An Unorthodox Introduction to QCD

These are lecture notes presented at the 2017 CTEQ Summer School at the University of Pittsburgh and the 2018 CTEQ Summer School at the University of Puerto Rico, Mayaguez. The title is a reference to hep-th/0309149 and introduces perturbative QCD and its application to jet substructure from a bottom-up perspective based on the approximation of QCD as a weakly-coupled, conformal field theory. Using this approach, a simple derivation of the Sudakov form factor with soft gluon emission modeled as a Poisson process is presented. Topics of the identification and discrimination of quark- versus gluon-initiated jets and jet grooming are also discussed.Comment: 16 pages, 18 figures. Comments welcome!, v2: updated to include both lectures from the 2018 CTEQ schoo

Unique genes differentially expressed during Incipient CLAD vs. No CLAD.

<p>Unique genes differentially expressed during Incipient CLAD vs. No CLAD.</p

Principal component analysis.

<p>Principal component analysis based on the 40 differentially expressed candidate genes demonstrates modest separation of incipient CLAD and CLAD free groups. The percentage of total variance accounted for by the first principal component was 63.2%, and for the second principal component was 15.1%.</p

Hierarchical clustering and heat map.

<p>Hierarchical clustering and heat map based on the expression index of n = 40 candidate genes.</p

Volcano plot visualization of differential gene expression.

<p>DAE generated a candidate list of 55 probe sets, 51 over- and 4 under-expressed in the incipient CLAD as compared to the CLAD free group.</p

Clinical characteristics of the CLAD Free and Incipient CLAD cohorts.

<p>Clinical characteristics of the CLAD Free and Incipient CLAD cohorts.</p

Sample selection flow chart.

<p>LTR, lung transplant recipient. BAL, bronchoalveolar lavage. CLAD, chronic lung allograft dysfunction. RIN, RNA integrity number.</p

Enriched Pathways among Differentially Expressed Genes in Incipient CLAD.

<p>Enriched Pathways among Differentially Expressed Genes in Incipient CLAD.</p

BAL cell differential.

<p>(A) Percentage of neutrophils among the BAL cells by sample. (B) Percent neutrophils analysis (Mann Whitney test) by CLAD Free versus Incipient CLAD group. (C) Percentage of lymphocytes among the BAL cells by sample. (D) Percent lymphocytes analysis (Mann Whitney test) by CLAD Free versus Incipient CLAD group.</p

The prognostic importance of CXCR3 chemokine during organizing pneumonia on the risk of chronic lung allograft dysfunction after lung transplantation

<div><p>Rationale</p><p>Since the pathogenesis of chronic lung allograft dysfunction (CLAD) remains poorly defined with no known effective therapies, the identification and study of key events which increase CLAD risk is a critical step towards improving outcomes. We hypothesized that bronchoalveolar lavage fluid (BALF) CXCR3 ligand concentrations would be augmented during organizing pneumonia (OP) and that episodes of OP with marked chemokine elevations would be associated with significantly higher CLAD risk.</p><p>Methods</p><p>All transbronchial biopsies (TBBX) from patients who received lung transplantation between 2000 to 2010 were reviewed. BALF concentrations of the CXCR3 ligands (CXCL9, CXCL10 and CXCL11) were compared between episodes of OP and “healthy” biopsies using linear mixed-effects models. The association between CXCR3 ligand concentrations during OP and CLAD risk was evaluated using proportional hazards models with time-dependent covariates.</p><p>Results</p><p>There were 1894 bronchoscopies with TBBX evaluated from 441 lung transplant recipients with 169 (9%) episodes of OP and 907 (49%) non-OP histopathologic injuries. 62 (37%) episodes of OP were observed during routine surveillance bronchoscopy. Eight hundred thirty-eight (44%) TBBXs had no histopathology and were classified as “healthy” biopsies. There were marked elevations in BALF CXCR3 ligand concentrations during OP compared with “healthy” biopsies. In multivariable models adjusted for other injury patterns, OP did not significantly increase the risk of CLAD when BAL CXCR3 chemokine concentrations were not taken into account. However, OP with elevated CXCR3 ligands markedly increased CLAD risk in a dose-response manner. An episode of OP with CXCR3 concentrations greater than the 25^th, 50^th and 75^th percentiles had HRs for CLAD of 1.5 (95% CI 1.0–2.3), 1.9 (95% CI 1.2–2.8) and 2.2 (95% CI 1.4–3.4), respectively.</p><p>Conclusions</p><p>This study identifies OP, a relatively uncommon histopathologic finding after lung transplantation, as a major risk factor for CLAD development when considered in the context of increased allograft expression of interferon-γ inducible ELR- CXC chemokines. We further demonstrate for the first time, the prognostic importance of BALF CXCR3 ligand concentrations during OP on subsequent CLAD risk.</p></div