"I am your mother and your father!": In vitro derived gametes and the ethics of solo reproduction

In this paper, we will discuss the prospect of human reproduction achieved with gametes originating from only one person. According to statements by a minority of scientists working on the generation of gametes in vitro, it may become possible to create eggs from men’s non-reproductive cells and sperm from women’s. This would enable, at least in principle, the creation of an embryo from cells obtained from only one individual: ‘solo reproduction’. We will consider what might motivate people to reproduce in this way, and the implications that solo reproduction might have for ethics and policy. We suggest that such an innovation is unlikely to revolutionise reproduction and parenting. Indeed, in some respects it is less revolutionary than in vitro fertilisation as a whole. Furthermore, we show that solo reproduction with in vitro created gametes is not necessarily any more ethically problematic than gamete donation—and probably less so. Where appropriate, we draw parallels with the debate surrounding reproductive cloning. We note that solo reproduction may serve to perpetuate reductive geneticised accounts of reproduction, and that this may indeed be ethically questionable. However, in this it is not unique among other technologies of assisted reproduction, many of which focus on genetic transmission. It is for this reason that a ban on solo reproduction might be inconsistent with continuing to permit other kinds of reproduction that also bear the potential to strengthen attachment to a geneticised account of reproduction. Our claim is that there are at least as good reasons to pursue research towards enabling solo reproduction, and eventually to introduce solo reproduction as an option for fertility treatment, as there are to do so for other infertility related purposes

A taxonomy of dignity: a grounded theory study

Abstract Background This paper has its origins in Jonathan Mann's insight that the experience of dignity may explain the reciprocal relationships between health and human rights. It follows his call for a taxonomy of dignity: "a coherent vocabulary and framework to characterize dignity." Methods Grounded theory procedures were use to analyze literature pertaining to dignity and to conduct and analyze 64 semi-structured interviews with persons marginalized by their health or social status, individuals who provide health or social services to these populations, and people working in the field of health and human rights. Results The taxonomy presented identifies two main forms of dignity–human dignity and social dignity–and describes several elements of these forms, including the social processes that violate or promote them, the conditions under which such violations and promotions occur, the objects of violation and promotion, and the consequences of dignity violation. Together, these forms and elements point to a theory of dignity as a quality of individuals and collectives that is constituted through interaction and interpretation and structured by conditions pertaining to actors, relationships, settings, and the broader social order. Conclusion The taxonomy has several implications for work in health and human rights. It suggests a map to possible points of intervention and provides a language in which to talk about dignity

Aggressive fibromatosis of the head and neck: a new classification based on a literature review over 40 years (1968-2008)

BACKGROUND: Fibromatosis is an aggressive fibrous tumor of unknown etiology that is, in some cases, lethal. Until now, there has been no particular classification for the head and neck. Therefore, the aim of the present study was to review the current literature in order to propose a new classification for future studies. METHODS: An evidence-based literature review was conducted from the last 40 years regarding aggressive fibromatosis in the head and neck. Studies that summarized patients' data without including individual data were excluded. RESULTS: Between 1968 and 2008, 179 cases with aggressive fibromatosis of the head and neck were published. The male to female ratio was 91 to 82 with a mean age of 16.87 years, and 57.32% of the described cases that involved the head and neck were found in patients under 11 years. The most common localization was the mandible, followed by the neck. All together, 143 patients were followed up, and in 43 (30.07%), a recurrence was seen. CONCLUSION: No clear prognostic factors for recurrence (age, sex, or localization) were observed. A new classification with regard to hormone receptors and bone involvement could improve the understanding of risk factors and thereby assist in future studies

Bmi-1 Absence Causes Premature Brain Degeneration

Bmi-1, a polycomb transcriptional repressor, is implicated in cell cycle regulation and cell senescence. Its absence results in generalized astrogliosis and epilepsy during the postnatal development, but the underlying mechanisms are poorly understood. Here, we demonstrate the occurrence of oxidative stress in the brain of four-week-old Bmi-1 null mice. The mice showed various hallmarks of neurodegeneration including synaptic loss, axonal demyelination, reactive gliosis and brain mitochondrial damage. Moreover, astroglial glutamate transporters and glutamine synthetase decreased in the Bmi-1 null hippocampus, which might contribute to the sporadic epileptic-like seizures in these mice. These results indicate that Bmi-1 is required for maintaining endogenous antioxidant defenses in the brain, and its absence subsequently causes premature brain degeneration

Enhancing Chemotherapy Response with Bmi-1 Silencing in Ovarian Cancer

Undoubtedly ovarian cancer is a vexing, incurable disease for patients with recurrent cancer and therapeutic options are limited. Although the polycomb group gene, Bmi-1 that regulates the self-renewal of normal stem and progenitor cells has been implicated in the pathogenesis of many human malignancies, yet a role for Bmi-1 in influencing chemotherapy response has not been addressed before. Here we demonstrate that silencing Bmi-1 reduces intracellular GSH levels and thereby sensitizes chemoresistant ovarian cancer cells to chemotherapeutics such as cisplatin. By exacerbating ROS production in response to cisplatin, Bmi-1 silencing activates the DNA damage response pathway, caspases and cleaves PARP resulting in the induction apoptosis in ovarian cancer cells. In an in vivo orthotopic mouse model of chemoresistant ovarian cancer, knockdown of Bmi-1 by nanoliposomal delivery significantly inhibits tumor growth. While cisplatin monotherapy was inactive, combination of Bmi-1 silencing along with cisplatin almost completely abrogated ovarian tumor growth. Collectively these findings establish Bmi-1 as an important new target for therapy in chemoresistant ovarian cancer

On the origin of glioma

Glioma is the most frequent primary brain tumor of adults that has a presumably glial origin. Although our knowledge regarding molecular mechanisms and signaling pathways involved in gliomagenesis has increased immensely during the past decade, high-grade glioma remains a lethal disease with dismal prognosis. The failure of current therapies has to a large extent been ascribed the functional heterogeneity of glioma cells. One reason for this heterogeneity is most certainly the large number of variations in genetic alterations that can be found in high-grade gliomas. Another factor that may influence glioma heterogeneity could be the cell type from which the glioma is initiated. The cell of origin for glioma is still undefined, and additional knowledge about this issue may prove critical for a more complete understanding of glioma biology. Based on information from patients, developmental biology, and experimental glioma models, the most putative target cells include astrocytes, neural stem cells, and oligodendrocyte precursor cells, which are all discussed in more detail in this article. Animal modeling of glioma suggests that these three cell types have the capability to be the origin of glioma, and we have reason to believe that, depending on the initiating cell type, prognosis and response to therapy may be significantly different. Thus, it is essential to explore further the role of cellular origin in glioma