Cytosolic phospholipase A2α–deficient mice are resistant to experimental autoimmune encephalomyelitis

Experimental autoimmune encephalomyelitis (EAE), a Th1-mediated inflammatory disease of the central nervous system (CNS), is a model of human multiple sclerosis. Cytosolic phospholipase A2α (cPLA2α), which initiates production of prostaglandins, leukotrienes, and platelet-activating factor, is present in EAE lesions. Using myelin oligodendrocyte glycoprotein (MOG) immunization, as well as an adoptive transfer model, we showed that cPLA2α−/− mice are resistant to EAE. Histologic examination of the CNS from MOG-immunized mice revealed extensive inflammatory lesions in the cPLA2α+/− mice, whereas the lesions in cPLA2α−/− mice were reduced greatly or completely absent. MOG-specific T cells generated from WT mice induced less severe EAE in cPLA2α−/− mice compared with cPLA2α+/− mice, which indicates that cPLA2α plays a role in the effector phase of EAE. Additionally, MOG-specific T cells from cPLA2α−/− mice, transferred into WT mice, induced EAE with delayed onset and lower severity compared with EAE that was induced by control cells; this indicates that cPLA2α also plays a role in the induction phase of EAE. MOG-specific T cells from cPLA2α−/− mice were deficient in production of Th1-type cytokines. Consistent with this deficiency, in vivo administration of IL-12 rendered cPLA2α−/− mice susceptible to EAE. Our data indicate that cPLA2α plays an important role in EAE development and facilitates differentiation of T cells toward the Th1 phenotype

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

FACTORS AND MECHANISMS OF CELEBRITY WORSHIP SYNDROME IN THE CONTEXT OF THE ABSORPTION-ADDICTION MODEL

Bachelor'sBachelor of Social Sciences (Honours

FREE CENTRE-BY-(ABELIAN-BY-EXPONENT 2) GROUPS

We study free centre-by-(abelian-by-exponent 2) groups. Our main result is a complete description of the centre. It is isomorphic to a direct sum of a free abelian group and a torsion subgroup. The latter is a direct sum of cyclic groups of order two and cyclic groups of order four. We exhibit a generating set consisting of elements of innite order, order 2, and order 4, such that the centre is the direct sum of cyclic subgroups generated by those generators. Our approach makes essential use of homological methods

Design of an aerosol mass spectral interface

Issued as final reportThis item was temporarily removed from SMARTech at the request of the Georgia Tech Research Institute on May 8, 2009

Group B Streptococcus Serotype III Sequence Type 283 Bacteremia Associated with Consumption of Raw Fish, Singapore

We conducted a retrospective study of 40 case-patients and 58 controls as part of a nationwide investigation of a group B Streptococcus outbreak in Singapore in 2015. Eating a Chinese-style raw fish dish (yusheng) was a major risk factor for bacteremia, particularly caused by serotype III sequence type 283

Relationship of percent body fat (PBF) with body adiposity index (BAI) and body mass index (BMI) in men and women.

<p>A. BAI versus PBF. B. BMI versus PBF. The graphs are generated on untransformed data for the BAI and BMI variables, while the main analyses in our study are based on log transformations of these variables. Therefore, the correlation coefficients (r) here are slightly different than those reported elsewhere in the text.</p

Clinical characteristics of the study cohort.

<p>Data are medians (interquartile range).</p><p>BAI, body adiposity index; BMI, body mass index; Carotid IMT, carotid intima-media thickness; CRP, C-reactive protein; DBP, diastolic blood pressure; HDL-C, high density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol; MCRI, metabolic clearance rate of insulin; M/I, insulin sensitivity index from the euglycemic-hyperinsulinemic clamp; PAI-1, plasminogen activator inhibitor-1; PBF, percent total body fat; SBP, systolic blood pressure; TG, triglycerides.</p

Correlations of anthropometric measurements with cardiometabolic risk factors.

<p>Data are correlation coefficients with <i>P</i> values in parentheses.</p

Comparison of correlation coefficients between cardiometabolic risk factors and BMI versus BAI.

<p>Correlation coefficients that are significantly greater are highlighted in bold.</p>a<p><i>P</i> values from Hotelling’s T-test.</p