Altitude dependence of atmospheric temperature trends: Climate models versus observation

As a consequence of greenhouse forcing, all state of the art general circulation models predict a positive temperature trend that is greater for the troposphere than the surface. This predicted positive trend increases in value with altitude until it reaches a maximum ratio with respect to the surface of as much as 1.5 to 2.0 at about 200 to 400 hPa. However, the temperature trends from several independent observational data sets show decreasing as well as mostly negative values. This disparity indicates that the three models examined here fail to account for the effects of greenhouse forcings.Comment: 9 pages, 3 figure

A quantification of uncertainties in historical tropical tropospheric temperature trends from radiosondes

The consistency of tropical tropospheric temperature trends with climate model expectations remains contentious. A key limitation is that the uncertainties in observations from radiosondes are both substantial and poorly constrained. We present a thorough uncertainty analysis of radiosonde‐based temperature records. This uses an automated homogenization procedure and a previously developed set of complex error models where the answer is known a priori. We perform a number of homogenization experiments in which error models are used to provide uncertainty estimates of real‐world trends. These estimates are relatively insensitive to a variety of processing choices. Over 1979–2003, the satellite‐equivalent tropical lower tropospheric temperature trend has likely (5–95% confidence range) been between −0.01 K/decade and 0.19 K/decade (0.05–0.23 K/decade over 1958–2003) with a best estimate of 0.08 K/decade (0.14 K/decade). This range includes both available satellite data sets and estimates from models (based upon scaling their tropical amplification behavior by observed surface trends). On an individual pressure level basis, agreement between models, theory, and observations within the troposphere is uncertain over 1979 to 2003 and nonexistent above 300 hPa. Analysis of 1958–2003, however, shows consistent model‐data agreement in tropical lapse rate trends at all levels up to the tropical tropopause, so the disagreement in the more recent period is not necessarily evidence of a general problem in simulating long‐term global warming. Other possible reasons for the discrepancy since 1979 are: observational errors beyond those accounted for here, end‐point effects, inadequate decadal variability in model lapse rates, or neglected climate forcings

Identification and Comparative Expression Analysis of Interleukin 2/15 Receptor β Chain in Chickens Infected with E. tenella

BACKGROUND: Interleukin (IL) 2 and IL15 receptor β chain (IL2/15Rβ, CD122) play critical roles in signal transduction for the biological activities of IL2 and IL15. Increased knowledge of non-mammalian IL2/15Rβ will enhance the understanding of IL2 and IL15 functions. METHODOLOGY/PRINCIPAL FINDINGS: [corrected] Chicken IL2/15Rβ (chIL2/15Rβ) cDNA was cloned using 5'/3'-RACE. The predicted protein sequence contained 576 amino acids and typical features of the type-I cytokine receptor family. COS-7 cells transfected with chIL2/15Rβ produced proteins of approximately 75 and 62.5 kDa under normal and tunicamycin-treated conditions, respectively. The genomic structure of chIL2/15Rβ was similar to its mammalian counterparts. chIL2/15Rβ transcripts were detected in the lymphoblast cell line CU205 and in normal lymphoid organs and at moderate levels in bursa samples. Expression profiles of chIL2/15Rβ and its related cytokines and receptors were examined in ConA-stimulated splenic lymphocytes and in ceca-tonsils of Eimeria tenella-infected chickens using quantitative real-time PCR. Expression levels of chIL2/15Rβ, chIL2Rα, and chIL15Rα were generally elevated in ceca-tonsils and ConA-activated splenic lymphocytes. However, chIL2 and chIL15 expression levels were differentially regulated between the samples. chIL2 expression was upregulated in ConA-activated splenic lymphocytes, but not in ceca-tonsils. In constrast, chIL15 expression was upregulated in ceca-tonsils, but not in ConA-activated splenic lymphocytes. CONCLUSIONS/SIGNIFICANCE: We identified an avian form of IL2/15Rβ and compared its gene expression pattern with those of chIL2, chIL15, chIL2Rα, and chIL15Rα. Our observations suggest that chIL15 and its receptors, including chIL2/15Rβ, play important roles in mucosal immunity to intestinal intracellular parasites such as Eimeria

East Coast Fever Caused by Theileria parva Is Characterized by Macrophage Activation Associated with Vasculitis and Respiratory Failure

Respiratory failure and death in East Coast Fever (ECF), a clinical syndrome of African cattle caused by the apicomplexan parasite Theileria parva, has historically been attributed to pulmonary infiltration by infected lymphocytes. However, immunohistochemical staining of tissue from T. parva infected cattle revealed large numbers of CD3- and CD20-negative intralesional mononuclear cells. Due to this finding, we hypothesized that macrophages play an important role in Theileria parva disease pathogenesis. Data presented here demonstrates that terminal ECF in both Holstein and Boran cattle is largely due to multisystemic histiocytic responses and resultant tissue damage. Furthermore, the combination of these histologic changes with the clinical findings, including lymphadenopathy, prolonged pyrexia, multi-lineage leukopenia, and thrombocytopenia is consistent with macrophage activation syndrome. All animals that succumbed to infection exhibited lymphohistiocytic vasculitis of small to medium caliber blood and lymphatic vessels. In pulmonary, lymphoid, splenic and hepatic tissues from Holstein cattle, the majority of intralesional macrophages were positive for CD163, and often expressed large amounts of IL-17. These data define a terminal ECF pathogenesis in which parasite-driven lymphoproliferation leads to secondary systemic macrophage activation syndrome, mononuclear vasculitis, pulmonary edema, respiratory failure and death. The accompanying macrophage phenotype defined by CD163 and IL-17 is presented in the context of this pathogenesis