Proposing a Crisis Portfolio for Telecommunications Companies

The aim of the current paper is to classify crises that threaten the telecommunications sector. The design of the crisis portfolio is based on managers’ assessments. Forty eight middle and senior managers working for the three major telecommunications companies in Greece were asked to rate the 16 crises on three major criteria: predictability, severity of consequences/ impact and probability to occur. Based on the results, a bubble chart was created. The present study engages three classification criteria, namely the predictability of a crisis, the impact/severity of consequences and the probability of a crisis occurring. Based on the above criteria, a new typology of totally four crises groups that has been adapted to the telecommunications industry is introduced and discussed. The concept of a crisis portfolio could strongly assist managers in preparing for and coping with crises because being prepared for one crisis in each cluster may provide valuable information for each of the other crises in the same cluster

Intracellular iron uptake is favored in Hfe-KO mouse primary chondrocytes mimicking an osteoarthritis-related phenotype

HFE-hemochromatosis is a disease characterized by a systemic iron overload phenotype mainly associated with mutations in the HFE protein (HFE) gene. Osteoarthritis (OA) has been reported as one of the most prevalent complications in HFE-hemochromatosis patients, but the mechanisms associated with its onset and progression remain incompletely understood. In this study, we have characterized the response to high iron concentrations of a primary culture of articular chondrocytes isolated from newborn Hfe-KO mice and compared the results with that of a similar experiment developed in cells from C57BL/6 wild-type (wt) mice. Our data provide evidence that both wt- and Hfe-KO-derived chondrocytes, when exposed to 50 mu M iron, develop characteristics of an OA-related phenotype, such as an increased expression of metalloproteases, a decreased extracellular matrix production, and a lower expression level of aggrecan. In addition, Hfe-KO cells also showed an increased expression of iron metabolism markers and MMP3, indicating an increased susceptibility to intracellular iron accumulation and higher levels of chondrocyte catabolism. Accordingly, upon treatment with 50 mu M iron, these chondrocytes were found to preferentially differentiate toward hypertrophy with increased expression of collagen I and transferrin and downregulation of SRY (sex-determining region Y)-box containing gene 9 (Sox9). In conclusion, high iron exposure can compromise chondrocyte metabolism, which, when simultaneously affected by an Hfe loss of function, appears to be more susceptible to the establishment of an OA-related phenotype.European Regional Development FundEuropean Union (EU) [EMBRC.PT Alg-01-0145-FEDER-022121, Norte-01-0145-FEDER-000012]Fundacao para a Ciencia e a TecnologiaPortuguese Foundation for Science and Technology [SFRH/BD/77056/2011]Portuguese Foundation for Science and TechnologyPortuguese Foundation for Science and TechnologyPortuguese Science and Technology FoundationPortuguese Foundation for Science and Technologyinfo:eu-repo/semantics/publishedVersio

Association of nadph oxidase p22phox gene C242T, A640G and - 930A/G polymorphisms and MMP1 gene -1607 1G/2G polymorphisms with primary knee osteoarthritis in the greek population

Introduction. Osteoarthritis (OA) is the most common form of arthritis with still unknownpathogenic etiology and considerable contribution of genetic factors. Recently,a new emerging role of oxidative stress in the pathology of OA has beenreported, lacking however elucidation of the underlying mechanism.Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase being acomplex enzyme produced by chondrocytes, presents the major source ofreactive oxygen species (ROS) and main contributor of increased oxidativestress. One of the reasons of cartilage degradation in OA is enzymaticproteolysis of the extracellular matrix by metalloproteinases (MMPs). MMP-1,produced by chondrocytes and synovial cells, is a major proteinase of theMMPs family. The present study aims to evaluate the association of NADPHoxidase p22phox gene C242T, A640G and -A930G polymorphisms andMMP1 gene -1607 1G/2G polymorphism with primary knee OA in the Greekpopulation.Materials and MethodsOne hundred fifty five patients with primary symptomatic knee OA participatedin the study along with 139 matched controls. Genotypes were determinedusing polymerase chain reaction and restriction fragment lengthpolymorphism (PCR - RLFP) technique. Allelic and genotypic frequencieswere compared between both study groups.ResultsNo significant difference was detected for NADPH p22phox C242T andA640G polymorphisms (P>0.05). –A930G polymorphism was significantly associated with knee OA in the crude analysis (P= 0.018). The associationbetween –A930G polymorphism and knee OA disappeared when the resultswere adjusted for obesity (P= 0.078, OR: 0.54, 95%CI: 0.272-1.071). Therewas no significant association between MMP1 -1607 1G/2G polymorphismand knee OA, in crude analysis; however after multiple logistic regressionanalysis, 1G/2G was associated with reduced odds of knee OA by 75% inmales, compared to genotypes 1G/1G+2G/2G, adjusting for age and BMI(adjusted OR: 0.25, 95% CI: 0.069, 0.910, p-value=0.035). The interactionbetween all four polymorphisms was not significant.ConclusionsThe present study shows that NADPH oxidase p22phox gene C242T andA640G are not risk factors for knee OA susceptibility in the Greek population.–A930G and MMP1 -1607 1G/2G polymorphisms might contribute to knee OApathogenesis. Further studies are needed to give a global view of theimportance of this polymorphisms in the pathogenesis of OA

ROS/oxidative stress signaling in osteoarthritis

Osteoarthritis is the most common joint disorder with increasing prevalence due to aging of the population. Its multi-factorial etiology includes oxidative stress and the overproduction of reactive oxygen species, which regulate intracellular signaling processes, chondrocyte senescence and apoptosis, extracellular matrix synthesis and degradation along with synovial inflammation and dysfunction of the subchondral bone. As disease-modifying drugs for osteoarthritis are rare, targeting the complex oxidative stress signaling pathways would offer a valuable perspective for exploration of potential therapeutic strategies in the treatment of this devastating disease. © 2016 Elsevier B.V

Redox and NF-κB signaling in osteoarthritis

Human cells have to deal with the constant production of reactive oxygen species (ROS). Although ROS overproduction might be harmful to cell biology, there are plenty of data showing that moderate levels of ROS control gene expression by maintaining redox signaling. Osteoarthritis (OA) is the most common joint disorder with a multi-factorial etiology including overproduction of ROS. ROS overproduction in OA modifies intracellular signaling, chondrocyte life cycle, metabolism of cartilage matrix and contributes to synovial inflammation and dysfunction of the subchondral bone. In arthritic tissues, the NF-κB signaling pathway can be activated by pro-inflammatory cytokines, mechanical stress, and extracellular matrix degradation products. This activation results in regulation of expression of many cytokines, inflammatory mediators, transcription factors, and several matrix-degrading enzymes. Overall, NF-κB signaling affects cartilage matrix remodeling, chondrocyte apoptosis, synovial inflammation, and has indirect stimulatory effects on downstream regulators of terminal chondrocyte differentiation. Interaction between redox signaling and NF-κB transcription factors seems to play a distinctive role in OA pathogenesis. © 2018 Elsevier Inc

Patient-Related Factors Affecting the Sensitivity of Sonication of Removed Hip and Knee Implants Against Conventional Tissue Cultures for Diagnosis of Prosthetic Joint Infections

Despite its decreasing incidence, prosthesis-related infections remain a research, diagnostic, therapeutic and cost-related problem. Our study aim was to compare the diagnostic accuracy of conventional periprosthetic tissue culture and culture of sonication fluid of the explanted hardware and to investigate the role of patientrelated factors affecting the sensitivity of the sonication method. We investigated 70 patients undergoing revision hip or knee arthroplasty, at our institution. Patients’ medical history and demographic characteristics were recorded. We compared the culture of samples obtained by sonication of explanted hip and knee prostheses with conventional culture of periprosthetic tissue for the microbiological diagnosis of prosthetic-joint infection. Thirty-two patients had septic loosening and 38 aseptic loosening (48 hip prostheses and 22 knee prostheses). The sensitivities of sonication fluid culture and conventional tissue cultures were 81.25% and 56.25%, respectively (p-value = 0.043). The sensitivity of the sonication method was statistically higher in obese, diabetic patients, with age above 60, in uncemented arthroplasties and in arthroplasties because of primary osteoarthritis (p-values &lt; 0.05). The sonication method has a greater sensitivity than the conventional periprosthetic tissue cultures for the periprosthetic infections, especially in obese, diabetic patients, with age above 60, in uncemented arthroplasties and in arthroplasties because of primary osteoarthritis. </jats:p