Spectrum Sharing For Information Freshness: A Repeated Games Perspective

We consider selfish sources that send updates to a monitor over a shared wireless access. The sources would like to minimize the age of their information at the monitor. Our goal is to devise strategies that incentivize such sources to use the shared spectrum cooperatively. Earlier work has modeled such a setting using a non-cooperative one-shot game, played over a single access slot, and has shown that under certain access settings the dominant strategy of each source is to transmit in any slot, resulting in packet collisions between the sources' transmissions and causing all of them to be decoded in error at the monitor. We capture the interaction of the sources over an infinitely many medium access slots using infinitely repeated games. We investigate strategies that enable cooperation resulting in an efficient use of the wireless access, while disincentivizing any source from unilaterally deviating from the strategy. Formally, we are interested in strategies that are a subgame perfect Nash equilibrium (SPNE). We begin by investigating the properties of the one-stage (slot) optimal and access-fair correlated strategies. We then consider their many-slot variants, the age-fair and access-fair strategies, in the infinitely repeated game model. We prove that the access-fair and age-fair strategies are SPNEs for when collision slots are longer than successful transmission slots. Otherwise, neither is a SPNE. We end with simulations that shed light on a possible SPNE for the latter case.Comment: Accepted for publication in IEEE Global Communications Conference (GLOBECOM) 202

The novel link between inflammatory enzyme C2GNT and the shedding of syndecan-1 in podocyte dysfunction

Syndecan-1 is known to be a potential contributor to sub-clinical inflammation in diabetic nephropathy (DN). Loss of syndecan-1 from the surface of podocytes is thought to lead to cell dysfunction, which leads to the detachment of viable podocytes from the glomerulus, an early feature of DN. Although the mechanisms of constitutive syndecan-1 shedding have been addressed by several studies, the pathological mechanisms are less elucidated. The aim of this investigation is to consider the role of the O-glycosylating enzyme C2GNT in syndecan-1 shedding by podocytes. Conditionally immortalised human podocytes were used to study the effect of hyperglycaemia and C2GNT knock-down on syndecan-1 shedding by these cells. Hyperglycaemia induced C2GNT activity in podocytes results in increased O-glycosylation on the surface syndecan-1 in cells treated with high glucose compared to percentage of normal glucose (219.5±145.7 vs . 100%, P<0.05). This increase in O-glycosylation is associated with an increase in the shedding of the syndecan-1 ectodomain by podocytes treated with high glucose compared to percentage of normal glucose (118.2±7.1 vs. 100%, P<0.05). Moreover, podocytes manipulated for C2GNT knockdown show reduced syndecan-1 shedding when treated with high glucose compared to wild type cells treated with high glucose (89.97±11.95 vs. 118.2±7.17, P<0.05). Our findings suggest that the activity of o-glycosylating enzyme C2GNT is raised in podocytes under diabetic conditions. We demonstrate for the first time a novel mecha nism of pathological syndecan-1 shedding induced by C2GNT activity. This excess syndecan-1 shedding by podocytes can contribute to podocyte dysfunction

Non-destructive Micro-structural Characterization of Metallic Specimens with a Portable X-ray Diffraction based Residual Stress Analyzer

Non-destructive characterization of surface microstructure of an engineering component is an important parameter to assess its fitness to function in the given service conditions. The paper describes various case studies performed in authors’ laboratory involving use of portable X-ray diffraction based residual stress analysis system to examine and understand the micro-structural state of the investigated surface. A significant decrease in full width at half maximum (FWHM) of gamma(311) diffraction peak from about 4.2° in the cold worked state to about 2.5° in the annealed/surface melted state was recorded for austenitic stainless steel. In case of 0.4% carbon steel there is sharp increase in FWHM of alpha(211) diffraction peak from about 2° in the as received condition to about 5-6° in the laser hardened condition. Crystallographic texture developed during electro-plating of chromium on stainless steel, could be detected from the strong intensity of alpha (211) peak of chromium at about 19° to the surface normal with respect to all other X-ray inclination angles (ѱ) during residual stress measurement. The results show that FWHM and intensity variation of the diffraction peak are two sensitive parameters for characterization of surface microstructure. Change in FWHM has been used to detect machining-induced cold deformation and evolution of re-crystallized grains in austenitic stainless steel and formation of hard martensite in laser transformation hardened ferritic steel. Variation in the intensity of diffracted peak with respect to X-ray inclination angle provided valuable information regarding crystallographic texture in hard chrome plated deposits

Higher incidence of persistent chronic infection of Chlamydia pneumoniae among coronary artery disease patients in India is a cause of concern

<p>Abstract</p> <p>Background</p> <p>There is growing evidence that <it>Chlamydia pneumoniae </it>may be involved in the pathogenesis of atherosclerosis, as several studies have demonstrated the presence of the organism in atherosclerotic lesions. <it>C. pneumoniae </it>infections, which are especially persistent infections, have been difficult to diagnose either by serological methods or isolation of the organism from the tissue. Nucleic Acid Amplification tests (NAATs) has emerged as an important method for detecting <it>C. pneumoniae</it>. Inspite of high prevalence of <it>C. pneumoniae </it>specific antibodies in coronary heart disease patients, direct detection of <it>C. pneumoniae </it>in circulating blood of coronary artery disease (CAD) patients by sensitive nucleic acid amplification tests nested PCR (nPCR), multiplex PCR (mPCR) has not been carried out is required. Further correlation of the presence of <it>C. pneumoniae </it>in blood of CAD patients with <it>C. pneumoniae </it>specific IgA and IgG antibodies, which may indicative of the status of infection with the progression of atherosclerosis. This will help in order to prepare strategies for the antibiotic intervention to avoid the progression towards CAD.</p> <p>Methods</p> <p>Venous blood was obtained from 91 CAD patients and 46 healthy controls. Nucleic acid amplification tests <it>viz</it>. nested -, semi-nested – and multiplex PCR were used for detection of <it>C. pneumoniae</it>. ELISA carried out prevalence of <it>C. pneumoniae </it>specific IgG and IgA antibodies.</p> <p>Results</p> <p>29.67% (27/91) patients were positive for <it>C. pneumoniae </it>using nested PCR. The sensitivity and specificity of semi-nested and multiplex PCR were 37.03%, 96.96% and 22.22%, 100% with respect to nested PCR. Positive nPCR patients were compared with presence of <it>C. pneumoniae </it>specific IgA, IgA+IgG and IgG antibodies. Among 27 (29.67%) nPCR <it>C. pneumoniae </it>positive CAD patients, 11(12%) were IgA positive, 13(14.2%) were IgA+IgG positive and only1 (1.1%) was IgG positive. A significant presence of <it>C. pneumoniae </it>was detected in heavy smokers, non-alcoholics and with family histories of diabetes and blood pressure group of CAD patients by nPCR.</p> <p>Conclusion</p> <p>The results indicate synergistic association of <it>C. pneumoniae </it>infection and development of CAD with other risk factors. We also detected increased positivity for <it>C. pneumoniae </it>IgA than IgG in nPCR positive CAD patients. Positive nPCR findings in conjunction with persisting high <it>C. pneumoniae </it>specific antibody strongly suggest an ongoing infection.</p

Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

As mortality rates decline, life expectancy increases, and populations age, non-fatal outcomes of diseases and injuries are becoming a larger component of the global burden of disease. The Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) provides a comprehensive assessment of prevalence, incidence, and years lived with disability (YLDs) for 328 causes in 195 countries and territories from 1990 to 2016

Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990–2017: A systematic analysis for the Global Burden of Disease Study 2017

Background: The Global Burden of Diseases, Injuries, and Risk Factors Study 2017 (GBD 2017) includes a comprehensive assessment of incidence, prevalence, and years lived with disability (YLDs) for 354 causes in 195 countries and territories from 1990 to 2017. Previous GBD studies have shown how the decline of mortality rates from 1990 to 2016 has led to an increase in life expectancy, an ageing global population, and an expansion of the non-fatal burden of disease and injury. These studies have also shown how a substantial portion of the world's population experiences non-fatal health loss with considerable heterogeneity among different causes, locations, ages, and sexes. Ongoing objectives of the GBD study include increasing the level of estimation detail, improving analytical strategies, and increasing the amount of high-quality data. Methods: We estimated incidence and prevalence for 354 diseases and injuries and 3484 sequelae. We used an updated and extensive body of literature studies, survey data, surveillance data, inpatient admission records, outpatient visit records, and health insurance claims, and additionally used results from cause of death models to inform estimates using a total of 68 781 data sources. Newly available clinical data from India, Iran, Japan, Jordan, Nepal, China, Brazil, Norway, and Italy were incorporated, as well as updated claims data from the USA and new claims data from Taiwan (province of China) and Singapore. We used DisMod-MR 2.1, a Bayesian meta-regression tool, as the main method of estimation, ensuring consistency between rates of incidence, prevalence, remission, and cause of death for each condition. YLDs were estimated as the product of a prevalence estimate and a disability weight for health states of each mutually exclusive sequela, adjusted for comorbidity. We updated the Socio-demographic Index (SDI), a summary development indicator of income per capita, years of schooling, and total fertility rate. Additionally, we calculated differences between male and female YLDs to identify divergent trends across sexes. GBD 2017 complies with the Guidelines for Accurate and Transparent Health Estimates Reporting. Findings: Globally, for females, the causes with the greatest age-standardised prevalence were oral disorders, headache disorders, and haemoglobinopathies and haemolytic anaemias in both 1990 and 2017. For males, the causes with the greatest age-standardised prevalence were oral disorders, headache disorders, and tuberculosis including latent tuberculosis infection in both 1990 and 2017. In terms of YLDs, low back pain, headache disorders, and dietary iron deficiency were the leading Level 3 causes of YLD counts in 1990, whereas low back pain, headache disorders, and depressive disorders were the leading causes in 2017 for both sexes combined. All-cause age-standardised YLD rates decreased by 3·9% (95% uncertainty interval [UI] 3·1-4·6) from 1990 to 2017; however, the all-age YLD rate increased by 7·2% (6·0-8·4) while the total sum of global YLDs increased from 562 million (421-723) to 853 million (642-1100). The increases for males and females were similar, with increases in all-age YLD rates of 7·9% (6·6-9·2) for males and 6·5% (5·4-7·7) for females. We found significant differences between males and females in terms of age-standardised prevalence estimates for multiple causes. The causes with the greatest relative differences between sexes in 2017 included substance use disorders (3018 cases [95% UI 2782-3252] per 100 000 in males vs 1400 [1279-1524] per 100 000 in females), transport injuries (3322 [3082-3583] vs 2336 [2154-2535]), and self-harm and interpersonal violence (3265 [2943-3630] vs 5643 [5057-6302]). Interpretation: Global all-cause age-standardised YLD rates have improved only slightly over a period spanning nearly three decades. However, the magnitude of the non-fatal disease burden has expanded globally, with increasing numbers of people who have a wide spectrum of conditions. A subset of conditions has remained globally pervasive since 1990, whereas other conditions have displayed more dynamic trends, with different ages, sexes, and geographies across the globe experiencing varying burdens and trends of health loss. This study emphasises how global improvements in premature mortality for select conditions have led to older populations with complex and potentially expensive diseases, yet also highlights global achievements in certain domains of disease and injury