Organized competitive sportfishing has been a growing use of fishery resources for at least the last 20 years. We conducted a survey of fishery agencies in Canada, the United States, District of Columbia, Puerto Rico, and U.S. Virgin Islands to estimate the numbers and types of competitive fishing events in inland and marine waters and to determine fishery agency perceptions of the benefits and problems associated with these events. Based on survey responses, there were 20,697 competitive fishing events annually. Adjusting for agencies that did not provide estimates and incomplete reporting, we estimated that there were at least 31,000 competitive fishing events annually. Most competitive fishing events were for black bass in inland waters and billfish in marine waters, but events targeted many species of fish. In inland waters, events for species other than black bass appear to be increasing. Prevalent problems of competitive fishing perceived by fishery management agencies were stimulation and concentration of fishing effort, conflicts among user groups, and impeded access. Prevalent benefits of competitive fishing were economical acquisition of catch and biological data, promotion of recreational fishing, and communication between agencies and anglers. Our survey indicated the need for accurate (rather than estimated) and current data about competitive fishing and further investigations of sociological aspects, economic values, and biological impacts of competitive fishing events.

Competitive fishing is a large and growing use of fishery resources that offers benefits and creates problems for fishery managers. Successful integration of competitive fishing with noncompetitive anglers and other aquatic resource users will require current and comprehensive data about competitive fishing events and additional information about sociological aspects, economic values, and biological effects of competitive fishing. In this paper we summarize available sociological, economic, and biological information about competitive fishing and suggest directions for future research. We suggest a permit system to obtain needed data about competitive fishing events and minimize social and biological problems associated with them. Competitive fishing provides communication channels between fishery managers and anglers. Integration of competitive fishing with other aquatic resource uses will require effective communication programs.

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Irofulven (6-hydroxymethylacylfulvene, HMAF, MGI 114) is one of a new class of anticancer agents that are semisynthetic derivatives of the mushroom toxin illudin S. Preclinical studies and clinical trials have demonstrated that irofulven is effective against several tumor types. Mechanisms of action studies indicate that irofulven induces DNA damage, MAPK activation, and apoptosis. In this study we found that in ovarian cancer cells, CHK2 kinase is activated by irofulven while CHK1 kinase is not activated even when treated at higher concentrations of the drug. By using GM00847 human fibroblast expressing tetracycline-controlled, FLAG-tagged kinase-dead ATR (ATR.kd), it was demonstrated that ATR kinase does not play a major role in irofulveninduced CHK2 activation. Results from human fibroblasts proficient or deficient in ATM function (GM00637 and GM05849) indicated that CHK2 activation by irofulven is mediated by the upstream ATM kinase. Phosphorylation of ATM on Ser 1981 , which is critical for kinase activation, was observed in ovarian cancer cell lines treated with irofulven. RNA interference results confirmed that CHK2 activation was inhibited after introducing siRNA for ATM. Finally, experiments done with human colon cancer cell line HCT116 and its isogenic CHK2 knockout derivative; and experiments done by expressing kinase-dead CHK2 in an ovarian cancer cell line demonstrated that CHK2 activation contributes to irofulven-induced S phase arrest. In addition, it was shown that NBS1, SMC1, and p53 were phosphorylated in an ATM-dependent manner, and p53 phosphorylation on serine 20 is dependent on CHK2 after irofulven treatment. In summary, we found that the anticancer agent, irofulven, activates the ATM-CHK2 DNA damage-signaling pathway, and CHK2 activation contributes to S phase cell cycle arrest induced by irofulven.Irofulven 1 (6-hydroxymethylacylfulvene, HMAF, MGI 114) is one of a new class of anticancer agents that are analogs of mushroom-derived illudin toxins. Preclinical studies and clinical trials have demonstrated that irofulven is effective against several tumor types (1-17). Studies of mechanisms of irofulven action suggest that it induces DNA damage, MAP kinase activation and apoptosis (18 -20). It is also suggested that irofulven-elicited DNA lesions are mainly repaired by transcriptioncoupled nucleotide excision repair (TC-NER) (21).In response to DNA damage, the cell evokes signal transduction pathways to arrest at G 1 /S, S, or G 2 /M checkpoints, allowing time to deal with the insult (22, 23). It has been well documented that DNA damage activates ATM (ataxia telangiectasia-mutated), and/or ATR (ATM-RAD3-related) kinases, two apical protein kinases of the DNA damage response pathways. ATM and ATR phosphorylate downstream effector kinases, CHK1 and CHK2. It is generally believed that ATM is the kinase mainly responding to ionizing radiation (IR)-induced DNA double strand breaks, while ATR responds to the formation of DNA adducts and stalled replication induced by UV, genotoxic drugs, and radia...

Combination of chemotherapeutic agents and angiogenesis inhibitors is now commonly employed in the clinic to treat cancer. Here, we used angiostatic agents anginex and 0118, in combination with the chemotherapeutic irofulven, to treat human ovarian tumor xenografts in mice. General linear mixed models were used to statistically analyze tumor growth curves. Overall, combination of a low, non-toxic dose of irofulven with either angiogenesis inhibitor was more effective at inhibiting tumor growth than any of the single-agent therapies. For example, the anginex/irofulven and 0118/irofulven combinations inhibited tumor growth relative to controls by 92% (p<0.0001) and 96% (p<0.0001), respectively, with the 0118/irofulven combinations yielding 100% complete responses. This study suggests that combination therapy of 0118 or anginex and irofulven may be highly effective in the clinical setting.