A Study of investor behavior in purchasing financial assets

This study investigated whether the process of purchasing financial assets follows a rational decision-making process using Engel-Blackwell-Miniard (EBM) model. The method of investigation was a questionnaire survey of Malaysian individual investors. The sample consisted of 223 responses collected through convenience sampling and online survey. The data was analyzed using factor analysis, reliability analysis, path analysis, and multivariate analysis of variance. The results show that investors' decision-making process of purchasing financial assets is in line with a rational decision-making process in EBM Model. However, the tendency for irrational investment behaviors also exists at the same time. The findings imply that irrational investment behaviors may still occur even though the decision-making process is rational. We also found significant differences in the tendencies for herding, disposition effect and over-confidence based on gender and age

Mechanisms of polyglutamine expanded huntingtin induced toxicity

Huntington's Disease (HD) belongs to the CAG repeat family of neurodegenerative diseases and is characterized by the presence of an expanded polyglutamine (polyQ) repeat in the huntingtin (htt) gene product. PolyQ-expanded htt accumulates within large aggregates in various subcellular compartments, but are more often localized within the nucleus. The sequestration of proteins essential to cell viability may be one mechanism that accounts for toxicity generated by polyQ-expanded proteins. Nuclear inclusions containing polyQ-expanded htt recruit the transcriptional cofactor, CREB-binding protein (CBP). PolyQ toxicity appears to involve alterations of gene transcription and reduced neuronal cell viability. In the HT22 hippocampal cell line, we found that toxicity within individual cells induced by polyQ-expanded htt was associated with the localization of the mutant htt within either nuclear or perinuclear aggregates. However, in addition to CBP recruitment, we found that CBP ubiquitylation and degradation can be selectively enhanced by polyQ-expanded htt. Thus, selected substrates may be directed to the ubiquitin/proteasome-dependent protein degradation pathway (UPP) in response to polyQ-expanded htt within the nucleus. While both the polyQ domain and the histone acetyltransferase domain (HAT) of CBP have been found to interact with polyQ-expanded htt, deletion of either domain does not affect its enhanced degradation in the presence of polyQ-expanded htt in HT22 cells. Thus, enhanced degradation of CBP in cells expressing polyQ-expanded htt may not involve a direct interaction between CBP and htt. It seems likely specific enzymes in the UPP may be activated by htt and selectively target proteins such as CBP for degradation. Since molecular chaperones are found in the aggregates containing polyQ-expanded proteins, misfolding of polyQ-expanded proteins may play a key role in polyglutamine disease pathogenesis. In a number of some studies, HDJ-2, a member of DnaJ family molecular chaperones, was found to reduce aggregation and toxicity induced by polyQ-expanded proteins. In contrast, we show that HDJ-2 is unable to rescue aggregate formation of polyQ-expanded htt in transfected HEK293 fibroblast cells, nor is it recruited into these aggregates in vivo in a HD transgenic mouse model. Thus, molecular chaperone effects on polyQ-expanded protein induced toxicity could be cell-type specific or influenced by the developmental state of the culturable cells. These factors must be considered in any attempts to use chaperones as potential therapeutic targets in polyglutamine diseases

Accessibility and the evaluation of investments on the Beijing subway

This study measures the job and population accessibility via transit for Beijing using the cumulative opportunity metric. It is shown that transit accessibility varies widely across Beijing, but is highly focused on subway stations. Early lines added far more accessibility than more recently planned lines.Jiang, Haibing; Levinson, David. (2017). Accessibility and the evaluation of investments on the Beijing subway. Retrieved from the University Digital Conservancy, 10.5198/jtlu.2016.884

White Matter Abnormalities in Major Depression: A Tract-Based Spatial Statistics and Rumination Study

Increasing evidence indicates that major depressive disorder (MDD) is usually accompanied by altered white matter in the prefrontal cortex, the parietal lobe and the limbic system. As a behavioral abnormity of MDD, rumination has been believed to be a substantial indicator of the mental state of the depressive state. So far, however, no report that we are aware of has evaluated the relationship between white matter alterations and the ruminative state. In this study, we first explored the altered white matter using a tract-based spatial statistics (TBSS) method based on diffusion tensor imaging of 19 healthy and 16 depressive subjects. We then investigated correlations between the altered white matter microstructure in the identified altered regions and the severity of ruminations measured by the ruminative response scale. Our results demonstrated altered white matter microstructure in circuits connecting the prefrontal lobe, the parietal lobe and the limbic system (p<0.005, uncorrected), findings which support previous research. More importantly, the result also indicated that a greater alteration in the white matter is associated with a more ruminative state (p<0.05, Bonferroni corrected). The detected abnormalities in the white matter should be interpreted cautiously because of the small sample size in this study. This finding supports the psychometric significance of white matter deficits in MDD

Kansas City Cardiomyopathy Questionnaire Utility in Prediction of 30-Day Readmission Rate in Patients with Chronic Heart Failure

Background. Heart failure (HF) is one of the most common diagnoses associated with hospital readmission. We designed this prospective study to evaluate whether Kansas City Cardiomyopathy Questionnaire (KCCQ) score is associated with 30-day readmission in patients hospitalized with decompensated HF. Methods and Results. We enrolled 240 patients who met the study criteria. Forty-eight (20%) patients were readmitted for decompensated HF within thirty days of hospital discharge, and 192 (80%) patients were not readmitted. Compared to readmitted patients, nonreadmitted patients had a higher average KCCQ score (40.8 versus 32.6, P = 0.019) before discharge. Multivariate analyses showed that a high KCCQ score was associated with low HF readmission rate (adjusted OR = 0.566, P = 0.022). The c-statistic for the base model (age + gender) was 0.617. The combination of home medication and lab tests on the base model resulted in an integrated discrimination improvement (IDI) increase of 3.9%. On that basis, the KCQQ further increased IDI of 2.7%. Conclusions. The KCCQ score determined before hospital discharge was significantly associated with 30-day readmission rate in patients with HF, which may provide a clinically useful measure and could significantly improve readmission prediction reliability when combined with other clinical components

Integrative analysis of chloroplast genome, chemicals, and illustrations in Bencao literature provides insights into the medicinal value of Peucedanum huangshanense

The genus Peucedanum L. (Apiaceae) is a large group comprising more than 120 species distributed worldwide. Many plants of the genus Peucedanum have been studied and used in traditional Chinese medicine. In 2020, a new species, Peucedanum huangshanense Lu Q. Huang, H. S. Peng &amp; S. S. Chu, was found in the Huangshan Mountains of Anhui Province, China. However, little is known about its medicinal properties. Thus, the objective of this study is to explore the potential medicinal value of P. huangshanense and its relationship with other Peucedanum species. Through textual research on illustrations of Qianhu in Bencao literature, it can be inferred that at least five species of genus Peucedanum have been used in Chinese medicine. Therefore, we chose these five species of Peucedanum and P. huangshanense together for subsequent research. We conducted morphological, chloroplast genome, and chemical analyses of six Peucedanum species, including the newly discovered P. huangshanense. The chloroplast genomes of Peucedanum showed a typical tetrad structure, and the gene structure and content were similar and conservative. There were significant differences in genome size and the expansion of the inverted repeat boundary. Through nucleotide polymorphism analysis, we screened 14 hotspot mutation regions that have the potential to be used as specific molecular markers for the taxonomy of Peucedanum. Our results showed an inversion of the trnD-trnY-trnE gene in the P. huangshanense chloroplast genome, which can be developed as a specific molecular marker for species identification. Phylogenetic analysis showed that the phylogenetic trees had high support and resolution, which strongly supports the view that Peucedanum is not a monophyletic group. P. huangshanense had the closest genetic relationship to P. ampliatum K. T. Fu, followed by P. harry-smithii Fedde ex Wolff. Furthermore, the main coumarins of P. huangshanense were most similar to those of P. japonicum Thunb. and P. harry-smithii. In summary, our research lays a foundation for the systematic classification of Peucedanum and sheds light on the medicinal value of P. huangshanense

Phosphorylation of p66Shc and forkhead proteins mediates Aβ toxicity

Excessive accumulation of amyloid β-peptide (Aβ) plays an early and critical role in synapse and neuronal loss in Alzheimer's Disease (AD). Increased oxidative stress is one of the mechanisms whereby Aβ induces neuronal death. Given the lessened susceptibility to oxidative stress exhibited by mice lacking p66Shc, we investigated the role of p66Shc in Aβ toxicity. Treatment of cells and primary neuronal cultures with Aβ caused apoptotic death and induced p66Shc phosphorylation at Ser36. Ectopic expression of a dominant-negative SEK1 mutant or chemical JNK inhibition reduced Aβ-induced JNK activation and p66Shc phosphorylation (Ser36), suggesting that JNK phosphorylates p66Shc. Aβ induced the phosphorylation and hence inactivation of forkhead transcription factors in a p66Shc-dependent manner. Ectopic expression of p66ShcS36A or antioxidant treatment protected cells against Aβ-induced death and reduced forkhead phosphorylation, suggesting that p66Shc phosphorylation critically influences the redox regulation of forkhead proteins and underlies Aβ toxicity. These findings underscore the potential usefulness of JNK, p66Shc, and forkhead proteins as therapeutic targets for AD