Privatization and regulation in Turkish telecommunications

Version of RecordThe importance of efficient workings of network industries and the markets in which they operate has long been recognized in the literature. In a parallel fashion, policy makers around the world initiated various restructuring efforts focusing on these sectors. However, the issues of privatization and much needed subsequent regulatory framework face considerable challenges in developing countries. Both political opposition and difficulties encountered in the process of privatization caused major delays in overall privatization and restructuring efforts of these countries. This paper focuses on the telecommunications sector and the Turk Telekom case, in particular, assessing the prospects for its much-debated divestiture, evaluating the company specifics and subsequent regulatory agenda. In doing that, it emphasizes the current "telecom meltdown" in international markets, and compares telecommunications privatizations of various nations. Additionally, the study reviews major regulatory methods and draws on some recommendations for policy makers in the light of the U.S experience in this sector.Aybar, C. B., Guney, S., & Suel, H. (2001, March). Privatization and regulation in Turkish telecommunications: A critical assessment (Working Paper). Manchester, NH: Southern New Hampshire University. Retrieved from http://academicarchive.snhu.ed

Transfusion-transmitted virus prevalence in subjects at high risk of sexually transmitted infection in Turkey

ObjectiveTo assess the possible sexual transmission of virus and to identify the prevalence of TTV viremia in Turkey and its association with other hepatotropic viruses.MethodsSerum samples were collected from 81 subjects (74 prostitutes and seven homosexual men) at high risk of sexually transmitted infection and from 81 healthy controls (74 females and seven males). Sera of patients and controls were tested for TTV, hepatitis A virus, hepatitis B virus, hepatitis C virus, and human immunodeficiency virus. Also, serum alanine and aspartate aminotransferases were measured.ResultsThe prevalence rates of TTV viremia in the risk group and control group were 86.4% and 82.7%, respectively. There was a statistical difference in mean age between TTV-infected and uninfected subjects (38.6 ± 9.9 versus 32.2 ± 6.1 years, respectively, P < 0.001). Prevalence rates of TTV infection in subjects with positive anti-HAV and positive anti-HBc were high when compared with subjects who were negative for these.ConclusionWe suggest that TTV infection has a diverse route of transmission, and its prevalence increases with age; also, the prevalence rate of TTV is high in certain risk groups. The prevalence rates of TTV in the group at risk for sexual transmission (86.4%) and in the control group (82.7%) were among the highest ever reported in the world. Also, we suggest that TTV generally does not cause clinical disease, in spite of this high prevalence

miR-34a-FOXP1 Loop in Ovarian Cancer

Ovarian cancer (OC) is the main cause of gynecological cancer mortality in most developed countries. microRNA (miR) expression dysregulation has been highlighted in human cancers, and miR-34a is found to be downregulated and associated with inhibition of tumor growth and invasion in several malignancies, including OC. The winged helix transcription factor forkhead box P1 (FOXP1) is reported as either an oncogene or tumor suppressor in various cancers. This study aimed to elucidate potential clinical and biological associations of miR-34a and transcription factor FOXP1 in OC. We investigated nine OC patients’ blood samples and two OC cell lines (SKOV-3 and OVCAR-3) using quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR) to determine both miR-34a and FOXP1 expressions. We have found that miR-34a and FOXP1 are reversely correlated in both in vitro and in vivo. Inhibition of miR-34a transiently led to upregulation of FOXP1 mRNA expression and increased cellular invasion in vitro. Our data indicate that miR-34a could be a potential biomarker for improving the diagnostic efficiency of OC, and miR-34a overexpression may reduce OC pathogenesis by targeting FOXP1

Influence of different glycoproteins and of the virion core on SERINC5 antiviral activity [preprint]

Host plasma membrane protein SERINC5 is incorporated into budding retrovirus particles where it blocks subsequent entry into susceptible target cells. Three accessory proteins encoded by diverse retroviruses, HIV-1 Nef, EIAV S2, and MLV Glycogag, each independently disrupt SERINC5 antiviral activity, by redirecting SERINC5 from the site of virion assembly on the plasma membrane to an internal RAB7+ endosomal compartment. Pseudotyping retroviruses with particular glycoproteins, e.g., the vesicular stomatitis glycoprotein (VSV G), renders the infectivity of particles resistant to inhibition by virion-associated SERINC5. To better understand viral determinants for SERINC5-sensitivity, the effect of SERINC5 was assessed using HIV-1, MLV, and M-PMV virion cores, pseudotyped with glycoproteins from Arenavirus, Coronavirus, Filovirus, Rhabdovirus, Paramyxovirus, and Orthomyxovirus genera. Infectivity of particles, pseudotyped with HIV-1, amphotropic-MLV, or influenza virus glycoproteins, was decreased by SERINC5, whether the core was provided by HIV-1, MLV, or M-PMV. Particles generated by all three cores, and pseudotyped with glycoproteins from either avian leukosis virus-A, human endogenous retrovirus K (HERV-K), ecotropic-MLV, HTLV-1, Measles morbillivirus, lymphocytic choriomeningitis mammarenavirus (LCMV), Marburg virus, Ebola virus, severe acute respiratory syndrome-related coronavirus (SARS-CoV), or VSV, were insensitive to SERINC5. In contrast, particles pseudotyped with M-PMV, RD114, or rabies virus (RABV) glycoproteins were sensitive to SERINC5, but only with particular retroviral cores. Resistance to SERINC5 by particular glycoproteins did not correlate with reduced SERINC5 incorporation into particles or with the route of viral entry. These findings indicate that some non-retroviruses may be sensitive to SERINC5 and that, in addition to the viral glycoprotein, the retroviral core influences sensitivity to SERINC5

Amplification of Earthquake Ground Motions in Washington, DC, and Implications for Hazard Assessments in Central and Eastern North America

The extent of damage in Washington, DC, from the 2011 MW 5.8 Mineral, VA, earthquake was surprising for an epicenter 130 km away; U.S. Geological Survey “Did-You-Feel-It” reports suggest that Atlantic Coastal Plain and other unconsolidated sediments amplified ground motions in the city. We measure this amplification relative to bedrock sites using earthquake signals recorded on a temporary seismometer array. The spectral ratios show strong amplification in the 0.7 to 4 Hz frequency range for sites on sediments. This range overlaps with resonant frequencies of buildings in the city as inferred from their heights, suggesting amplification at frequencies to which many buildings are vulnerable to damage. Our results emphasize that local amplification can raise moderate ground motions to damaging levels in stable continental regions, where low attenuation extends shaking levels over wide areas and unconsolidated deposits on crystalline metamorphic or igneous bedrock can result in strong contrasts in near-surface material properties

Partition-of-unity finite-element method for large scale quantum molecular dynamics on massively parallel computational platforms

Over the course of the past two decades, quantum mechanical calculations have emerged as a key component of modern materials research. However, the solution of the required quantum mechanical equations is a formidable task and this has severely limited the range of materials systems which can be investigated by such accurate, quantum mechanical means. The current state of the art for large-scale quantum simulations is the planewave (PW) method, as implemented in now ubiquitous VASP, ABINIT, and QBox codes, among many others. However, since the PW method uses a global Fourier basis, with strictly uniform resolution at all points in space, and in which every basis function overlaps every other at every point, it suffers from substantial inefficiencies in calculations involving atoms with localized states, such as first-row and transition-metal atoms, and requires substantial nonlocal communications in parallel implementations, placing critical limits on scalability. In recent years, real-space methods such as finite-differences (FD) and finite-elements (FE) have been developed to address these deficiencies by reformulating the required quantum mechanical equations in a strictly local representation. However, while addressing both resolution and parallel-communications problems, such local real-space approaches have been plagued by one key disadvantage relative to planewaves: excessive degrees of freedom (grid points, basis functions) needed to achieve the required accuracies. And so, despite critical limitations, the PW method remains the standard today. In this work, we show for the first time that this key remaining disadvantage of real-space methods can in fact be overcome: by building known atomic physics into the solution process using modern partition-of-unity (PU) techniques in finite element analysis. Indeed, our results show order-of-magnitude reductions in basis size relative to state-of-the-art planewave based methods. The method developed here is completely general, applicable to any crystal symmetry and to both metals and insulators alike. We have developed and implemented a full self-consistent Kohn-Sham method, including both total energies and forces for molecular dynamics, and developed a full MPI parallel implementation for large-scale calculations. We have applied the method to the gamut of physical systems, from simple insulating systems with light atoms to complex d- and f-electron systems, requiring large numbers of atomic-orbital enrichments. In every case, the new PU FE method attained the required accuracies with substantially fewer degrees of freedom, typically by an order of magnitude or more, than the current state-of-the-art PW method. Finally, our initial MPI implementation has shown excellent parallel scaling of the most time-critical parts of the code up to 1728 processors, with clear indications of what will be required to achieve comparable scaling for the rest. Having shown that the key remaining disadvantage of real-space methods can in fact be overcome, the work has attracted significant attention: with sixteen invited talks, both domestic and international, so far; two papers published and another in preparation; and three new university and/or national laboratory collaborations, securing external funding to pursue a number of related research directions. Having demonstrated the proof of principle, work now centers on the necessary extensions and optimizations required to bring the prototype method and code delivered here to production applications

Primate immunodeficiency virus Vpx and Vpr counteract transcriptional repression of proviruses by the HUSH complex [preprint]

Drugs that inhibit HIV-1 replication and prevent progression to AIDS do not eliminate HIV-1 proviruses from the chromosomes of long-lived CD4+ memory T cells. To escape eradication by these antiviral drugs, or by the host immune system, HIV-1 exploits poorly defined host factors that silence provirus transcription. These same factors, though, must be overcome by all retroviruses, including HIV-1 and other primate immunodeficiency viruses, in order to activate provirus transcription and produce new virus. Here we show that Vpx and Vpr, proteins from a wide range of primate immunodeficiency viruses, activate provirus transcription in human CD4+ T cells. Provirus activation required the DCAF1 adaptor that links Vpx and Vpr to the CUL4A/B ubiquitin ligase complex, but did not require degradation of SAMHD1, a well-characterized target of Vpx and Vpr. A loss-of-function screen for transcription silencing factors that mimic the effect of Vpx on provirus silencing identified all components of the Human Silencing Hub (HUSH) complex, FAM208A (TASOR/RAP140), MPHOSPH8 (MPP8), PPHLN1 (PERIPHILIN), and MORC2. Vpx associated with the HUSH complex components and decreased steady-state levels of these proteins in a DCAF-dependent manner. Finally, vpx and FAM208A knockdown accelerated HIV-1 and SIVMAC replication kinetics in CD4+ T cells to a similar extent, and HIV-2 replication required either vpx or FAM208A disruption. These results demonstrate that the HUSH complex restricts transcription of primate immunodeficiency viruses and thereby contributes to provirus latency. To counteract this restriction and activate provirus expression, primate immunodeficiency viruses encode Vpx and Vpr proteins that degrade HUSH complex components

A simple analytical expression for the gradient induced potential on active implants during MRI

During magnetic resonance imaging, there is an interaction between the time-varying magnetic fields and the active implantable medical devices (AIMD). In this study, in order to express the nature of this interaction, simplified analytical expressions for the electric fields induced by time-varying magnetic fields are derived inside a homogeneous cylindrical volume. With these analytical expressions, the gradient induced potential on the electrodes of the AIMD can be approximately calculated if the position of the lead inside the body is known. By utilizing the fact that gradient coils produce linear magnetic field in a volume of interest, the simplified closed form electric field expressions are defined. Using these simplified expressions, the induced potential on an implant electrode has been computed approximately for various lead positions on a cylindrical phantom and verified by comparing with the measured potentials for these sample conditions. In addition, the validity of the method was tested with isolated frog leg stimulation experiments. As a result, these simplified expressions may help in assessing the gradient-induced stimulation risk to the patients with implants. © 1964-2012 IEEE