Die anthropologische Gutachter_innentätigkeit bei Landrechtsfällen im Spannungsfeld zwischen wissenschaftlicher Verantwortung und juristischer Verpflichtung

Das Erkenntnisinteresse dieser Diplomarbeit liegt in der Ergründung der Auswirkungen des Spannungsfelds zwischen Recht und Anthropologie auf die anthropologische Gutachter_innentätigkeit bei Landrechtsfällen. Besonderes Augenmerk wird dabei auf Australien gelegt, wo Recht und Anthropologie bei Native Title-Verfahren aufeinandertreffen. Dieses Aufeinandertreffen birgt dabei nicht nur Auswirkungen auf die anthropologische Gutachter_innentätigkeit, sondern auch auf die indigenen Antragsteller_innen sowie auf die australische Anthropologie und ihr Selbstverständnis als sozialwissenschaftliche Disziplin.The knowledge being sought in this thesis lies within the anlaysis of the effects the tense field between law and anthropology has on anthropologists being expert witnesses in litigations about indigenous landrights. Particular attention is paid to Australia, where law and anthropology interact in native title litigations. This interaction implies not only effects on anthropological expert witnesses, but also on the indigenous claimants and the australian anthropology and its self-conception as a socio-scientific discipline

Eliminating HIV-1 Packaging Sequences from Lentiviral Vector Proviruses Enhances Safety and Expedites Gene Transfer for Gene Therapy

Lentiviral vector genomic RNA requires sequences that partially overlap wild-type HIV-1 gag and env genes for packaging into vector particles. These HIV-1 packaging sequences constitute 19.6% of the wild-type HIV-1 genome and contain functional cis elements that potentially compromise clinical safety. Here, we describe the development of a novel lentiviral vector (LTR1) with a unique genomic structure designed to prevent transfer of HIV-1 packaging sequences to patient cells, thus reducing the total HIV-1 content to just 4.8% of the wildtype genome. This has been achieved by reconfiguring the vector to mediate reverse-transcription with a single strand transfer, instead of the usual two, and in which HIV-1 packaging sequences are not copied. We show that LTR1 vectors offer improved safety in their resistance to remobilization in HIV-1 particles and reduced frequency of splicing into human genes. Following intravenous luciferase vector administration to neonatal mice, LTR1 sustained a higher level of liver transgene expression than an equivalent dose of a standard lentivirus. LTR1 vectors produce reverse-transcription products earlier and start to express transgenes significantly quicker than standard lentiviruses after transduction. Finally, we show that LTR1 is an effective lentiviral gene therapy vector as demonstrated by correction of a mouse hemophilia B model

Regulation of the double-stranded RNA-dependent protein kinase PKR by RNAs encoded by a repeated sequence in the Epstein-Barr virus genome.

During the initial infection of B lymphocytes by Epstein-Barr virus (EBV) only a few viral genes are expressed, six of which encode the EBV nuclear antigens, EBNAs 1-6. The majority of EBNA mRNAs share common 5'-ends containing a variable number of two alternating and repeated exons transcribed from the BamHI W major internal repeats of the viral DNA. These sequences can also exist as independent small RNA species in some EBV-infected cell types. We present evidence that transcripts from these W repeat regions can exert a trans-acting effect on protein synthesis, through their ability to activate the dsRNA-dependent protein kinase PKR. UV cross-linking and filter binding assays have demonstrated that the W transcripts bind specifically to PKR and can compete with another EBV-encoded small RNA, EBER-1, which was shown previously to bind this kinase. In the reticulocyte lysate system the W RNAs shut off protein synthesis through an ability to activate PKR. In contrast to EBER-1, the W RNAs are unable to block the dsRNA-dependent activation of PKR. Using a purified preparation of the protein kinase we have shown that the W transcripts directly activate PKR in vitro. The results suggest that EBV has the ability both to activate and to inhibit PKR through the actions of different products of viral transcription