Combination of Multiple Bipartite Ranking for Web Content Quality Evaluation

Web content quality estimation is crucial to various web content processing applications. Our previous work applied Bagging + C4.5 to achive the best results on the ECML/PKDD Discovery Challenge 2010, which is the comibination of many point-wise rankinig models. In this paper, we combine multiple pair-wise bipartite ranking learner to solve the multi-partite ranking problems for the web quality estimation. In encoding stage, we present the ternary encoding and the binary coding extending each rank value to $L - 1$ (L is the number of the different ranking value). For the decoding, we discuss the combination of multiple ranking results from multiple bipartite ranking models with the predefined weighting and the adaptive weighting. The experiments on ECML/PKDD 2010 Discovery Challenge datasets show that \textit{binary coding} + \textit{predefined weighting} yields the highest performance in all four combinations and furthermore it is better than the best results reported in ECML/PKDD 2010 Discovery Challenge competition.Comment: 17 pages, 8 figures, 2 table

A Taxonomy of Hyperlink Hiding Techniques

Hidden links are designed solely for search engines rather than visitors. To get high search engine rankings, link hiding techniques are usually used for the profitability of black industries, such as illicit game servers, false medical services, illegal gambling, and less attractive high-profit industry, etc. This paper investigates hyperlink hiding techniques on the Web, and gives a detailed taxonomy. We believe the taxonomy can help develop appropriate countermeasures. Study on 5,583,451 Chinese sites' home pages indicate that link hidden techniques are very prevalent on the Web. We also tried to explore the attitude of Google towards link hiding spam by analyzing the PageRank values of relative links. The results show that more should be done to punish the hidden link spam.Comment: 12 pages, 2 figure

The effect of periodic segmentation cracks on the interfacial debonding: Study on interfacial stresses

Abstract Hard coatings on relatively soft substrate always face the danger of debonding along the interface. Interfacial stresses are considered to be the initial driving force for the interfacial debonding of the relatively strong bonded coatings. Interfacial stresses due to the mismatch of strain between the coating and substrate are simulated with FEM firstly. The distribution of the interfacial stresses is achieved, which confirms an excessive stresses concentration near the interface end. Subsequently, the redistribution of interfacial stresses is calculated for a coating with periodic segmentation cracks. Results indicate that the distribution of interfacial stresses is altered greatly with the periodic segmentation cracks. To reveal the effect of the spacing of the periodic segmentation cracks on the distribution of interfacial stresses, different crack density is modeled within the coating. It is found that that the peak values of the interfacial stresses decrease with the increase of crack density, i.e. with reduction of spacing of segmentation cracks

Upregulation of CCNB2 and Its Perspective Mechanisms in Cerebral Ischemic Stroke and All Subtypes of Lung Cancer: A Comprehensive Study

Cyclin B2 (CCNB2) belongs to type B cell cycle family protein, which is located on chromosome 15q22, and it binds to cyclin-dependent kinases (CDKs) to regulate their activities. In this study, 103 high-throughput datasets related to all subtypes of lung cancer (LC) and cerebral ischemic stroke (CIS) with the data of CCNB2 expression were collected. The analysis of standard mean deviation (SMD) and summary receiver operating characteristic (SROC) reflecting expression status demonstrated significant up-regulation of CCNB2 in LC and CIS (Lung adenocarcinoma: SMD = 1.40, 95%CI [0.98–1.83], SROC = 0.92, 95%CI [0.89–0.94]. Lung squamous cell carcinoma: SMD = 2.56, 95%CI [1.64–3.48]. SROC = 0.97, 95%CI [0.95–0.98]. Lung small cell carcinoma: SMD = 3.01, 95%CI [2.01–4.01]. SROC = 0.98, 95%CI [0.97–0.99]. CIS: SMD = 0.29, 95%CI [0.05–0.53], SROC = 0.68, 95%CI [0.63–0.71]). Simultaneously, protein-protein interaction (PPI) analysis indicated that CCNB2 is the hub molecule of crossed high-expressed genes in CIS and LC. Through Multiscale embedded gene co-expression network analysis (MEGENA), a gene module of CIS including 76 genes was obtained and function enrichment analysis of the CCNB2 module genes implied that CCNB2 may participate in the processes in the formation of CIS and tissue damage caused by CIS, such as “cell cycle,” “protein kinase activity,” and “glycosphingolipid biosynthesis.” Afterward, via single-cell RNA-seq analysis, CCNB2 was found up-regulated on GABAergic neurons in brain organoids as well as T cells expressing proliferative molecules in LUAD. Concurrently, the expression of CCNB2 distributed similarly to TOP2A as a module marker of cell proliferation in cell cluster. These findings can help in the field of the pathogenesis of LC-related CIS and neuron repair after CIS damage

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field