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Results for “Genetic Enhancement”

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At least 19 recordsLinked to original sources
PubMed1995

Can human genetic enhancement be prohibited?

This article seeks to reframe the ethical discussion of genetic enhancement, which is the use of genetic engineering to supply a characteristic that a parent might want in a child that does not involve the treatment or prevention of disease. I consider whether it is likely that enhancement can be successfully prohibited. If genetic enhancement is feasible, it is likely that there will be demand for it because parents compete to produce able children and nations compete to accumulate human capital in skilled workers. If some parents or nations begin using genetic enhancement, this will change these competitions in ways that increase the incentives for others to use it. Therefore, a ban on genetic enhancement would be unstable, because once the ban was breached by defectors the motivation of others to uphold it would weaken, making the ban liable to collapse. The argument provides a new perspective on slippery slopes to dangerous technology.

Adult↗
PubMed1999

Does justice require genetic enhancements?

It is argued that justice in some cases provides a pro tanto reason genetically to enhance victims of the genetic lottery. Various arguments--both to the effect that justice provides no such reason and to the effect that while there may be such reasons, they are overridden by certain moral constraints--are considered and rejected. Finally, it is argued that justice provides stronger reasons to perform more traditional medical tasks (treatments), and that therefore genetic enhancements should not play an important role in a public health care system.

Adolescent↗
PubMed2001

When norms normalize: the case of genetic "enhancement".

As the possibility of genetic intervention becomes more concrete, defining and regulating ethically permissible interventions must include a consideration of the implicit as well as explicit consequences. These include the moral implications of defining "enhancement" by reference to a standard of normality. Some authors have called into question the standard ethical concerns about genetic enhancement, but the distinction between enhancing and therapeutic interventions is still structured as relatively unproblematic. However, determining the boundary between therapy and enhancement will have feedback effects on the socially implemented definitions of what counts as normal in human embodiment. Positioning the interface between permissible and nonpermissible interventions at the same place as the boundaries between therapy and enhancement, and between normal and abnormal embodiment, (1) uses biology to justify a moral evaluation, (2) privileges the single standpoint of the genetically canonical person, and (3) enhances the dichotomy between "normal" and "not normal". Assuming that the limit of permissibility along the interventional continuum is coterminous with the definitions of enhancement and of normality, distracts from the work of uncovering the real grounds to setting limits to genetic manipulation.

Ethics, Medical↗
PubMed1999

Thinking theologically about reproductive and genetic enhancements: the challenge.

Current philosophical and legal bioethical reflections on reprogenetics provides little more than a rationalization of the interests of science. There are two reasons for this. First, bioethicists attempt to address ethical issues in a "language of precision" that characterizes science, and this works against analogical and narratological modes of discourse that have traditionally provided guidance for understanding human nature and purpose. Second, the current ethical and legal debate is framed by a public/private distinction that banishes robust norms to the private realm, and leaves a minimalist public discourse of harm avoidance that is insuffucient for regulating the science. In this essay, I argue that Mark Hanson's account of anxiety provides a valuable starting point for addressing deficiencies in the current philosophical and legal debate, and it highlights the need for a theological discourse on genetic enhancements. Through an assessment of Joel Shuman's criticism of the public/private distinction, I show how the needed theological discourse should be situated in the context of robust communities, and how such a communitarian inter-ethic is compatible with a variant of liberalism. Finally, I critically assess James Keenan's account of virtue and perfection, in order to outline what a sufficient discourse on reproductive and genetic enhancements requires.

Anthropology↗
PubMed1999

Genetic enhancement and theosis: two models of therapy.

The author argues that to think theologically about genetic enhancement is to think prayerfully about how to locate all one's uses of medicine, recognizing that they must all be lodged in the Christian struggle to holiness. He is critical of the essays in this issue because they often appear to take on a scholastic life of their own outside of the all-consuming struggle to salvation of Christians across the millennia.

Christianity↗
PubMed1999

Human genetic enhancement: is it really a matter of perfection? A dialog with Hanson, Keenan, and Shuman.

The author reviews the arguments made by Mark Hanson, James Keenan, S.J., and Joel Shuman in this issue. In the first section, she argues that they offer a significant contribution toward an understanding of the inner logic of a new trend in contemporary medicine, genetic engineering. However, she criticizes the authors for relying excessively on procedural guidelines and for failing to bring the practical realities of medicine and technology to bear on theory. She argues that more concrete guidelines, which are ultimately grounded in a Christian conception of the person and on the commandment to love, are necessary. Writing from the Roman Catholic perspective, the author argues that the distinction between genetic enhancement and gene therapy is essential, despite the criticisms which have been offered of this distinction. Understanding this distinction will be critical for identifying as licit only those forms of genetic manipulation which respect the dignity of the human person.

Anthropology↗
PubMed1981

Murine immune memory to a TI-2 antigen, DNP-Ficoll: carrier-specificity, genetic enhancement and phenotypic dominant inheritance.

C3H/HeN x NZB/BIN F1 mice were primed and challenged with DNP-Ficoll, a thymic independent (TI-2) antigen. They developed strong IgM and IgG carrier-specific memory responses: DNP-pneumococcal polysaccharide or DNP-haemocyanin challenge did not elicit memory responses. The IgG response component appeared to be inherited dominantly from the C3H/HeN parent. The IgM component resulted from genetic enhancement.

Animals↗
PubMed1999

Genetic enhancement of learning and memory in mice.

Hebb's rule (1949) states that learning and memory are based on modifications of synaptic strength among neurons that are simultaneously active. This implies that enhanced synaptic coincidence detection would lead to better learning and memory. If the NMDA (N-methyl-D-aspartate) receptor, a synaptic coincidence detector, acts as a graded switch for memory formation, enhanced signal detection by NMDA receptors should enhance learning and memory. Here we show that overexpression of NMDA receptor 2B (NR2B) in the forebrains of transgenic mice leads to enhanced activation of NMDA receptors, facilitating synaptic potentiation in response to stimulation at 10-100 Hz. These mice exhibit superior ability in learning and memory in various behavioural tasks, showing that NR2B is critical in gating the age-dependent threshold for plasticity and memory formation. NMDA-receptor-dependent modifications of synaptic efficacy, therefore, represent a unifying mechanism for associative learning and memory. Our results suggest that genetic enhancement of mental and cognitive attributes such as intelligence and memory in mammals is feasible.

Animals↗
PubMed1997

Genetic enhancers of sem-5 define components of the gonad-independent guidance mechanism controlling sex myoblast migration in Caenorhabditis elegans hermaphrodites.

The migrations of the sex myoblasts in Caenorhabditis elegans hermaphrodites involve two guidance mechanism: a gonad-dependent attraction that confers precise positioning of the sex myoblasts and a gonad-independent mechanism that is sufficient for coarse positioning in the absence of the gonad (Thomas et al., 1990). Here we show that mutations in unc-53, unc-71, and unc-73 disrupt sex myoblast positioning in the absence of the gonad, while they do not affect positioning in the presence of the gonad. Thus, mutations in these genes appear to compromise the gonad-independent mechanism without affecting motility or the gonad-dependent attraction. Mutations in sem-5 confer dramatic sex myoblast positioning defects in double mutant combinations with unc-53, unc-71, or unc-73 mutations, even in the presence of the gonad. This suggests that sem-5 is required for the gonad-dependent attractive mechanism. Mutations in let-60 ras and let-341 also confer sex myoblast migration defects in an unc-53 background, implicating these genes in gonad-dependent positioning as well.

Animals↗
PubMed2000

Genetic enhancement of fracture repair: healing of an experimental segmental defect by adenoviral transfer of the BMP-2 gene.

This study evaluated the ability of gene transfer to enhance bone healing. Segmental defects were created surgically in the femora of New Zealand white rabbits. First generation adenoviruses were used as vectors to introduce into the defects genes encoding either human bone morphogenetic protein-2 (BMP-2) or, as a negative control, firefly luciferase. Representative specimens were evaluated histologically after 8 weeks. Healing of the defects was monitored radiographically for 12 weeks, after which time the repair tissue was evaluated biomechanically. By radiological criteria, animals receiving the BMP-2 gene had healed their osseous lesions after 7 weeks, whereas those receiving the luciferase gene had not. Histologic examination of representative rabbits at 8 weeks confirmed ossification across the entire defect in response to the BMP-2 gene, whereas the control defect was predominantly fibrotic and sparsely ossified. At the end of the 12-week experiment, the control femora still showed no radiological signs of stable healing. The difference in radiologically defined healing between the experimental and control groups was statistically significant (P < 0. 002). Biomechanical testing of the femora at 12 weeks demonstrated statistically significant increases in the mean bending strength (P < 0.005) and bending stiffness (P < 0.05) of the animals treated with the BMP-2 gene. Direct, local adenoviral delivery of an osteogenic gene thus led to the healing of an osseous lesion that otherwise would not do so. These promising data encourage the further development of genetic approaches to enhancing bone healing. Gene Therapy (2000) 7, 734-739.

Adenoviridae↗
PubMed2001

Genetic enhancement of inflammatory pain by forebrain NR2B overexpression.

N-methyl-D-aspartate (NMDA) receptors contribute to many brain functions. We studied the effect of forebrain-targeted overexpression of the NMDA receptor subunit NR2B on the response of mice to tissue injury and inflammation. Transgenic mice exhibited prominent NR2B expression and enhanced NMDA receptor-mediated synaptic responses in two pain-related forebrain areas, the anterior cingulate cortex and insular cortex, but not in the spinal cord. Although transgenic and wild type mice were indistinguishable in tests of acute pain, transgenic mice exhibited enhanced responsiveness to peripheral injection of two inflammatory stimuli, formalin and complete Freund's adjuvant. Genetic modification of forebrain NMDA receptors can therefore influence pain perception, which suggests that forebrain-selective NMDA receptor antagonists, including NR2B-selective agents, may be useful analgesics for persistent pain.

Animals↗
PubMed1986

Factors enhancing genetic transformation of intact yeast cells modify cell wall porosity.

Genetic transformation of intact cells of Saccharomyces cerevisiae, achieved by incubating the cells with plasmid DNA in the presence of PEG, could be enhanced, not only by pretreatment of the cells with Li+ and 2-mercaptoethanol, as has been reported previously, but also by pretreatment with proteolytic enzymes. The efficiency of transformation with 2-mercaptoethanol rose dramatically when the pretreated cells had been handled in osmotically stabilized media. Following all the pretreatments the cells became leaky for nucleic acids as detected by the presence of endogenous RNAs in the medium. The pretreatments evidently facilitated the passage of transforming DNA across the cell wall.

Cell Survival↗