleic acid was sustained. In conclusion, our results indicate that unsaturated fatty acids regulate ABCA1 expression in HepG2 and FHs 74 Int cells at the posttranscriptional level, and PKCδ is likely to be involved in maintaining ABCA1 protein levels

Lipid Extract of \u3ci\u3eNostoc commune\u3c/i\u3e var. \u3ci\u3esphaeroides\u3c/i\u3e Kützing, a Blue-Green Alga, Inhibits the Activation of Sterol Regulatory Element Binding Proteins in HepG2 Cells

Nostoc commune var. sphaeroides Kützing (N. commune), a blue-green alga, has been used as both a food ingredient and in medicine for centuries. To determine the effect of N. commune on cholesterol metabolism, N. commune lipid extract was incubated at increasing concentrations (25–100 mg/L) with HepG2 cells, a human hepatoma cell line. The addition of N. commune lipid extract markedly reduced mRNA abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) and LDL receptor (LDLR) (P \u3c 0.05), with a concomitant decrease in their protein expression (P \u3c 0.001). Reduced HMGR activity by 90% with N. commune lipid extract confirmed the inhibitory role of N. commune in cholesterol synthesis (P \u3c 0.006). To elucidate a molecular mechanism underlying the repression of HMGR and LDLR by N. commune lipid extract, expression of sterol regulatory element binding protein 2 (SREBP-2) was assessed. Whereas mRNA for SREBP-2 remained unchanged, SREBP-2 mature protein was reduced by N. commune (P \u3c 0.009). In addition, N. commune lipid extract also decreased SREBP-1 mature protein by ~30% (P \u3c 0.002) and reduced the expression of SREBP-1-responsive genes such as fatty acid synthase and stearoyl CoA desaturase 1 (SCD-1) (P \u3c 0.05). Therefore, our results demonstrate that N. commune lipid extract inhibits the maturation process of both SREBP-1 and -2, resulting in a decrease in expression of genes involved in cholesterol and fatty acid metabolism

Improvement of Subjective Well-Being by Ranolazine in Patients with Chronic Angina and Known Myocardial Ischemia (IMWELL Study)

Introduction: We aimed to assess if ranolazine would improve angina symptoms among patients with documented myocardial ischemia. Methods: Eligible subjects had chronic stable angina and at least one coronary stenosis with fractional flow reserve (FFR) ≤0.80 or at least one chronic total occlusion (CTO) without attempted revascularization. Subjects were randomized to oral ranolazine 500 mg twice daily for 1 week, then ranolazine 1000 mg twice daily for 15 weeks versus matching placebo. The primary end point was change in angina at 16 weeks as assessed by the Seattle Angina Questionnaire (SAQ). Results: Between September 2014 and January 2016, 25 subjects were randomized to ranolazine versus 25 to placebo. The most common reason for eligibility was CTO (72%), while the remainder had myocardial ischemia documented by low FFR. The mean FFR was 0.57 ± 0.12. Sixty-eight percent of subjects were on two or more anti-angina medications at baseline. Study medication was discontinued in 32% (eight of 25) of the ranolazine group versus 36% (nine of 25) of the placebo group. By intention-to-treat, 46 subjects had baseline and follow-up SAQ data completed. Ranolazine was not associated with an improvement in angina compared with placebo at 16 weeks. The results were similar among 33 subjects that completed study medication. The incidence of ischemia-driven hospitalization or catheterization was 12% (three of 25) of the ranolazine group versus 20% (five of 25) in the placebo group (p \u3e 0.05). Conclusions: In subjects with chronic stable angina and documented myocardial ischemia, ranolazine did not improve angina symptoms at 16 weeks

Hypocholesterolemic effect of \u3ci\u3eNostoc commune\u3c/i\u3e var. \u3ci\u3esphaeroides\u3c/i\u3e Kützing, an edible blue-green alga

Background Intake of an edible blue-green alga Nostoc commune var. sphaeroides Kützing (N. commune) has been shown to lower plasma total cholesterol concentration, but the mechanisms behind the hypocholesterolemic effect have not been elucidated. Aim of the study To elucidate the mechanisms underlying the cholesterol-lowering effect of N. commune in mice. Methods Male C57BL/6J mice were fed the AIN-93 M diet supplemented with 0 or 5% (wt/wt) dried N. commune for 4 weeks. Lipid levels in the plasma and liver, intestinal cholesterol absorption, and fecal sterol excretion were measured. Expression of hepatic and intestinal genes involved in cholesterol metabolism was evaluated by quantitative realtime PCR. Results N. commune supplementation significantly reduced total plasma cholesterol and triglyceride concentrations by ~20% compared to controls. Intestinal cholesterol absorption was significantly decreased, while fecal neutral sterol output was significantly increased in N. commune–fed mice. mRNA levels of the cholesterol transporters such as Niemann Pick C1 Like 1, scavenger receptor class B type 1, ATP-binding cassette transporters G5 and A1 in small intestine were not significantly different between two groups. Hepatic lipid contents including total cholesterol, triglyceride and free cholesterol in N. commune–fed mice were not significantly altered. However, the expression of cholesterol-modulating genes including sterol regulatory element binding protein-2 and 3-hydroxy-3-methylglutaryl coenzyme A reductase were significantly increased in mice fed N. commune. Conclusions N. commune supplementation exerted a hypocholesterolemic effect in mice, largely in part, by reducing intestinal cholesterol absorption and promoting fecal neutral sterol excretion

Repression of Proinflammatory Gene Expression by Lipid Extract of \u3ci\u3eNostoc commune\u3c/i\u3e var \u3ci\u3esphaeroides\u3c/i\u3e Kützing, a Blue-green Alga, via Inhibition of Nuclear Factor-κB in RAW 264.7 Macrophages

We investigated whether lipid extract from a blue-green alga, N. commune, modulates proinflammatory gene expression in RAW 264.7 macrophages. The cells were incubated with N. commune lipid extract (0–100 μg/mL) and subsequently activated by LPS (100 ng/mL). Quantitative real-time PCR analysis showed that mRNA abundance of proinflammatory mediators, including TNF-α, COX-2, IL-1β, IL-6, and iNOS, was significantly reduced by N. commune lipid extract in a dose-dependent manner. Secretion of TNF-α and IL-1β into cell culture medium was also significantly decreased by N. commune lipid extract. Thin-layer chromatography-densitometry analysis showed that N. commune lipid extract contained approximately 15% of fatty acids. To determine whether the inhibition of proinflammatory mediator production by N. commune lipid extract is primarily conferred by fatty acids in the lipid extract, macrophages were incubated with 100 μg/mL of N. commune lipid extract or 15 μg/mL of a fatty acid mixture, which was formulated to reflect the fatty acid composition of N. commune lipid extract. The fatty acid mixture significantly reduced RNA abundance of TNF-α and COX-2, but to a lesser extent than did the N. commune lipid extract, suggesting the presence of additional bioactive compounds with an anti-inflammatory property in the lipid extract. As NF-κB is a major regulator for the proinflammatory gene expression, we measured its DNA-binding activity. DNA-binding activity of NF-κB was significantly reduced by N. commune lipid extract. In conclusion, our study suggests that N. commune lipid extract represses the expression of proinflammatory genes in RAW 264.7 macrophages, at least in part, by inhibiting the activation of NF-κB pathway