Strengthening Families: Parents' Voices on Discipline and Child Rearing

This qualitative study conducted semi-structured, multi-session focus groups and interviews with twenty-seven participants to explore in-depth, participant constructs of child discipline and punishment methods and reasons for the continuing support for corporal punishment of U.S. children. The research assumed that parents want to parent well and utilized the strengths perspective as the instrument to listen to participants' voices. Narratives revealed that participants were thoughtful about discipline and parenting strategies and viewed their parent role as a serious commitment. Non-violent discipline strategies, particularly communication, were often used. However, parents generally framed use of physical punishment as “when children need spanking” versus articulating the view that corporal punishment is a choice. Parents were unfamiliar with risks associated with physical punishment and only three parents, as a result of their foster parent training, had ever heard, “Do not spank.” Participants enumerated services and recommendations that would support and inform their own parenting, as well as, benefit children and the eighty percent of women and men in the United States who become mothers and fathers. Recommendations included: creation of a national campaign to build on parent strengths and the intentionality of effective parenting; child development education and increased public awareness of positive discipline methods; parenting supports, including respite and venues for dialogue and discourse about parenting. Recommendations are intended to inform child welfare practice and policy, particularly child abuse prevention. Creating, funding, and implementing a national campaign as described would challenge the dominant child welfare paradigm from one currently perceived as punitive and focused on parents' deficits to a strengths-based paradigm that provides supports and assistance to parents and children.

Chromosomal control of the dominant suppression of {\it ras\/}-mediated transformation

The role of tumor suppressor function in the multistep process of carcinogenesis was studied in the human teratocarcinoma cell line PA-1. Early passage PA-1 cells ($<$P100) are preneoplastic while late passage ($>$P100) PA-1 cells are spontaneously transformed. Previous work demonstrated a causal role for the N-ras oncogene in the neoplastic transformation of this cell line and the gene was cloned. A clonal cell line established at passage 40 has been shown to suppress the neoplastic transformation potential of the PA-1 N-ras oncogene in gene transfer experiments. This phenotype has been termed SRT+ for suppression of ras transformation. A clonal cell line established at passage 63 is neoplastically transformed by the N-ras in similar gene transfer experiments and is regarded as srt$-$. Somatic cell hybrids were formed between the SRT+ cell and two different N-ras transformed srt$-$ cells. The results indicate that five of the seven independent hybrid clones, and all 14 subclones, failed to form tumors in the nude mouse tumor assay. Chromosomal analysis of rare neoplastic segregants which arose from suppressed hybrid populations demonstrate that the general loss of chromosomes correlates with the reemergence of neoplastic transformation. Karyotype analyses demonstrate a statistically correlative loss of chromosomes 1, 4, 19, and to a lesser extent 11, 14, and 16. DNA hybridization analysis demonstrates a single copy of the intact N-ras oncogene in parental cells, suppressed hybrids, and neoplastically transformed hybrids. These results indicate that functional ras transformation suppression is a trans-dominant trait which may be controlled by sequences residing on particular chromosomes in the human genome. Furthermore, the suppression of ras transformation results from a unique step in the multistep process of carcinogenesis that is different from the induction of immortality. Thus, the neoplastic process of the PA-1 cell line involves at least three steps: (1) induction of immortality, (2) activation of the N-ras oncogene, and (3) loss of tumor suppressor function. ^

The story of RP10: A positional cloning approach to the identification of an autosomal dominant retinitis pigmentosa gene

Retinitis pigmentosa (RP) is an inherited retinal degenerative disease that is the leading cause of inherited blindness worldwide. Characteristic features of the disease include night blindness, progressive loss of visual fields, and deposition of pigment on the retina in a bone spicule-like pattern. RP is marked by extreme genetic heterogeneity with at least 19 autosomal dominant, autosomal recessive and X-linked loci identified. RP10, which maps to chromosome 7q, was the fifth autosomal dominant RP locus identified, and accounts for the early-onset disease in two independent families. Extensive linkage and haplotype analyses have been performed in these two families which have allowed the assignment of the disease locus to a 5-cM region on chromosome 7q31.3. In collaboration with Dr. Eric Green (National Center for Human Genome Research, National Institutes of Health), a well-characterized physical map of the region was constructed which includes YAC, BAC and cosmid coverage. The entire RP10 critical region resides within a 9-Mb well-characterized YAC contig. These physical maps not only provided the resources to undertake the CAIGES (cDNA amplification for identification of genomic expressed sequences) procedure for identification of retinal candidate genes within the critical region, but also identified a number of candidate genes, including transducin-$\gamma$ and blue cone pigment genes. All candidate genes examined were excluded. In addition, a number of ESTs were mapped within the critical region. EST20241, which was isolated from an eye library, corresponded to the 3$\sp\prime$ region of the ADP-ribosylation factor (ARF) 5 gene. ARF5, with its role in vesicle transport and possible participation in the regulation of the visual transduction pathway, became an extremely interesting candidate gene. Using a primer walking approach, the entire 3.2 kb genomic sequence of the ARF5 gene was generated and developed intronic primers to screen for coding region mutations in affected family members. No mutations were found in the ARF5 gene, however, a number of additional ESTs have been mapped to the critical region, and, as the large-scale sequencing projects get underway, megabases of raw sequence data from the RP10 region are becoming available. These resources will hasten the isolation and characterization of the RP10 gene. ^

Race and discourse analysis: Building a dialogue in health service research and health care settings

Using a framework for discourse analysis developed by Van Dijk, the investigator will pinpoint the pathological forms of discourse on race, defined as 'race talk' in three professional domains: health services research, public health provider organizations, and literature on multiculturalism. Attention will then turn to developing an analytical strategy for building more meaningful dialogue on race. The retrieval of potential resources for dialogue will be drawn from the third domain. Analysis will focus on enhancing the prospects of converting 'race talk' into dialogue. This will be accomplished by characterizing the normative preconditions as formal procedural requirements for dialogue and then supplementing these conditions with others related specifically to race. From here, the practical implications of combining procedural requirements and resources in each of the domains will be considered. Finally, the author will attempt to determine how these selected resources might be employed to transform 'race talk' in practice and lay the groundwork for a dialogue of understanding. ^

A discourse-theoretic perspective on the bioethical-legal framework of genetic counseling

The reflexive nature of reason and the unique relationship reason shares with autonomy in Kant's philosophy is the theoretical basis of this dissertation. The principle of respect for autonomy undergirds the two main legal and ethical tenets of genetic counseling, an emerging profession trying to accommodate the sweeping changes that have occurred in clinical genetics, clinical ethics, and case law applicable to medicine. These two tenets of the counseling profession, informed consent and nondirectiveness, both share a principlist interpretation of autonomy that I argue is flawed due to its connection to: instrumental forms of reasoning, empirical theories of action supporting rational choice, and a liberal paradigm of law. I offer an alternative bioethical-legal framework that is based in the Kantian tradition in law and ethics through the complex theories of Jurgen Habermas. Following Habermas's reconstruction of the mutually constituting notions of private and public autonomy, I will argue for a richer conceptualization of autonomy that can have significant implications for the legal and bioethical concepts supporting the profession of genetic counseling, and which can ultimately change counseling practice. ^

A discourse-theoretic approach to negotiated rulemaking

In 1996 and in 1997, Congress ordered the Secretary of Health and Human Services to undertake a process of negotiated rulemaking, which is authorized under the Negotiated Rulemaking Act of 1990, on three separate rulemaking matters. Other Federal agencies, including the Environmental Protection Agency and the Occupational Health and Safety Administration, have also made use of this procedure. As part of the program to reinvent government, President Clinton has issued an executive order requiring federal agencies to engage in some negotiated rulemaking procedures. I present an analytic, interpretative and critical approach to looking at the statutory and regulatory provisions for negotiated rulemaking as related to issues of democratic governance surrounding the problem of delegation of legislative power. The paradigm of law delineated by Jürgen Habermas, which sets law the task of achieving social or value integration as well as integration of systems, provides the background theory for a critique of such processes. My research questions are two. First, why should a citizen obey a regulation which is the result of negotiation by directly interested parties? Second, what is the potential effect of negotiated rulemaking on other institutions for deliberative democracy? For the internal critique I argue that the procedures for negotiated rulemaking will not produce among the participants the agreement and cooperation which is the legislative intent. For the external critique I argue that negotiated rulemaking will not result in democratically-legitimated regulation. In addition, the practice of negotiated rulemaking will further weaken the functioning of the public sphere, as Habermas theorizes it, as the central institution of deliberative democracy. The primary implication is the need to mitigate further development of administrative agencies as isolated, self-regulating systems, which have been loosened from the controls of democratic governance, through the development of a robust public sphere in which affected persons may achieve mutual understanding. ^

CHROMOSOMAL MAPPING, LINKAGE RELATIONSHIPS, AND EVOLUTIONARY STUDIES OF THE HUMAN ANONYMOUS DNA CLONE D1S1 (IN SITU HYBRIDIZATION, PRIMATES, GENE MAPPING, AUTOSOMAL DOMINANT RETINITIS PIGMENTOSA, GENE DUPLICATION)

D1S1, an anonymous human DNA clone originally called (lamda)Ch4-H3 or (lamda)H3, was the first single copy mapped to a human chromosome (1p36) by in situ hybridization. The chromosomal assignment has been confirmed in other laboratories by repeating the in situ hybridization but not by another method. In the present study, hybridization to a panel of hamster-human somatic cell hybrids revealed copies of D1S1 on both chromosomes 1 and 3. Subcloning D1S1 showed that the D1S1 clone itself is from chromosome 3, and the sequence detected by in situ hybridization is at least two copies of part of the chromosome 3 copy. This finding demonstrates the importance of verifying gene mapping with two methods and questions the accuracy of in situ hybridization mapping.^ Non-human mammals have only one copy of D1S1, and the non-human primate D1S1 map closely resembles the human chromosome 3 copy. Thus, the human chromosome 1 copies appear to be part of a very recent duplication that occurred after the divergence between humans and the other great apes.^ A moderately informative HindIII D1S1 RFLP was mapped to chromosome 3. This marker and 12 protein markers were applied to a linkage study of autosomal dominant retinitis pigmentosa (ADRP). None of the markers proved linkage, but adding the three families examined to previously published data raises the ADRP:Rh lod score to 1.92 at (THETA) = 0.30. ^