Renormalization Group Improved Exponentiation of Soft Gluons in QCD

We extend the methods of Yennie, Frautschi and Suura to QCD for the summation of soft gluon effects in which infrared singularities are cancelled to all orders in $\alpha_s$. An explicit formula for the respective \rngp improved exponentiated cross section is obtained for q+\bbar{{q'}}\to q+\bbar{{q'}}+ n(G) at SSC energies. Possible applications are discussed.Comment: 7 pages (1 figure not included, available on request) LATEX, UTHEP-93-040

Multiple photon effects in pppp scattering at SSC energies

The Monte Carlo program SSCYFS2 is used in conjunction with available parton distribution functions to calculate the effects of multiple photon radiation on pp scattering at SSC energies. Effects relevant to precision SSC physics such as Higgs discovery and exploration are illustrated.Comment: LaTeX file, uses phyzzx, 7pp + 5 LaTeX figure

Closed Strings with Low Harmonics and Kinks

Low-harmonic formulas for closed relativistic strings are given. General parametrizations are presented for the addition of second- and third-harmonic waves to the fundamental wave. The method of determination of the parametrizations is based upon a product representation found for the finite Fourier series of string motion in which the constraints are automatically satisfied. The construction of strings with kinks is discussed, including examples. A procedure is laid out for the representation of kinks that arise from self-intersection, and subsequent intercommutation, for harmonically parametrized cosmic strings.Comment: 39, CWRUTH-93-

Cumulative Human Immunodeficiency Viremia, Antiretroviral Therapy, and Incident Myocardial Infarction

Background: People living with HIV are at risk of increased myocardial infarction (MI). Cumulative HIV viral load (VL) has been proposed as a better measure of HIV inflammation than other measures of VL, like baseline VL, but its associations with MI are not known. Methods: The multisite Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) cohort includes clinical data and centrally adjudicated MI with distinction between atheroembolic MI (type 1) and MI related to supply-demand mismatch (type 2). We examined CNICS participants who were not on antiretroviral therapy (ART) at enrollment. Cumulative VL (copy-days of virus) from 6 months after enrollment was estimated with a time-weighted sum using the trapezoidal rule. We modeled associations of cumulative and baseline VL with MI by type using marginal structural Cox models. We contrasted the 75% percentile of the VL distribution with the 25% percentile. Results: Among 11,324 participants, 218 MIs occurred between 1996 and 2016. Higher cumulative VL was associated with risk of all MI (hazard ratio [HR] = 1.72; 95% confidence interval [CI] = 1.26, 2.36), type 1 MI (HR = 1.23; 95% CI = 0.78, 1.96), and type 2 MI (HR = 2.52; 95% CI = 1.74, 3.66). While off ART, cumulative VL had a stronger association with type 1 MI (HR = 2.13; 95% CI = 1.15, 3.94) than type 2 MI (HR = 1.25; 95% CI = 0.70, 2.25). Baseline VL was associated with all MI (HR = 1.60; 95% CI = 1.28, 2.01), type 1 MI (HR = 1.73; 95% CI = 1.26, 2.38), and type 2 MI (HR = 1.51; 95% CI = 1.10, 2.08). Conclusions: Higher cumulative and baseline VL is associated with all MI, with a particularly strong association between cumulative VL and type 2 MI

Rescue of beta-amyloid\u2013induced alterations in cerebrovascular protein expression by pioglitazone in APP mice: Link to functional recovery in the cerebrovasculature

Cerebrovascular dysfunction appears prior to A\u3b2-plaque deposition and measurable mnemonic impairment in Alzheimer's disease (AD) patients and amyloid precursor protein (APP)-expressing transgenic mice. The soluble, highly toxic A\u3b2-fragment generated from the amyloidogenic processing of APP is likely the primary instigator of chronic cerebrovascular insufficiency in APP mice. We recently demonstrated that the PPAR-gamma agonist, pioglitazone, is a potent drug for reversing cerebrovascular impairment at all stages of A\u3b2-induced pathology in APP mice. Our aims are to (a) characterize the effect of A\u3b2-overproduction on the cerebrovascular proteome of APP mice; (b) determine the extent to which pioglitazone rescues the A\u3b2-altered cerebrovascular proteome; and (c) determine the link between protein expression rescue by pioglitazone and functional recovery in the cerebrovasculature.Peer reviewed: YesNRC publication: Ye

A male with unilateral microphthalmia reveals a role for TMX3 in eye development.

Anophthalmia and microphthalmia are important birth defects, but their pathogenesis remains incompletely understood. We studied a patient with severe unilateral microphthalmia who had a 2.7 Mb deletion at chromosome 18q22.1 that was inherited from his mother. In-situ hybridization showed that one of the deleted genes, TMX3, was expressed in the retinal neuroepithelium and lens epithelium in the developing murine eye. We re-sequenced TMX3 in 162 patients with anophthalmia or microphthalmia, and found two missense substitutions in unrelated patients: c.116G>A, predicting p.Arg39Gln, in a male with unilateral microphthalmia and retinal coloboma, and c.322G>A, predicting p.Asp108Asn, in a female with unilateral microphthalmia and severe micrognathia. We used two antisense morpholinos targeted against the zebrafish TMX3 orthologue, zgc:110025, to examine the effects of reduced gene expression in eye development. We noted that the morphant larvae resulting from both morpholinos had significantly smaller eye sizes and reduced labeling with islet-1 antibody directed against retinal ganglion cells at 2 days post fertilization. Co-injection of human wild type TMX3 mRNA rescued the small eye phenotype obtained with both morpholinos, whereas co-injection of human TMX3(p.Arg39Gln) mutant mRNA, analogous to the mutation in the patient with microphthalmia and coloboma, did not rescue the small eye phenotype. Our results show that haploinsufficiency for TMX3 results in a small eye phenotype and represents a novel genetic cause of microphthalmia and coloboma. Future experiments to determine if other thioredoxins are important in eye morphogenesis and to clarify the mechanism of function of TMX3 in eye development are warranted