Noise and the Law: A Survey

The subject of noise and the law has received extensive comment recently as a consequence of a more general concern with environmental protection. Although a certain amount of redundancy, therefore, cannot be avoided in treating this subject, the purpose of this article is to set forth the state of the law with respect to problems of noise. Consideration will first be given to the private remedies available to persons whose personal or property rights are adversely affected by noise. Secondly, the law of public nuisance will be explored as a transitional concept from private remedy to public regulation. The various types of public regulation will then be discussed. Finally, certain conclusions about the manner in which the law seeks to deal with problems of noise and the direction of prospective legislation and programs of noise control will be made

Occupational Therapy’s Psychosocial Role for Young Children Transitioning out of Foster Care

Background: Unmet needs for children in the foster care system lead to hardships with social participation, healthy relationships, and occupational engagement. Despite an understanding of these needs, there is minimal research on occupational therapy’s role for young children transitioning from foster care back to their biological parents. Method: A single case report was completed via occupational-based interventions focused on psychosocial development, such as emotional regulation and appropriate social skills. All nine interventions were intended to be provided via 45-min individual treatment sessions followed by biological parent coaching for 15 min with strategies such as role-playing, sensory techniques, and trauma-informed care. Emotional regulation and appropriate social skills were tracked through Goal Attainment Scaling, the Canadian Occupational Performance Measure, the Developmental Assessment of Young Children- Second Edition, and a parent interview. Results: All assessments provided significant results in the improvement of child engagement in social participation, education, and play. The parent interview demonstrated increased biological parent knowledge and decreased stress. Conclusion: Overall, the child’s occupational engagement and biological parent’s satisfaction enhanced their skill sets to improve their quality of life, occupational participation, and relationship quality. Through a coaching strategy, the biological parent gained confidence to take on social-emotional challenges during the child’s transitional phase

Localization of complement factor H gene expression and protein distribution in the mouse outer retina.

To determine the localization of complement factor H (Cfh) mRNA and its protein in the mouse outer retina.Quantitative real-time PCR (qPCR) was used to determine the expression of Cfh and Cfh-related (Cfhr) transcripts in the RPE/choroid. In situ hybridization (ISH) was performed using the novel RNAscope 2.0 FFPE assay to localize the expression of Cfh mRNA in the mouse outer retina. Immunohistochemistry (IHC) was used to localize Cfh protein expression, and western blots were used to characterize CFH antibodies used for IHC.Cfh and Cfhr2 transcripts were detected in the mouse RPE/choroid using qPCR, while Cfhr1, Cfhr3, and Cfhrc (Gm4788) were not detected. ISH showed abundant Cfh mRNA in the RPE of all mouse strains (C57BL/6, BALB/c, 129/Sv) tested, with the exception of the Cfh(-/-) eye. Surprisingly, the Cfh protein was detected by immunohistochemistry in photoreceptors rather than in RPE cells. The specificity of the CFH antibodies was tested by western blotting. Our CFH antibodies recognized purified mouse Cfh protein, serum Cfh protein in wild-type C57BL/6, BALB/c, and 129/Sv, and showed an absence of the Cfh protein in the serum of Cfh(-/-) mice. Greatly reduced Cfh protein immunohistological signals in the Cfh(-/-) eyes also supported the specificity of the Cfh protein distribution results.Only Cfh and Cfhr2 genes are expressed in the mouse outer retina. Only Cfh mRNA was detected in the RPE, but no protein. We hypothesize that the steady-state concentration of Cfh protein is low in the cells due to secretion, and therefore is below the detection level for IHC

Rapid alteration in circulating free thyroxine modulates pituitary type II 5\u27 deiodinase and basal thyrotropin secretion in the rat

TSH secretion is decreased by both T4 and T3. This negative feedback control of TSH secretion has been correlated with an increase in pituitary nuclear T3 content, and it is not clear whether T4 exerts its effect directly on the thyrotroph or after its deiodination to T3. However, levels of the pituitary enzyme catalyzing T4 to T3 conversion, 5\u27D-II, are decreased in the presence of an increased amount of T4. Thus, it is unclear why the thyrotroph would have a mechanism for modulating the production of T3, if T3 is, in fact, the sole bioactive signal providing negative feedback inhibition. To examine this apparent paradox, we administered EMD 21388, a compound which inhibits the binding of T4 to transthyretin resulting in a rapid increase in circulating free T4 levels, to rats pretreated with radiolabeled T4 and T3. We observed increases in pituitary and liver T4 content of greater than 150%, without increases in the respective tissue T3 contents. The EMD 21388-treated rats also exhibited a 25% decrease in pituitary 5\u27D-II activity (103.8 +/- 15.8 fmol 125I released.mg protein-1.h-1, vs. control, 137.4 +/- 15.9, mean +/- SE), as did rats treated with sodium salicylate, another compound that inhibits T4-TTR binding (100.8 +/- 7.1). TSH levels significantly decreased 2 h after the administration of EMD 21388. These data demonstrate that despite a T4-mediated decrease in pituitary 5\u27D-II activity, an increase in T4 independently decreases TSH secretion

ROGUE:an R Shiny app for RNA sequencing analysis and biomarker discovery

Background: The growing power and ever decreasing cost of RNA sequencing (RNA-Seq) technologies have resulted in an explosion of RNA-Seq data production. Comparing gene expression values within RNA-Seq datasets is relatively easy for many interdisciplinary biomedical researchers; however, user-friendly software applications increase the ability of biologists to efficiently explore available datasets. Results: Here, we describe ROGUE (RNA-Seq Ontology Graphic User Environment, https://marisshiny.research.chop.edu/ROGUE/), a user-friendly R Shiny application that allows a biologist to perform differentially expressed gene analysis, gene ontology and pathway enrichment analysis, potential biomarker identification, and advanced statistical analyses. We use ROGUE to identify potential biomarkers and show unique enriched pathways between various immune cells. Conclusions: User-friendly tools for the analysis of next generation sequencing data, such as ROGUE, will allow biologists to efficiently explore their datasets, discover expression patterns, and advance their research by allowing them to develop and test hypotheses.</p

The human CHRNA7 and CHRFAM7A genes: A review of the genetics, regulation, and function

The human α7 neuronal nicotinic acetylcholine receptor gene (CHRNA7) is ubiquitously expressed in both the central nervous system and in the periphery. CHRNA7 is genetically linked to multiple disorders with cognitive deficits, including schizophrenia, bipolar disorder, ADHD, epilepsy, Alzheimer's disease, and Rett syndrome. The regulation of CHRNA7 is complex; more than a dozen mechanisms are known, one of which is a partial duplication of the parent gene. Exons 5–10 of CHRNA7 on chromosome 15 were duplicated and inserted 1.6 Mb upstream of CHRNA7, interrupting an earlier partial duplication of two other genes. The chimeric CHRFAM7A gene product, dupα7, assembles with α7 subunits, resulting in a dominant negative regulation of function. The duplication is human specific, occurring neither in primates nor in rodents. The duplicated α7 sequence in exons 5–10 of CHRFAM7A is almost identical to CHRNA7, and thus is not completely queried in high throughput genetic studies (GWAS). Further, pre-clinical animal models of the α7nAChR utilized in drug development research do not have CHRFAM7A (dupα7) and cannot fully model human drug responses. The wide expression of CHRNA7, its multiple functions and modes of regulation present challenges for study of this gene in disease