Anaesthetic management of laparoscopic assisted bilateral adrenalectomy in a five-year-old child with Cushing’s disease

A five-year-old girl, weighing 42 kg and with a diagnosis of Cushing’s disease, presented for bilateral, laparoscopic adrenalectomy.South Afr J Anaesth Analg 2011;17(6):396-39

Simulations of Cold Electroweak Baryogenesis: quench from portal coupling to new singlet field

We compute the baryon asymmetry generated from Cold Electroweak Baryogenesis, when a dynamical Beyond-the-Standard-Model scalar singlet field triggers the spinodal transition. Using a simple potential for this additional field, we match the speed of the quench to earlier simulations with a "by-hand" mass flip. We find that for the parameter subspace most similar to a by-hand transition, the final baryon asymmetry shows a similar dependence on quench time and is of the same magnitude. For more general parameter choices the Higgs-singlet dynamics can be very complicated, resulting in an enhancement of the final baryon asymmetry. Our results validate and generalise results of simulations in the literature and open up the Cold Electroweak Baryogenesis scenario to further model building

Bi-galileon theory II: phenomenology

We continue to introduce bi-galileon theory, the generalisation of the single galileon model introduced by Nicolis et al. The theory contains two coupled scalar fields and is described by a Lagrangian that is invariant under Galilean shifts in those fields. This paper is the second of two, and focuses on the phenomenology of the theory. We are particularly interesting in models that admit solutions that are asymptotically self accelerating or asymptotically self tuning. In contrast to the single galileon theories, we find examples of self accelerating models that are simultaneously free from ghosts, tachyons and tadpoles, able to pass solar system constraints through Vainshtein screening, and do not suffer from problems with superluminality, Cerenkov emission or strong coupling. We also find self tuning models and discuss how Weinberg's no go theorem is evaded by breaking Poincar\'e invariance in the scalar sector. Whereas the galileon description is valid all the way down to solar system scales for the self-accelerating models, unfortunately the same cannot be said for self tuning models owing to the scalars backreacting strongly on to the geometry

Cancer Biomarker Discovery: The Entropic Hallmark

Background: It is a commonly accepted belief that cancer cells modify their transcriptional state during the progression of the disease. We propose that the progression of cancer cells towards malignant phenotypes can be efficiently tracked using high-throughput technologies that follow the gradual changes observed in the gene expression profiles by employing Shannon's mathematical theory of communication. Methods based on Information Theory can then quantify the divergence of cancer cells' transcriptional profiles from those of normally appearing cells of the originating tissues. The relevance of the proposed methods can be evaluated using microarray datasets available in the public domain but the method is in principle applicable to other high-throughput methods. Methodology/Principal Findings: Using melanoma and prostate cancer datasets we illustrate how it is possible to employ Shannon Entropy and the Jensen-Shannon divergence to trace the transcriptional changes progression of the disease. We establish how the variations of these two measures correlate with established biomarkers of cancer progression. The Information Theory measures allow us to identify novel biomarkers for both progressive and relatively more sudden transcriptional changes leading to malignant phenotypes. At the same time, the methodology was able to validate a large number of genes and processes that seem to be implicated in the progression of melanoma and prostate cancer. Conclusions/Significance: We thus present a quantitative guiding rule, a new unifying hallmark of cancer: the cancer cell's transcriptome changes lead to measurable observed transitions of Normalized Shannon Entropy values (as measured by high-throughput technologies). At the same time, tumor cells increment their divergence from the normal tissue profile increasing their disorder via creation of states that we might not directly measure. This unifying hallmark allows, via the the Jensen-Shannon divergence, to identify the arrow of time of the processes from the gene expression profiles, and helps to map the phenotypical and molecular hallmarks of specific cancer subtypes. The deep mathematical basis of the approach allows us to suggest that this principle is, hopefully, of general applicability for other diseases

EFHC1 interacts with microtubules to regulate cell division and cortical development

Mutations in the EFHC1 gene are linked to juvenile myoclonic epilepsy (JME), one of the most frequent forms of idiopathic generalized epilepsies. JME is associated with subtle alterations of cortical and subcortical architecture, but the underlying pathological mechanism remains unknown. We found that EFHC1 is a microtubule-associated protein involved in the regulation of cell division. In vitro, EFHC1 loss of function disrupted mitotic spindle organization, impaired M phase progression, induced microtubule bundling and increased apoptosis. EFHC1 impairment in the rat developing neocortex by ex vivo and in utero electroporation caused a marked disruption of radial migration. We found that this effect was a result of cortical progenitors failing to exit the cell cycle and defects in the radial glia scaffold organization and in the locomotion of postmitotic neurons. Therefore, we propose that EFHC1 is a regulator of cell division and neuronal migration during cortical development and that disruption of its functions leads to JM