One of the most remarkable predictions of the physics of strong interactions, and quantum chromodynamics (QCD) in particular, is gluon saturation. It is observed that the gluon density in hadrons, ...such as the proton, grows with energy, or equivalently with decreasing Bjorken-x (the fraction of the hadron momentum carried by the parton). At some point this growth exceeds the unitarity limit and some new phenomena such as non-linear effects must set in. Data on the proton structure function, and on exclusive vector-meson photoproduction from the electron-proton collider HERA, which ended operations in 2007, have been inconclusive on whether or not gluon saturation has been observed. The search for non-linear QCD effects such as gluon saturation in both the proton and the nucleus is one of the main lines of research in high energy nuclear physics today. In nuclei the quantum fluctuations ought to be stronger than in protons. Recently, it has been found that the Quark Gluon Plasma (QGP) created in nucleus-nucleus collisions at RHIC and LHC expands with very little dissipation. The quantum fluctuations of the initial state described by the overlap of two highly Lorentz-contracted nuclei traveling on light-cone trajectories are probably imprinted upon the distribution of particles created in the QGP. Without assessing these quantum fluctuations in nuclei, fundamental properties of the QGP such as its viscosity-to-entropy ratio cannot be determined to a high precision. In this thesis we have studied, for the first time, the angular correlations of photoproduced dijets in ultra-peripheral Pb+Pb collisions at √ sNN = 5.02 TeV. This process has been suggested as a way to extract information of the nuclear gluon density in the Pb target, and thus provide information about the initial state of high energy nucleus-nucleus collisions.
Familial hypercholesterolaemia (FH) is a common genetic cause of premature coronary heart disease (CHD). Globally, one baby is born with FH every minute. If diagnosed and treated early in childhood, ...individuals with FH can have normal life expectancy. This consensus paper aims to improve awareness of the need for early detection and management of FH children. Familial hypercholesterolaemia is diagnosed either on phenotypic criteria, i.e. an elevated low-density lipoprotein cholesterol (LDL-C) level plus a family history of elevated LDL-C, premature coronary artery disease and/or genetic diagnosis, or positive genetic testing. Childhood is the optimal period for discrimination between FH and non-FH using LDL-C screening. An LDL-C ≥5 mmol/L (190 mg/dL), or an LDL-C ≥4 mmol/L (160 mg/dL) with family history of premature CHD and/or high baseline cholesterol in one parent, make the phenotypic diagnosis. If a parent has a genetic defect, the LDL-C cut-off for the child is ≥3.5 mmol/L (130 mg/dL). We recommend cascade screening of families using a combined phenotypic and genotypic strategy. In children, testing is recommended from age 5 years, or earlier if homozygous FH is suspected. A healthy lifestyle and statin treatment (from age 8 to 10 years) are the cornerstones of management of heterozygous FH. Target LDL-C is <3.5 mmol/L (130 mg/dL) if >10 years, or ideally 50% reduction from baseline if 8-10 years, especially with very high LDL-C, elevated lipoprotein(a), a family history of premature CHD or other cardiovascular risk factors, balanced against the long-term risk of treatment side effects. Identifying FH early and optimally lowering LDL-C over the lifespan reduces cumulative LDL-C burden and offers health and socioeconomic benefits. To drive policy change for timely detection and management, we call for further studies in the young. Increased awareness, early identification, and optimal treatment from childhood are critical to adding decades of healthy life for children and adolescents with FH.
Endothelial injury makes the vessel wall vulnerable to cardiovascular diseases. Injured endothelium regenerates by collective sheet migration, that is, the endothelial cells coordinate their motion ...and regrow as a sheet of cells with retained cell‐cell contacts into the wounded area. Leukocytes appear to be involved in endothelial repair in vivo; however, little is known about their identity and role in the reparative sheet migration process. To address these questions, we developed a high‐quality en face technique that enables visualizing of leukocytes and endothelial cells simultaneously following an endoluminal scratch wound injury of the mouse carotid artery. We discovered that regrowing endothelium forms a broad proliferative front accompanied by CD11c+ leukocytes. Functionally, the leukocytes were dispensable for the initial migratory response of the regrowing endothelial sheet, but critical for the subsequent formation and maintenance of a front zone with high cellular density. Marker expression analyses, genetic fate mapping, phagocyte targeting experiments, and mouse knock‐out experiments indicate that the CD11c+ leukocytes were mononuclear phagocytes with an origin from both Ly6Chigh and Ly6Clow monocytes. In conclusion, CD11c+ mononuclear phagocytes are essential for a proper endothelial regrowth following arterial endoluminal scratch injury. Promoting the endothelial‐preserving function of CD11c+ leukocytes may be a strategy to enhance endothelial repair following surgical and endovascular procedures.
CD11c+ mononuclear phagocytes are recruited specifically to regenerating endothelium following vascular injury to orchestrate endothelial sheet migration.
Expression of the Helicobacter pylori blood group antigen binding adhesin A (BabA) is more common in strains isolated from patients with peptic ulcer disease or gastric cancer, rather than ...asymptomatic colonization. Here we used mouse models to examine host determinants that affect H. pylori BabA expression. BabA expression was lost by phase variation as frequently in WT mice as in RAG2-/- mice that do not have functional B or T cells, and in MyD88-/-, TLR2-/- and TLR4-/- mice that are defective in toll like receptor signaling. The presence of other bacteria had no effect on BabA expression as shown by infection of germ free mice. Moreover, loss of BabA expression was not dependent on Le
expression or the capacity of BabA to bind Le
. Surprisingly, gender was the host determinant most associated with loss of BabA expression, which was maintained to a greater extent in male mice and was associated with greater bacterial load. These results suggest the possibility that loss of BabA expression is not driven by adaptive immunity or toll-like receptor signaling, and that BabA may have other, unrecognized functions in addition to serving as an adhesin that binds Le
.
Book review section Kennicott, Patrick C.; Brown, Herbert H.; Hicks, Mason A. ...
Today's Speech,
11/1/1968, 1968-11-00, Letnik:
16, Številka:
4
Book Review
POLITICS AND COMMUNICATION. By Richard R. Fagen. Boston: Little Brown, 1966. pp. x+162. Paper $2.50.
THE NEW POLITICS. By James M. Perry. New York: Clarkson N. Potter, Inc., 1968. pp. viii+230. ...$4.95.
THE LIFE OF POLITICS. By Henry Fairlie. New York: Basic Books, Inc., 1968; pp. 271. $5.95.
THE GREAT SOCIETY. By Glenn R. Capp, Dickenson Publishing Company, Inc., Belmont, California, 1967, pp. 195.
POLITICS AND POWER: THE UNITED STATES SENATE, 1869-1901. By David J. Rothman. Cambridge, Mass.: Harvard University Press, 1966. pp. 348. $6.95.
DIRTY POLITICS. By Bruce L. Felknor. New York: W. W. Norton & Company, Inc., 1966; pp. 295, $5.95.
QUOTEMANSHIP: THE USE AND ABUSE OF QUOTATIONS FOR POLEMICAL AND OTHER PURPOSES. By Paul F. Boiler, Jr. Dallas: Southern Methodist University Press, 1967; pp. xiii+454. $7.95.
LANGUAGE AND POLITICS. By Thomas P. Brockway, ed. Boston: D. C. Heath and Company, 1965. pp. 97+ study aids. Paper $1.50.
THE WORD WAR. By Thomas C. Sorensen (Foreword by Robert F. Kennedy) New York: Harper and Row, Publishers, 1968; pp. xi+337.
BULLETIN FROM DALLAS: THE PRESIDENT IS DEAD. By John B. Mayo, Jr. New York: Exposition Press. 1967; pp. 157. $6.00.
POLITICAL TELEVISION. By Bernard Rubin. Belmont, California: Wadsworth Publishing Company. 1967; pp. 200. $4.50.
ETHICS OF SPEECH COMMUNICATION. By Thomas R. Nilsen. Indianapolis: Bobbs-Merrill, 1966; pp. xii+98. Paper $1.25.
SENATOR FULBRIGHT: PORTRAIT OF A PUBLIC PHILOSOPHER. By Tristram Coffin. New York: E. P. Dutton and Company, 1966; pp. 378. $6.95.
AN ANALYSIS OF LINCOLN AND DOUGLAS AS PUBLIC SPEAKERS AND DEBATERS. By Lionel Crocker. Springfield, Illinois: Charles C. Thomas, 1968, pp. 550. $16.50.
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