bluuebunny/crossref_metadata_2025_split huggingface dataset:
RSV infection modulates IL-15 production and MICA levels in respiratory epithelial cells
Authors: Zdrenghea M.T. , Telcian A.G. , Laza-Stanca V. , Bellettato C.M. , Edwards M.R. , Nikonova A. , Khaitov M.R. , Azimi N. , Groh V. , Mallia P. , Johnston S.L. , Stanciu L.A. 
Published: August 2011

The cytokine interleukin (IL)-15, major histocompatibility complex (MHC) class I molecules and MHC class I chain-related proteins (MIC) A and B are involved in cellular immune responses to virus infections but their role in respiratory syncytial virus (RSV) infection has not been studied. We aimed to determine how RSV infection modulates IL-15 production, MHC class I and MICA expression in respiratory epithelial cells, the molecular pathways implicated in virus-induced IL-15 production and how interferon (IFN)-γ alters RSV-induced IL-15 production and MHC class I and MICA expression.We infected respiratory epithelial cell lines (A549 and BEAS-2B cells) and primary bronchial epithelial cells with RSV and measured production of IL-15, expression of MHC I and MICA and the role of the transcription factor nuclear factor (NF)-κB.We report here that RSV increases IL-15 in respiratory epithelial cellsviavirus replication and NF-κB-dependent mechanisms. Furthermore, RSV infection of epithelial cells upregulated cell surface expression of MICA and levels of soluble MICA. IFN-γ upregulated RSV induction of soluble IL-15 but inhibited induction of MICA.Upregulation of IL-15, MHC I and MICA are likely to be important mechanisms in activating immune responses to RSV by epithelial cells.
Cigarette smoke inhibits lung fibroblast proliferation by translational mechanisms
Authors: Miglino N. , Roth M. , Lardinois D. , Sadowski C. , Tamm M. , Borger P. 
Published: August 2011

Cigarette smoke is a major cause of chronic obstructive pulmonary disease (COPD) and emphysema. Although cigarette smoke represses cellular proliferation, the molecular mechanisms underlying this phenomenon are unknown. CCAAT/enhancer-binding proteins (C/EBPs) are key regulators of cell cycle progression, differentiation and pro-inflammatory gene expression, are regulated predominantly at the translational level and may be involved in the pathogenesis of COPD. The aim of this study was to assess the effect of cigarette smoke on proliferation and the expression and translational regulation of C/EBPα and C/EBPβ in nondiseased primary human lung fibroblasts.Fibroblasts were exposed to cigarette smoke-conditioned medium (10% and 20% for 24 h). Proliferation was determined by [3H]thymidine incorporation. Protein expression levels were determined by immunoblotting and translation was monitored using a translation control reporter system.Cigarette smoke significantly reduced fibroblast proliferation and significantly upregulated full-length C/EBPα and C/EBPβ proteins due to a shift in the translational control ofCEBPAandCEBPBmRNAs. This shift involved the re-initiation of mRNA translationviathe regulatory upstream open reading frame, which coincided with increased interleukin-8 release and a decrease in functional elastin level.These findings provide a novel mechanism to understanding the tissue remodelling observed in the lungs of COPD patients.
Home telemonitoring (forced expiratory volume in 1 s) in children with severe asthma does not reduce exacerbations
Authors: Deschildre A. , Béghin L. , Salleron J. , Iliescu C. , Thumerelle C. , Santos C. , Hoorelbeke A. , Scalbert M. , Pouessel G. , Gnansounou M. , Edmé J-L. , Matran R. 
Published: August 2011

Some children with severe asthma develop frequent exacerbations despite intensive treatment.We sought to assess the outcome (severe exacerbations and healthcare use, lung function, quality of life and maintenance treatment) of a strategy based on daily home spirometry with teletransmission to an expert medical centre and whether it differs from that of a conventional strategy.50 children with severe uncontrolled asthma were enrolled in a 12-month prospective study and were randomised into two groups: 1) treatment managed with daily home spirometry and medical feedback (HM) and 2) conventional treatment (CT).The children’s mean age was 10.9 yrs (95% confidence interval 10.2–11.6). 44 children completed the study (21 in the HM group and 23 in the CT group). The median number of severe exacerbations per patient was 2.0 (interquartile range 1.0–4.0) in the HM group and 3.0 (1.0–4.0) in the CT group (p=0.38 with adjustment for age). There were no significant differences between the two groups for unscheduled visits (HM 5.0 (3.0–7.0), CT 3.0 (2.0–7.0); p=0.30), lung function (pre-β2-agonist forced expiratory volume in 1 s (FEV1) p=0.13), Paediatric Asthma Quality of Life Questionnaire scores (p=0.61) and median daily dose of inhaled corticosteroids (p=0.86).A treatment strategy based on daily FEV1monitoring with medical feedback did not reduce severe asthma exacerbations.
Rapid early weight gain is associated with wheeze and reduced lung function in childhood
Authors: van der Gugten A.C. , Koopman M. , Evelein A.M.V. , Verheij T.J.M. , Uiterwaal C.S.P.M. , van der Ent C.K. 
Published: August 2011

The aim of our study was to investigate the association between rapid weight gain in the first 3 months of life and the prevalence of wheeze in the first years of life and lung function at 5 yrs of age.The infants selected were participating in an ongoing birth cohort. Information on growth and respiratory symptoms was collected during the first year of life, and on primary care consultations during total follow-up. Forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25–75% of forced vital capacity (FEF25–75%) were measured at 5 yrs of age.Information on growth and respiratory symptoms was obtained for 1,431 infants, out of whom 235 children had already had 5 yrs of follow-up. Every one-point z-score increase in weight gain resulted in a 37% increase in days with wheeze (incidence rate ratio 1.37, 95% CI 1.27–1.47; p<0.001) and in associated consultations by 16% (incidence rate ratio 1.16, 95% CI 1.01–1.34; p=0.04). Children with rapid weight gain reported significantly more physician-diagnosed asthma. FEV1and FEF25–75%were reduced by 34 mL (adjusted regression coefficient -0.034, 95% CI -0.056– -0.013; p=0.002) and 82 mL (adjusted regression coefficient -0.082, 95% CI -0.140– -0.024; p=0.006) per every one-point z-score increase in weight gain, respectively. These associations were independent of birthweight.Rapid early weight gain is a risk factor for clinically relevant wheezing illnesses in the first years of life and lower lung function in childhood.
Valproic acid inhibits neural progenitor cell death by activation of NF-κB signaling pathway and up-regulation of Bcl-XL
Authors: Go Hyo Sang , Seo Jung Eun , Kim Ki Chan , Han So Min , Kim Pitna , Kang Young Sun , Han Seol Heui , Shin Chan Young , Ko Kwang Ho 
Published: August 2011

AbstractBackgroundAt the beginning of neurogenesis, massive brain cell death occurs and more than 50% of cells are eliminated by apoptosis along with neuronal differentiation. However, few studies were conducted so far regarding the regulation of neural progenitor cells (NPCs) death during development. Because of the physiological role of cell death during development, aberration of normal apoptotic cell death is detrimental to normal organogenesis.Apoptosis occurs in not only neuron but also in NPCs and neuroblast. When growth and survival signals such as EGF or LIF are removed, apoptosis is activated as well as the induction of differentiation. To investigate the regulation of cell death during developmental stage, it is essential to investigate the regulation of apoptosis of NPCs.MethodsNeural progenitor cells were cultured from E14 embryonic brains of Sprague-Dawley rats. Forin vivoVPA animal model, pregnant rats were treated with VPA (400 mg/kg S.C.) diluted with normal saline at E12. To analyze the cell death, we performed PI staining and PARP and caspase-3 cleavage assay. Expression level of proteins was investigated by Western blot and immunocytochemical assays. The level of mRNA expression was investigated by RT-PCR. Interaction of Bcl-XL gene promoter and NF-κB p65 was investigated by ChIP assay.ResultsIn this study, FACS analysis, PI staining and PARP and caspase-3 cleavage assay showed that VPA protects cultured NPCs from cell death after growth factor withdrawal both in basal and staurosporine- or hydrogen peroxide-stimulated conditions. The protective effect of prenatally injected VPA was also observed in E16 embryonic brain. Treatment of VPA decreased the level of IκBα and increased the nuclear translocation of NF-κB, which subsequently enhanced expression of anti-apoptotic protein Bcl-XL.ConclusionTo the best of our knowledge, this is the first report to indicate the reduced death of NPCs by VPA at developmentally critical periods through the degradation of IκBα and the activation of NF-κB signaling. The reduced NPCs death might underlie the neurodevelopmental defects collectively called fetal valproate syndrome, which shows symptoms such as mental retardation and autism-like behavior.
High efficient isolation and systematic identification of human adipose-derived mesenchymal stem cells
Authors: Yang Xu-Fang , He Xu , He Jian , Zhang Li-Hong , Su Xue-Jin , Dong Zhi-Yong , Xu Yun-Jian , Li Yan , Li Yu-Lin 
Published: August 2011

Abstract

Background
Developing efficient methods to isolate and identify human adipose-derived mesenchymal stem cells (hADSCs) remains to be one of the major challenges in tissue engineering.

Methods
We demonstrate here a method by isolating hADSCs from abdominal subcutaneous adipose tissue harvested during caesarian section. The hADSCs were isolated from human adipose tissue by collagenase digestion and adherence to flasks.

Results
The yield reached around 1 × 106 hADSCs per gram adipose tissue. The following comprehensive identification and characterization illustrated pronounced features of mesenchymal stem cells (MSCs). The fibroblast-like hADSCs exhibited typical ultrastructure details for vigorous cell activities. Karyotype mapping showed normal human chromosome. With unique immunophenotypes they were positive for CD29, CD44, CD73, CD105 and CD166, but negative for CD31, CD34, CD45 and HLA-DR. The growth curve and cell cycle analysis revealed high capability for self-renewal and proliferation. Moreover, these cells could be functionally induced into adipocytes, osteoblasts, and endothelial cells in the presence of appropriate conditioned media.

Conclusion
The data presented here suggest that we have developed high efficient isolation and cultivation methods with a systematic strategy for identification and characterization of hADSCs. These techniques will be able to provide safe and stable seeding cells for research and clinical application.
A first-generation integrated tammar wallaby map and its use in creating a tammar wallaby first-generation virtual genome map
Authors: Wang Chenwei , Deakin Janine E , Rens Willem , Zenger Kyall R , Belov Katherine , Marshall Graves Jennifer A , Nicholas Frank W 
Published: August 2011

Abstract

Background
The limited (2X) coverage of the tammar wallaby (Macropus eugenii) genome sequence dataset currently presents a challenge for assembly and anchoring onto chromosomes. To provide a framework for this assembly, it would be a great advantage to have a dense map of the tammar wallaby genome. However, only limited mapping data are available for this non-model species, comprising a physical map and a linkage map.

Results
We combined all available tammar wallaby mapping data to create a tammar wallaby integrated map, using the Location DataBase (LDB) strategy. This first-generation integrated map combines all available information from the second-generation tammar wallaby linkage map with 148 loci, and extensive FISH mapping data for 492 loci, especially for genes likely to be located at the ends of wallaby chromosomes or at evolutionary breakpoints inferred from comparative information. For loci whose positions are only approximately known, their location in the integrated map was refined on the basis of comparative information from opossum (Monodelphis domestica) and human. Interpolation of segments from the opossum and human assemblies into the integrated map enabled the subsequent construction of a tammar wallaby first-generation virtual genome map, which comprises 14336 markers, including 13783 genes recruited from opossum and human assemblies. Both maps are freely available at http://compldb.angis.org.au.

Conclusions
The first-generation integrated map and the first-generation virtual genome map provide a backbone for the chromosome assembly of the tammar wallaby genome sequence. For example, 78% of the 10257 gene-scaffolds in the Ensembl annotation of the tammar wallaby genome sequence (including 10522 protein-coding genes) can now be given a chromosome location in the tammar wallaby virtual genome map.
Testing the importance of jasmonate signalling in induction of plant defences upon cabbage aphid (Brevicoryne brassicae) attack
Authors: Kuśnierczyk Anna , Tran Diem HT , Winge Per , Jørstad Tommy S , Reese John C , Troczyńska Joanna , Bones Atle M 
Published: August 2011

Abstract

Background
Phloem-feeding aphids deprive plants of assimilates, but mostly manage to avoid causing the mechanical tissue damage inflicted by chewing insects. Nevertheless, jasmonate signalling that is induced by infestation is important in mediating resistance to phloem feeders. Aphid attack induces the jasmonic acid signalling pathway, but very little is known about the specific impact jasmonates have on the expression of genes that respond to aphid attack.

Results
We have evaluated the function that jasmonates have in regulating Arabidopsis thaliana responses to cabbage aphid (Brevicoryne brassicae) by conducting a large-scale transcriptional analysis of two mutants: aos, which is defective in jasmonate production, and fou2, which constitutively induces jasmonic acid biosynthesis. This analysis enabled us to determine which genes' expression patterns depend on the jasmonic acid signalling pathway. We identified more than 200 genes whose expression in non-challenged plants depended on jasmonate levels and more than 800 genes that responded differently to infestation in aos and fou2 plants than in wt. Several aphid-induced changes were compromised in the aos mutant, particularly genes connected to regulation of transcription, defence responses and redox changes. Due to jasmonate-triggered pre-activation of fou2, its transcriptional profile in non-challenged plants mimicked the induction of defence responses in wt. Additional activation of fou2 upon aphid attack was therefore limited. Insect fitness experiments revealed that the physiological consequences of fou2 mutation contributed to more effective protection against B. brassicae. However, the observed resistance of the fou2 mutant was based on antibiotic rather than feeding deterrent properties of the mutant as indicated by an analysis of aphid feeding behaviour.

Conclusions
Analysis of transcriptional profiles of wt, aos and fou2 plants revealed that the expression of more than 200 genes is dependent on jasmonate status, regardless of external stimuli. Moreover, the aphid-induced response of more than 800 transcripts is regulated by jasmonate signalling. Thus, in plants lacking jasmonates many of the defence-related responses induced by infestation in wt plants are impaired. Constant up-regulation of jasmonate signalling as evident in the fou2 mutant causes reduction in aphid population growth, likely as a result of antibiotic properties of fou2 plants. However, aos mutation does not seem to affect aphid performance when the density of B. brassicae populations on plants is low and aphids are free to move around.
In Mycoplasma hoministhe OppA-mediated cytoadhesion depends on its ATPase activity
Authors: Hopfe Miriam , Dahlmanns Theresa , Henrich Birgit 
Published: August 2011

AbstractBackgroundInMycoplasma hominis, a facultative human pathogen of the human genital tract, OppA, the substrate-binding domain of the oligopeptide permease, is a multifunctional protein involved in nutrition uptake, cytoadhesion and hydrolysis of extracellular ATP.ResultsTo map the function-related protein regions the ATPase activity and adhesive behavior of OppA mutants were analyzed. Mutations of the Walker BA motifs resulted in an inhibition of up to 8% of the OppA ATPase activity, whereas deletion of the N-terminal CS1 or the CS2 region, structural motifs that are conserved in bacterial OppA proteins, reduced ATPase activity to 60% and deletion of CS3, the third conserved region adjacent to the Walker B motif led to a reduction to 42% ATPase activity.Interestingly, adhesion of the OppA mutants to immobilized HeLa cells demonstrated that two distal regions are mainly involved in adherence of OppA: the CS1 region, deletion of which led to 35% of the cytoadhesion, and the Walker BA with the adjacent upstream region CS3, deletion of which led to 25% of the cytoadhesion. The influence of the ATPase activity on the adherence ofM. hoministo HeLa cells was confirmed by the use of ATPase inhibitors which reduced mycoplasmal cytoadhesion to 50%.ConclusionsThese findings suggest that the OppA-mediated cytoadherence ofMycoplasma hominis depends on both, the topology of the neighbouring CS1 and ATPase domain regions and the functionality of the ecto-ATPase activity in addition.
A bacterial PriB with weak single-stranded DNA binding activity can stimulate the DNA unwinding activity of its cognate PriA helicase
Authors: Feng Cui , Sunchu Bharath , Greenwood Mallory E , Lopper Matthew E 
Published: August 2011

Abstract

Background
Bacterial DNA replication restart pathways facilitate reinitiation of DNA replication following disruptive encounters of a replisome with DNA damage, thereby allowing complete and faithful duplication of the genome. In Neisseria gonorrhoeae, the primosome proteins that catalyze DNA replication restart differ from the well-studied primosome proteins of E. coli with respect to the number of proteins involved and the affinities of their physical interactions: the PriA:PriB interaction is weak in E. coli, but strong in N. gonorrhoeae, and the PriB:DNA interaction is strong in E. coli, but weak in N. gonorrhoeae. In this study, we investigated the functional consequences of this affinity reversal.

Results
We report that N. gonorrhoeae PriA's DNA binding and unwinding activities are similar to those of E. coli PriA, and N. gonorrhoeae PriA's helicase activity is stimulated by its cognate PriB, as it is in E. coli. This finding is significant because N. gonorrhoeae PriB's single-stranded DNA binding activity is weak relative to that of E. coli PriB, and in E. coli, PriB's single-stranded DNA binding activity is important for PriB stimulation of PriA helicase. Furthermore, a N. gonorrhoeae PriB variant defective for binding single-stranded DNA can stimulate PriA's helicase activity, suggesting that DNA binding by PriB might not be important for PriB stimulation of PriA helicase in N. gonorrhoeae. We also demonstrate that N. gonorrhoeae PriB stimulates ATP hydrolysis catalyzed by its cognate PriA. This activity of PriB has not been observed in E. coli, and could be important for PriB stimulation of PriA helicase in N. gonorrhoeae.

Conclusions
The results of this study demonstrate that a bacterial PriB homolog with weak single-stranded DNA binding activity can stimulate the DNA unwinding activity of its cognate PriA helicase. While it remains unclear if N. gonorrhoeae PriB's weak DNA binding activity is required for PriB stimulation of PriA helicase, the ability of PriB to stimulate PriA-catalyzed ATP hydrolysis could play an important role. Thus, the weak interaction between N. gonorrhoeae PriB and DNA might be compensated for by the strong interaction between PriB and PriA, which could result in allosteric activation of PriA's ATPase activity.
Prevalence and antimicrobial resistance of Salmonella isolated from lactating cows and in contact humans in dairy farms of Addis Ababa: a cross sectional study
Authors: Addis Zelalem , Kebede Nigatu , Sisay Zufan , Alemayehu Haile , Wubetie Alehegne , Kassa Tesfu 
Published: August 2011

Abstract

Background

Salmonella are the major pathogenic bacteria in humans as well as in animals. Salmonella species are leading causes of acute gastroenteritis in several countries and salmonellosis remains an important public health problem worldwide, particularly in the developing countries. The situation is more aggravated by the ever increasing rate of antimicrobial resistance strains. Cattle have been implicated as a source of human infection with antimicrobial resistant Salmonella through direct contact with livestock and through the isolation of antimicrobial resistant Salmonella from raw milk, cheddar cheese, and hamburger meat traced to dairy farms. Despiite the presence of many studies on the prevalence and antimicrobial susceptibility pattern of Salmonella in Ethiopia, nothing has been said on the degree of the situation among apparently healthy lactating cows and in contact humans. Hence this study was conducted to determine the prevalence and antimicrobial resistance pattern of Salmonella isolates from lactating cows and in contact humans in dairy farms of Addis Ababa.

Methods
a cross sectional study was conducted in Addis Ababa by collecting milk and faecal samples from lactating cows and stool samples from humans working in dairy farms. Samples were pre-enriched in buffered peptone water followed by selective enrichment using selenite cysteine and Rapaport-Vassilidis broths. Isolation and identification was made by inoculating the selectively enriched sample on to Xylose Lysine Deoxycholate agar followed by confirmation of presumptive colonies using different biochemical tests. The Kibry Bauer disk diffusion method was used for antimicrobial sensitivity testing.

Results
10.7% (21/195) of cows and 13.6% (3/22) of the human subjects sheded Salmonella. 83% resistance to two or more antimicrobials and 100% resistance to ampicillin were observed. Most of the isolates were relatively sensitive to ciprofloxacin, cotrimoxazole, and chloramphenicol.

Conclusion
High proportion of Salmonella isolates developed resistance to the commonly prescribed antimicrobials and this may be a considerable risk in the treatment of clinical cases. So, wise use of antimicrobials must be practiced to combat the ever increasing situation of antimicrobial resistance.