Study of the process e+e−→ppˉe^+e^-\to p\bar{p} in the c.m. energy range from threshold to 2 GeV with the CMD-3 detector

Using a data sample of 6.8 pb$^{-1}$ collected with the CMD-3 detector at the VEPP-2000 $e^+e^-$ collider we select about 2700 events of the $e^+e^- \to p\bar{p}$ process and measure its cross section at 12 energy ponts with about 6\% systematic uncertainty. From the angular distribution of produced nucleons we obtain the ratio $|G_{E}/G_{M}| = 1.49 \pm 0.23 \pm 0.30$

Measurement of the e+e−→K+K−π+π−e^+e^- \to K^+K^-\pi^+\pi^- cross section with the CMD-3 detector at the VEPP-2000 collider

The process $e^+e^- \to K^+K^-\pi^+\pi^-$ has been studied in the center-of-mass energy range from 1500 to 2000\,MeV using a data sample of 23 pb$^{-1}$ collected with the CMD-3 detector at the VEPP-2000 $e^+e^-$ collider. Using about 24000 selected events, the $e^+e^- \to K^+K^-\pi^+\pi^-$ cross section has been measured with a systematic uncertainty decreasing from 11.7\% at 1500-1600\,MeV to 6.1\% above 1800\,MeV. A preliminary study of $K^+K^-\pi^+\pi^-$ production dynamics has been performed

P-P Total Cross Sections at VHE from Accelerator Data

Comparison of P-P total cross-sections estimations at very high energies - from accelerators and cosmic rays - shows a disagreement amounting to more than 10 %, a discrepancy which is beyond statistical errors. Here we use a phenomenological model based on the Multiple-Diffraction approach to successfully describe data at accelerator energies. The predictions of the model are compared with data On the basis of regression analysis we determine confident error bands, analyzing the sensitivity of our predictions to the employed data for extrapolation. : using data at 546 and 1.8 TeV, our extrapolations for p-p total cross-sections are only compatible with the Akeno cosmic ray data, predicting a slower rise with energy than other cosmic ray results and other extrapolation methods. We discuss our results within the context of constraints in the light of future accelerator and cosmic ray experimental results.Comment: 26 pages aqnd 11 figure

Phenotypic Modulation of Smooth Muscle Cells in Atherosclerosis Is Associated With Downregulation of LMOD1, SYNPO2, PDLIM7, PLN, and SYNM

OBJECTIVE: Key augmented processes in atherosclerosis have been identified, whereas less is known about downregulated pathways. Here, we applied a systems biology approach to examine suppressed molecular signatures, with the hypothesis that they may provide insight into mechanisms contributing to plaque stability. APPROACH AND RESULTS: Muscle contraction, muscle development, and actin cytoskeleton were the most downregulated pathways (false discovery rate=6.99e-21, 1.66e-6, 2.54e-10, respectively) in microarrays from human carotid plaques (n=177) versus healthy arteries (n=15). In addition to typical smooth muscle cell (SMC) markers, these pathways also encompassed cytoskeleton-related genes previously not associated with atherosclerosis. SYNPO2, SYNM, LMOD1, PDLIM7, and PLN expression positively correlated to typical SMC markers in plaques (Pearson r>0.6, P0.8, P<0.0001). By immunohistochemistry, the proteins were expressed in SMCs in normal vessels, but largely absent in human plaques and intimal hyperplasia. Subcellularly, most proteins localized to the cytoskeleton in cultured SMCs and were regulated by active enhancer histone modification H3K27ac by chromatin immunoprecipitation-sequencing. Functionally, the genes were downregulated by PDGFB (platelet-derived growth factor beta) and IFNg (interferron gamma), exposure to shear flow stress, and oxLDL (oxidized low-density lipoprotein) loading. Genetic variants in PDLIM7, PLN, and SYNPO2 loci associated with progression of carotid intima-media thickness in high-risk subjects without symptoms of cardiovascular disease (n=3378). By eQTL (expression quantitative trait locus), rs11746443 also associated with PDLIM7 expression in plaques. Mechanistically, silencing of PDLIM7 in vitro led to downregulation of SMC markers and disruption of the actin cytoskeleton, decreased cell spreading, and increased proliferation. CONCLUSIONS: We identified a panel of genes that reflect the altered phenotype of SMCs in vascular disease and could be early sensitive markers of SMC dedifferentiation

The state of the Martian climate

60°N was +2.0°C, relative to the 1981–2010 average value (Fig. 5.1). This marks a new high for the record. The average annual surface air temperature (SAT) anomaly for 2016 for land stations north of starting in 1900, and is a significant increase over the previous highest value of +1.2°C, which was observed in 2007, 2011, and 2015. Average global annual temperatures also showed record values in 2015 and 2016. Currently, the Arctic is warming at more than twice the rate of lower latitudes

Measurement of the e+e−→π+π−e^+e^-\to\pi^+\pi^- cross section from threshold to 1.2 GeV with the CMD-3 detector

The cross section of the process $e^+e^-\to\pi^+\pi^-$ has been measured in the center of mass energy range from 0.32 to 1.2 GeV with the CMD-3 detector at the electron-positron collider VEPP-2000. The measurement is based on a full dataset collected below 1 GeV during three data taking seasons, corresponding to an integrated luminosity of about 62 pb$^{-1}$. In the dominant $\rho$-resonance region, a systematic uncertainty of 0.7% has been reached. At energies around $\phi$-resonance the $\pi^+\pi^-$ production cross section was measured for the first time with high energy resolution. The forward-backward charge asymmetry in the $\pi^+\pi^-$ production has also been measured. It shows the strong deviation from the theoretical prediction based on conventional sQED framework and is in good agreement with GVDM and dispersive-based predictions. The impact of presented results on the evaluation of the hadronic contribution to the anomalous magnetic moment of muon is discussed.Comment: 52 pages, 36 figures; cosmetic changes of the text, fix fig.2 , fix comment on used selection cuts in the attached radiative correction tabl

Proteoglycan 4 modulates osteogenic smooth muscle cell differentiation during vascular remodeling and intimal calcification

Calcification is a prominent feature of late-stage atherosclerosis, but the mechanisms driving this process are unclear. Using a biobank of carotid endarterectomies, we recently showed that Proteoglycan 4 (PRG4) is a key molecular signature of calcified plaques, expressed in smooth muscle cell (SMC) rich regions. Here, we aimed to unravel the PRG4 role in vascular remodeling and intimal calcification. PRG4 expression in human carotid endarterectomies correlated with calcification assessed by preoperative computed tomographies. PRG4 localized to SMCs in early intimal thickening, while in advanced lesions it was found in the extracellular matrix, surrounding macro-calcifications. In experimental models, Prg4 was upregulated in SMCs from partially ligated ApoE(-/-) mice and rat carotid intimal hyperplasia, correlating with osteogenic markers and TGFb1. Furthermore, PRG4 was enriched in cells positive for chondrogenic marker SOX9 and around plaque calcifications in ApoE(-/-) mice on warfarin. In vitro, PRG4 was induced in SMCs by IFNg, TGFb1 and calcifying medium, while SMC markers were repressed under calcifying conditions. Silencing experiments showed that PRG4 expression was driven by transcription factors SMAD3 and SOX9. Functionally, the addition of recombinant human PRG4 increased ectopic SMC calcification, while arresting cell migration and proliferation. Mechanistically, it suppressed endogenous PRG4, SMAD3 and SOX9, and restored SMC markers' expression. PRG4 modulates SMC function and osteogenic phenotype during intimal remodeling and macro-calcification in response to TGFb1 signaling, SMAD3 and SOX9 activation. The effects of PRG4 on SMC phenotype and calcification suggest its role in atherosclerotic plaque stability, warranting further investigations.Vascular Surger