12 research outputs found

    Manufacturing and the q-factor pricing model

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    This thesis looks at the differences between the q-factor asset pricing model (Hou, Xue, and Zhang, 2015) factors constructed from manufacturing sector stocks and the factors created from the non-manufacturing stocks. The differences between the corresponding factors were tested with the paired sample t-test. The differences between the market, the size, and the investment factors were not found to be statistically significant at any reasonable level, neither in the shorter sample 1992-2019, nor in the longer period 1967-2019, which was used as a robustness check. The profitability factor created from the manufacturing stocks had on average lower returns than that created from the non-manufacturing stocks. This difference was statistically significant at 5% level in the short sample, but it was not significant during the longer sample period

    Unmasking Differential Effects of Rosiglitazone and Pioglitazone in the Combination Treatment with n-3 Fatty Acids in Mice Fed a High-Fat Diet

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    Combining pharmacological treatments and life style interventions is necessary for effective therapy of major diseases associated with obesity, which are clustered in the metabolic syndrome. Acting via multiple mechanisms, combination treatments may reduce dose requirements and, therefore, lower the risk of adverse side effects, which are usually associated with long-term pharmacological interventions. Our previous study in mice fed high-fat diet indicated additivity in preservation of insulin sensitivity and in amelioration of major metabolic syndrome phenotypes by the combination treatment using n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFA) and rosiglitazone, i.e. an anti-diabetic drug of the thiazolidinedione (TZD) family. We investigated here whether pioglitazone, a TZD-drug in clinical use, could elicit the additive beneficial effects when combined with n-3 LC-PUFA. Adult male mice (C57BL/6N) were fed an obesogenic corn oil-based high-fat diet (cHF) for 8 weeks, or randomly assigned to various dietary treatments (i) cHF+F, cHF with n-3 LC-PUFA concentrate replacing 15% of dietary lipids; (ii) cHF+ROSI, cHF with 10 mg rosiglitazone/kg diet; (iii) cHF+F+ROSI; (iv) cHF+PIO, cHF with 50 mg pioglitazone/kg diet; and (v) cHF+F+PIO, or chow-fed. Plasma concentrations of 163 metabolites were evaluated using a targeted metabolomics approach. Both TZDs preserved glucose homeostasis and normal plasma lipid levels while inducing adiponectin, with pioglitazone showing better effectiveness. The beneficial effects of TZDs were further augmented by the combination treatments. cHF+F+ROSI but not cHF+F+PIO counteracted development of obesity, in correlation with inducibility of fatty acid β-oxidation, as revealed by the metabolomic analysis. By contrast, only cHF+F+PIO eliminated hepatic steatosis and this treatment also reversed insulin resistance in dietary obese mice. Our results reveal differential effects of rosiglitazone and pioglitazone, unmasked in the combination treatment with n-3 LC-PUFA, and support the notion that n-3 LC-PUFA could be used as add-on treatment to TZDs in order to improve diabetic patient's therapy

    Prenatal diagnosis of Pallister-Killian syndrome in pregnancy with normal CVS result and abnormal ultrasound findings in the second trimester

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    Objective: To highlight importance of detailed ultrasound examination in fetuses with known normal karyotype (and micro-array result) from CVS. In case of markedly abnormal ultrasound result repeated karyotyping by amniocentesis should be considered. Sample should be analyzed by routine cytogenetic techniques, however also micro-array and targeted FISH should be added in order to achieve most accurate diagnosis. Case report: We report prenatal diagnosis of Pallister-Killian Syndrome (PKS) at 18 gestational weeks. The mother asked us for second opinion scan in our centre due to finding of seven soft markers of chromosomal defects in fetus with normal CVS result. Our examination revealed asymmetrical fetal growth, normohydramnion, spastic fetal movements and several abnormalities: nuchal edema, mild bilateral hydronephrosis, omphalocoele and facial anomalies. We asked for targeted genetic analysis for PKS. Amniocentesis with repeated genetic analysis confirmed PKS (80% mosaicism of tetrasomy 12p). Conclusion: Diagnosis of PKS led mother to terminate pregnancy. Keywords: Pallister-Killian syndrome, Prenatal diagnosis, 2D-3D ultrasound, FISH, Micro-arra
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