Bark Beetle and Wood Borer Infestation in the Greater Yellowstone Area During Four Postfire Years

Extensive surveys of bark beetles and wood bores in the Greater Yellowstone area were conducted in 1991 through 1993. The study objectives were to determine the effect of delayed tree mortality following the 1988 fires on mosaics of fire-killed and green tree stands, the relationship between fire injury and subsequent infestation, and the effect of insect buildup in fire injured trees on infestation rates for uninjured trees. Surveys were conducted adjacent to roads, and plots wee selected randomly. In 1991, 321 plots were measured, 198 plots in 1992, and 127 plots in 1993. Insects killed 12.6 percent of the Douglas-fir, 17.9 percent of the lodgepole pine, 6.6 percent of the Engelmann spruce, 7.5 percent of the subalpine fire, and 2.8 percent of the whitebark pine. Delayed mortality attributed to fire injury accounted for more mortality than insects. Both types of mortality greatly altered the original fire-killed/green tree mosaics that were apparent immediately after the 1988 fires. Insect infestation was strongly and positively correlated with the percent of the basal circumference of the tree that was fire killed in the species, except in Engelmann spruce where infestation peaked in the middle fire-injury class. Infestation in Douglas-fir, lodgepole pine, and Engelmann spruce increased through 1992 then declined in 1993. Although it cannot be said with certainty that insects built up in fire-injured trees and then caused increased infestation of uninjured trees, the high level of infestation suggests this is the case

Carbon Monoxide Blocks Lipopolysaccharide-Induced Gene Expression by Interfering with Proximal TLR4 to NF-κB Signal Transduction in Human Monocytes

Carbon monoxide (CO) is an endogenous messenger that suppresses inflammation, modulates apoptosis and promotes vascular remodeling. Here, microarrays were employed to globally characterize the CO (250 ppm) suppression of early (1 h) LPS-induced inflammation in human monocytic THP-1 cells. CO suppressed 79 of 101 immediate-early genes induced by LPS; 19% (15/79) were transcription factors and most others were cytokines, chemokines and immune response genes. The prototypic effects of CO on transcription and protein production occurred early but decreased rapidly. CO activated p38 MAPK, ERK1/2 and Akt and caused an early and transitory delay in LPS-induced JNK activation. However, selective inhibitors of these kinases failed to block CO suppression of LPS-induced IL-1β, an inflammation marker. Of CO-suppressed genes, 81% (64/79) were found to have promoters with putative NF-κB binding sites. CO was subsequently shown to block LPS-induced phosphorylation and degradation of IκBα in human monocytes, thereby inhibiting NF-κB signal transduction. CO broadly suppresses the initial inflammatory response of human monocytes to LPS by reshaping proximal events in TLR4 signal transduction such as stress kinase responses and early NF-κB activation. These rapid, but transient effects of CO may have therapeutic applications in acute pulmonary and vascular injury

Biomarker Discovery in Serum from Patients with Carotid Atherosclerosis

www.karger.com/cee This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License (www.karger.com/OA-license), applicable to the online version of the article only. Distribution for non-commercial purposes only

Whole Blood Gene Expression and Atrial Fibrillation: The Framingham Heart Study

Background: Atrial fibrillation (AF) involves substantial electrophysiological, structural and contractile remodeling. We hypothesize that characterizing gene expression might uncover important pathways related to AF. Methods and Results: We performed genome-wide whole blood transcriptomic profiling (Affymetrix Human Exon 1.0 ST Array) of 2446 participants (mean age 66±9 years, 55% women) from the Offspring cohort of Framingham Heart Study. The study included 177 participants with prevalent AF, 143 with incident AF during up to 7 years follow up, and 2126 participants with no AF. We identified seven genes statistically significantly up-regulated with prevalent AF. The most significant gene, PBX1 (P = 2.8×10−7), plays an important role in cardiovascular development. We integrated differential gene expression with gene-gene interaction information to identify several signaling pathways possibly involved in AF-related transcriptional regulation. We did not detect any statistically significant transcriptomic associations with incident AF. Conclusion: We examined associations of gene expression with AF in a large community-based cohort. Our study revealed several genes and signaling pathways that are potentially involved in AF-related transcriptional regulation

Impact of animal strain on gene expression in a rat model of acute cardiac rejection

<p>Abstract</p> <p>Background</p> <p>The expression levels of many genes show wide natural variation among strains or populations. This study investigated the potential for animal strain-related genotypic differences to confound gene expression profiles in acute cellular rejection (ACR). Using a rat heart transplant model and 2 different rat strains (Dark Agouti, and Brown Norway), microarrays were performed on native hearts, transplanted hearts, and peripheral blood mononuclear cells (PBMC).</p> <p>Results</p> <p>In heart tissue, strain alone affected the expression of only 33 probesets while rejection affected the expression of 1368 probesets (FDR 10% and FC ≥ 3). Only 13 genes were affected by both strain and rejection, which was < 1% (13/1368) of all probesets differentially expressed in ACR. However, for PBMC, strain alone affected 265 probesets (FDR 10% and FC ≥ 3) and the addition of ACR had little further effect. Pathway analysis of these differentially expressed strain effect genes connected them with immune response, cell motility and cell death, functional themes that overlap with those related to ACR. After accounting for animal strain, additional analysis identified 30 PBMC candidate genes potentially associated with ACR.</p> <p>Conclusion</p> <p>In ACR, genetic background has a large impact on the transcriptome of immune cells, but not heart tissue. Gene expression studies of ACR should avoid study designs that require cross strain comparisons between leukocytes.</p

Contesting the psychiatric framing of ME / CFS

ME/CFS is a medically contested illness and its understanding, framing and treatment has been the subject of heated debate. This paper examines why framing the condition as a psychiatric issue—what we refer to as ‘psychiatrisation’—has been so heavily contested by patients and activists. We argue that this contestation is not simply about stigmatising mental health conditions, as some have suggested, but relates to how people diagnosed with mental illness are treated in society, psychiatry and the law. We highlight the potentially harmful consequences of psychiatrisation which can lead to people’s experiential knowledge being discredited. This stems, in part, from a psychiatric-specific form of ‘epistemic injustice’ which can result in unhelpful, unwanted and forced treatments. This understanding helps explain why the psychiatrisation of ME/CFS has become the focus of such bitter debate and why psychiatry itself has become such a significant field of contention, for both ME/CFS patients and mental health service users/survivors. Notwithstanding important differences, both reject the way psychiatry denies patient explanations and understandings, and therefore share a collective struggle for justice and legitimation. Reasons why this shared struggle has not resulted in alliances between ME and mental health activists are noted