The Evolving Role of Semiconductor Consortia in the United States and Japan

This article examines the interactions between public and private actors as cooperation in the semiconductor industry becomes increasingly international. The latest manifestations of multilateral collaboration are two consortia: I300I based in the United States and Selete based in Japan. Through an analysis of their structures and their origins, this article provides a deeper understanding of the complexities facing industry-wide consortia, the role of the government in promoting or inhibiting cooperation, and the lingering rivalries that impede truly global cooperation in a dynamic, high-technology industry

Distinctive Collections: The Space Between “General” and “Special” Collections and Implications for Collection Development

Many libraries separate collection development activities into two broad categories, that of “general” collections versus “special” collections. Although this makes for a clean distinction between two areas of library activity (roughly the work of librarians as distinct and separate from that of archivists), in between these two poles lie “distinctive collections”—items that are neither especially rare nor unique (special), but are also not run-of-the-mill monographs or journals. Government documents, numeric datasets, ephemera, area collections, audiovisual media, born-digital materials—these are all recognized subsets of library collections with their own frameworks (more or less developed) for acquisition, cataloging/metadata, preservation, inter-institutional collaboration. Falling as they do somewhere between general and the special collections, these distinctive collections are often overlooked in traditional collection development and public service activities. This session presents an overview of how distinctive collections and their management fit into the overall collection profile of a library

Lifetime Exposure to Adverse Events and Reinforcement Sensitivity in Obsessive-Compulsive Prone Individuals

A diathesis-stress perspective of obsessive-compulsive symptoms (OCS) predicts that exposure to adverse events and personality dispositions jointly influence OCS. Gray and McNaughton's (2000) model of personality posits that, faced with challenging circumstances, individuals with a high sensitivity to punishment (SP) will be more prone to OCS because they cannot avoid the downward spiral into anxiety. The current study investigates OCS severity in relation to lifetime exposure to adverse events (AE), SP, and sensitivity to reward (SR) in 122 nonclinical adults. The results indicate that OCS severity is predicted by AE, SP and SR. Interestingly, the impact of adverse experiences is moderated by SR and not SP. These findings suggest that: (1) exposure to adverse events and SP are independent OCS risk factors, and (2) exposure to adverse events is more critical for reward dependent people. This is discussed in light of responsibility and ‘not just right experiences' in OCS, along with the role of impulsivity in the obsessive-compulsive disorder spectru

Knockdown of menin affects pre-mRNA processing and promoter fidelity at the interferon-gamma inducible IRF1 gene

<p>Abstract</p> <p>Background</p> <p>The tumor suppressor menin (<it>MEN1</it>) is mutated in the inherited disease multiple endocrine neoplasia type I, and has several documented cellular roles, including the activation and repression of transcription effected by several transcription factors. As an activator, MEN1 is a component of the Set1-like mixed lineage leukemia (MLL) MLL1/MLL2 methyltransferase complex that methylates histone H3 lysine 4 (H3K4). MEN1 is localized to the signal transducer and activator of transcription 1 (STAT1)-dependent gene, interferon regulatory factor 1 (<it>IRF1)</it>, and is further recruited when <it>IRF1 </it>transcription is triggered by interferon-γ signaling.</p> <p>Results</p> <p>RNAi-mediated knockdown of MEN1 alters the H3K4 dimethylation and H3 acetylation profiles, and the localization of histone deacetylase 3, at <it>IRF1</it>. While MEN1 knockdown does not impact the rate of transcription, <it>IRF1 </it>heteronuclear transcripts become enriched in MEN1-depleted cells. The processed mRNA and translated protein product are concomitantly reduced, and the antiviral state is attenuated. Additionally, the transcription start site at the <it>IRF1 </it>promoter is disrupted in the MEN1-depleted cells. The H3K4 demethylase, lysine specific demethylase 1, is also associated with <it>IRF1</it>, and its inhibition alters H3K4 methylation and disrupts the transcription start site as well.</p> <p>Conclusions</p> <p>Taken together, the data indicate that MEN1 contributes to STAT1-activated gene expression in a novel manner that includes defining the transcription start site and RNA processing.</p

Lifetime Exposure to Adverse Events and Reinforcement Sensitivity in Obsessive–Compulsive Prone Individuals

A diathesis-stress perspective of obsessive compulsive symptoms (OCS) predicts that exposure to adverse events and personality dispositions jointly influence OCS. Gray and McNaughton's (2000) model of personality posits that, faced with challenging circumstances, individuals with a high sensitivity to punishment (SP) will be more prone to OCS because they cannot avoid the downward spiral into anxiety. The current study investigates OCS severity in relation to lifetime exposure to adverse events (AE), SP, and sensitivity to reward (SR) in 122 nonclinical adults. The results indicate that OCS severity is predicted by AE, SP and SR. Interestingly, the impact of adverse experiences is moderated by SR and not SR These findings suggest that: (1) exposure to adverse events and SP are independent OCS risk factors, and (2) exposure to adverse events is more critical for reward dependent people. This is discussed in light of responsibility and 'not just right experiences' in OCS, along with the role of impulsivity in the obsessive-compulsive disorder spectrum

Children's Budget 2008

Examines trends in mandatory and discretionary federal spending on children by tracking funding from fiscal year 2004 through 2009 for specific programs in child welfare, education, health, housing, income support, nutrition, safety, and training

Endurance Exercise Training Programs Intestinal Lipid Metabolism in a Rat Model of Obesity and Type 2 Diabetes

Endurance exercise has been shown to improve metabolic outcomes in obesity and type 2 diabetes; however, the physiological and molecular mechanisms for these benefits are not completely understood. Although endurance exercise has been shown to decrease lipogenesis, promote fatty acid oxidation (FAO), and increase mitochondrial biosynthesis in adipose tissue, muscle, and liver, its effects on intestinal lipid metabolism remain unknown. The absorptive cells of the small intestine, enterocytes, mediate the highly efficient absorption and processing of nutrients, including dietary fat for delivery throughout the body. We investigated how endurance exercise altered intestinal lipid metabolism in obesity and type 2 diabetes using Otsuka Long-Evans Tokushima Fatty (OLETF) rats. We assessed mRNA levels of genes associated with intestinal lipid metabolism in nonhyperphagic, sedentary Long-Evans Tokushima Otsuka (LETO) rats (L-Sed), hyperphagic, sedentary OLETF rats (O-Sed), and endurance exercised OLETF rats (O-EndEx). O-Sed rats developed hyperphagia-induced obesity (HIO) and type 2 diabetes compared with L-Sed rats. O-EndEx rats gained significantly less weight and fat pad mass, and had improved serum metabolic parameters without change in food consumption compared to O-Sed rats. Endurance exercise resulted in dramatic up-regulation of a number of genes in intestinal lipid metabolism and mitochondrial content compared with sedentary rats. Overall, this study provides evidence that endurance exercise programs intestinal lipid metabolism, likely contributing to its role in improving metabolic outcomes in obesity and type 2 diabetes

Adenosine A2A receptor activation reduces hepatic ischemia reperfusion injury by inhibiting CD1d-dependent NKT cell activation

Ischemia reperfusion injury results from tissue damage during ischemia and ongoing inflammation and injury during reperfusion. Liver reperfusion injury is reduced by lymphocyte depletion or activation of adenosine A2A receptors (A2ARs) with the selective agonist 4- {3-[6-amino-9-(5-ethylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]- prop-2-ynyl}-cyclohexanecarboxylic acid methyl ester (ATL146e). We show that NKT cells are stimulated to produce interferon (IFN)-γ by 2 h after the initiation of reperfusion, and the use of antibodies to deplete NK1.1-positive cells (NK and NKT) or to block CD1d-mediated glycolipid presentation to NKT cells replicates, but is not additive to, the protection afforded by ATL146e, as assessed by serum alanine aminotransferase elevation, histological necrosis, neutrophil accumulation, and serum IFN-γ elevation. Reduced reperfusion injury observed in RAG-1 knockout (KO) mice is restored to the wild-type (WT) level by adoptive transfer of NKT cells purified from WT or A2AR KO mice but not IFN-γ KO mice. Additionally, animals with transferred A2AR−/− NKT cells are not protected from hepatic reperfusion injury by ATL146e. In vitro, ATL146e potently inhibits both anti-CD3 and α-galactosylceramide–triggered production of IFN-γ by NKT cells. These findings suggest that hepatic reperfusion injury is initiated by the CD1d-dependent activation of NKT cells, and the activation of these cells is inhibited by A2AR activation

Trauma exposure interacts with impulsivity in predicting emotion regulation and depressive mood.

BACKGROUND: Traumatic exposure may modulate the expression of impulsive behavioral dispositions and change the implementation of emotion regulation strategies associated with depressive mood. Past studies resulted in only limited comprehension of these relationships, especially because they failed to consider impulsivity as a multifactorial construct. OBJECTIVE: Based on Whiteside and Lynam's multidimensional model that identifies four distinct dispositional facets of impulsive-like behaviors, namely urgency, (lack of) premeditation, (lack of) perseverance, and sensation seeking (UPPS), the current study used a sample of community volunteers to investigate whether an interaction exists between impulsivity facets and lifetime trauma exposure in predicting cognitive emotion regulation and depressive mood. METHODS: Ninety-three adults completed questionnaires measuring lifetime trauma exposure, impulsivity, cognitive emotion regulation, and depressive mood. RESULTS: Results showed that trauma-exposed participants with a strong disposition toward urgency (predisposition to act rashly in intense emotional contexts) tended to use fewer appropriate cognitive emotion regulation strategies than other individuals. Unexpectedly, participants lacking in perseverance (predisposition to have difficulties concentrating on demanding tasks) used more appropriate emotion regulation strategies if they had experienced traumatic events during their life than if they had not. Emotion regulation mediated the path between these two impulsivity facets and depressive mood. CONCLUSIONS: Together, these findings suggest that impulsivity has a differential impact on emotion regulation and depressive mood depending on lifetime exposure to environmental factors, especially traumatic events