CONSUMER CREDIT DELINQUENCY AND BANKRUPTCY FORECASTING USING ADVANCED ECONOMETRC MODELING

This research paper empirically shows that unemployment is significant in determining both consumer bankruptcy filings and delinquency even after controlling for household demographics. Furthermore, I show that unemployment and the debt/wealth ratio also affect the choice of whether to file for bankruptcy under chapter 7 or chapter 13, after controlling for demographics. The paper then points out some of the implications the empirical results have for policy-makers and banking regulators.consumer credit risk; delinquency; bankruptcy; advanced empirical econometrics; financial economics; consumer finance

CONSUMER CREDIT DELINQUENCY AND BANKRUPTCY FORECASTING USING ADVANCED ECONOMETRC MODELING

This research paper empirically shows that unemployment is significant in determining both consumer bankruptcy filings and delinquency even after controlling for household demographics. Furthermore, I show that unemployment and the debt/wealth ratio also affect the choice of whether to file for bankruptcy under chapter 7 or chapter 13, after controlling for demographics. The paper then points out some of the implications the empirical results have for policy-makers and banking regulators

Essays on consumer portfolio choice and credit risk

Three essays comprise this dissertation. The first essay uses panel data to show that labor income risk alone cannot explain limited stock market participation. However, transaction costs and household demographics, considered jointly, can determine both the discrete choice of whether to hold stock and the amount held, conditional on whether the household is already investing in the stock market. Transaction costs are proxied by state-level number of brokers per capita. The second essay builds on the first essay. I measure two different covariance terms. One is between self-evaluated house value and uninsurable labor income risk. The other is between housing investment return and stock return. The results show that homeownership has a diversification effect on stock holdings. This effect occurs because adding a house to the household portfolio can significantly decrease the overall risk of the portfolio. The last essay empirically shows that unemployment is significant in determining both consumer bankruptcy filings and delinquency even after controlling for household demographics. Furthermore, I show that unemployment and the debt/wealth ratio also affect the choice of whether to file for bankruptcy under chapter 7 or chapter 13, after controlling for demographics. The paper then points out some of the implications the empirical results have for policy-makers and banking regulators

Ultra-narrowband interference circuits enable low-noise and high-rate photon counting for InGaAs/InP avalanche photodiodes

Afterpulsing noise in InGaAs/InP single photon avalanche photodiodes (APDs) is caused by carrier trapping and can be suppressed successfully through limiting the avalanche charge via sub-nanosecond gating. Detection of faint avalanches requires an electronic circuit that is able to effectively remove the gate-induced capacitive response while keeping photon signals intact. Here we demonstrate a novel ultra-narrowband interference circuit (UNIC) that can reject the capacitive response by up to 80 dB per stage with little distortion to avalanche signals. Cascading two UNIC's in a readout circuit, we were able to enable high count rate of up to 700 MC/s and low afterpulsing of 0.5 % at a detection efficiency of 25.3 % for 1.25 GHz sinusoidally gated InGaAs/InP APDs. At -30 degree C, we measured 1 % afterpulsing at a detection efficiency of 21.2 %

Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells

Wnt1-inducible signaling pathway protein-1 is a cysteine-rich protein that belongs to the CCN family, which has been implicated in mediating the occurrence and progression through distinct molecular mechanisms in several tumor types. However, the association of Wnt1-inducible signaling pathway protein-1 with gastric cancer and the related molecular mechanisms remain to be elucidated. Therefore, this study aimed to clarify the biological role of Wnt1-inducible signaling pathway protein-1 in the proliferation, migration, and invasion in gastric cancer cells and further investigated the associated molecular mechanism on these biological functions. We first detected the expression level of Wnt1-inducible signaling pathway protein-1 in gastric cancer, and the reverse transcription polymerase chain reaction have shown that Wnt1-inducible signaling pathway protein-1 expression levels were upregulated in gastric cancer tissues. The expression of Wnt1-inducible signaling pathway protein-1 in gastric cancer cell lines was also detected by quantitative real-time polymerase chain reaction and Western blotting. Furthermore, two gastric cancer cell lines with high expression of Wnt1-inducible signaling pathway protein-1 were selected to explore the biological function of Wnt1-inducible signaling pathway protein-1 in gastric cancer. Function assays indicated that knockdown of Wnt1-inducible signaling pathway protein-1 suppressed cell proliferation, migration, and invasion in BGC-823 and AGS gastric cancer cells. Further investigation of mechanisms suggested that cyclinD1 was identified as one of Wnt1-inducible signaling pathway protein-1 related genes to accelerate proliferation in gastric cancer cells. In addition, one pathway of Wnt1-inducible signaling pathway protein-1 induced migration and invasion was mainly through the enhancement of epithelial-to-mesenchymal transition progression. Taken together, our findings presented the first evidence that Wnt1-inducible signaling pathway protein-1 was upregulated in gastric cancer and acted as an oncogene by promoting proliferation, migration, and invasion in gastric cancer cells

Pharmacokinetic comparisons of S-oxiracetam and R-oxiracetam in beagle dogs

A pharmacokinetic comparison and conformational stability study of S-oxiracetam (S-ORT) and R-oxiracetam (R-ORT) in beagle dogs was used to investigate the possible mechanism of different effects of two oxiracetam enantiomers through a random crossover design. After drug administration to beagle dogs, blood samples were collected at different time points for pharmacokinetic analysis using the UPLC-ESI-MS/MS method. Parts of plasma samples were used for conformation transformation studies using a normal phase high performance liquid chromatographic (NP HPLC) method. The study showed that oxiracetam enantiomers maintained their original conformation when administered orally to beagle dogs. Concentrations of S-ORT were significantly higher than R-ORT 1.5 and 2 h after administration; the AUC0-∞ of S-ORT after oral administration tended to be higher than that of R-ORT, which showed that the different effects between S-ORT and R-ORT may be partly associated with their distinctive absorption at least

BCS-BEC crossover in a quasi-two-dimensional Fermi superfluid

We study the crossover from the Bardeen-Cooper-Shrieffer (BCS) regime to the Bose-Einstein-condensation (BEC) regime in a quasi-two-dimensional quantum gas of ultracold fermionic atoms. Using an effective two-dimensional Hamiltonian with renormalized interactions between atoms and dressed molecules within a Gaussian pair fluctuation theory, we investigate how Fermi superfluidity is affected by reduced dimensionality at zero temperature in a wide range of crossover. We observe that the order parameter and pair size show universal relations with the chemical potential on the BCS side, irrespective of dimensionality. However, such universal dependences break down towards the BEC limit with increasing interaction strength. This results reveal the notable effect of reduced dimenionality on pairing physics, which can also be observed in the sound velocity and convexity parameter of the Goldstone mode. We compare our results with the latest experiments in both ${}^{6}$Li atomic gases and layered nitrides LixZrNCl and find good agreements.Comment: 11 pages, 7 fugure

TNFα induces Ca2+ influx to accelerate extrinsic apoptosis in hepatocellular carcinoma cells

BACKGROUND: Tumor necrosis factor-α has been proven an effective anticancer agent in preclinical studies. However, the translation of TNFα from research to clinic has been blocked by significant systemic toxicity and limited efficacy at maximal tolerated dose, which need urgently to be solved. METHODS: The level of cytosolic Ca RESULTS: Here, we demonstrated that TNFα induced extracellular Ca CONCLUSIONS: Our study provides the evidence supporting a novel mechanism by which TNFα induces extracellular C

Shikonin suppresses the proliferation and colony formation of gastric cancer cells by regulating miR96/SOCS4 pathway

Purpose: To investigate whether shikonin is able to inhibit cell proliferation and colony formation in gastric cancer (GC) cells and to elucidate the molecular mechanism. Methods: Gastric cancer (GC) cell line SGC-7901 was used. The effects of shikonin on SGC-7901 cells were evaluated using Cell Counting Kit-8 (CCK-8) and soft-agar colony formation assays, respectively. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was employed to measure miR-96 expression levels. The regulatory effect of miR-96 on SOCS4 was determined by luciferase activity assay, while the effect of shikonin and miR-96 overexpression on proliferating cell nuclear antigen (PCNA), cyclin D1, suppressor of cytokine signaling 4 (SOCS4), and JAK/STAT pathwayrelated protein expression levels were analyzed by western blots. Results: The results show that shikonin dose-dependently suppressed the proliferation and colony formation of SGC-7901 cells. Western blot analysis revealed that PCNA and cyclin D1 were downregulated by shikonin treatment. Luciferase activity assay demonstrated that miR-96 is directly bound to SOCS4. Further results showed that miR-96 mimics reversed the effects of shikonin on SOCS4 and JAK/STAT pathway-related protein expression levels. Conclusion: Shikonin suppresses proliferation and colony formation by regulating miR-96/SOCS4 pathway in SGC-7901 cells, providing a potential therapeutic target for GC