bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endobronchial ultrasound‐guided transbronchial needle aspiration (EBUS‐TBNA): Applications in chest disease
Authors: MEDFORD Andrew R.L. , BENNETT Jonathan A. , FREE Catherine M. , AGRAWAL Sanjay 
Published: November 2009

ABSTRACTEndobronchial ultrasound‐guided transbronchial needle aspiration (EBUS‐TBNA) offers a minimally invasive option for staging the mediastinum in suspect lung cancer but also in the diagnosis of mediastinal lesions accessible from the airway. This review is aimed at centres considering establishing an EBUS service that may not be so familiar with the technique. It focuses primarily on technical aspects of EBUS‐TBNA, training issues, cost considerations, indications, advantages and disadvantages compared with other mediastinal sampling techniques as well as some reference to its performance in clinical studies.In summary, EBUS‐TBNA is primarily used for staging non‐small cell lung cancer, especially for bulky mediastinal disease and discrete N2 or N3 disease on CT, but also used for the diagnosis of unexplained mediastinal lymphadenopathy. For radical treatment staging, mediastinoscopy is still used at many centres and negative EBUS‐TBNA results should be corroborated by mediastinoscopy. In the future, EBUS‐TBNA may be used for staging the radiologically normal mediastinum and in re‐staging. It is a procedure that can be taught with ease by an experienced operator, has numerous advantages over mediastinoscopy and is potentially cost saving by reducing the number of mediastinoscopies and associated peri‐operative support required.
Age‐associated mitochondrial DNA mutations lead to small but significant changes in cell proliferation and apoptosis in human colonic crypts
Authors: Nooteboom Marco , Johnson Riem , Taylor Robert W. , Wright Nicholas A. , Lightowlers Robert N. , Kirkwood Thomas B. L. , Mathers John C. , Turnbull Doug M. , Greaves Laura C. 
Published: October 2009

SummaryMitochondrial DNA (mtDNA) mutations are a cause of human disease and are proposed to have a role in human aging. Clonally expanded mtDNA point mutations have been detected in replicating tissues and have been shown to cause respiratory chain (RC) defects. The effect of these mutations on other cellular functions has not been established. Here, we investigate the consequences of RC deficiency on human colonic epithelial stem cells and their progeny in elderly individuals. We show for the first time in aging human tissue that RC deficiency attenuates cell proliferation and increases apoptosis in the progeny of RC deficient stem cells, leading to decreased crypt cell population.
Genetic variation in the murine lifespan response to dietary restriction: from life extension to life shortening
Authors: Liao Chen‐Yu , Rikke Brad A. , Johnson Thomas E. , Diaz Vivian , Nelson James F. 
Published: October 2009

SummaryChronic dietary restriction (DR) is considered among the most robust life‐extending interventions, but several reports indicate that DR does not always extend and may even shorten lifespan in some genotypes. An unbiased genetic screen of the lifespan response to DR has been lacking. Here, we measured the effect of one commonly used level of DR (40% reduction in food intake) on mean lifespan of virgin males and females in 41 recombinant inbred strains of mice. Mean strain‐specific lifespan varied two to threefold under ad libitum (AL) feeding and 6‐ to 10‐fold under DR, in males and females respectively. Notably, DR shortened lifespan in more strains than those in which it lengthened life. Food intake and female fertility varied markedly among strains under AL feeding, but neither predicted DR survival: therefore, strains in which DR shortened lifespan did not have low food intake or poor reproductive potential. Finally, strain‐specific lifespans under DR and AL feeding were not correlated, indicating that the genetic determinants of lifespan under these two conditions differ. These results demonstrate that the lifespan response to a single level of DR exhibits wide variation amenable to genetic analysis. They also show that DR can shorten lifespan in inbred mice. Although strains with shortened lifespan under 40% DR may not respond negatively under less stringent DR, the results raise the possibility that life extension by DR may not be universal.
Autoimmunity against type VII collagen in inflammatory bowel disease
Authors: Hundorfean Gheorghe , Neurath Markus F. , Sitaru Cassian 
Published: October 2009

Abstract

Introduction
The autoantigen: type VII collagen
Autoimmunity to type VII collagen
Inflammatory bowel disease
Autoimmune phenomena in IBD
Association of IBD with autoimmune diseases
Autoimmunity to type VII collagen in IBD
Autoimmunity against type VII collagen and EBA show a strong association with IBD
Sequence of occurrence of skin blistering and bowel disease in IBD associated with EBA
Initiation of the type VII collagen‐specific autoimmune response in IBD
Response of EBA and IBD to treatment
Implications for the practical management of IBD and EBA
Concluding remarks and perspectives

Autoimmunity against type VII collagen, an adhesion molecule of the extracellular matrix in epithelial basement membranes, is causing the rare organ‐specific epidermolysis bullosa acquisita (EBA). An intriguing association between EBA and inflammatory bowel disease (IBD) has been extensively documented over the last decades, but, because of the very low incidence of EBA, received little attention from physicians involved in the care of patients with IBD. More recently, autoantibodies against type VII collagen have been detected in up to 68% of IBD patients. Although these findings suggest that chronic intestinal inflammation in IBD predisposes for autoimmunity against type VII collagen, their relevance for the pathogenesis of both IBD and EBA is still unclear. In this review article, the main features of the association between IBD and EBA are presented and pathomechanistic hypotheses as well as future lines of investigation in this area are discussed. Future research should provide new pathomechanistic insights and will likely facilitate the development of more specific and effective immunotherapeutic strategies for both conditions.
The phenotypic profile of dermatomyositis and lupus erythematosus: a comparative analysis
Authors: Magro Cynthia M. , Segal Jeremy P. , Crowson A. Neil , Chadwick Paul 
Published: November 2009

Background: The mechanisms which regulate cutaneous inflammation in the setting of collagen vascular disease have been a topic of recent interest; emphasis has been placed on type I interferon‐associated recruitment of CXCR3+ lymphocytes in dermatomyositis (DM). Methods: On a total of 42 biopsies from patients with DM, systemic lupus erythematosus (SLE), discoid lupus erythematosus (DLE) and subacute cutaneous lupus erythematosus (SCLE) comprehensive phenotypic studies were performed to explore the practical value of phenotypic analysis in the subclassification of lesions of collagen vascular disease. Results: The infiltrate in DM was of mild intensity compared to lupus erythematosus (LE). The dominant mononuclear cell in DM exhibited a CD4/CXCR3‐positive phenotype while biopsies of SLE typically showed a dearth of CXCR3‐positive cells. CD8 and CD20 lymphocytes were greatest in SLE and DLE, respectively. CD123 plasmacytoid dendritic cells, seen in most cases, were most frequent in cases of SCLE; CD83 expression was minimal. Endothelial MXA expression was a characteristic feature of DM. CD123 and MXA expression within inflammatory cells and keratinocytes was most conspicuous in areas of interface injury. Cutaneous lymphocyte antigen (CLA) expression was diminished in the dermal infiltrate in most cases of DM and LE. T regulatory cells never exceeded 15% of the infiltrate and were the least in the setting of DM and LE. Conclusions: An interferon‐α‐inducible cytokine milieu is common in SLE, DLE, SCLE and DM. In addition, there are phenotypic differences as alluded to above that may be of some practical value in separating these distinctive subsets. Features not previously emphasized such as MXA endothelial cell staining in DM and the lack of staining for CD83 and CLA in lesions of collagen vascular disease may be of diagnostic value.Magro CM, Segal JP, Crowson AN, Chadwick P. The phenotypic profile of dermatomyositis and lupus erythematosus: a comparative analysis.
The Triad of Impairment in Autism Revisited
Authors: Cashin Andrew , Sci Dip App , Barker Philip 
Published: November 2009

TOPIC:  The triad of impairment referred to at present in the autism‐related literature is a behavioral triad. This paper extends this thinking of the triad of impairment to the triad that underlies the behavioral manifestation. The real triad of impairment.PURPOSE:  This paper considers the thinking and information processing style of autism and takes the next transitional step in understanding the triad of impairment.SOURCES USED:  Contemporary literature on autism and information processing.CONCLUSIONS:  Exceptional pioneering work in the late 1970s gave rise to the concept of the triad of impairments as the central plank of the construct of autism: impaired communication; impaired social skills; and a restricted and repetitive way of being‐in‐the‐world. This clear articulation of the structures of the phenomena allowed a new way for professionals and families to see and understand autism, and to relate to those with autism. Like the evolution of many concepts, this was a transitional idea. The original triad of impairments described the behavioral manifestation; the actual triad of impairments is at the level of cognitive processing. The actual triad of impairment is static and ubiquitous unlike the variable and fluctuating behavioral manifestation. The actual triad of impairment in autism is visual as opposed to linguistic processing, impaired abstraction, and lack of theory of mind. The actual triad is central to all diagnosis that together makes up the autism spectrum.
Korean American Adolescents' and Their Parents' Perceptions of Acculturative Stress
Authors: Choi Heeseung , Dancy Barbara L. 
Published: November 2009

PROBLEM: The purpose of this study was to describe Korean American adolescents' (KAAs') and their parents' perceptions of KAAs' experiences with acculturative stress and to examine the congruity between their perceptions.METHOD: This study used the qualitative descriptive method. Twenty KAAs aged 11–14 years and their 21 parents participated in in‐depth, face‐to‐face interviews.FINDINGS: Qualitative content analysis revealed that KAAs and their parents reported similar views regarding acculturative stress experienced by KAAs: peer relationships, being treated differently or unfairly, pressure to excel academically and be successful, and strained parent–child relationships.CONCLUSION: Culturally and developmentally relevant interventions focusing on strengthening peer relationships and parent–child relationships are needed for this population.
Coral reef quality and recreation fees in marine protected areas
Authors: Wielgus Jeffrey , Balmford Andrew , Lewis Tiffany B. , Mora Camilo , Gerber Leah R. 
Published: November 2009

AbstractThe recreational use of marine protected areas (MPAs) is a potential source of funding for MPAs in developing countries, for instance given the willingness of international divers to pay considerably higher diving fees than they currently pay. We conducted a global survey of MPAs containing coral reefs to investigate what factors are important in determining the size of fees charged to recreational SCUBA divers. The survey suggests that a negative perception about diving fees by managers is a more important predictor of fee size than the quality of diving, which can help explain the prevalently low size of diving fees. Decentralized fee systems and higher diving fees can help capture some of the surplus willingness to pay for diving in MPAs, but an excessive reliance on tourism for funding MPA management could expose coral reefs to damages.
Differential Expression of Virulence and Stress Fitness Genes between
Escherichia coli
O157:H7 Strains with Clinical or Bovine-Biased Genotypes
Authors: Vanaja Sivapriya Kailasan , Springman Amber C. , Besser Thomas E. , Whittam Thomas S. , Manning Shannon D. 
Published: October 2009

ABSTRACT

Escherichia coli
O157:H7 strains can be classified into different genotypes based on the presence of specific Shiga toxin-encoding bacteriophage insertion sites. Certain O157:H7 genotypes predominate among human clinical cases (clinical genotypes), while others are more frequently found in bovines (bovine-biased genotypes). To determine whether inherent differences in gene expression explain the variation in infectivity of these genotypes, we compared the expression patterns of clinical genotype 1 strains with those of bovine-biased genotype 5 strains using microarrays. Important O157:H7 virulence factors, including locus of enterocyte effacement genes, the enterohemolysin, and several pO157 genes, showed increased expression in the clinical versus bovine-biased genotypes. In contrast, genes essential for acid resistance (e.g.,
gadA
,
gadB
, and
gadC
) and stress fitness were upregulated in bovine-biased genotype 5 strains. Increased expression of acid resistance genes was confirmed functionally using a model stomach assay, in which strains of bovine-biased genotype 5 had a 2-fold-higher survival rate than strains of clinical genotype 1. Overall, these results suggest that the increased prevalence of O157:H7 illness caused by clinical genotype 1 strains is due in part to the overexpression of key virulence genes. The bovine-biased genotype 5 strains, however, are more resistant to adverse environmental conditions, a characteristic that likely facilitates O157:H7 colonization of bovines.
Roles of the Snf1-Activating Kinases during Nitrogen Limitation and Pseudohyphal Differentiation in
Saccharomyces cerevisiae
Authors: Orlova Marianna , Ozcetin Hamit , Barrett LaKisha , Kuchin Sergei 
Published: October 2009

ABSTRACT

In
Saccharomyces cerevisiae
, Snf1 protein kinase is important for growth on carbon sources that are less preferred than glucose. When glucose becomes limiting, Snf1 undergoes catalytic activation, which requires phosphorylation of its T-loop threonine (Thr210). Thr210 phosphorylation can be performed by any of three Snf1-activating kinases: Sak1, Tos3, and Elm1. These kinases are redundant in that all three must be eliminated to confer
snf1
Δ-like growth defects on nonpreferred carbon sources. We previously showed that in addition to glucose signaling, Snf1 also participates in nitrogen signaling and is required for diploid pseudohyphal differentiation, a filamentous-growth response to nitrogen limitation. Here, we addressed the roles of the Snf1-activating kinases in this process. Loss of Sak1 caused a defect in pseudohyphal differentiation, whereas Tos3 and Elm1 were dispensable. Sak1 was also required for increased Thr210 phosphorylation of Snf1 under nitrogen-limiting conditions. Expression of a catalytically hyperactive version of Snf1 restored pseudohyphal differentiation in the
sak1
Δ/
sak1
Δ mutant. Thus, while the Snf1-activating kinases exhibit redundancy for growth on nonpreferred carbon sources, the loss of Sak1 alone produced a significant defect in a nitrogen-regulated phenotype, and this defect resulted from deficient Snf1 activation rather than from disruption of another pathway. Our results suggest that Sak1 is involved in nitrogen signaling upstream of Snf1.
The Silicon Layer Supports Acid Resistance of
Bacillus cereus
Spores
Authors: Hirota Ryuichi , Hata Yumehiro , Ikeda Takeshi , Ishida Takenori , Kuroda Akio 
Published: October 2009

ABSTRACT

Silicon (Si) is considered to be a “quasiessential” element for most living organisms. However, silicate uptake in bacteria and its physiological functions have remained obscure. We observed that Si is deposited in a spore coat layer of nanometer-sized particles in
Bacillus cereus
and that the Si layer enhances acid resistance. The novel acid resistance of the spore mediated by Si encapsulation was also observed in other
Bacillus
strains, representing a general adaptation enhancing survival under acidic conditions.
Thermococcus kodakar
ensis
Mutants Deficient in Di-
myo
-Inositol Phosphate Use Aspartate To Cope with Heat Stress
Authors: Borges Nuno , Matsumi Rie , Imanaka Tadayuki , Atomi Haruyuki , Santos Helena 
Published: October 2009

ABSTRACT

Many of the marine microorganisms which are adapted to grow at temperatures above 80°C accumulate di-
myo
-inositol phosphate (DIP) in response to heat stress. This led to the hypothesis that the solute plays a role in thermoprotection, but there is a lack of definitive experimental evidence. Mutant strains of
Thermococcus kodakar
ensis
(formerly
Thermococcus kodakaraensis
), manipulated in their ability to synthesize DIP, were constructed and used to investigate the involvement of DIP in thermoadaptation of this archaeon. The solute pool of the parental strain comprised DIP, aspartate, and α-glutamate. Under heat stress the level of DIP increased 20-fold compared to optimal conditions, whereas the pool of aspartate increased 4.3-fold in response to osmotic stress. Deleting the gene encoding the key enzyme in DIP synthesis, CTP:inositol-1-phosphate cytidylyltransferase/CDP-inositol:inositol-1-phosphate transferase, abolished DIP synthesis. Conversely, overexpression of the same gene resulted in a mutant with restored ability to synthesize DIP. Despite the absence of DIP in the deletion mutant, this strain exhibited growth parameters similar to those of the parental strain, both at optimal (85°C) and supraoptimal (93.7°C) temperatures for growth. Analysis of the respective solute pools showed that DIP was replaced by aspartate. We conclude that DIP is part of the strategy used by
T. kodakarensis
to cope with heat stress, and aspartate can be used as an alternative solute of similar efficacy. This is the first study using mutants to demonstrate the involvement of compatible solutes in the thermoadaptation of (hyper)thermophilic organisms.
Endogenous Phenazine Antibiotics Promote Anaerobic Survival of
Pseudomonas aeruginosa
via Extracellular Electron Transfer
Authors: Wang Yun , Kern Suzanne E. , Newman Dianne K. 
Published: October 2009

ABSTRACT

Antibiotics are increasingly recognized as having other, important physiological functions for the cells that produce them. An example of this is the effect that phenazines have on signaling and community development for
Pseudomonas aeruginosa
(L. E. Dietrich, T. K. Teal, A. Price-Whelan, and D. K. Newman, Science 321:1203-1206, 2008). Here we show that phenazine-facilitated electron transfer to poised-potential electrodes promotes anaerobic survival but not growth of
Pseudomonas aeruginosa
PA14 under conditions of oxidant limitation. Other electron shuttles that are reduced but not made by PA14 do not facilitate survival, suggesting that the survival effect is specific to endogenous phenazines.
Implication of Serine Residues 271, 273, and 275 in the Human Immunodeficiency Virus Type 1 Cofactor Activity of Lens Epithelium-Derived Growth Factor/p75
Authors: Garcia-Rivera Jose A. , Bueno Murilo T. D. , Morales Elisa , Kugelman Jeffrey R. , Rodriguez Daniel F. , Llano Manuel 
Published: November 2009

ABSTRACT
Lens epithelium-derived growth factor (LEDGF)/p75 is a cellular cofactor for HIV-1 DNA integration. It is well established that the simultaneous binding of LEDGF/p75 to chromatin and to HIV-1 integrase is required for its cofactor activity. However, the exact molecular mechanism of LEDGF/p75 in HIV-1 integration is not yet completely understood. Our hypothesis is that evolutionarily conserved regions in LEDGF/p75 exposed to solvent and harboring posttranslational modifications may be involved in its HIV-1 cofactor activity. Therefore, a panel of LEDGF/p75 deletion mutants targeting these protein regions were evaluated for their HIV-1 cofactor activity, chromatin binding, integrase interaction, and integrase-to-chromatin-tethering activity by using different cellular and biochemical approaches. The deletion of amino acids 267 to 281 reduced the cofactor activity of LEDGF/p75 to levels observed for chromatin-binding-defective mutants. This region contains a serine cluster (residues 271, 273, and 275) recurrently found to be phosphorylated in both human and mouse cells. Importantly, the conversion of these Ser residues to Ala was sufficient to impair the ability of LEDGF/p75 to mediate HIV-1 DNA integration, although these mutations did not alter chromatin binding, integrase binding, or the integrase-to-chromatin-tethering capability of LEDGF/p75. These results clearly indicated that serine residues 271, 273, and 275 influence the HIV-1 cofactor activity of integrase-to-chromatin-tethering-competent LEDGF/p75.
Integrity of the Early Secretory Pathway Promotes, but Is Not Required for, Severe Acute Respiratory Syndrome Coronavirus RNA Synthesis and Virus-Induced Remodeling of Endoplasmic Reticulum Membranes
Authors: Knoops Kèvin , Swett-Tapia Cindy , van den Worm Sjoerd H. E. , te Velthuis Aartjan J. W. , Koster Abraham J. , Mommaas A. Mieke , Snijder Eric J. , Kikkert Marjolein 
Published: November 2009

ABSTRACT
To accommodate its RNA synthesis in the infected cell, severe acute respiratory syndrome coronavirus (SARS-CoV) induces a cytoplasmic reticulovesicular network (RVN) that is derived from endoplasmic reticulum (ER) membranes. We set out to investigate how the early secretory pathway interacts with the RVN and the viral replication/transcription complex (RTC) that is anchored to it. When the secretory pathway was disrupted by brefeldin A (BFA) treatment at the start of infection, RVN formation and viral RTC activity were not blocked and continued up to 11 h postinfection, although RNA synthesis was reduced by ca. 80%. In vitro RTC assays, using membrane fractions from infected cells, demonstrated that BFA does not directly interfere with the activity of the viral RNA-synthesizing enzymes. Confocal microscopy studies showed that early secretory pathway components are not associated with SARS-CoV-induced replication sites, although our studies revealed that infection induces a remarkable redistribution of the translocon subunit Sec61α. Ultrastructural studies, including electron tomography, revealed that the formation of the RVN and all its previously documented features can occur in the presence of BFA, despite differences in the volume and morphology of the network. We therefore conclude that early secretory pathway proteins do not play a direct role in RVN morphogenesis or the functionality of the SARS-CoV RTC. The BFA-induced disruption of ER integrity and functionality probably affects the overall quality of the membrane scaffold that is needed to support the viral RTC and/or the availability of specific host factors, which in turn compromises viral RNA synthesis.