ENVIRONMENTAL REGULATORY POLICY: POLITICAL ECONOMY, INDUSTRIAL GEOGRAPHY, AND INTERGOVERNMENTAL FISCAL EFFECTS

Environmental regulatory policy in the U.S. is a mixture of federal, state, and local activity and impacts. This is true of air quality regulations, which are governed at the federal level by the Clean Air Act. This dissertation analyzes both the political economy of federal environmental regulations and the empirical effects of ozone regulations under the Clean Air Act.A political economy model is developed that offers a motivation for political support of national environmental policy that regulates strictly local pollution. Altering local environmental policies in other jurisdictions will cause capital migration, which may increase local welfare. Thus, individuals have an incentive to influence local policies in other jurisdictions. National environmental policy then becomes a potential tool for inter-jurisdictional competition.The empirical impacts of ground-level ozone regulations under the Clean Air Act are also analyzed. The Clean Air Act established minimum air quality standards; localities failing to meet the established standards are classified as nonattainment areas and are subject to additional environmental regulations. These new regulations have a direct impact on polluting industries, and therefore also an indirect impact on the revenues and expenditures of local governments.First, nonattainment status is seen to alter regional industrial geography. Overall economic activity declines in both nonattainment areas and the surrounding jurisdictions. Gaining attainment status partially mitigates these impacts, although to some extent theeconomic impacts in both nonattainment areas and the surrounding jurisdictions do permanently persist. I also find evidence that manufacturing activity relocates from nonattainment areas to surrounding areas that face more lenient air quality regulations.Ozone nonattainment status is also seen to produce fiscal effects for local governments as changes in industrial geography alter local tax bases. Revenues and expenditures decline in regulated population centers, while they increase in surrounding areas. These increases diminish with distance from the urban center. Also, the fiscal impacts persist even after attainment status has been gained

Exploring joint hypermobility syndrome, developmental coordination disorder and pain

INTRODUCTION Floppy, clumsy, hypermobile children are increasingly referred to occupational and physical therapy under the label of dyspraxia. Motor impairments associated with the umbrella diagnosis of developmental coordination disorder (DCD) have been reported as persisting into adolescence and adulthood and subsequently affecting functional abilities (Cousins and Smyth 2003). Within this heterogeneous condition the underlying mechanisms causing the motor difficulties remains unclear. Ayers (1985) hypothesised that some individuals might have somatosensory processing issues contributing to their poor motor planning and coordination difficulties. Similarities in functional difficulties have been noted in children with a diagnosis of DCD and joint hypermobility syndrome (JHS) (Kirby and Davies 2006). There is limited understanding of the relationship between the two conditions. JHS is a multisystemic inherited connective tissue disorder, in which hypermobile joints, pain, clumsiness, poor proprioception and dislocations are familiar features (Grahame and Hakim 2006; Adib et al 2005). It has been suggested that adults with JHS show poor movement patterns which contribute to biomechanical dysfunction and continuing pain (Clark et al 2009). Pain and disability reported in adults with JHS often leads to anxiety, depression, work incapacity and social isolation (Grahame and Hakim 2006). The purpose of this study was to explore the association between adults with JHS and DCD and long term pain. METHODOLOGY/ METHODS A mixed methods design influenced by a pragmatic paradigm was utilised. Subjects: 90 patients with JHS (18-65 years) recruited from a hypermobility clinic were compared, using a questionnaire, with 113 healthy volunteers (18-65 years) with no pain recruited from a university. Analysis: Quantitative data were described and examined by regression, odds ratios were calculated. Qualitative data was analysed thematically FINDINGS The percentage of subjects who reported DCD in patients with JHS and healthy volunteers were 56% and 19% respectively. A significant association between patients with JHS and DCD was noted, chi square = 30.11, p < .001. Patients with JHS were 6 times [95% CI 2.9 – 10.3] more likely to report DCD than healthy volunteers. Pain was a significant feature with an average of 9.8 pain sites reported (out of a total of 17). Open ended questions revealed many patients recalling pain starting in early childhood and adolescence. DISCUSSION These results suggest a significant association between patients with JHS and DCD and the reporting of long term pain. Early recognition and understanding of the needs of children with DCD who present with somatosensory impairment, pain modulation and JHS is therefore essential. Sensory integration therapy as part of a comprehensive early intervention program has the potential to mitigate long term problems. A multidisciplinary approach which involves health professionals and teachers is also recommended. CONCLUSION This research may be considered an early step in the identification of an association of DCD and JHS. Further studies are required to explore somatosensory processing issues experienced by those with DCD and JHS as this might be an important underlying mechanism

Cloning and characterisation of the rad9 DNA repair gene from Schizosaccharomyces pombe

The rad9.192 DNA repair mutant from the fission yeast, Schizosaccharomyces pombe, is sensitive to both UV and ionising radiation. The rad9 gene has been cloned by complementation of the gamma-ray sensitivity of the mutant cell line. A 4.3kb HindIII fragment was found to confer resistance to both types of radiation. The region of complementation was further localised to a 2.6kb HindIII-EcoRV fragment, which, by DNA sequence analysis, was found to contain sequences capable of coding for a 427 amino acid protein, if three introns were postulated to remove stop codons. The introns were confirmed by sequence analysis of cDNA clones and PCR products derived from cDNA. The product of transcription is a 1.6kb mRNA of low abundance. The putative rad9 protein shows no homology to any published sequence. A truncated protein is capable of complementing the radiation sensitivity of the rad9.192 mutant. Deletion of the gene is not lethal and the null allele has a similar phenotype to the rad9.192 mutant

Book review of Linley, A. & Joseph, S. (2004) Positive Psychology in Practice

In the preface to this volume Martin Seligman notes that ‘the scientific psychological literature of the 20th century is littered with well-done analytic science that applied to nothing at all, and this is a fate positive psychology must avoid.’ Alex Linley and Stephen Joseph in their volume Positive Psychology Practice have taken an important step in diverting positive psychology from this undesirable fate. They have edited a compendium of scholarly chapters on practical applications of the science of positive psychology to important social issues

Evolutionary conservation of excision repair in Schizosaccharomyces pombe: Evidence for a family of sequences related to the Saccharomyces cerevisiae RAD2 gene

Cells mutated at the rad13 locus in the fission yeast, Schizosaccharomyces pombe are deficient in excision-repair of UV damage. We have cloned the S.pombe rad13 gene by its ability to complement the UV sensitivity of a rad13 mutant. The gene is not essential for cell proliferation. Sequence analysis of the cloned gene revealed an open reading-frame of 1113 amino acids with structural homology to the RAD2 gene of the distantly related Saccharomyces cerevisiae. The sequence similarity is confined to three domains, two close to the N-terminus of the encoded protein, the third being close to the C-terminus. The central region of about 500 amino acids shows little similarity between the two organisms. The first and third domains are also found in a related yet distinct pair of homologous S.pombe/S.cerevisiae DNA repair genes (rad2/YKL510), which have only a very short region between these two conserved domains. Using the polymerase chain reaction with degenerate primers, we have isolated fragments from a gene homologous to rad13/RAD2 from Aspergillus nidulans. These findings define new functional domains involved in excision-repair, as well as identifying a conserved family of genes related to RAD2

Cloning and characterisation of the S.pombe rad15 gene, a homologue to the S.cerevisiae RAD3 and human ERCC2 genes

The RAD3 gene of Saccharomyces cerevisiae encodes an ATP-dependent 5' - 3' DNA helicase, which is involved in excision repair of ultraviolet radiation damage. By hybridisation of a Schizosaccharomyces pombe genomic library with a RAD3 gene probe we have isolated the S.pombe homologue of RAD3. We have also cloned the rad15 gene of S.pombe by complementation of radiation-sensitive phenotype of the rad15 mutant. Comparison of the restriction map and DNA sequence, shows that the S.pombe rad15 gene is identical to the gene homologous to S.cerevisiae RAD3, identified by hybridisation. The S.pombe rad15.P mutant is highly sensitive to UV radiation, but only slightly sensitive to ionising radiation, as expected for a mutant defective in excision repair. DNA sequence analysis of the rad15 gene indicates an open reading frame of 772 amino acids, and this is consistent with a transcript size of 2.6kb as detected by Northern analysis. The predicted rad15 protein has 65% identity to RAD3 and 55% identity to the human homologue ERCC2. This homology is particularly striking in the regions identified as being conserved in a group of DNA helicases. Gene deletion experiments indicate that, like the S.cerevisiae RAD3 gene, the S.pombe rad15 gene is essential for viability, suggesting that the protein product has a role in cell proliferation and not solely in DNA repair