bluuebunny/crossref_metadata_2025_split huggingface dataset:
Unveiling Unusual Features of Formation of Septal Partition and Constriction in Mycobacteria—an Ultrastructural Study
Authors: Vijay Srinivasan , Anand Deepak , Ajitkumar Parthasarathi 
Published: November 2011

ABSTRACT

The ultrastructural functions of the electron-dense glycopeptidolipid-containing outermost layer (OL), the arabinogalactan-mycolic acid-containing electron-transparent layer (ETL), and the electron-dense peptidoglycan layer (PGL) of the mycobacterial cell wall in septal growth and constriction are not clear. Therefore, using transmission electron microscopy, we studied the participation of the three layers in septal growth and constriction in the fast-growing saprophytic species
Mycobacterium smegmatis
and the slow-growing pathogenic species
Mycobacterium xenopi
and
Mycobacterium tuberculosis
in order to document the processes in a comprehensive and comparative manner and to find out whether the processes are conserved across different mycobacterial species. A complete septal partition is formed first by the fresh synthesis of the septal PGL (S-PGL) and septal ETL (S-ETL) from the envelope PGL (E-PGL) in
M. smegmatis
and
M. xenopi
. The S-ETL is not continuous with the envelope ETL (E-ETL) due to the presence of the E-PGL between them. The E-PGL disappears, and the S-ETL becomes continuous with the E-ETL, when the OL begins to grow and invaginate into the S-ETL for constriction. However, in
M. tuberculosis
, the S-PGL and S-ETL grow from the E-PGL and E-ETL, respectively, without a separation between the E-ETL and S-ETL by the E-PGL, in contrast to the process in
M. smegmatis
and
M. xenopi
. Subsequent growth and invagination of the OL into the S-ETL of the septal partition initiates and completes septal constriction in
M. tuberculosis
. A model for the conserved sequential process of mycobacterial septation, in which the formation of a complete septal partition is followed by constriction, is presented. The probable physiological significance of the process is discussed. The ultrastructural features of septation and constriction in mycobacteria are unusually different from those in the well-studied organisms
Escherichia coli
and
Bacillus subtilis
.
CitA/CitB Two-Component System Regulating Citrate Fermentation in Escherichia coli and Its Relation to the DcuS/DcuR System
In Vivo
Authors: Scheu P. D. , Witan J. , Rauschmeier M. , Graf S. , Liao Y.-F. , Ebert-Jung A. , Basché T. , Erker W. , Unden G. 
Published: November 2011

ABSTRACT

Citrate fermentation by
Escherichia coli
requires the function of the citrate/succinate antiporter CitT (
citT
gene) and of citrate lyase (
citCDEFXG
genes). Earlier experiments suggested that the two-component system CitA/CitB, consisting of the membrane-bound sensor kinase CitA and the response regulator CitB, stimulates the expression of the genes in the presence of citrate, similarly to CitA/CitB of
Klebsiella pneumoniae
. In this study, the expression of a chromosomal
citC-lacZ
gene fusion was shown to depend on CitA/CitB and citrate. CitA/CitB is related to the DcuS/DcuR two-component system which induces the expression of genes for fumarate respiration in response to C
4
-dicarboxylates and citrate. Unlike DcuS, CitA required none of the cognate transporters (CitT, DcuB, or DcuC) for function, and the deletion of the corresponding genes showed no effect on the expression of
citC-lacZ
. The
citAB
operon is preceded by a DcuR binding site. Phosphorylated DcuR bound specifically to the promoter region, and the deletion of
dcuS
or
dcuR
reduced the expression of
citC
. The data indicate the presence of a regulatory cascade consisting of DcuS/DcuR modulating
citAB
expression (and CitA/CitB levels) and CitA/CitB controlling the expression of the
citCDEFXGT
gene cluster in response to citrate.
In vivo
fluorescence resonance energy transfer (FRET) and the bacterial two-hybrid system (BACTH) showed interaction between the DcuS and CitA proteins. However, BACTH and expression studies demonstrated the lack of interaction and cross-regulation between CitA and DcuR or DcuS and CitB. Therefore, there is only linear phosphoryl transfer (DcuS→DcuR and CitA→CitB) without cross-regulation between DcuS/DcuR and CitA/CitB.
Patient safety in patients who occupy beds on clinically inappropriate wards: a qualitative interview study with NHS staff
Authors: Goulding Lucy , Adamson Joy , Watt Ian , Wright John 
Published: November 2011

ObjectiveTo explore NHS staff members' perceptions and experiences of the contributory factors that may underpin patient safety issues in those who are placed on a hospital ward that would not normally treat their illness (such patients are often called ‘outliers’ ‘sleep outs’ or ‘boarders’).DesignQualitative study using semi-structured interviews.SettingA single large teaching hospital in the north of England.Participants29 members of NHS staff (doctors, nurses and non-clinical or management staff).ResultsFive themes describing contributory factors underlying safety issues were identified: competing demands on staff time created by having patients on inappropriate wards and patients who are on the correct specialty ward to care for; poor communication between the correct specialty ward and the clinically inappropriate ward; lack of knowledge or specialist expertise on clinically inappropriate wards; an unsuitable ward environment for patients on inappropriate wards; and the characteristics of patients who are placed on clinically inappropriate wards (specifically staff perceive patients on inappropriate wards to be medically fit and therefore of lower priority and moving patients between wards may disorientate confused or impaired patients). Examples of how these contributory factors may lead to safety issues are given.ConclusionsNHS staff report that placement of patients on clinically inappropriate wards is a specific patient safety concern. The application of James Reason's Swiss cheese model of accident causation suggests that placement on an inappropriate ward constitutes a ‘latent condition’ which may expose patients to contributory factors that underlie adverse events.
Stress-Regulated Transcription Factor ATF4 Promotes Neoplastic Transformation by Suppressing Expression of the INK4a/ARF Cell Senescence Factors
Authors: Horiguchi Michiko , Koyanagi Satoru , Okamoto Akinori , Suzuki Satoshi O. , Matsunaga Naoya , Ohdo Shigehiro 
Published: November 2011

Abstract
Many cancers overexpress ATF4, a stress-induced transcription factor that promotes cell survival under hypoxic conditions and other stresses of the tumor microenvironment, but the potential contributions of ATF4 to oncogenesis itself have been little explored. Here, we report that ATF4 promotes oncogene-induced neoplastic transformation by suppressing the expression of cellular senescence-associated genes. Strikingly, primary embryo fibroblasts from ATF4-deficient mice were resistant to transformation by coexpression of H-rasV12 and SV40 large T antigen. In wild-type cells these oncogenes induced expression of the murine Atf4 gene along with the cyclin-dependent kinase inhibitor Cdkn2a, which encodes the cell senescence-associated proteins p16INK4 and p19ARF. Elevated levels of ATF4 were sufficient to suppress expression of these proteins and drive oncogenic transformation. Conversely, genetic ablation of ATF4 led to constitutive expression of p16INK4a and p19ARF, triggering cellular senescence. Our findings define a central function for ATF4 in promoting oncogenic transformation by suppressing a central pathway of cellular senescence. Cancer Res; 72(2); 395–401. ©2011 AACR.
A Large Candidate Gene Survey Identifies the
KCNE1
D85N Polymorphism as a Possible Modulator of Drug-Induced Torsades de Pointes
Authors: Kääb Stefan , Crawford Dana C. , Sinner Moritz F. , Behr Elijah R. , Kannankeril Prince J. , Wilde Arthur A.M. , Bezzina Connie R. , Schulze-Bahr Eric , Guicheney Pascale , Bishopric Nanette H. , Myerburg Robert J. , Schott Jean-Jacques , Pfeufer Arne , Beckmann Britt-Maria , Martens Eimo , Zhang Taifang , Stallmeyer Birgit , Zumhagen Sven , Denjoy Isabelle , Bardai Abdennasser , Van Gelder Isabelle C. , Jamshidi Yalda , Dalageorgou Chrysoula , Marshall Vanessa , Jeffery Steve , Shakir Saad , Camm A. John , Steinbeck Gerhard , Perz Siegfried , Lichtner Peter , Meitinger Thomas , Peters Annette , Wichmann H.-Erich , Ingram Christiana , Bradford Yuki , Carter Shannon , Norris Kris , Ritchie Marylyn D. , George Alfred L. , Roden Dan M. 
Published: November 2011

Background—
Drug-induced long-QT syndrome (diLQTS) is an adverse drug effect that has an important impact on drug use, development, and regulation. We tested the hypothesis that common variants in key genes controlling cardiac electric properties modify the risk of diLQTS.

Methods and Results—

In a case-control setting, we included 176 patients of European descent from North America and Europe with diLQTS, defined as documented torsades de pointes during treatment with a QT-prolonging drug. Control samples were obtained from 207 patients of European ancestry who displayed <50 ms QT lengthening during initiation of therapy with a QT-prolonging drug and 837 control subjects from the population-based KORA study. Subjects were successfully genotyped at 1424 single-nucleotide polymorphisms (SNPs) in 18 candidate genes including 1386 SNPs tagging common haplotype blocks and 38 nonsynonymous ion channel gene SNPs. For validation, we used a set of cases (n=57) and population-based control subjects of European descent. The SNP
KCNE1
D85N (rs1805128), known to modulate an important potassium current in the heart, predicted diLQTS with an odds ratio of 9.0 (95% confidence interval, 3.5–22.9). The variant allele was present in 8.6% of cases, 2.9% of drug-exposed control subjects, and 1.8% of population control subjects. In the validation cohort, the variant allele was present in 3.5% of cases and in 1.4% of control subjects.

Conclusions—
This high-density candidate SNP approach identified a key potassium channel susceptibility allele that may be associated with the rare adverse drug reaction torsades de pointes.
Burden of informal care giving to patients with psychoses: A descriptive and methodological study
Authors: Flyckt Lena , Löthman Anna , Jörgensen Leif , Rylander Anders , Koernig Thomas 
Published: November 2011

Background: There is a lack of studies of the size of burden associated with informal care giving in psychosis. Aims: To evaluate the objective and subjective burden of informal care giving to patients with psychoses, and to compare a diary and recall method for assessments of objective burden. Method: Patients and their informal caregivers were recruited from nine Swedish psychiatric outpatient centres. Subjective burden was assessed at inclusion using the CarerQoL and COPE index scales. The objective burden (time and money spent) was assessed by the caregivers daily using diaries over four weeks and by recall at the end of weeks 1 and 2. Results: One-hundred and seven patients (53% females; mean age 43 ± 11) and 118 informal caregivers (67%; 58 ± 15 years) were recruited. Informal caregivers spent 22.5 hours/week and about 14% of their gross income on care-related activities. The time spent was underestimated by two to 20 hours when assessed by recall than by daily diary records. The most prominent aspects of the subjective burden were mental problems. Conclusion: Despite a substantial amount of time and money spent on care giving, the informal caregivers perceived the mental aspects of burden as the most troublesome. The informal caregiver burden is considerable and should be taken into account when evaluating effects of health care provided to patients with psychoses.
Sources of parental burden in a UK sample of first-generation North Indian Punjabi Sikhs and their white British counterparts
Authors: Lloyd Helen , Singh Pratima , Merritt Rowena , Shetty Adarsh , Singh Swaran , Burns Tom 
Published: November 2011

Objective: The correlates of parental burden in schizophrenia may differ between ethnic groups, but few studies have examined this in a UK setting. Our aim was to identify the correlates of burden in a UK sample of first-generation North Indian Punjabi Sikh parents and their white British counterparts. Method: Test the association of burden with a series of clinical, social and service use variables and control for potential confounding factors in a model predicting drivers of burden in a combined sample of the above. Results: The strongest correlates of burden were patient symptoms and parental distress. Differences in correlates of burden between the groups emerged when individual components of service use and parental social network were tested. The group comparisons also revealed differences in expressed emotion (EE) and social networks. Conclusion: The similarities in sources of burden between the groups could be explained by a commonality of sociocultural and economic experience, resulting from the successful acculturation and affluence of this British Sikh group. The differences between the groups may be related to enduring cultural factors such as kin support, since larger family groups were associated with low burden in the British Sikh group. The nature of EE in this British Sikh group may explain why it was not associated with burden in this sample.
Desialylation accelerates platelet clearance after refrigeration and initiates GPIbα metalloproteinase-mediated cleavage in mice
Authors: Jansen A. J. Gerard , Josefsson Emma C. , Rumjantseva Viktoria , Liu Qiyong Peter , Falet Hervé , Bergmeier Wolfgang , Cifuni Stephen M. , Sackstein Robert , von Andrian Ulrich H. , Wagner Denisa D. , Hartwig John H. , Hoffmeister Karin M. 
Published: November 2011

AbstractWhen refrigerated platelets are rewarmed, they secrete active sialidases, including the lysosomal sialidase Neu1, and express surface Neu3 that remove sialic acid from platelet von Willebrand factor receptor (VWFR), specifically the GPIbα subunit. The recovery and circulation of refrigerated platelets is greatly improved by storage in the presence of inhibitors of sialidases. Desialylated VWFR is also a target for metalloproteinases (MPs), because GPIbα and GPV are cleaved from the surface of refrigerated platelets. Receptor shedding is inhibited by the MP inhibitor GM6001 and does not occur in Adam17ΔZn/ΔZn platelets expressing inactive ADAM17. Critically, desialylation in the absence of MP-mediated receptor shedding is sufficient to cause the rapid clearance of platelets from circulation. Desialylation of platelet VWFR therefore triggers platelet clearance and primes GPIbα and GPV for MP-dependent cleavage.
Ionizing radiation–induced expression of INK4a/ARF in murine bone marrow–derived stromal cell populations interferes with bone marrow homeostasis
Authors: Carbonneau Cynthia L. , Despars Geneviève , Rojas-Sutterlin Shanti , Fortin Audrey , Le Oanh , Hoang Trang , Beauséjour Christian M. 
Published: November 2011

Abstract
Alterations of the BM microenvironment have been shown to occur after chemoradiotherapy, during aging, and after genetic manipulations of telomere length. Nevertheless, whether BM stromal cells adopt senescent features in response to these events is unknown. In the present study, we provide evidence that exposure to ionizing radiation (IR) leads murine stromal BM cells to express senescence markers, namely senescence-associated β-galactosidase and increased p16INK4a/p19ARF expression. Long (8 weeks) after exposure of mice to IR, we observed a reduction in the number of stromal cells derived from BM aspirates, an effect that we found to be absent in irradiated Ink4a/arf-knockout mice and to be mostly independent of the CFU potential of the stroma. Such a reduction in the number of BM stromal cells was specific, because stromal cells isolated from collagenase-treated bones were not reduced after IR. Surprisingly, we found that exposure to IR leads to a cellular nonautonomous and Ink4a/arf-dependent effect on lymphopoiesis. Overall, our results reveal the distinct sensitivity of BM stromal cell populations to IR and suggest that long-term residual damage to the BM microenvironment can influence hematopoiesis in an Ink4a/arf-dependent manner.
The recombinant lectin-like domain of thrombomodulin inhibits angiogenesis through interaction with Lewis Y antigen
Authors: Kuo Cheng-Hsiang , Chen Po-Ku , Chang Bi-Ing , Sung Meng-Chen , Shi Chung-Sheng , Lee Jeng-Shin , Chang Chuan-Fa , Shi Guey-Yueh , Wu Hua-Lin 
Published: November 2011

AbstractLewis Y Ag (LeY) is a cell-surface tetrasaccharide that participates in angiogenesis. Recently, we demonstrated that LeY is a specific ligand of the recombinant lectin-like domain of thrombomodulin (TM). However, the biologic function of interaction between LeY and TM in endothelial cells has never been investigated. Therefore, the role of LeY in tube formation and the role of the recombinant lectin-like domain of TM—TM domain 1 (rTMD1)—in antiangiogenesis were investigated. The recombinant TM ectodomain exhibited lower angiogenic activity than did the recombinant TM domains 2 and 3. rTMD1 interacted with soluble LeY and membrane-bound LeY and inhibited soluble LeY-mediated chemotaxis of endothelial cells. LeY was highly expressed on membrane ruffles and protrusions during tube formation on Matrigel. Blockade of LeY with rTMD1 or Ab against LeY inhibited endothelial tube formation in vitro. Epidermal growth factor (EGF) receptor in HUVECs was LeY modified. rTMD1 inhibited EGF receptor signaling, chemotaxis, and tube formation in vitro, and EGF-mediated angiogenesis and tumor angiogenesis in vivo. We concluded that LeY is involved in vascular endothelial tube formation and rTMD1 inhibits angiogenesis via interaction with LeY. Administration of rTMD1 or recombinant adeno-associated virus vector carrying TMD1 could be a promising antiangiogenesis strategy.
Induction of acute GVHD by sex-mismatched H-Y antigens in the absence of functional radiosensitive host hematopoietic–derived antigen-presenting cells
Authors: Toubai Tomomi , Tawara Isao , Sun Yaping , Liu Chen , Nieves Evelyn , Evers Rebecca , Friedman Thea , Korngold Robert , Reddy Pavan 
Published: November 2011

AbstractIt is currently thought that acute GVHD cannot be elicited in the absence of Ag presentation by radiosensitive host hematopoietic-derived APCs after allogeneic BM transplantation. Because clinical data suggest that sex-mismatched H-Y Ags may be important minor histocompatibility Ags for GVH responses, we directly tested their relevance and ability to initiate GVHD when presented by either the hematopoietic- (host or donor) or the nonhematopoietic-derived APCs. H-Y minor Ag incompatibility elicited both CD4+ and CD8+ T-cell driven GVHD lethality. Studies with various well-established BM chimera recipients, in contrast to the current views, have reported that in the absence of functional radiosensitive host hematopoietic-derived APCs, H-Y Ag presentation by either the donor hematopoietic-derived or the host nonhematopoietic-derived APCs is sufficient for inducing GVHD. Our data further suggest that infusion of sufficient numbers of alloreactive donor T cells will induce GVHD in the absence of radiosensitive host hematopoietic-derived APCs.
Strategies to facilitate the development of uncloned or cloned infectious full-length viral cDNAs: Apple chlorotic leaf spot virus as a case study
Authors: Youssef Fater , Marais Armelle , Faure Chantal , Gentit Pascal , Candresse Thierry 
Published: November 2011

Abstract

Background
Approaches to simplify and streamline the construction of full-length infectious cDNA clones (FL-cDNAs) are needed. Among desirable improvements are the ability to use total nucleic acids (TNA) extracts from infected hosts (to bypass viral purification limitations) for the direct one-step amplification of large FL-cDNAs, the possibility to inoculate plants with uncloned FL-cDNAs and the simplified cloning of these large molecules.

Results
Using the 7.55 kb genome of Apple chlorotic leaf spot trichovirus (ACLSV) approaches allowing the rapid generation from TNA extracts of FL-cDNAs under the control of the T7 promoter and the successful inoculation of plants using in vitro transcripts obtained from these uncloned amplification products have been developed. We also show that the yeast homologous recombination system permits efficient cloning of FL-cDNAs and the simultaneous one-step tailoring of a ternary Yeast-Escherichia coli-Agrobacterium tumefaciens shuttle vector allowing efficient inoculation of both herbaceous and woody host plants by agroinfiltration.

Conclusions
The fast and efficient strategies described here should have broad applications, in particular for the study of "difficult" plant viruses, such as those infecting woody hosts, and potentially for other, non plant-infecting viral agents.
Bioinformatics analysis of rabbit haemorrhagic disease virus genome
Authors: Tian Xiao-ting , Li Bao-yu , Zhang Liang , Jiao Wen-qiang , Liu Ji-xing 
Published: November 2011

Abstract

Background
Rabbit haemorrhagic disease virus (RHDV), as the pathogeny of Rabbit haemorrhagic disease, can cause a highly infectious and often fatal disease only affecting wild and domestic rabbits. Recent researches revealed that it, as one number of the Caliciviridae, has some specialties in its genome, its reproduction and so on.

Results
In this report, we firstly analyzed its genome and two open reading frameworks (ORFs) from this aspect of codon usage bias. Our researches indicated that mutation pressure rather than natural is the most important determinant in RHDV with high codon bias, and the codon usage bias is nearly contrary between ORF1 and ORF2, which is maybe one of factors regulating the expression of VP60 (encoding by ORF1) and VP10 (encoding by ORF2). Furthermore, negative selective constraints on the RHDV whole genome implied that VP10 played an important role in RHDV lifecycle.

Conclusions
We conjectured that VP10 might be beneficial for the replication, release or both of virus by inducing infected cell apoptosis initiate by RHDV. According to the results of the principal component analysis for ORF2 of RSCU, we firstly separated 30 RHDV into two genotypes, and the ENC values indicated ORF1 and ORF2 were independent among the evolution of RHDV.