Landing bulletins provide records of amounts and values of various living marine resources taken by California's commercial fisheries, and summarize catches made by the partyboat sportfishing industry. They also detail the small quantities of freshwater fish taken commercially in inland areas. These data provide the basic background for managing California's marine fishery resources. The published figures are of local, national, and international significance, and are used by fisheries scientists, legislators, educators, members of the fishing industry, and others interested in California fisheries.

This report for 1970 is the 30th in the series of landing bulletins. The first, published in 1929, contained the records of the 1926 and 1927 commercial fish landings.

California's fishery statistics are based on a system whereby fish dealers, processors, and partyboat operators send duplicate copies of their landing records to the Department. The statistical system and methods used to collect the records were fully described in Fish Bulletin 86, which reported the catch for 1950. In the intervening years, methods and equipment have been modified as conditions warranted, but the basic principles have remained unchanged.

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Guided by Uncertainty Management Theory (UMT) (Brashers, 2001), the objective of this dissertation was to develop and test a model of the effects of contradictory health information on uncertainty and information seeking, dubbed therein as The Contradictory Health Information Processing (CHIP) Model. Three empirical studies were conducted to accomplish this objective. In the first investigation, the model of the effects of uncertainty-arousing nutrition information was developed and tested. Generic measures that can be used across a range of health topics were also developed for each of the CHIP model’s concepts. These measures enabled the three experiments that comprise this dissertation. In Study 2, a revised CHIP model and several moderators of the causal relations identified in Study 1 were tested in the nutrition context. Finally, Study 3 tested the most recent version of the CHIP model, but in the context of a completely different kind of health topic, consumer health product safety. This third study also tested the moderating role of health self-efficacy and cognitive outcome expectations for the purpose of assessing the relationship between threat emotions and information-seeking intentions. Overall, the findings from these three studies support the CHIP model.

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Cis-regulatory element (cRE) mutations underlie hereditary cancers and may contribute significantly to sporadic cancer, but cancer genetics research to date has primarily focused on the protein coding exome. Non-coding mutations can contribute to tumorigenesis by altering transcription factor (TF) binding and the expression level of their target gene(s). Determining which cRE mutations are functional and act as drivers of a malignant phenotype in part depends on the cell type-specific chromatin state and the presence of relevant transcription factors. Only a fraction of cREs in the genome are active in a given cell type, and many show little conservation between species, making their identification difficult using comparative genomics alone. Recent advances in mapping histone modifications using ChIP-seq allows for the rapid identification of active cREs in any accessible tissue type. We generated these “chromatin state” maps from primary Glioblastoma (GBM) and adult normal brain tissues, and intersected publicly available GBM whole genome and transcriptome sequencing data to identify novel mutations in cREs. We identified the TERT promoter to be the most commonly mutated cRE in GBM patients. TERT gene expression is critical for the modulation of telomerase activity, the enzyme responsible for telomere maintenance, and TERT promoter mutations are among the most common genetic alterations observed across multiple cancer types. We identify the functional consequence of these mutations in GBM to be recruitment of the multimeric GABP transcription factor specifically to the mutant promoter. Allelic recruitment of GABP is consistently observed across four cancer types, highlighting a shared mechanism underlying TERT reactivation. This study provides an experimental and computational framework to identify driver cRE mutations that is widely applicable to most other tumor types.