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In common with several other autoimmune diseases, autoimmune Addison's disease (AAD) is thought to be caused by a combination of deleterious susceptibility polymorphisms in several genes, together with undefined environmental factors and stochastic events. To date, the strongest genomic association with AAD has been with alleles at the HLA locus, DR3-DQ2 and DR4. The contribution of other genetic variants has been inconsistent. We have studied the association of 16 single-nucleotide polymorphisms (SNPs) within the CD28-CTLA-4-ICOS genomic locus, in a cohort comprising 691 AAD patients of Norwegian and UK origin with matched controls. We have also performed a meta-analysis including 1002 patients from European countries. The G-allele of SNP rs231775 in CTLA-4 is associated with AAD in Norwegian patients (odds ratio (OR)=1.35 (confidence interval (CI) 1.10-1.66), P=0.004), but not in UK patients. The same allele is associated with AAD in the total European population (OR=1.37 (CI 1.13-1.66), P=0.002). A three-marker haplotype, comprising PROMOTER_1661, rs231726 and rs1896286 was found to be associated with AAD in the Norwegian cohort only (OR 2.43 (CI 1.68-3.51), P=0.00013). This study points to the CTLA-4 gene as a susceptibility locus for the development of AAD, and refines its mapping within the wider genomic locus.
Transport processes across the membrane are essential to ensure survival of every living cell. Therefore, the exchange of membrane impermeable molecules is mediated by specific transport proteins, which are embedded in the lipid bilayer.
One important class comprises secondary active transporters, which couple very efficiently the uphill transport of the main substrate against its concentration gradient to the downhill transport of an additional substrate. These transporters are widely distributed among all kingdoms of life and accomplish many crucial functions. One function is to counteract the deleterious effect of hyperosmotic stress in bacteria. Several members of the BCCT (betaine-choline-carnitinetransport) family of secondary transporters mediate osmostress protection by the accumulation of the compatible solute betaine or its precursor choline (Lamark et al., 1991; Peter et al., 1996; Ziegler et al., 2010). Besides osmo-dependent sodium or proton-coupled symporters, the BCCT family includes few rare representatives of osmo-independent transporters such as the substrate:product antiporter CaiT from E. coli (Jung et al., 2002; Ziegler et al., 2010).
The best-characterized member of the BCCT family is the sodium-coupled betaine transporter BetP from Corynebacterium glutamicum. BetP together with the ABCtransporter OpuA and the H+-solute symporter ProP, became a paradigm for osmoregulated osmolyte transport. Although, all three transporters were extensively studied, the general mechanism of osmoregulation is still far from being understood. Thus, one task of this thesis was to elucidate further the regulatory properties of BetP.
BetP is tightly regulated by osmotic stress and is able to increase its basal betaine uptake activity dramatically upon elevated osmolalities within one second (Peter et al., 1998a). The osmotic stress is sensed by BetP via two stimuli, one is the increase of the internal K+ concentration above a threshold of 220 mM (Rübenhagen et al., 2001), the second is related to a change in the physical state of the membrane (Maximov et al., 2014). So far, several solved crystal structures in combination with functional and computational analysis provided insights into the coupling mechanism of betaine and its co-substrate sodium (Khafizov et al., 2012; Perez et al., 2012). Despite the wealth of data, the precise regulatory mechanism of trimeric BetP is still unclear.
Novel insights into the regulation of cyclooxygenase-2 expression by platelet-cancer cell cross-talk
(2015)
Platelets are activated by the interaction with cancer cells and release enhanced levels of lipid mediators [such as thromboxane (TX)A2 and prostaglandin (PG)E2, generated from arachidonic acid (AA) by the activity of cyclooxygenase (COX)-1], granule content, including ADP and growth factors, chemokines, proteases and Wnt proteins. Moreover, activated platelets shed different vesicles, such as microparticles (MPs) and exosomes (rich in genetic material such as mRNAs and miRNAs). These platelet-derived products induce several phenotypic changes in cancer cells which confer high metastatic capacity. A central event involves an aberrant expression of COX-2 which influences cell-cycle progression and contribute to the acquisition of a cell migratory phenotype through the induction of epithelial mesenchymal transition genes and down-regulation of E-cadherin expression. The identification of novel molecular determinants involved in the cross-talk between platelets and cancer cells has led to identify novel targets for anti-cancer drug development.
Introduction: ameloblastoma is a slow growing, painless odontogenic swelling which can attain sizes that result in severe deformities of the craniofacial complex. It is the most commonly encountered odontogenic tumor in Nigeria. Surgical intervention is currently the method of treatment; however identification of altered molecular pathways may inform chemotherapeutic potential. The Protein Patched homolog 1 (PTCH-1) is overexpressed in ameloblastoma. Also, mutation in the MDM2 gene can reduce the tumor suppressor function of p53 and promote ameloblastoma growth. No study however has characterized the molecular profile of African cases of ameloblastoma with a view to developing chemotherapeutic alternatives. The objective was to characterize the PTCH-1 genetic profile of Ameloblastoma in Nigerian patients as a first step in investigating its potential for chemotherapeutic intervention.
Methods: twenty-eight FFPE blocks of ameloblastoma cases from Nigerian patients were prepared for antibody processing to PTCH-1 (Polyclonal Anti-PTCH antibody ab39266) and MDM2 (Monoclonal Anti-MDM2 antibody (2A10) ab16895). Cytoplasmic brown staining was considered as positive for PTCH while nuclear staining was positive for MDM2.
Results: moderate and strong expressions for PTCH in ameloblast and stellate reticulum were 78.6% and 60.7% respectively. Only 3 (10.7%) cases expressed MDM2.
Conclusion: the importance of our study is that it supports, in theory, anti-PTCH/SHH chemotherapeutics for Nigerian ameloblastoma cases and also infers the possible additional use of anti-p53 agents.
This article discusses the interrelation between transculturality and transmediality with an emphasis on processes of translation. It focuses on two examples of transcultural and transmedial writing taken from contemporary Cuban literature in Paris: Miguel Sales's recontextualization of Cuban popular music in Paris and William Navarrete's ekphrastic reinscription of his island into the realm of French romantic painting. The case studies are significant in this context because they show how cultural borders are simultaneously set and transgressed at medial crossings—between music and poetry, text, and image. Thus, cultural translations go hand in hand with medial transpositions that include forms of rewriting, recomposition, and revisualization. The connection between moving cultures and moving media also points to the question of “travelling memory” in diaspora.
Protein turnover and quality control by the proteasome is of paramount importance for cell homeostasis. Dysfunction of the proteasome is associated with aging processes and human diseases such as neurodegeneration, cardiomyopathy, and cancer. The regulation, i.e. activation and inhibition of this fundamentally important protein degradation system, is still widely unexplored. We demonstrate here that the evolutionarily highly conserved type II triple-A ATPase VCP and the proteasome inhibitor PSMF1/PI31 interact directly, and antagonistically regulate proteasomal activity. Our data provide novel insights into the regulation of proteasomal activity.
The Fisher information constitutes a natural measure for the sensitivity of a probability distribution with respect to a set of parameters. An implementation of the stationarity principle for synaptic learning in terms of the Fisher information results in a Hebbian self-limiting learning rule for synaptic plasticity. In the present work, we study the dependence of the solutions to this rule in terms of the moments of the input probability distribution and find a preference for non-Gaussian directions, making it a suitable candidate for independent component analysis (ICA). We confirm in a numerical experiment that a neuron trained under these rules is able to find the independent components in the non-linear bars problem. The specific form of the plasticity rule depends on the transfer function used, becoming a simple cubic polynomial of the membrane potential for the case of the rescaled error function. The cubic learning rule is also an excellent approximation for other transfer functions, as the standard sigmoidal, and can be used to show analytically that the proposed plasticity rules are selective for directions in the space of presynaptic neural activities characterized by a negative excess kurtosis.