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Cardiovascular and respiratory responses of the ghost shrimp, Callianassa californiensis Dana, to the pesticide carbaryl and its hydrolytic product 1-naphthol
Many environmental factors influence cardiovascular and
respiratory activities of crustaceans. The effects of natural
stressors (hypoxia, low salinity, high temperature) have been well
studied, but the effects of pollutants upon these two organ systems
have received less attention. The presence of the pesticide
carbaryl (Sevin, Union Carbide, Inc.) and its degradation product,
1-naphthol, in Northwestern rivers and bays has resulted from
intentional application to commercial oyster beds and through
careless handling during other spraying operations. In this study,
the burrowing thalassinid ghost shrimp, Callianassa californiensis
was exposed to sublethal levels of the two toxicants to assess their
influence on the cardiovascular and respiratory performance of these
tidal mudflat dwellers.
Both carbaryl and 1-naphthol altered the behavior of exposed
ghost shrimp, causing hyperactivity, convulsions and paralysis.
During these changes oxygen consumption was increased two-fold. In
carbaryl-treated ghost shrimp, normally occurring periods of apnea
were abolished and replaced with high frequency scaphognathite
beating. The heart rate, however, was not substantially increased.
Once carbaryl treatment was discontinued, scaphognathite rates
declined and heart rates became elevated. During 1-naphthol
exposure, neither heart nor scaphognathite activities were
consistently altered. Both toxicants stimulated the secretion of
mucosubstances by the shrimp, however, the source of these
secretions is not known.
The responses of ghost shrimp to carbaryl and 1-naphthol may
be due, in part, to the ability of these compounds to reversibly
inhibit acetylcholinesterase, the enzyme which degrades
acetylcholine at cholinergic nerve synapses. Although the exact
mode of action of these two toxicants in ghost shrimp is not known,
it is clear that any substance which would alter their behavior and
increase their metabolic demands might seriously affect the ability
of the ghost shrimp to survive in the hypoxic mudflat environment
The Public Health Exposome: A Population-Based, Exposure Science Approach to Health Disparities Research
The lack of progress in reducing health disparities suggests that new approaches are needed if we are to achieve meaningful, equitable, and lasting reductions. Current scientific paradigms do not adequately capture the complexity of the relationships between environment, personal health and population level disparities. The public health exposome is presented as a universal exposure tracking framework for integrating complex relationships between exogenous and endogenous exposures across the lifespan from conception to death. It uses a social-ecological framework that builds on the exposome paradigm for conceptualizing how exogenous exposures “get under the skin”. The public health exposome approach has led our team to develop a taxonomy and bioinformatics infrastructure to integrate health outcomes data with thousands of sources of exogenous exposure, organized in four broad domains: natural, built, social, and policy environments. With the input of a transdisciplinary team, we have borrowed and applied the methods, tools and terms from various disciplines to measure the effects of environmental exposures on personal and population health outcomes and disparities, many of which may not manifest until many years later. As is customary with a paradigm shift, this approach has far reaching implications for research methods and design, analytics, community engagement strategies, and research training
BMQ
BMQ: Boston Medical Quarterly was published from 1950-1966 by the Boston University School of Medicine and the Massachusetts Memorial Hospitals
Mastermind Mutations Generate a Unique Constellation of Midline Cells within the Drosophila CNS
Background: The Notch pathway functions repeatedly during the development of the central nervous system in metazoan organisms to control cell fate and regulate cell proliferation and asymmetric cell divisions. Within the Drosophila midline cell lineage, which bisects the two symmetrical halves of the central nervous system, Notch is required for initial cell specification and subsequent differentiation of many midline lineages. Methodology/Principal Findings: Here, we provide the first description of the role of the Notch co-factor, mastermind, in the central nervous system midline of Drosophila. Overall, zygotic mastermind mutations cause an increase in midline cell number and decrease in midline cell diversity. Compared to mutations in other components of the Notch signaling pathway, such as Notch itself and Delta, zygotic mutations in mastermind cause the production of a unique constellation of midline cell types. The major difference is that midline glia form normally in zygotic mastermind mutants, but not in Notch and Delta mutants. Moreover, during late embryogenesis, extra anterior midline glia survive in zygotic mastermind mutants compared to wild type embryos. Conclusions/Significance: This is an example of a mutation in a signaling pathway cofactor producing a distinct centra
A method for the direct measurement of mRNA in discrete regions of mammalian brain
A rapid and nearly quantitative method for the direct analysis of steady-state mRNA levels in microgram quantities of frozen mammalian brain is described. Briefly, tissue punches 0.5-1.0 mm in diameter were sampled from 250-microns-thick cryostat sections of rat brain (approximately 50-200 micrograms tissue). The samples were homogenized in 50 microliters of a denaturing gel loading buffer and applied directly to a 2.2 M formaldehyde-agarose gel for electrophoresis and subsequent RNA blot analysis. The method is extremely rapid, results in excellent recovery of intact RNA, and allows the direct assay of mRNA levels in discrete subregions of the mammalian brain
MINUARTIA DRUMMONDII (CARYOPHYLLACEAE) AND GRATIOLA FLAVA (PLANTAGINACEAE) REDISCOVERED IN LOUISIANA AND GRATIOLA FLAVA HISTORICALLY IN ARKANSAS
Volume: 1Start Page: 763End Page: 76
Positive- and negative-acting promoter sequences regulate cell type-specific expression of the rat synapsin I gene
The phosphoprotein synapsin I is expressed exclusively in neuronal cells. We are interested in elucidating the promoter sequences involved in cell type-specific expression of the synapsin I gene. The PC12 cell line expresses the 3.4 kb and 4.5 kb synapsin I mRNAs and is used to analyze cell type-specific gene expression. A series of deletion fragments of the rat synapsin I gene promoter were fused to the promoterless reporter gene encoding bacterial chloramphenicol acetyltransferase (CAT) for transfection analysis in PC12 cells and in HeLa cells, which do not express the gene. A -349 bp to +110 bp rat synapsin I promoter fragment contains a positive regulator, shown to be 33-times more active in PC12 cells than HeLa cells. Transfection of reporter plasmids containing up to 4.4 kb of rat synapsin I gene promoter sequences exhibit significantly reduced CAT activity in PC12 cells. The reduction in CAT expression was attributed to a negative regulator located between -349 bp and -1341 bp in the rat synapsin I promoter. Our results suggest that both positive and negative-acting sequence elements regulate cell type-specific expression of the rat synapsin I gene