Therapeutic Uses Of Adventure-Challenge-Outdoor-Wilderness: Theory and Research

This article contains the text of a keynote presentation at the Inaugural Symposium at Bradford Woods, January 1992, which focused on research into therapeutic recreation

A Research Update of Adventure Therapy (1992-1995): Challenge Activities and Ropes Courses, Wilderness Expeditions, and Residential Camping Programs

n 1992 a review of research in adventure therapy offered a perspective that utilized work in psy­chotherapy as a lens to view the current state of the field. From that review, several recommenda­tions were made to gain respect within the field of traditional mental health. This update examines the recommendations made in 1992 and updates them utilizing research that has taken place in adventure therapy and borrowing liberally from suggestions made for enhancing the field of psy­chotherapy. The article makes the following points. First, the field of adventure therapy must cre­ate a collective document that addresses its accomplishments and effectiveness. Technology al­lows world wide web connections that can facilitate the process of communication at levels we were unaware of in 1992. Second, the clinically significant events of adventure therapy need to be examined through a massive survey of consumers of our service in order to achieve credibility with mental health and those who hold the purse strings. If we do not do so, we risk benefiting our potential consumers, those who may not be able to access adventure therapy as a viable approach to treatment. Finally, the time is ripe with possibilities for researchers and several avenues are ex­plored for shaping the future of the field

Psychological Rationale for Adventure Therapy with Hospitalized Adolescents

Inpatient and residential therapeutic programs for adolescents are often fairly generic in format relying heavily on traditional, insight-Oriented approaches to treatment without regard to how the intellectual functioning of the adolescent might impact upon therapeutic effectiveness. This study examined the WISC-R profiles of two treatment populations and presented a theoretical rationale for using adventure based treatment based upon the participants performance on verbal and performance subscales. It is hoped that the article might be used to help justify the implementation of adventure therapy in psychiatric treatment facilities and lead to further research to test the proposed hypotheses

Books

Valuable distillations of other people's experiencesHow To Do It. Vol. 3. Pp. x + 203. Illustrated. £9 (including postage by air). London: BMJ. 1990. (Also available from Libriger Book Distributors, Bloemfontein.)Medical dictionaryConcise Medical Dictionary. 3rd ed. Ed. By Elizabeth A. Martin. Pp. 1-759. Oxford: Oxford University Press. 1990.Paediatric cardiologyPrevention in Childhood and Youth of Adult Cardiovascular Diseases: Time for Action. Ed. by WHO Expert Committee. Pp. 1 - 105. Illustrated. Sw. Fr. 12. Geneva: WHO.1990.Contraceptive safety Safety Requirements for Contraceptive Steroids. Ed. by F. Michal. pp. xv - 467. Illustrated. £65,00. Cambridge: Cambridge University Press. 1989.Psychiatry Textbook of Psychiatry. Ed. by P. J. V. Beumont and R. B. Hampshire. Pp. x + 520. Illustrated. PriCe £29,50. Oxford: Blackwell Scientific Publications. 1989

The Genetic Age: Who Owns the Genome?: A Symposium on Intellectual Property and the Human Genome, 2 J. Marshall Rev. Intell. Prop. L. 6 (2002)

A Symposium on Intellectual Property Co-Sponsored by The Woodrow Wilson Center. Featuring the remarks of Scott A. Brown, J.D.; Q. Todd Dickinson, J.D.; Stephen P.A. Fodor, Ph.D.; Justin Gillis; Hon. Lee H. Hamilton; Eric S. Lander, Ph.D.; and Pilar Ossorio, Ph.D., J.D

A modifier of Huntington's disease onset at the MLH1 locus

Huntington’s disease (HD) is a dominantly inherited neurodegenerative disease caused by an expanded CAG repeat in HTT. Many clinical characteristics of HD such as age at motor onset are determined largely by the size of HTT CAG repeat. However, emerging evidence strongly supports a role for other genetic factors in modifying the disease pathogenesis driven by mutant huntingtin. A recent genome-wide association analysis to discover genetic modifiers of HD onset age provided initial evidence for modifier loci on chromosomes 8 and 15 and suggestive evidence for a locus on chromosome 3. Here, genotyping of candidate single nucleotide polymorphisms in a cohort of 3,314 additional HD subjects yields independent confirmation of the former two loci and moves the third to genome-wide significance at MLH1, a locus whose mouse orthologue modifies CAG length-dependent phenotypes in a Htt-knock-in mouse model of HD. Both quantitative and dichotomous association analyses implicate a functional variant on 32% of chromosomes with the beneficial modifier effect that delays HD motor onset by 0.7 years/allele. Genomic DNA capture and sequencing of a modifier haplotype localize the functional variation to a 78 kb region spanning the 3’end of MLH1 and the 5’end of the neighboring LRRFIP2, and marked by an isoleucinevaline missense variant in MLH1. Analysis of expression Quantitative Trait Loci (eQTLs) provides modest support for altered regulation of MLH1 and LRRFIP2, raising the possibility that the modifier affects regulation of both genes. Finally, polygenic modification score and heritability analyses suggest the existence of additional genetic modifiers, supporting expanded, comprehensive genetic analysis of larger HD datasets

Haplotype-based stratification of Huntington's disease

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease caused by expansion of a CAG trinucleotide repeat in HTT, resulting in an extended polyglutamine tract in huntingtin. We and others have previously determined that the HD-causing expansion occurs on multiple different haplotype backbones, reflecting more than one ancestral origin of the same type of mutation. In view of the therapeutic potential of mutant allele-specific gene silencing, we have compared and integrated two major systems of HTT haplotype definition, combining data from 74 sequence variants to identify the most frequent disease-associated and control chromosome backbones and revealing that there is potential for additional resolution of HD haplotypes. We have used the large collection of 4078 heterozygous HD subjects analyzed in our recent genome-wide association study of HD age at onset to estimate the frequency of these haplotypes in European subjects, finding that common genetic variation at HTT can distinguish the normal and CAG-expanded chromosomes for more than 95% of European HD individuals. As a resource for the HD research community, we have also determined the haplotypes present in a series of publicly available HD subject-derived fibroblasts, induced pluripotent cells, and embryonic stem cells in order to facilitate efforts to develop inclusive methods of allele-specific HTT silencing applicable to most HD patients. Our data providing genetic guidance for therapeutic gene-based targeting will significantly contribute to the developments of rational treatments and implementation of precision medicine in HD

Haplotype-based stratification of Huntington's disease

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease caused by expansion of a CAG trinucleotide repeat in HTT, resulting in an extended polyglutamine tract in huntingtin. We and others have previously determined that the HD-causing expansion occurs on multiple different haplotype backbones, reflecting more than one ancestral origin of the same type of mutation. In view of the therapeutic potential of mutant allele-specific gene silencing, we have compared and integrated two major systems of HTT haplotype definition, combining data from 74 sequence variants to identify the most frequent disease-associated and control chromosome backbones and revealing that there is potential for additional resolution of HD haplotypes. We have used the large collection of 4078 heterozygous HD subjects analyzed in our recent genome-wide association study of HD age at onset to estimate the frequency of these haplotypes in European subjects, finding that common genetic variation at HTT can distinguish the normal and CAG-expanded chromosomes for more than 95% of European HD individuals. As a resource for the HD research community, we have also determined the haplotypes present in a series of publicly available HD subject-derived fibroblasts, induced pluripotent cells, and embryonic stem cells in order to facilitate efforts to develop inclusive methods of allele-specific HTT silencing applicable to most HD patients. Our data providing genetic guidance for therapeutic gene-based targeting will significantly contribute to the developments of rational treatments and implementation of precision medicine in HD

Thermochemistry of Microhydration of Sodiated and Potassiated Monosaccharides

The thermochemical properties ΔHon , ΔSon, and ΔGon for the hydration of sodiated and potassiated monosaccharides (Ara = arabinose, Xyl = xylose, Rib = ribose, Glc = glucose, and Gal = galactose) have been experimentally studied in the gas phase at 10 mbar by equilibria measurements using an electrospray high-pressure mass spectrometer equipped with a pulsed ion beam reaction chamber. The hydration enthalpies for sodiated complexes were found to be between −46.4 and −57.7 kJ/mol for the first, and −42.7 and −52.3 kJ/mol for the second water molecule. For potassiated complexes, the water binding enthalpies were similar for all studied systems and varied between −48.5 and −52.7 kJ/mol. The thermochemical values for each system correspond to a mixture of the α and β anomeric forms of monosaccharide structures involved in their cationized complexes

Parity nonconservation in deuteron photoreactions

We calculate the asymmetries in parity nonconserving deuteron photodisintegration due to circularly polarized photons gamma+d to n+p with the photon laboratory energy ranging from the threshold up to 10 MeV and the radiative capture of thermal polarized neutrons by protons n+p to gamma+d. We use the leading order electromagnetic Hamiltonian neglecting the smaller nuclear exchange currents. Comparative calculations are done by using the Reid93 and Argonne v18 potentials for the strong interaction and the DDH and FCDH "best" values for the weak couplings in a weak one-meson exchange potential. A weak NDelta transition potential is used to incorporate also the Delta(1232)-isobar excitation in the coupled-channels formalism.Comment: 14 pages, 13 figures (18 eps files), LaTeX2