Automated Detection of EUV Polar Coronal Holes During Solar Cycle 23

A new method for automated detection of polar coronal holes is presented. This method, called perimeter tracing, uses a series of 171, 195, and 304 \AA\ full disk images from the Extreme ultraviolet Imaging Telescope (EIT) on SOHO over solar cycle 23 to measure the perimeter of polar coronal holes as they appear on the limbs. Perimeter tracing minimizes line-of-sight obscurations caused by the emitting plasma of the various wavelengths by taking measurements at the solar limb. Perimeter tracing also allows for the polar rotation period to emerge organically from the data as 33 days. We have called this the Harvey rotation rate and count Harvey rotations starting 4 January 1900. From the measured perimeter, we are then able to fit a curve to the data and derive an area within the line of best fit. We observe the area of the northern polar hole area in 1996, at the beginning of solar cycle 23, to be about 4.2% of the total solar surface area and about 3.6% in 2007. The area of the southern polar hole is observed to be about 4.0% in 1996 and about 3.4% in 2007. Thus, both the north and south polar hole areas are no more than 15% smaller now than they were at the beginning of cycle 23. This compares to the polar magnetic field measured to be about 40% less now than it was a cycle ago.Comment: 18 pagers, 7 figures, accepted to Solar Physic

Global energy budgets and ‘Trenberth diagrams’ for the climates of terrestrial and gas giant planets

The climate on Earth is generally determined by the amount and distribution of incoming solar radiation, which must be balanced in equilibrium by the emission of thermal radiation from the surface and atmosphere. The precise routes by which incoming energy is transferred from the surface and within the atmosphere and back out to space, however, are important features that characterize the current climate. This has been analysed in the past by several groups over the years, based on combinations of numerical model simulations and direct observations of the Earths climate system. The results are often presented in schematic form to show the main routes for the transfer of energy into, out of and within the climate system. Although relatively simple in concept, such diagrams convey a great deal of information about the climate systemin a compact form. Such an approach has not so far been widely adopted in any systematic way for other planets of the Solar System, let alone beyond, although quite detailed climate models of several planets are now available, constrained by many new observations and measurements. Here we present an analysis of the global transfers of energy within the climate systems of a range of planets within the Solar System, including Mars, Titan, Venus and Jupiter, as modelled by relatively comprehensive radiative transfer and (in some cases) numerical circulationmodels. These results are presented in schematic form for comparison with the classical global energy budget analyses (e.g. Trenberth et al. 2009; Stephens et al. 2012; Wild et al. 2013; IPCC 2013) for the Earth, highlighting important similarities and differences. We also take the first steps towards extending this approach to other Solar System and extra-solar planets, including Mars, Venus, Titan, Jupiter and the ‘hot Jupiter’ exoplanet HD189733b, presenting a synthesis of both previously published and new calculations for all of these planets

CDK-Mediated Regulation of Cell Functions via c-Jun Phosphorylation and AP-1 Activation

Cyclin-dependent kinases (CDKs) and their targets have been primarily associated with regulation of cell-cycle progression. Here we identify c-Jun, a transcription factor involved in the regulation of a broad spectrum of cellular functions, as a newly recognized CDK substrate. Using immune cells from mouse and human, and several complementary in vitro and in vivo approaches including dominant negative protein expression, pharmacologic inhibitors, kinase assays and CDK4 deficient cells, we demonstrate the ability of CDK4 to phosphorylate c-Jun. Additionally, the activity of AP-1, a ubiquitous transcription factor containing phosphorylated c-Jun as a subunit, was inhibited by abrogating CDK4. Surprisingly, the regulation of c-Jun phosphorylation by CDK4 occurred in non-dividing cells, indicating that this pathway is utilized for cell functions that are independent of proliferation. Our studies identify a new substrate for CDK4 and suggest a mechanism by which CDKs can regulate multiple cellular activation functions, not all of which are directly associated with cell cycle progression. These findings point to additional roles of CDKs in cell signaling and reveal potential implications for therapeutic manipulations of this kinase pathway

Silent brain infarct

Akutni infarkt mozga svojim nastupom i simptomima uzrokuje relativno jasnu i prepoznatljivu kliničku sliku, no postoje kronične pojedinačne i/ili difuzne ishemične lezije mozga koje su klinički asimptomatske i duže vremena se ne prepoznaju. Termin tihi infarkt mozga često se koristi za opis infarkta mozga koji se slučajno utvrdi u osoba koje nikad ranije u svojoj povijesti bolesti nisu imale kliničke simptome tranzitorne ishemijske atake ili moždanog udara. Može ga se utvrditi obdukcijom ili neuroradiološkim pretragama, kompjutoriziranom tomografijom i magnetskom rezonancijom mozga. Radi se najčešće o malom infarktu u dubokim subkortikalnim regijama mozga i morfološki je sličan simptomatskom lakunarnom infarktu. Lakunarna ishemična lezija mozga posljedica je okluzije duboke, penetrantne arterije u čijoj se osnovi uglavnom nalazi hipertenzivna moždana mikroangiopatija. Tihom infarktu mozga posljednje se desetljeće pridaje velika pažnja jer su studije pokazale da prisutnost tihog infarkta mozga dvostruko povećava rizik nastanka simptomatskog moždanog udara i demencije. U ovom preglednom članku prikazujemo epidemiologiju, patofiziološka obilježja, čimbenike rizika i moguće posljedice tihog infarkta mozga.With its onset and symptoms the acute brain stroke causes relatively clear and recognizable clinical features. However, there are chronic, single and/or diffuse ischemic brain lesions which are clinically asymptomatic and which take longer to recognize. The term ”silent brain infarct” is frequently used to describe the brain infarct which is determined with the autopsy by chance or which could be determined with computerized tomography. Such brain infarct could also be determined using the brain magnetic resonance imaging on people who never before had clinical symptoms transient ischemic attack or brain stroke in their lives. For the most of the time this is about small infarct in deep sub-cortical brain regions. It is morphologically similar to symptomatic lacunar infarct. Lacunar ischemic brain lesion is the consequence of the deep, perforating artery occlusion. Its base is mainly the hypertensive brain microangiopathy. The silent brain infarct is given great attention in the last decade because the studies show the silent brain infarct presence doubles the symptomatic brain stroke and dementia risk. In this review we show the epidemiology, the pathophysiologic attributes, the risk factors and possible silent brain infarct consequences

Atmospheric electrification in dusty, reactive gases in the solar system and beyond

Detailed observations of the solar system planets reveal a wide variety of local atmospheric conditions. Astronomical observations have revealed a variety of extrasolar planets none of which resembles any of the solar system planets in full. Instead, the most massive amongst the extrasolar planets, the gas giants, appear very similar to the class of (young) Brown Dwarfs which are amongst the oldest objects in the universe. Despite of this diversity, solar system planets, extrasolar planets and Brown Dwarfs have broadly similar global temperatures between 300K and 2500K. In consequence, clouds of different chemical species form in their atmospheres. While the details of these clouds differ, the fundamental physical processes are the same. Further to this, all these objects were observed to produce radio and X-ray emission. While both kinds of radiation are well studied on Earth and to a lesser extent on the solar system planets, the occurrence of emission that potentially originate from accelerated electrons on Brown Dwarfs, extrasolar planets and protoplanetary disks is not well understood yet. This paper offers an interdisciplinary view on electrification processes and their feedback on their hosting environment in meteorology, volcanology, planetology and research on extrasolar planets and planet formation

Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes

BACKGROUND: Data are lacking on the long-term effect on cardiovascular events of adding sitagliptin, a dipeptidyl peptidase 4 inhibitor, to usual care in patients with type 2 diabetes and cardiovascular disease. METHODS: In this randomized, double-blind study, we assigned 14,671 patients to add either sitagliptin or placebo to their existing therapy. Open-label use of antihyperglycemic therapy was encouraged as required, aimed at reaching individually appropriate glycemic targets in all patients. To determine whether sitagliptin was noninferior to placebo, we used a relative risk of 1.3 as the marginal upper boundary. The primary cardiovascular outcome was a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. RESULTS: During a median follow-up of 3.0 years, there was a small difference in glycated hemoglobin levels (least-squares mean difference for sitagliptin vs. placebo, -0.29 percentage points; 95% confidence interval [CI], -0.32 to -0.27). Overall, the primary outcome occurred in 839 patients in the sitagliptin group (11.4%; 4.06 per 100 person-years) and 851 patients in the placebo group (11.6%; 4.17 per 100 person-years). Sitagliptin was noninferior to placebo for the primary composite cardiovascular outcome (hazard ratio, 0.98; 95% CI, 0.88 to 1.09; P<0.001). Rates of hospitalization for heart failure did not differ between the two groups (hazard ratio, 1.00; 95% CI, 0.83 to 1.20; P = 0.98). There were no significant between-group differences in rates of acute pancreatitis (P = 0.07) or pancreatic cancer (P = 0.32). CONCLUSIONS: Among patients with type 2 diabetes and established cardiovascular disease, adding sitagliptin to usual care did not appear to increase the risk of major adverse cardiovascular events, hospitalization for heart failure, or other adverse events