Quark-gluon vertex in general kinematics

The original publication can be found at www.springerlink.com Submitted to Cornell University’s online archive www.arXiv.org in 2007 by Jon-Ivar Skullerud. Post-print sourced from www.arxiv.org.We compute the quark–gluon vertex in quenched lattice QCD in the Landau gauge, using an off-shell mean-field O(a)-improved fermion action. The Dirac-vector part of the vertex is computed for arbitrary kinematics. We find a substantial infrared enhancement of the interaction strength regardless of the kinematics.Ayse Kizilersu, Derek B. Leinweber, Jon-Ivar Skullerud and Anthony G. William

Prions fail to activate B cells with or without T cell help.

<p>A simplified model of T cell-dependent and independent B cell activation. Binding of antigen to IgM on the surface of B cells provides the first activation signal. (A) T cells that recognize antigen processed by the B cell and presented in MHC II molecules provide the second signal, typically through its CD40 ligand binding CD40 on the B cell during infections with classic pathogens. (B) Prion-specific T cells are absent during prion infection. Other innate immune receptors, like CD21 or TLRs, can provide secondary signals without T cells in response to (C) bacteria, but not to (D) prions.</p

Antigen processing and presentation of classic pathogens and prions.

<p>A simplified model showing a macrophage processing and presenting viral (A) and prion (B) antigens. Each panel depicts typical antigen processing of (1) exogenous pathogens via endocytosis and fusion with acidified lysosomes, which degrade proteins into small peptides. Endolysosomes then fuse to vesicles containing MHC II molecules, which load peptides into their antigen binding clefts. Vesicles containing loaded MHC II molecules traffic to and fuse with the plasma membrane, depositing the loaded MHC II molecule on the cell surface. (2) Ubiquitin chains mark endogenous pathogens for degradation by the proteosome, which process proteins into peptides. Multiple proteins, including TAP and Calreticulin, help load peptides onto MHC I molecules and transport them to the cell surface. (3) Autophagy can degrade cellular proteins derived from the host and pathogens into peptides that can be presented by MHC I molecules. Cross presentation of (4) endogenous pathogens by MHC II and (5) exogenous pathogens by MHC I molecules via processing through the autophagosome and the proteosome occur less frequently. Prions likely constipate antigen processing at multiple points in these pathways, preventing presentation of prion-specific antigens.</p

Preferential use of unmutated immunoglobulin heavy variable region genes in Boxer dogs with chronic lymphocytic leukemia

<div><p>Human chronic lymphocytic leukemia (CLL) is a clinically heterogeneous disease, and immunoglobulin heavy variable region (IGHV) gene mutational status is an important prognostic marker. IGHV mutational status has not been previously examined in canine CLL. We sequenced the IGHV-D-J rearrangements from 55 canine patients with CLL, including 36 non-Boxer and 19 Boxer dogs. The majority of non-Boxers (75%) had mutated IGHV genes, whereas the majority of Boxers (79%) had unmutated IGHV genes. IGHV3-41 and IGHV3-67 gene usage was significantly higher in Boxers with CLL compared to non-Boxers. Additionally, 11 Boxers with large B-cell lymphoma and the normal IGHV repertoire of six control dogs (three Boxers and three non-Boxers) were sequenced. IGHV3-41 was preferentially used in Boxers with other forms of lymphoma and without lymphoproliferative disease. However, preferential use of unmutated IGHV genes was unique to Boxers with CLL, suggesting Boxers may be a valuable model to investigate unmutated CLL.</p></div

PCR amplification primer sequences and cycling conditions for IGHV sequencing.

<p>PCR amplification primer sequences and cycling conditions for IGHV sequencing.</p

Antibody panels used for immunophenotyping.

<p>Antibody panels used for immunophenotyping.</p

Distribution of IGHV gene usage and mutational status in (A) non-Boxer dogs with CLL (n = 36), (B) Boxer dogs with CLL (n = 19), and (C) Boxer dogs with large B-cell lymphoma (n = 11).

<p>IGHV gene usage is reported as the percentage of patients using an IGHV gene within that cohort. There were significant differences in the IGHV gene usage between non-Boxers and Boxers with CLL for IGHV3-67 (p = 0.037) and IGHV3-41 (p<0.001). There were significantly more unmutated cases in the Boxer CLL cohort, compared to non-Boxers with CLL (p<0.001) and Boxers with large B-cell lymphoma (p = 0.026).</p

Breed, mutational status, and IGHV gene rearrangements in 55 canine patients with chronic lymphocytic leukemia.

<p>Breed, mutational status, and IGHV gene rearrangements in 55 canine patients with chronic lymphocytic leukemia.</p

Dog IG V-REGION depictions in germline genomic DNA (A) and rearranged genomic DNA (B).

<p>(A) The V-DOMAIN of canine IGHV3-38 is shown as an example. IMGT standardized labels are shown, including framework regions (FR), complementarity determining regions (CDR), and the four conserved positions: 23 (1st-CYS), 41 (CONSERVED-TRP), 89 (hydrophobic) and 104 (2nd-CYS). Other labels include: the OCTAMER in the 5’UTR of the V-GENE; INIT-CODON, initiation codon (ATG sequence); L-PART1, first exon of the leader sequence; DONOR and ACCEPTOR SPLICE sites flanking the INTRON; L-PART2, second part of the leader sequence; V-HEPTAMER and V-NONAMER, recombination sites. (B) An IGHV-D-J rearrangement from a CLL case is shown as an example. The location of the PCR sequencing primers are shown, including the forward primer (used for both amplification protocols) and the reverse primers for protocol 1 (reverse 1) and protocol 2 (reverse 2)(see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0191205#pone.0191205.t001" target="_blank">Table 1</a>). Below, the genomic sequence and amino acid translation are shown for a portion of the rearrangement. The conserved position, 118 (J-PHE or J-TRP), and G-X-G motif of the J-REGION are shown.</p

List of significantly associated haplotypes.

<p>List of significantly associated haplotypes.</p