Monopolistic Competition with Two-Part Tariffs

Non-uniform pricing equilibria are shown to dominate uniform pricing equilibria in free entry, monopolistically competitive markets with identical consumers. The non-uniform pricing equilibrium is welfare optimal. Comparisons of Cournot and non-uniform pricing equilibria in terms of the equilibrium number of firms and sales per firm show that the positioning of Cournot equilibria relative to the welfare optimal configuration of firms and outputs depends on the relative curvatures of inverse demand and average cost functions, entry-induced rotation of inverse demand functions, and the relative price effects of changes in own and other firms outputs. The choice between the non-uniform and uniform pricing interpretations of equilibria in differentiated product markets may have important implications for policy analysis

Crafting a Systematic Literature Review on Open-Source Platforms

This working paper unveils the crafting of a systematic literature review on open-source platforms. The high-competitive mobile devices market, where several players such as Apple, Google, Nokia and Microsoft run a platforms- war with constant shifts in their technological strategies, is gaining increasing attention from scholars. It matters, then, to review previous literature on past platforms-wars, such as the ones from the PC and game-console industries, and assess its implications to the current mobile devices platforms-war. The paper starts by justifying the purpose and rationale behind this literature review on open-source platforms. The concepts of open-source software and computer-based platforms were then discussed both individually and in unison, in order to clarify the core-concept of 'open-source platform' that guides this literature review. The detailed design of the employed methodological strategy is then presented as the central part of this paper. The paper concludes with preliminary findings organizing previous literature on open-source platforms for the purpose of guiding future research in this area.Comment: As presented in 10th IFIP WG 2.13 International Conference on Open Source Systems, OSS 2014, San Jos\'e, Costa Rica, May 6-9, 201

The prohibitin-repressive interaction with E2F1 is rapidly inhibited by androgen signalling in prostate cancer cells

Prohibitin (PHB) is a tumour suppressor molecule with pleiotropic activities across several cellular compartments including mitochondria, cell membrane and the nucleus. PHB and the steroid-activated androgen receptor (AR) have an interplay where AR downregulates PHB, and PHB represses AR. Additionally, their cellular locations and chromatin interactions are in dynamic opposition. We investigated the mechanisms of cell cycle inhibition by PHB and how this is modulated by AR in prostate cancer. Using a prostate cancer cell line overexpressing PHB, we analysed the gene expression changes associated with PHB-mediated cell cycle arrest. Over 1000 gene expression changes were found to be significant and gene ontology analysis confirmed PHB-mediated repression of genes essential for DNA replication and synthesis, for example, MCMs and TK1, via an E2F1 regulated pathway-agreeing with its G1/S cell cycle arrest activity. PHB is known to inhibit E2F1-mediated transcription, and the PHB:E2F1 interaction was seen in LNCaP nuclear extracts, which was then reduced by androgen treatment. Upon two-dimensional western blot analysis, the PHB protein itself showed androgen-mediated charge differentiation (only in AR-positive cells), indicating a potential dephosphorylation event. Kinexus phosphoprotein array analysis indicated that Src kinase was the main interacting intracellular signalling hub in androgen-treated LNCaP cells, and that Src inhibition could reduce this AR-mediated charge differentiation. PHB charge change may be associated with rapid dissociation from chromatin and E2F1, allowing the cell cycle to proceed. The AR and androgens may deactivate the repressive functions of PHB upon E2F1 leading to cell cycle progression, and indicates a role for AR in DNA replication licensing

Iron deposits in the knee joints of a thalassemic patient

The overall prognosis for patients with β-thalassemia has improved considerably during the past decades mainly due to regular blood transfusions, improvements in chelation therapy, and enhanced surveillance with imaging studies examining iron overload and other clinical complications. However, the prolonged survival of these patients leads to the development of other health problems including degenerative diseases such as arthropathies, which require further attention since they have a significant impact on the quality of life. In the current case report, we present a 45-year-old white man with β-thalassemia complaining of non-traumatic pain and restriction in the range of motion of both knees. Magnetic resonance imaging (MRI) revealed a tear in the medial meniscus of the left knee as well as iron deposits in both knees. Histological findings confirmed the presence of hemosiderin in both joints. To our knowledge, this is the first reported case of macroscopically documented iron deposits in the knee joints of a patient with β-thalassemia using MRI

Biocytin Recovery and 3D Reconstructions of Filled Hippocampal CA2 Interneurons

How cortical network activity processes information is of importance to a large number of basic 26 and clinical scientific questions. The protocol described here identifies the basic building blocks 27 of this circuitry. The in-depth studies of cortical regions will ultimately provide other scientists 28 with the circuit components needed for an understanding of how the brain acquires, processes 29 and stores information and what goes wrong in disease, while the electrophysiological and morphological data are widely used by computational neuroscientists in the construction of model networks that explore information processing. The protocol outlined here describes how biocytin-filled cells recorded in the CA2 region of the hippocampus are recovered and then reconstructed in 3D. Additionally, the protocol describes the demonstration of calcium binding protein or peptide content in recorded interneurons

Diversity, equity, and inclusion in engineering education: an exploration of European higher education institutions’ strategic frameworks, resources, and initiatives

Significant efforts have been made to promote gender equality in higher education (HE) in Europe. Examples include the establishment of the Athena Swan Charter in the UK in 2005 and the 2019 launch of the Irène Curie Fellowship scheme by Eindhoven University of Technology. But which initiatives address broader diversity, equity, and inclusion (DEI) challenges in HE? And which are specifically focused on engineering education? This exploratory study aims to improve our understanding of the ways in which a set of European HE Institutions engaged in engineering education address DEI at an organisation level, and how this is communicated within the public domain. The analysis of online data provided by a purposive sample of institutions is guided by the following research questions (RQ): 1. How is DEI addressed and defined in institution-wide strategic frameworks? 2. How many institutions describe having an institution-wide DEI organization? 3. What specific policies around DEI are being developed, and what areas are mentioned, defined, and prioritized? 4. What structures and resources noted as part of their DEI activities are specific to engineering faculties and departments? 5. What engineering-specific DEI initiatives exist that are not available in the public domain or are not written in English? Our sample is composed of the host institutions of the authors of the paper, and represent different European countries: Belgium, Denmark, France, Ireland, Portugal, Switzerland, and the UK. The findings of this exploratory study will be used to inform the design of a large-scale survey to identify DEI practices across the SEFI community

Society of pediatric liver transplantation: Current registry status 2011‐2018

BackgroundSPLIT was founded in 1995 in order to collect comprehensive prospective data on pediatric liver transplantation, including waiting list data, transplant, and early and late outcomes. Since 2011, data collection of the current registry has been refined to focus on prospective data and outcomes only after transplant to serve as a foundation for the future development of targeted clinical studies.ObjectiveTo report the outcomes of the SPLIT registry from 2011 to 2018.MethodsThis is a multicenter, cross‐sectional analysis characterizing patients transplanted and enrolled in the SPLIT registry between 2011 and 2018. All patients, <18 years of age, received a first liver‐only, a combined liver‐kidney, or a combined liver‐pancreas transplant during this study period.ResultsA total of 1911 recipients from 39 participating centers in North America were registered. Indications included biliary atresia (38.5%), metabolic disease (19.1%), tumors (11.7%), and fulminant liver failure (11.5%). Greater than 50% of recipients were transplanted as either Status 1A/1B or with a MELD/PELD exception score. Incompatible transplants were performed in 4.1%. Kaplan‐Meier estimates of 1‐year patient and graft survival were 97.3% and 96.6%. First 30 days of surgical complications included reoperation (31.7%), hepatic artery thrombosis (6.3%), and portal vein thrombosis (3.2%). In the first 90 days, biliary tract complications were reported in 13.6%. Acute cellular rejection during first year was 34.7%. At 1 and 2 years of follow‐up, 39.2% and 50.6% had normal liver tests on monotherapy (tacrolimus or sirolimus). Further surgical, survival, allograft function, and complications are detailed.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/153657/1/petr13605_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/153657/2/petr13605.pd

Sostdc1 deficiency accelerates fracture healing by promoting the expansion of periosteal mesenchymal stem cells

Loss of Sostdc1, a growth factor paralogous to Sost, causes the formation of ectopic incisors, fused molars, abnormal hair follicles, and resistance to kidney disease. Sostdc1 is expressed in the periosteum, a source of osteoblasts, fibroblasts and mesenchymal progenitor cells, which are critically important for fracture repair. Here, we investigated the role of Sostdc1 in bone metabolism and fracture repair. Mice lacking Sostdc1 (Sostdc1−/−) had a low bone mass phenotype associated with loss of trabecular bone in both lumbar vertebrae and in the appendicular skeleton. In contrast, Sostdc1−/− cortical bone measurements revealed larger bones with higher BMD, suggesting that Sostdc1 exerts differential effects on cortical and trabecular bone. Mid-diaphyseal femoral fractures induced in Sostdc1−/− mice showed that the periosteal population normally positive for Sostdc1 rapidly expands during periosteal thickening and these cells migrate into the fracture callus at 3 days post fracture. Quantitative analysis of mesenchymal stem cell (MSC) and osteoblast populations determined that MSCs express Sostdc1, and that Sostdc1−/− 5 day calluses harbor > 2-fold more MSCs than fractured wildtype controls. Histologically a fraction of Sostdc1-positive cells also expressed nestin and α-smooth muscle actin, suggesting that Sostdc1 marks a population of osteochondral progenitor cells that actively participate in callus formation and bone repair. Elevated numbers of MSCs in D5 calluses resulted in a larger, more vascularized cartilage callus at day 7, and a more rapid turnover of cartilage with significantly more remodeled bone and a thicker cortical shell at 21 days post fracture. These data support accelerated or enhanced bone formation/remodeling of the callus in Sostdc1−/− mice, suggesting that Sostdc1 may promote and maintain mesenchymal stem cell quiescence in the periosteum