Finite Horizon Portfolio Selection with Transaction Costs

Ph.DDOCTOR OF PHILOSOPH

Ethyl 2-benzyl-1-propyl-1H-indole-3-carboxyl­ate

In the title compound, C21H23NO2, the dihedral angle between the indole ring system and the benzyl ring is 75.92 (9)°. The crystal packing is controlled by C—H⋯O and C—H⋯π inter­actions

(Z)-Ethyl 2,4-diphenyl-3-(propyl­amino)­but-2-enoate

The title compound, C21H25NO2, adopts a Z conformation about the C=C double bond. The mol­ecular structure is stabilized by an intra­molecular N—H⋯O hydrogen bond and the dihedral angle between the aromatic ring planes is 76.04 (12)°. The atoms of the ethyl substituent are disordered over two sets of sites in a 0.60 (2):0.40 (2) ratio

Metoprolol, N-Acetylcysteine, and Escitalopram Prevents Chronic Unpredictable Mild Stress-Induced Depression by Inhibition of Endoplasmic Reticulum Stress

Background: Endoplasmic reticulum stress (ERS) has been recently suggested to be activated in the major depressive disorder (MDD). However, whether ERS is a potential therapeutic target for MDD is largely unknown. Here we attempted to assess the preventive effect of metoprolol (MET), N-acetylcysteine (NAC), and escitalopram (ESC) on chronic unpredictable mild stress (CUMS)-induced depression and investigate whether ERS mediates the antidepressant role of these drugs.Method: Forty-five sprague-dawley rats were randomly divided into five groups: control, CUMS, CUMS+ESC, CUMS+NAC, and CUMS+MET. Weight measurement, open field activity and sucrose preference were performed before and after stress. Hippocampal nerve cells and capillary ultrastructure were observed by transmission electron microscope, and hippocampal cells apoptosis were detected by flow cytometry. Furthermore, expression of ERS markers glucose-regulated protein 78 (GRP78), C/EBP-homologous protein (CHOP), and caspase-12 were measured by western blot and qRT-PCR.Results: The CUMS-induced rats showed significantly increased depressive-like behaviors including decreased open field activity and sucrose preference. Moreover, CUMS-exposed rats exhibited significantly increased hippocampal cell apoptosis, and showed damage in hippocampal nerve cells and capillary ultrastructure. Furthermore, ESC and NAC not only mitigated depressive-like behaviors, but also decreased apoptosis and pathologies, while MET fail to decrease apoptosis. Moreover, CUMS stimulation significantly elevated ERS by increasing the levels of GRP78, CHOP, and decreasing the level of caspase-12, while ESC, NAC, and MET significantly decreased the ERS.Conclusion: ESC, NAC, and MET might prevent the MDD partly through inactivating the ERS. These findings demonstrated ERS as a novel treatment target for depression

Regional Cerebral Blood Flow in Mania: Assessment Using 320-Slice Computed Tomography

Objectives: While evidence that episodes of mania in bipolar I are associated with changes in bioenergetic and regional cerebral blood flow (rCBF) and cerebral blood flow velocity (rCBFV), both the regions and the extent of these changes have not yet been defined. Therefore, we determined the pattern of regional cerebral perfusion mania patients and using patients with major depressive disorder (MDD) as positive controls and healthy participants as negative controls.Methods: Twenty participants with mania, together with 22 MDD patients and 24 healthy volunteers, were recruited for this study. On all participants, Transcranial Doppler (TCD) was conducted to measure rCBFV parameters, 320-slice CT was conducted to measure rCBF in the different cerebral artery regions, and hematological parameters were assessed. ANOVA and Pearson's tests were used for the statistical analysis.Results: Our data indicated that rCBF in the medial temporal lobe and hippocampus, especially in the left medial temporal lobe and the right hippocampus, was increased in the mania group compared with the control and MDD groups (p < 0.01). In contrast, rCBF in the medial temporal lobe and hippocampus was decreased in the depression group (p < 0.01) compared with healthy controls. In addition, values of rCBFV in the bilateral internal carotid arteries (ICAs) and middle cerebral arteries (MCA) were increased in mania (p < 0.01) in comparison to the MDD group. Whole blood viscosity and hematocrit as well as red blood cell sedimentation rate remained unchanged in all group (p > 0.05).Conclusions: In mania, rCBF is increased in the medial temporal lobe and hippocampus, with a corresponding increase in rCBFV in the same regions

Risperidone induces apoptosis of human osteoblast cell line hFob1.19 through Wnt/β-catenin signaling pathway

Objective To investigate the effect of risperidone on the apoptosis of human osteoblast cell line hFob1.19 and analyze potential molecular mechanism based on Wnt/β-catenin signaling pathway. Methods hFob1.19 cells were divided into control group and risperidone intervention group (0, 5, 20, 40, 60, 80, 100 and 120 μmol/L). Cell viability was detected by CCK-8 assay. The apoptosis rate was detected by flow cytometry. RT-qPCR and Western blot was used to detect the mRNA and protein expression of BCL-2, MCL-1, BAX, and β-catenin. Results 1)Compared with the control group, the cell viability of the risperidone group decreased in a dose- and time-dependent manner (P＜0.05), while the apoptosis rate increased in a dose-dependent manner(P＜0.05). 2)Compared with the control group, the expression of pro-apoptotic gene BAX in risperidone group increased, while the expression of anti-apoptotic genes BCL-2 and MCL-1 decreased, and the expression of β-catenin decreased (P＜0.01). 3)Compared with the control group, the levels of pro-apoptotic proteins BAX and cleaved caspase-3 were increased, the levels of anti-apoptotic proteins BCL-2 and MCL-1 were decreased, and the expression of β-catenin protein was decreased in risperidone group (P＜0.01). 4) Compared with the control group, the expression of β-catenin protein in the nucleus and cytoplasm of risperidone group decreased (P＜0.05). Conclusions Risperidone induces apoptosis of hFob1.19 cells, and the mechanism may be related to the inhibition of β-catenin expression and nuclear translocation of β-catenin by risperidone, which leads to the disruption of the balance between anti-apoptotic and pro-apoptotic proteins

A lattice algorithm for pricing moving average barrier options

This paper presents a lattice algorithm for pricing both European- and American-style moving average barrier options (MABOs). We develop a finite-dimensional partial differential equation (PDE) model for discretely monitored MABOs and solve it numerically by using a forward shooting grid method. The modeling PDE for continuously monitored MABOs has infinite dimensions and cannot be solved directly by any existing numerical method. We find their approximate values indirectly by using an extrapolation technique with the prices of discretely monitored MABOs. Numerical experiments show that our algorithm is very efficient.Barrier option Moving average Lattice algorithm Forward shooting grid method Extrapolation

Efficacy of hearing aid treatment on sound perception and residual hearing preservation in patients with tinnitus and coexisting hearing loss: study protocol for a randomized controlled trial

Abstract Background Chronic subjective tinnitus poses significant challenges in clinical practice, and it is usually associated with hearing impairment, particularly with high-frequency sensorineural hearing loss (SNHL). Patients suffering from tinnitus with SNHL experience one of the most severe sensory disabilities, and this has devastating effects on their quality of life. Nowadays, mild to moderate SNHL can be managed with a properly fitted hearing aid (HA) that provides sound amplification, and several studies suggest that HAs may also benefit those with tinnitus. However, inadequate attention has been paid by medical personnel to the impact of HA use in residual hearing protection for patients with tinnitus and coexisting SNHL, and existing evidence is still at a preliminary stage. This study aims to identify and evaluate the efficacy of the use of HAs in both sound perception and residual hearing preservation among patients with tinnitus and coexisting SNHL. Methods and design The present study is a prospective, single-center, outcome assessor and data analyst-blinded, randomized, controlled trial. Eligible participants will be recruited and randomly allocated into the HA intervention group and the waiting list control group at a ratio of 1:1. The primary outcome is to evaluate the severity of tinnitus using the Tinnitus Handicap Inventory as a continuous variable at 6 months from randomization. Secondary outcome measures include changes in hearing status and mental states. The trial will last 6 months, with follow-up visits at 3 months and 6 months. Discussion This will be the first randomized, controlled trial to identify and evaluate HAs’ efficacy on residual hearing preservation among tinnitus patients with coexisting high-frequency SNHL in China. We are aiming for novelty and generalizability, and strengths of this study are that it will examine the effectiveness of HA in patients with tinnitus and hearing impairment and will further explore the residual hearing protection provided by HA treatment in the tinnitus group. Trial registration ClinicalTrials.gov NCT05343026. Registered on April 25, 202

Sirt-1 Regulates Physiological Process and Exerts Protective Effects against Oxidative Stress

Background. Recent studies suggest a correlation between the reduced Sirt-1 expression with Alzheimer’s diseases (AD) and depression, respectively, suggesting a possible pathogenic role of the altered Sirt-1 expression in neuronal degenerative diseases, such as AD and depression. However, the molecular mechanisms underlying how Sirt-1 reduction impairs neuronal functions remain unknown. Methods. We used the SK-N-SH neuroblastoma cells to study the role of Sirt-1 expression on physiological roles in neuronal cells. Gain of Sirt-1 was achieved by transiently transfecting Sirt-1 expression plasmid. Sirt-1-specific shRNA was used to elucidate the role of Sirt-1 loss of function. CCK-8 (Cell Counting Kit-8) assay and flow cytometry were used to evaluate cell proliferation. Semiquantitative western blotting was used to detect relative protein levels. A further luciferase reporter gene assay was employed to examine the effect of Sirt-1 expression on the transcriptional activity of p53. RT-qPCR was used to determine the mRNA levels of p21, Bax, and Bcl-2, which were the downstream target genes of p53. Results. Sirt-1 suppressed the p53 downstream gene p21 transcription, while shRNA-mediated Sirt-1 knockdown resulted in a significant increase in p21 expression, implying a possibility that Sirt-1 promotes neuron proliferation through suppressing p53 transcriptional activity. The mRNA and protein levels of p53 were not affected by the altered Sirt-1 expression, suggesting that Sirt-1 regulates the transcriptional regulatory activity of p53 rather than p53 expression. Indeed, we further confirmed that Sirt-1 appeared to inhibit p53 transcriptional activity by attenuating its acetylation and resulted in a decrease of p53’s binding to the p21 promoter. Overexpressed Sirt-1 scavenged reactive oxygen species (ROS) production in SK-N-SH with H2O2. Knockdown of Sirt-1 presented opposite effect; the addition of EX527 (Sirt-1 inhibitor) increased ROS accumulation. Conclusions. Oxidative stress induces Sirt-1 in neuron cells, and Sirt-1 promotes proliferation in SK-N-SH cells, which protects them from oxidative stress-induced cell death, potentially via suppressing the transcriptional activity of p53. These results provide a molecular explanation underlying how the reduced Sirt-1 potentially causes the AD and depression-related diseases, supporting the idea that Sirt-1 can possibly be used as a diagnostic biomarker and/or therapeutic drug target for the AD and depression-related diseases