Decomposing and valuing callable convertible bonds: a new method based on exotic options

In the framework of Black-Scholes-Merton option pricing models, by employing exotic options instead of plain options or warrants, this paper presents an equivalent decomposition method for usual Callable Convertible Bonds (CCB). Furthermore, the analytic valuation formulae for CCB are worked out by using the analytic formulae for those simpler securities decomposed from CCB. Moreover, this method is validated by comparing with Monte Carlo simulation. Besides, the effects of call clauses, coupon clauses and soft call condition clauses are analyzed respectively. These give lots of new insights into the valuation and analysis of CCB and much help to hedge their risks.Callable convertible bonds; Equivalent decomposition; Up-and-out calls; American binary calls; Derivative pricing

Decomposing and valuing callable convertible bonds: a new method based on exotic options

In the framework of Black-Scholes-Merton option pricing models, by employing exotic options instead of plain options or warrants, this paper presents an equivalent decomposition method for usual Callable Convertible Bonds (CCB). Furthermore, the analytic valuation formulae for CCB are worked out by using the analytic formulae for those simpler securities decomposed from CCB. Moreover, this method is validated by comparing with Monte Carlo simulation. Besides, the effects of call clauses, coupon clauses and soft call condition clauses are analyzed respectively. These give lots of new insights into the valuation and analysis of CCB and much help to hedge their risks

Decomposing and valuing callable convertible bonds: a new method based on exotic options

In the framework of Black-Scholes-Merton option pricing models, by employing exotic options instead of plain options or warrants, this paper presents an equivalent decomposition method for usual Callable Convertible Bonds (CCB). Furthermore, the analytic valuation formulae for CCB are worked out by using the analytic formulae for those simpler securities decomposed from CCB. Moreover, this method is validated by comparing with Monte Carlo simulation. Besides, the effects of call clauses, coupon clauses and soft call condition clauses are analyzed respectively. These give lots of new insights into the valuation and analysis of CCB and much help to hedge their risks

Inhibition of Phosphodiesterase-4 Reverses Aβ-Induced Memory Impairment by Regulation of HPA Axis Related cAMP Signaling

Beta amyloid peptides (Aβ) are found to be associated with dysfunction of hypothalamic-pituitary-adrenal axis (HPA axis) that leads to memory and cognitive deficits in patients with Alzheimer’s disease (AD). Phosphodiesterase 4 (PDE4) inhibitors increase the intracellular cAMP activities, which may ameliorate cognitive deficits associated with AD. However, it remains unclear whether PDE4-mediated reversal of cognitive impairment in mouse model of AD is related to HPA axis and downstream cAMP-dependent pathway. The present study investigated the effects of PDE4 inhibitor rolipram on Aβ1-42-induced cognitive dysfunction and its underlying mechanisms. The step-down passive avoidance (PA) and Morris water-maze (MWM) tests were conducted 1 week (1 W), 2 months (2 M), and 6 months (6 M) after intracerebroventricular microjection (i.c.v.) of Aβ1-42. The results suggested that memory impairment emerged as early as 1 W, peaked at 2 M, and lasted until 6 M after injection. Chronic treatment with rolipram (0.1, 0.5, 1.0 mg/kg/d, i.p.) for 2 weeks (i.e., treatment started at 1.5 months after Aβ1-42 microinjection) dose-dependently improved memory performance in both MWM and PA tests. Moreover, rolipram reversed the Aβ-induced increases in serum corticosterone (CORT), corticotropin-releasing factor, and glucocorticoid receptors (CRF-R and GR) levels, whereas it decreases in brain-derived neurotropic factor (BDNF) and the ratio of pCREB to CREB expression. These effects of rolipram were prevented by pre-treatment with PKA inhibitor H89. The findings indicated that the protective effects of rolipram against Aβ1-42-induced memory deficits might involve HPA axis and cAMP-CREB-BDNF signaling

Pure curcumin decreases the expression of WT1 by upregulation of miR-15a and miR-16-1 in leukemic cells

<p>Abstract</p> <p>Background</p> <p>Pure curcumin has been reported to down-regulate the expression of WT1 in leukemic cells. However, the molecular mechanism underlying the down-regulation of WT1 by curcumin is not completely delineated. The purpose of this present study is to identify a new miRNA-mediated mechanism which plays an important role in the anti-proliferation effects of curcumin in leukemic cells.</p> <p>Methods</p> <p>K562 and HL-60 cells were treated with different concentrations of curcumin for 24 and 48 hours, the level of miR-15a/16-1 and WT1 were detected by qRT-PCR and Western blotting. WT1 expression and cell proliferation were detected by Western blotting and CCK-8, after curcumin treated-K562 and HL-60 cells were transfected with anti-miR-15a/16-1 oligonucleotides.</p> <p>Results</p> <p>We found that pure curcumin upregulated the expression of miR-15a/16-1 and downregulated the expression of WT1 in leukemic cells and primary acute myeloid leukemia (AML) cells. Overexpression of miR-15a/16-1 deduced the protein level of WT1 in leukemic cells, but downregulation of WT1 by siRNA-WT1 could not increase the expression of miR-15a/16-1 in leukemic cells. These results reveal that curcumin induced-upregulation of miR-15a/16-1 is an early event upstream to downregulation of WT1. Furthermore, anti-miR-15a/16-1 oligonucleotides (AMO) partly reversed the downregulation of WT1 induced by pure curcumin in leukemic cells and AMO promoted the growth of curcumin treated-K562 and HL-60 cells.</p> <p>Conclusion</p> <p>Thus, these data suggest for the first time that pure curcumin downregulated the expression of WT1 partly by upregulating the expression of miR-15a/16-1 in leukemic cells. miR-15a/16-1 mediated WT1 downregulation plays an important role in the anti-proliferation effect of curcumin in leukemic cells.</p

Zfp322a Regulates Mouse ES Cell Pluripotency and Enhances Reprogramming Efficiency

Embryonic stem (ES) cells derived from the inner cell mass (ICM) of blastocysts are characterised by their ability to self-renew and their potential to differentiate into many different cell types. Recent studies have shown that zinc finger proteins are crucial for maintaining pluripotent ES cells. Mouse zinc finger protein 322a (Zfp322a) is expressed in the ICM of early mouse embryos. However, little is known regarding the role of Zfp322a in the pluripotency maintenance of mouse ES cells. Here, we report that Zfp322a is required for mES cell identity since depletion of Zfp322a directs mES cells towards differentiation. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays revealed that Zfp322a binds to Pou5f1 and Nanog promoters and regulates their transcription. These data along with the results obtained from our ChIP-seq experiment showed that Zfp322a is an essential component of mES cell transcription regulatory network. Targets which are directly regulated by Zfp322a were identified by correlating the gene expression profile of Zfp322a RNAi-treated mES cells with the ChIP-seq results. These experiments revealed that Zfp322a inhibits mES cell differentiation by suppressing MAPK pathway. Additionally, Zfp322a is found to be a novel reprogramming factor that can replace Sox2 in the classical Yamanaka's factors (OSKM). It can be even used in combination with Yamanaka's factors and that addition leads to a higher reprogramming efficiency and to acceleration of the onset of the reprogramming process. Together, our results demonstrate that Zfp322a is a novel essential component of the transcription factor network which maintains the identity of mouse ES cells

Temporal Changes of Lung Cancer Mortality in Korea

The lung cancer mortality in Korea has increased remarkably during the last 20 yr, and, it has become the first leading cause of cancer-related deaths since 2000. The aim of the current study was to examine time trends of lung cancer mortality during the period 1984-2003 in Korea, assessing the effects of age, period, and birth cohort. Data on the annual number of deaths due to lung cancer and on population statistics from 1984 to 2003 were obtained from the Korea National Statistical Office. A log-linear Poisson age-period-cohort model was used to estimate the effects of age, period, and birth cohort. The both trends of male and female lung cancer mortality were both explained by age-period-cohort models. The risks of lung cancer mortalities for both genders were shown to decline in recent birth cohorts. The decreasing trends begin with the 1939 birth cohort for men and 1959 for women. The mortality pattern of lung cancer was dominantly explained by a birth cohort effect, possibly related with the change in smoking pattern, for both men and women. Finally, the mortality of lung cancer in Korea is expected to further increase in both men and women for a while

PL - 038 Habitual swimming exercise induced partial resistance to rat Alzheimer's disease

Objective &nbsp;In MSSE, we&nbsp;have divided male 2.5-month-old Sprague-Dawley rats into the following 4 groups: control (C), habitual&nbsp;swimming (SW), Alzheimer’s disease (AD) induction without swimming (AD), and habitual swimming and then AD induction (SA), and found the perfect resistance of habitual swimming to AD induction by using the P value statistics of the 5 behavior parameters of rats and the 23 physiological and biochemical parameters of their hippocampus. The topological difference&nbsp; of four groups were further calculated in this paper by using quantitative difference (QD) and self-similar approach. Methods 1. The logarithm to base golden section τ&nbsp;(lt) is called golden logarithm. It was found that σ=ltσ&nbsp;≈&nbsp;0.710439287156503. 2. For a process from x1&nbsp;to x2, lx(1,2)=lt(x2/x1) and its absolute vale are called the process logarithm and its QD, QDx(1,2). There are&nbsp;QD threshold values (αx,βx,γx) of function x which can be calculated in terms of&nbsp;σ. The function x&nbsp;is kept to be constant&nbsp;if QDx(1,2) &lt; αx.&nbsp;A function in/far from its function-specific homeostasis&nbsp;is called a normal/dysfunctional function. A normal function can resist a disturbance under its threshold so that&nbsp;QDx(1,2) &lt; βx. A dysfunctional function is defined as the QD is significant if βx&nbsp;≦QDx(1,2) &lt; γx and extraordinarily significant if QDx(1,2) ≧&nbsp;γx.&nbsp;3. Self-similarity was&nbsp;studied&nbsp;in&nbsp;the fractal literature: a pattern is self-similar if it does not vary with spatial or temporal scale. First-order self-similarity condition leads to the power law between two data&nbsp;sets A = {xi}&nbsp;and B = {yi};&nbsp;yi&nbsp;= ai&nbsp;xi&nbsp;if the QDi&nbsp;of ai and the average of {ai} is smaller than βmin=min{βi} and the average QD of {QDi}&nbsp;is smaller than αmin=min{αi}. 4. The σ&nbsp;algorithm for integrative biology was established based on high-order self-similarity. Those parameters that contribute to&nbsp;the topological difference&nbsp;were the biomarkers. Results The 28 dimension data set consisted of all the 28 parameters. The first-order self-similarity held true for the 28 dimension data sets between groups C and SW.&nbsp;The topological algorithm of other groups suggested three AD biomarkers, protein&nbsp;carbonyl, granules density of presynaptic synaptophysin in the hippocampal CA1 and malondialdehyde intensity. The first two biomarkers were completely reversed by exercise pretreatment, but the third biomarker was partially reversed. Conclusions &nbsp;Exercise pretraining exerts partial&nbsp;benefits on AD that support its use as a promising new therapeutic option for prevention of neurodegeneration in the elderly and/or AD population.&nbsp

Cordycepin Suppresses Expression of Diabetes Regulating Genes by Inhibition of Lipopolysaccharide-induced Inflammation in Macrophages

Background: It has been recently noticed that type 2 dia-betes (T2D), one of the most common metabolic diseases, causes a chronic low-grade inflammation and activation of the innate immune system that are closely involved in the pathogenesis of T2D. Cordyceps militaris, a traditional me-dicinal mushroom, produces a component compound, cordy-cepin (3’-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immuno-logical stimulating, anti-cancer, and anti-infection activities. The molecular mechanisms of cordycepin in T2D are not clear. In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells. Methods: We confirmed the levels of diabetes regulating genes mRNA and protein of cytokines through RT-PCR and western blot analysis and fol