8 research outputs found
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Sportfishing creel census pilot study
The sportfishing creel census project was originated to obtain information relating to the use of the Corpus Christi Bay area for sportfishing, the amount of fish caught and other environmental information relating to the total productivity cycles of the bay system. The Census is to be conducted during the summer months of June, July and August 1974 and the pilot study was made during August 1973. The total catch will be used in a current project to assess carbon, nitrogen, phosporous input and output to the bay system.March 15, 1974To The Lower Nueces River Water Supply DistrictMarine Scienc
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Development of the methodology and analysis, Creel census of Corpus Christi Bay area, 1974 summer
A sportfishing creel census of Corpus Christi Bay area was conducted during the summer months of 1974. During the three months June, July, and August, 7,575 interviews of fishing parties with 22,313 persons were made. The data extrapolated to the total area and a full year indicate a catch from the bay of 2.87 million pounds of fish caught per year and a Gulf catch of 0.88 million pounds, Fishing yield per unit effort was greatest for the Gulf because of the summer runs of kingfish. The bay was divided into biotopes and related to fish catch. The poorest area was the fish pass. The most fish per hours fishing were caught in the bay oil platform or bulkhead biotopes, however, the size was small. Speckled trout and redfish were the major fish caught by weight in the Grassflats and shallow bay which is reflected in a large fishing effort. The open bay yielded higher numbers of fish per hour fishing (4.9 fish) than either the grassflat (3.0) or the shallow bay (2.0). If the fishing intensity was equal for the above biotopes the bay should have the best yield. The average boat fishing party lasted four hours. Boat fishing was generally better per party than shore fishing. The weight catch per person in boat fishing was approximately one pound per person per hour, and only 0.4 pounds per person per hour on the same basis for shore fishing. Fish yields in the Corpus area were related to Galveston Bay. The efficiency of various lures was discussed.April 22, 1976Marine Scienc
Loss-of-function HDAC8 mutations cause a phenotypic spectrum of Cornelia de Lange syndrome-like features, ocular hypertelorism, large fontanelle and X-linked inheritance
Cornelia de Lange syndrome (CdLS) is amultisystemgenetic disorder with distinct facies, growth failure, intellectual disability, distal limb anomalies, gastrointestinal and neurological disease. Mutations in NIPBL, encoding a cohesin regulatory protein, account for >80% of cases with typical facies. Mutations in the core cohesin complex proteins, encoded by the SMC1A, SMC3 and RAD21 genes, together account for ̃5% of subjects, often with atypical CdLS features. Recently, we identified mutations in the X-linked gene HDAC8 as the cause of a small number of CdLS cases. Here, we report a cohort of 38 individuals with an emerging spectrum of features caused by HDAC8 mutations. For several individuals, the diagnosis of CdLS was not considered prior to genomic testing. Most mutations identified are missense and de novo. Many cases are heterozygous females, each with marked skewing of X-inactivation in peripheral blood DNA.Wealso identified eight hemizygous males who are more severely affected. The craniofacial appearance caused by HDAC8 mutations overlaps that of typical CdLS but often displays delayed anterior fontanelle closure, ocular hypertelorism, hooding of the eyelids, a broader nose and dental anomalies, which may be useful discriminating features. HDAC8 encodes the lysine deacetylase for the cohesin subunit SMC3 and analysis of the functional consequences of the missense mutations indicates that all cause a loss of enzymatic function. These data demonstrate that loss-of-function mutations in HDAC8 cause a range of overlapping human developmental phenotypes, including a phenotypically distinct subgroup of CdLS. © The Author 2014. Published by Oxford University Press. All rights reserved.Published by Oxford University Press. All rights reserved
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Loss-of-function HDAC8 mutations cause a phenotypic spectrum of Cornelia de Lange syndrome-like features, ocular hypertelorism, large fontanelle and X-linked inheritance.
Cornelia de Lange syndrome (CdLS) is a multisystem genetic disorder with distinct facies, growth failure, intellectual disability, distal limb anomalies, gastrointestinal and neurological disease. Mutations in NIPBL, encoding a cohesin regulatory protein, account for >80% of cases with typical facies. Mutations in the core cohesin complex proteins, encoded by the SMC1A, SMC3 and RAD21 genes, together account for ∼5% of subjects, often with atypical CdLS features. Recently, we identified mutations in the X-linked gene HDAC8 as the cause of a small number of CdLS cases. Here, we report a cohort of 38 individuals with an emerging spectrum of features caused by HDAC8 mutations. For several individuals, the diagnosis of CdLS was not considered prior to genomic testing. Most mutations identified are missense and de novo. Many cases are heterozygous females, each with marked skewing of X-inactivation in peripheral blood DNA. We also identified eight hemizygous males who are more severely affected. The craniofacial appearance caused by HDAC8 mutations overlaps that of typical CdLS but often displays delayed anterior fontanelle closure, ocular hypertelorism, hooding of the eyelids, a broader nose and dental anomalies, which may be useful discriminating features. HDAC8 encodes the lysine deacetylase for the cohesin subunit SMC3 and analysis of the functional consequences of the missense mutations indicates that all cause a loss of enzymatic function. These data demonstrate that loss-of-function mutations in HDAC8 cause a range of overlapping human developmental phenotypes, including a phenotypically distinct subgroup of CdLS