The Impact of COVID-19 Pandemic on Government Bond Yields

The COVID-19 pandemic is a real shock to society and business and financial markets. The government bond market is an essential part of financial markets, especially in difficult times, because it is a source of government funding. The majority of existing ESG studies report positive impacts on corporate financial performance regarding environmental, social, and governance. Thus, understanding governments’ financial practices and their relevant ESG implications is insufficient. This research aims to value the impact of the COVID-19 pandemic on different government bond curve sectors. We try to identify the reactions to the COVID-19 pandemic in the government bond market and analyze separate tenors of government bond yields in different regions. We have chosen Germany and the United States government bond yields of 10, 5, and 3 years tenor for the analysis. As independent variables, we have chosen daily cases of COVID-19 and daily deaths from COVID-19 at the country and global levels. We used daily data from 02 January 2020–19 March 2021, and divided this period into three stages depending on the COVID-19 pandemic data. We employed the methods of correlation-regression analysis (ordinary least squares and least squares with breakpoints) and VAR-based impulse response functions to evaluate the effect of the COVID-19 pandemic on government bond yields both in the long and short run. Our analysis revealed the impact of the spread of the COVID-19 pandemic on government bond yields differs depending on the country and the assessment period. The short-term responses vary in direction, strength, and duration; the long-term response of Germany’s yields appeared to be more negative (indicating the decrease of the yields), while the response of the United States yields appeared to be more positive (i.e., increase of yields).</jats:p

A novel canine kidney cell line model for the evaluation of neoplastic development: karyotype evolution associated with spontaneous immortalization and tumorigenicity

The molecular mechanisms underlying spontaneous neoplastic transformation in cultured mammalian cells remain poorly understood, confounding recognition of parallels with the biology of naturally occurring cancer. The broad use of tumorigenic canine cell lines as research tools, coupled with the accumulation of cytogenomic data from naturally occurring canine cancers, makes the domestic dog an ideal system in which to investigate these relationships. We developed a canine kidney cell line, CKB1-3T7, which allows prospective examination of the onset of spontaneous immortalization and tumorigenicity. We documented the accumulation of cytogenomic aberrations in CKB1-3T7 over 24months in continuous culture. The majority of aberrations emerged in parallel with key phenotypic changes in cell morphology, growth kinetics, and tumor incidence and latency. Focal deletion of CDKN2A/B emerged first, preceding the onset and progression of tumorigenic potential, and progressed to a homozygous deletion across the cell population during extended culture. Interestingly, CKB1-3T7 demonstrated a tumorigenic phenotype in vivo prior to exhibiting loss of contact inhibition in vitro. We also performed the first genome-wide characterization of the canine tumorigenic cell line MDCK, which also exhibited CDKN2A/B deletion. MDCK and CKB1-3T7 cells shared several additional aberrations that we have reported previously as being highly recurrent in spontaneous canine cancers, many of which, as with CDKN2A/B deletion, are evolutionarily conserved in their human counterparts. The conservation of these molecular events across multiple species, in vitro and in vivo, despite their contrasting karyotypic architecture, is a powerful indicator of a common mechanism underlying emerging neoplastic activity. Through integrated cytogenomic and phenotypic characterization of serial passages of CKB1-3T7 from initiation to development of a tumorigenic phenotype, we present a robust and readily accessible model (to be made available through the American Type Culture Collection) of spontaneous neoplastic transformation that overcomes many of the limitations of earlier studies.Electronic supplementary materialThe online version of this article (doi:10.1007/s10577-015-9474-8) contains supplementary material, which is available to authorized users

A novel canine kidney cell line model for the evaluation of neoplastic development: karyotype evolution associated with spontaneous immortalization and tumorigenicity

The molecular mechanisms underlying spontaneous neoplastic transformation in cultured mammalian cells remain poorly understood, confounding recognition of parallels with the biology of naturally occurring cancer. The broad use of tumorigenic canine cell lines as research tools, coupled with the accumulation of cytogenomic data from naturally occurring canine cancers, makes the domestic dog an ideal system in which to investigate these relationships. We developed a canine kidney cell line, CKB1-3T7, which allows prospective examination of the onset of spontaneous immortalization and tumorigenicity. We documented the accumulation of cytogenomic aberrations in CKB1-3T7 over 24 months in continuous culture. The majority of aberrations emerged in parallel with key phenotypic changes in cell morphology, growth kinetics, and tumor incidence and latency. Focal deletion of CDKN2A/B emerged first, preceding the onset and progression of tumorigenic potential, and progressed to a homozygous deletion across the cell population during extended culture. Interestingly, CKB1-3T7 demonstrated a tumorigenic phenotype in vivo prior to exhibiting loss of contact inhibition in vitro. We also performed the first genome-wide characterization of the canine tumorigenic cell line MDCK, which also exhibited CDKN2A/B deletion. MDCK and CKB1-3T7 cells shared several additional aberrations that we have reported previously as being highly recurrent in spontaneous canine cancers, many of which, as with CDKN2A/B deletion, are evolutionarily conserved in their human counterparts. The conservation of these molecular events across multiple species, in vitro and in vivo, despite their contrasting karyotypic architecture, is a powerful indicator of a common mechanism underlying emerging neoplastic activity. Through integrated cytogenomic and phenotypic characterization of serial passages of CKB1-3T7 from initiation to development of a tumorigenic phenotype, we present a robust and readily accessible model (to be made available through the American Type Culture Collection) of spontaneous neoplastic transformation that overcomes many of the limitations of earlier studies. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10577-015-9474-8) contains supplementary material, which is available to authorized users

Non-Separation Radioassay for Cortisol Binding Capacity in Human Serum

Peer Reviewe

In Situ Study of the Oxygen-Induced Transformation of Pyrochlore Ce2Zr2O7+x to the k-Ce2Zr2O8-Phase

Temporary storage of oxygen in a solid catalyst is imperative for many important industrial oxidation reactions in the gas phase, for instance the post-treatment of automotive exhaust gas. A peculiar mixed Ce\u2013Zr (1:1) oxide, the ordered \u3ba-Ce2Zr2O8 phase, is a promising catalytic material exhibiting an extraordinarily high oxygen storage capacity (OSC) and high thermal and chemical stability. We elucidate the temperature-dependent transformation between the pyrochlore pyr-Ce2Zr2O7 and \u3ba-Ce2Zr2O8 phase upon oxygen uptake by in situ X-ray diffraction, X-ray absorption, and in situ Raman spectroscopy, providing insights into the electronic and structural changes on the atomic level, which are at the heart of the extraordinarily high OSC. We demonstrate that the Ce3+ concentration can be followed during transformation in situ by Raman spectroscopy of the electronic spin flip in the f-shell of Ce3+. The catalytic activity of the \u3ba-Ce2Zr2O8 phase was investigated without an additional active component such as noble metals (Pt, etc.). While the high OSC of the \u3ba-phase is beneficial for the oxidation of CO, the oxidation of HCl turns out to be unaffected by the high OSC

Identification of a high-affinity binding site involved in the transport of endocannabinoids

Phytocannabinoids, such as the principal bioactive component of marijuana, Δ(9)-tetrahydrocannabinol, have been used for thousands of years for medical and recreational purposes. Δ(9)-Tetrahydrocannabinol and endogenous cannabinoids (e.g., anandamide) initiate their agonist properties by stimulating the cannabinoid family of G protein-coupled receptors (CB(1) and CB(2)). The biosynthesis and physiology of anandamide is well understood, but its mechanism of uptake (resulting in signal termination by fatty acid amide hydrolase) has been elusive. Mounting evidence points to the existence of a specific anandamide transport protein; however, no direct evidence for this protein has been provided. Here, we use a potent, competitive small molecule inhibitor of anandamide uptake (LY2318912, IC(50) 7.27 ± 0.510 nM) to identify a high-affinity, saturable anandamide transporter binding site (LY2318912; K(d) = 7.62 ± 1.18 nM, B(max) = 31.6 ± 1.80 fmol/mg protein) that is distinct from fatty acid amide hydrolase. Systemic administration of the inhibitor into rodents elevates anandamide levels 5-fold in the brain and demonstrates efficacy in the formalin paw-licking model of persistent pain with no obvious adverse effects on motor function. Identification of the anandamide transporter binding site resolves a missing mechanistic link in endocannabinoid signaling, and in vivo results suggest that endocannabinoid transporter antagonists may provide a strategy for positive modulation of cannabinoid receptors