International Journal of Economics and Business Administration

The purpose of this study is to evaluate the impact of the country risk factors on the dispersion of the cost of bank borrowing within the euro area, during the period of the global financial and Eurozone debt crises. The main aim is to empirically evaluate the degree to which the cost of borrowing differentials of euro area countries can be explained by changing dispersion in country risk (measured by government bond spreads). The results using rolling estimations suggest that the impacts of bond yield spreads are not such a significant determinant of the observed dispersion of the cost of borrowing, a dispersion that has been worsen after the outbreak of the global financial crisis and the subsequent euro area debt crisis. Even in the cases where a significant association is found for some countries, it seems that it is weakening as we move further away from the beginning of the turbulent periods.peer-reviewe

An Investigation of Evaluation Metrics for Automated Medical Note Generation

Recent studies on automatic note generation have shown that doctors can save significant amounts of time when using automatic clinical note generation (Knoll et al., 2022). Summarization models have been used for this task to generate clinical notes as summaries of doctor-patient conversations (Krishna et al., 2021; Cai et al., 2022). However, assessing which model would best serve clinicians in their daily practice is still a challenging task due to the large set of possible correct summaries, and the potential limitations of automatic evaluation metrics. In this paper, we study evaluation methods and metrics for the automatic generation of clinical notes from medical conversations. In particular, we propose new task-specific metrics and we compare them to SOTA evaluation metrics in text summarization and generation, including: (i) knowledge-graph embedding-based metrics, (ii) customized model-based metrics, (iii) domain-adapted/fine-tuned metrics, and (iv) ensemble metrics. To study the correlation between the automatic metrics and manual judgments, we evaluate automatic notes/summaries by comparing the system and reference facts and computing the factual correctness, and the hallucination and omission rates for critical medical facts. This study relied on seven datasets manually annotated by domain experts. Our experiments show that automatic evaluation metrics can have substantially different behaviors on different types of clinical notes datasets. However, the results highlight one stable subset of metrics as the most correlated with human judgments with a relevant aggregation of different evaluation criteria.Comment: Accepted to ACL Findings 202

Investigating Multi-cancer Biomarkers and Their Cross-predictability in the Expression Profiles of Multiple Cancer Types

Microarray technology has been widely applied to the analysis of many malignancies, however, integrative analyses across multiple studies are rarely investigated. In this study we performed a meta-analysis on the expression profiles of four published studies analyzing organ donor, benign tissues adjacent to tumor and tumor tissues from liver, prostate, lung and bladder samples. We identified 99 distinct multi-cancer biomarkers in the comparison of all three tissues in liver and prostate and 44 in the comparison of normal versus tumor in liver, prostate and lung. The bladder samples appeared to have a different list of biomarkers from the other three cancer types. The identified multi-cancer biomarkers achieved high accuracy similar to using whole genome in the within-cancer-type prediction. They also performed superior than the one using whole genome in inter-cancer-type prediction. To test the validity of the multi-cancer biomarkers, 23 independent prostate cancer samples were evaluated and 96% accuracy was achieved in inter-study prediction from the original prostate, liver and lung cancer data sets respectively. The result suggests that the compact lists of multi-cancer biomarkers are important in cancer development and represent the common signatures of malignancies of multiple cancer types. Pathway analysis revealed important tumorogenesis functional categories

Protection against Fas-induced fulminant hepatic failure in liver specific integrin linked kinase knockout mice

Background\ud \ud Programmed cell death or apoptosis is an essential process for tissue homeostasis. Hepatocyte apoptosis is a common mechanism to many forms of liver disease. This study was undertaken to test the role of ILK in hepatocyte survival and response to injury using a Jo-2-induced apoptosis model.\ud Methods\ud \ud For survival experiments, ILK KO and WT mice received a single intraperitoneal injection of the agonistic anti-Fas monoclonal antibody Jo-2 at the lethal dose (0.4 μg/g body weight) or sublethal dose (0.16 μg/g body weight). For further mechanistic studies sublethal dose of Fas monoclonal antibody was chosen.\ud \ud Results\ud \ud There was 100% mortality in the WT mice as compared to 50% in the KO mice. We also found that hepatocyte specific ILK KO mice (integrin linked kinase) died much later than WT mice after challenge with a lethal dose of Fas agonist Jo-2. At sublethal dose of Jo-2, there was 20% mortality in KO mice with minimal apoptosis whereas WT mice developed extensive apoptosis and liver injury leading to 70% mortality due to liver failure at 12 h. Proteins known to be associated with cell survival/death were differentially expressed in the 2 groups. In ILK KO mice there was downregulation of proapoptotic genes and upregulation of antiapoptotic genes.\ud \ud Conclusions\ud \ud Mechanistic insights revealed that pro-survival pathways such as Akt, ERK1/2, and NFkB signaling were upregulated in the ILK KO mice. Inhibition of only NFkB and ERK1/2 signaling led to an increase in the susceptibility of ILK KO hepatocytes to Jo-2-induced apoptosis. These studies suggest that ILK elimination from hepatocytes protects against Jo-2 induced apoptosis by upregulating survival pathways. FAK decrease may also play a role in this process. The results presented show that the signaling effects of ILK related to these functions are mediated in part mediated through NFkB and ERK1/2 signaling

Role of PINCH and Its Partner Tumor Suppressor Rsu-1 in Regulating Liver Size and Tumorigenesis

Particularly interesting new cysteine-histidine-rich protein (PINCH) protein is part of the ternary complex known as the IPP (integrin linked kinase (ILK)-PINCH-Parvin-α) complex. PINCH itself binds to ILK and to another protein known as Rsu-1 (Ras suppressor 1). We generated PINCH 1 and PINCH 2 Double knockout mice (referred as PINCH DKO mice). PINCH2 elimination was systemic whereas PINCH1 elimination was targeted to hepatocytes. The genetically modified mice were born normal. The mice were sacrificed at different ages after birth. Soon after birth, they developed abnormal hepatic histology characterized by disorderly hepatic plates, increased proliferation of hepatocytes and biliary cells and increased deposition of extracellular matrix. After a sustained and prolonged proliferation of all epithelial components, proliferation subsided and final liver weight by the end of 30 weeks in livers with PINCH DKO deficient hepatocytes was 40% larger than the control mice. The livers of the PINCH DKO mice were also very stiff due to increased ECM deposition throughout the liver, with no observed nodularity. Mice developed liver cancer by one year. These mice regenerated normally when subjected to 70% partial hepatectomy and did not show any termination defect. Ras suppressor 1 (Rsu-1) protein, the binding partner of PINCH is frequently deleted in human liver cancers. Rsu-1 expression is dramatically decreased in PINCH DKO mouse livers. Increased expression of Rsu-1 suppressed cell proliferation and migration in HCC cell lines. These changes were brought about not by affecting activation of Ras (as its name suggests) but by suppression of Ras downstream signaling via RhoGTPase proteins. In conclusion, our studies suggest that removal of PINCH results in enlargement of liver and tumorigenesis. Decreased levels of Rsu-1, a partner for PINCH and a protein often deleted in human liver cancer, may play an important role in the development of the observed phenotype. © 2013 Donthamsetty et al