The Mathematical Programming and the Rule Extraction from Layered Feed-forward Neural Networks

We propose a mathematical programming methodology for identifying and examining regression rules extracted from layered feed-forward neural networks. The area depicted in the rule premise covers a convex polyhedron in the input space, and the adopted approximation function for the output value is a multivariate polynomial function of x, the outside stimulus input. The mathematical programming analysis, instead of a data analysis, is proposed for identifying the convex polyhedron associated with each rule. Moreover, the mathematical programming analysis is proposed for examining the extracted rules to explore features. An implementation test on bond pricing rule extraction lends support to the proposed methodology

A Pseudomonas syringae pv. tomato DC3000 mutant lacking the type III effector HopQ1-1 is able to cause disease in the model plant Nicotiana benthamiana

The model pathogen Pseudomonas syringae pv. tomato DC3000 causes bacterial speck in tomato and Arabidopsis, but Nicotiana benthamiana, an important model plant, is considered to be a non-host. Strain DC3000 injects approximately 28 effector proteins into plant cells via the type III secretion system (T3SS). These proteins were individually delivered into N. benthamiana leaf cells via T3SS-proficient Pseudomonas fluorescens, and eight, including HopQ1-1, showed some capacity to cause cell death in this test. Four gene clusters encoding 13 effectors were deleted from DC3000: cluster II (hopH1, hopC1), IV (hopD1, hopQ1-1, hopR1), IX (hopAA1-2, hopV1, hopAO1, hopG1), and native plasmid pDC3000A (hopAM1-2, hopX1, hopO1-1, hopT1-1). DC3000 mutants deleted for cluster IV or just hopQ1-1 acquired the ability to grow to high levels and produce bacterial speck lesions in N. benthamiana. HopQ1-1 showed other hallmarks of an avirulence determinant in N. benthamiana: expression in the tobacco wildfire pathogen P. syringae pv. tabaci 11528 rendered this strain avirulent in N. benthamiana, and elicitation of the hypersensitive response in N. benthamiana by HopQ1-1 was dependent on SGT1. DC3000 polymutants involving other effector gene clusters in a hopQ1-1-deficient background revealed that clusters II and IX contributed to the severity of lesion symptoms in N. benthamiana, as well as in Arabidopsis and tomato. The results support the hypothesis that the host ranges of P. syringae pathovars are limited by the complex interactions of effector repertoires with plant antieffector surveillance systems, and they demonstrate that N. benthamiana can be a useful model host for DC3000

A Pseudomonas syringae pv. tomato DC3000 mutant lacking the type III effector HopQ1-1 is able to cause disease in the model plant Nicotiana benthamiana

The model pathogen Pseudomonas syringae pv. tomato DC3000 causes bacterial speck in tomato and Arabidopsis, but Nicotiana benthamiana, an important model plant, is considered to be a non-host. Strain DC3000 injects approximately 28 effector proteins into plant cells via the type III secretion system (T3SS). These proteins were individually delivered into N. benthamiana leaf cells via T3SS-proficient Pseudomonas fluorescens, and eight, including HopQ1-1, showed some capacity to cause cell death in this test. Four gene clusters encoding 13 effectors were deleted from DC3000: cluster II (hopH1, hopC1), IV (hopD1, hopQ1-1, hopR1), IX (hopAA1-2, hopV1, hopAO1, hopG1), and native plasmid pDC3000A (hopAM1-2, hopX1, hopO1-1, hopT1-1). DC3000 mutants deleted for cluster IV or just hopQ1-1 acquired the ability to grow to high levels and produce bacterial speck lesions in N. benthamiana. HopQ1-1 showed other hallmarks of an avirulence determinant in N. benthamiana: expression in the tobacco wildfire pathogen P. syringae pv. tabaci 11528 rendered this strain avirulent in N. benthamiana, and elicitation of the hypersensitive response in N. benthamiana by HopQ1-1 was dependent on SGT1. DC3000 polymutants involving other effector gene clusters in a hopQ1-1-deficient background revealed that clusters II and IX contributed to the severity of lesion symptoms in N. benthamiana, as well as in Arabidopsis and tomato. The results support the hypothesis that the host ranges of P. syringae pathovars are limited by the complex interactions of effector repertoires with plant antieffector surveillance systems, and they demonstrate that N. benthamiana can be a useful model host for DC3000

Conflicts of Interest in Sell-side Research and The Moderating Role of Institutional Investors

Because sell-side analysts are dependent on institutional investors for performance ratings and trading commissions, we argue that analysts are less likely to succumb to investment banking or brokerage pressure in stocks highly visible to institutional investors. Examining a comprehensive sample of analyst recommendations over the 1994-2000 period, we find that analysts’ recommendations relative to consensus are positively associated with investment banking relationships and brokerage pressure, but negatively associated with the presence of institutional investor owners. The presence of institutional investors is also associated with more accurate earnings forecasts and more timely re-ratings following severe share price falls

On the Association between IPO Underpricing and Reversal and Taiwan‘s Regulatory Reforms for Mandatory Forecasts

The unique institutions in Taiwan may add to our understanding of the effect of initial public offering (IPO) firm disclosures. Consistent with the notion of market mispricing, most of Taiwan's IPOs were with consecutive up-limit hits followed by substantial price reversals. In this study, we decompose IPO underpricing into two components: pure underpricing and subsequent reversal, exploring the impact of the 1991 mandate that IPO firms should include their management forecasts in the prospectuses on these two anomaly measures. Our results support the notion that disclosure regulations ameliorate investors' mispricing the stocks. First, pure underpricing and reversal are significantly less (more) pronounced for post‐mandate (pre‐mandate) IPO stocks. In contrast, consistent with the cheap talk hypothesis, the pre‐mandate voluntary forecasters (non‐forecasters) appear to be more (less) underpriced. Second, the duration of underpricing for the post‐mandate (pre‐mandate) IPOs appears to be shorter (longer). Nevertheless, underpricing lasted relatively longer (shorter) for the pre‐mandate IPOs with (with no) voluntary disclosures