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Tagging systems allow users to interactively annotate a pool of shared resources using descriptive strings called tags. Tags are used to guide users to interesting resources and help them build communities that share their expertise and resources. As tagging systems are gaining in popularity, they become more susceptible to tag spam: misleading tags that are generated in order to increase the visibility of some resources or simply to confuse users. Our goal is to understand this problem better. In particular, we are interested in answers to questions such as: How many malicious users can a tagging system tolerate before results significantly degrade? What types of tagging systems are more vulnerable to malicious attacks? What would be the effort and the impact of employing a trusted moderator to find bad postings? Can a system automatically protect itself from spam, for instance, by exploiting user tag patterns? In a quest for answers to these questions, we introduce a framework for modeling tagging systems and user tagging behavior. We also describe a method for ranking documents matching a tag based on taggers' reliability. Using our framework, we study the behavior of existing approaches under malicious attacks and the impact of a moderator and our ranking method. [ABSTRACT FROM AUTHOR]

This article focuses on the emergence of Web spam with the move of spammers to undermine search engines by subverting search results to increase the visibility of their pages. The issue is that Web spam undermines the reputation of a trusted information source. Web spamming undermines the trustworthiness people have come to expect from search engines. Web spammers are counting on this trust and that more people will turn to search engines for their information needs. Those in the search engine community believe that Web spam will become increasingly prevalent and sophisticated. INSET: What Constitutes Web Spam?.

Methylnitrosourea (MNU) is a well-known pluripotent direct-acting carcinogen. Formation of MNU following incubation of various meats with additional nitrite under in vitro acidic conditions is possible. It is possible that many species, including humans, are exposed to carcinogenic MNU, generated in their alimentary tract. Previously, an animal model was developed by our research group to investigate the expression of three genes c-myc, Ha-ras and p53 as early molecular epidemiological biomarkers of carcinogenic exposure or carcinogenesis caused by DMBA (dimethylbenz[alpha]anthracene). The aim of this study was to investigate the early effect of MNU on the gene expression levels. MNU is a direct-acting carcinogen which spontaneously and rapidly degrades, so any effect on the gene expression is observed in 24 hours. Our results show the maximum effect in vivo on the gene expression at 12 hours after the MNU treatment; on the other hand, 24 hours after the treatment, the elevated gene expressions decreased in target organs (bone marrow, lung, lymph nodes). Our results correspond to "long-term" experiments of the carcinogenic effect of MNU in different target organs. Our findings suggest that MNU has an impact on the expression of c-myc, Ha-ras and p53 genes in 12 hours, especially in bone marrow. Overexpression of these genes occurs as an early biological effect of exposure to chemical carcinogens. According to our results, the high expression of these genes could indicate MNU exposure and these genes could take part in MNU-induced tumorigenesis.

For many years the molecular biology has been one of the most promising fields of science and its several methods have been used in practice. These new methods of molecular biology made impression on epidemiology and developed a new discipline, called molecular epidemiology. The molecular and predictive epidemiology play more and more important roles in the prevention of cancers. Early biomarkers could identify the high risk population to have the possibilities of primary preventive interventions. It uses both molecular biological methods and the elements of epidemiology. Its specificity is not high enough to establish the diagnosis but it can be used to follow the "minimal residual disease" and with markers of individual susceptibility, to assess the risk of tumors. As to the practice there are many problems because of the limited therapeutic possibilities, but the molecular and predictive epidemiology becomes an important part of medicine in the future.

According to recent publications 7,12-dimethylbenz[a]anthracene (DMBA) induces not only mammary cancer but also leukemia in Long-Evans (LE) rats. After treatment with DMBA, trisomy of the chromosome bearing N-ras and mutations in the codon 61 of different ras family genes are frequent. These alterations are already visible within 48 hours. Since there are very few data on ras genes' expression in the early stages of leukemogenesis, in our investigations LE rats were treated with DMBA and the expression of ras genes was measured within two days. DMBA was administered to outbred Long-Evans rats and the fluorescence intensity of the antibody recognizing the ras gene family was measured in femoral bone marrow cells 24 and 48 hours after the treatment. One of the bone marrow cell populations, separated by FSC and SSC, showed elevated ras gene expression at both 24 and 48 hours after the administration of the carcinogen. These results suggest that, besides the specific chromosomal aberrations and gene mutations, elevated ras gene expression could also be the marker of DMBA exposure.

The aim of the study was to monitor the early effect of cytostatics containing platinum on oncogenes in inbred CBA/Ca mice. In human head-neck tumors after treatment with the Cisplatin supplemented BVM (Bleomycin, Vincristine, Methotrexate) protocol, further surgeries are often necessary due to regional recurrence. Body weight equivalent amounts of human dose of Cisplatin were administered intraperitoneally to 6-8-week-old, inbred, female CBA/Ca mice. Twenty four 48 and 72 hours after the treatment RNA was isolated from the target organs and the quantitative expression of c-myc, Ha-ras and p53 genes was examined by dot-blotting in potential target tissues. Significant overexpression of Ha-ras and p53 genes was measured in the bone marrow. Regarding the expression of Ha-ras gene, a significant increase was also found in the lymph nodes after 48 hours. The p53 expression in the lungs was down-regulated compared to the control group. In the "short-term" in vivo test, 24-hour examination of gene expression and amplification is suitable for detecting the early effects of carcinogenetic exposure. Cisplatin-induced gene expression alterations call attention to its possible role in the development of regional recurrence in patients treated with cisplatin-containing regimens.

An understanding of the molecular changes occuring during exposure to a carcinogen enhances the possibility of cancer prevention. Molecular genetic-biological screening methods offer the potential for early diagnosis of high-risk groups, and identification of specific signals, as a major step in primary prevention. Recent investigations have suggested that oncogene or oncosuppressor gene expression investigation at the RNA level is a proper and early molecular epidemiological biomarker of carcinogen exposure and a tool for risk assessment. This is one way by which the high-risk groups could be recognized. At the protein level, the investigation of gene expression is very useful in molecular diagnosis and in molecular pathology.

Autooxidation of polyunsaturated fatty acids (PUFAs) of edible oils results in the formation of fatty acid hydroperoxides that can undergo further chemical transformations to yield a variety of re-arranged and chain-cleavage products. Since the oxidation products of PUFAs have been reported to have cytotoxic and mutagenic effects, the consumption of rancid oils and fats represents a possible health hazard for the population. Storage of corn oil at room temperature and in the refrigerator for a forty-eight month period resulted in two different qualities of oil samples, which were characterized by UV, titrimetric (peroxide value, acid value) and GC-MS methods. Earlier it was demonstrated that the increase of expression of certain oncogenes and tumor suppressor genes is a method of choice for the early detection of carcinogen exposure. Treatment of CBA/Calpha inbred mice with the two oil samples showed significantly increased expression of the Ha-ras gene in all the investigated organs (liver, lung, kidney, thymus and spleen) of the rancid corn oil-treated animals. Expression of the c-myc and the p53 genes was also increased after the rancid corn oil-treatment in all the organs but the thymus of the mice. The results suggest that rancid oils, rich in omega-6 unsaturated fatty acids, could be involved not only in tumor promotion but in initiation as well.