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Biomedical subjects

C Hue

Publications and source records attributed to C Hue.

5 recordsLinked to original sources
PubMed2001

From irreversibility to participation: towards a participatory foresight for the governance of collective environmental risks.

This paper presents a reflection on the introduction of methods and tools of "participative foresight" for scientific and technology policy as well as environmental policy fields. Future studies have recently made a comeback under the label of foresight. Future technology studies no longer claim to forecast the future, but are presented as a strategic tool for improving interaction between key actors and for anticipatory policy making. They can be defined as a "process by which one comes to a fuller understanding of the forces shaping the long term future which should be taken into account in policy formulation, planning and decision-making" [Foresight in Federal Government Policymaking, Futures Res. Quart. (1985) 29]. We discuss applications of this approach for perspectives on environmental policy and sustainable development. Foresight opens up the possibility of negotiating a new and more fruitful relationship or 'social contract' between science and technology, on the one hand, and society on the other. The focus has moved from merely scientific and industrial insights to social demand, thus emphasizing the importance of both the production and "supply" of innovation, and the "demand" as signaled in the views of citizens.

Decision Making↗
PubMed2001

Optimization of retroviral gene transfer protocol to maintain the lymphoid potential of progenitor cells.

We have attempted to improve retrovirus-mediated gene transfer efficacy into hematopoietic progenitor cells (HPCs) without causing them to lose their lymphoid potential. Highly purified CD34(+) cells on CH-296 fibronectin fragments have been transduced with three different cytokine combinations. Murine CD2 was used as a marker gene. Transgene expression was assayed by FACS analysis shortly after transduction of CD34(+) cells and after long-term culture (LTC) extended by differentiation of various lymphoid lineages: NK cells, B cells, and dendritic cells. Compared with the historical cytokine mix, i.e., SCF (stem cell factor) + IL-3 (interleukin 3) + IL-6, the combination SCF + FL (Flt-3 ligand) + M-GDF (megakaryocyte growth and differentiation factor) + IL-3 significantly improved the total number of viable cells and CD34(+) cells after transduction and the long term-cultured progenitors after 6 weeks. In addition, the combination of SCF + FL + M-GDF + IL-3 maintained more efficiently the lymphoid potential of the progeny of transduced long term-cultured CD34(+) cells, as attested by the significantly higher number of CD56(+), CD19(+), and CD1a(+) cells recovered when FL and M-GDF were added to SCF + IL-3. Thus, even though additional improvements may still be needed in transduction of HPCs, these conditions were adopted for a clinical trial of gene therapy for X-linked severe combined immunodeficiency.

Animals↗
PubMed2000

Gene therapy of human severe combined immunodeficiency (SCID)-X1 disease.

Severe combined immunodeficiency-X1 (SCID-X1) is an X-linked inherited disorder characterized by an early block in T and natural killer (NK) lymphocyte differentiation. This block is caused by mutations of the gene encoding the gammac cytokine receptor subunit of interleukin-2, -4, -7, -9, and -15 receptors, which participates in the delivery of growth, survival, and differentiation signals to early lymphoid progenitors. After preclinical studies, a gene therapy trial for SCID-X1 was initiated, based on the use of complementary DNA containing a defective gammac Moloney retrovirus-derived vector and ex vivo infection of CD34+ cells. After a 10-month follow-up period, gammac transgene-expressing T and NK cells were detected in two patients. T, B, and NK cell counts and function, including antigen-specific responses, were comparable to those of age-matched controls. Thus, gene therapy was able to provide full correction of disease phenotype and, hence, clinical benefit.

Antigens, CD34↗