bluuebunny/crossref_metadata_2025_split huggingface dataset:
Silencing of NADPH-Dependent Oxidoreductase Genes (yqhDanddkgA) in Furfural-Resistant EthanologenicEscherichia coli
Authors: Miller E. N. , Jarboe L. R. , Yomano L. P. , York S. W. , Shanmugam K. T. , Ingram L. O. 
Published: May 2009

ABSTRACTLow concentrations of furfural are formed as a side product during the dilute acid hydrolysis of hemicellulose. Growth is inhibited by exposure to furfural but resumes after the complete reduction of furfural to the less toxic furfuryl alcohol. Growth-based selection was used to isolate a furfural-resistant mutant of ethanologenicEscherichia coliLY180, designated strain EMFR9. Based on mRNA expression levels in the parent and mutant in response to furfural challenge, genes encoding 12 oxidoreductases were found to vary by more than twofold (eight were higher in EMFR9; four were higher in the parent). All 12 genes were cloned. When expressed from plasmids, none of the eight genes in the first group increased furfural tolerance in the parent (LY180). Expression of three of the silenced genes (yqhD,dkgA, andyqfA) in EMFR9 was found to decrease furfural tolerance compared to that in the parent. Purified enzymes encoded byyqhDanddkgAwere shown to have NADPH-dependent furfural reductase activity. Both exhibited lowKmvalues for NADPH (8 μM and 23 μM, respectively), similar to those of biosynthetic reactions. Furfural reductase activity was not associated withyqfA. DeletingyqhDanddkgAin the parent (LY180) increased furfural tolerance, but not to the same extent observed in the mutant EMFR9. Together, these results suggest that the process of reducing furfural by using an enzyme with a lowKmfor NADPH rather than a direct inhibitory action is the primary cause for growth inhibition by low concentrations of furfural.
Recovery Efficiency and Limit of Detection of Aerosolized
Bacillus anthracis
Sterne from Environmental Surface Samples
Authors: Estill Cheryl Fairfield , Baron Paul A. , Beard Jeremy K. , Hein Misty J. , Larsen Lloyd D. , Rose Laura , Schaefer Frank W. , Noble-Wang Judith , Hodges Lisa , Lindquist H. D. Alan , Deye Gregory J. , Arduino Matthew J. 
Published: May 2009

ABSTRACT

After the 2001 anthrax incidents, surface sampling techniques for biological agents were found to be inadequately validated, especially at low surface loadings. We aerosolized
Bacillus anthracis
Sterne spores within a chamber to achieve very low surface loading (ca. 3, 30, and 200 CFU per 100 cm
2
). Steel and carpet coupons seeded in the chamber were sampled with swab (103 cm
2
) or wipe or vacuum (929 cm
2
) surface sampling methods and analyzed at three laboratories. Agar settle plates (60 cm
2
) were the reference for determining recovery efficiency (RE). The minimum estimated surface concentrations to achieve a 95% response rate based on probit regression were 190, 15, and 44 CFU/100 cm
2
for sampling steel surfaces and 40, 9.2, and 28 CFU/100 cm
2
for sampling carpet surfaces with swab, wipe, and vacuum methods, respectively; however, these results should be cautiously interpreted because of high observed variability. Mean REs at the highest surface loading were 5.0%, 18%, and 3.7% on steel and 12%, 23%, and 4.7% on carpet for the swab, wipe, and vacuum methods, respectively. Precision (coefficient of variation) was poor at the lower surface concentrations but improved with increasing surface concentration. The best precision was obtained with wipe samples on carpet, achieving 38% at the highest surface concentration. The wipe sampling method detected
B. anthracis
at lower estimated surface concentrations and had higher RE and better precision than the other methods. These results may guide investigators to more meaningfully conduct environmental sampling, quantify contamination levels, and conduct risk assessment for humans.
Transcriptomic Response of
Lactococcus lactis
in Mixed Culture with
Staphylococcus aureus
Authors: Nouaille Sébastien , Even Sergine , Charlier Cathy , Le Loir Yves , Cocaign-Bousquet Muriel , Loubière Pascal 
Published: May 2009

ABSTRACT

The mechanisms of interaction between
Lactococcus lactis
and the food pathogen
Staphylococcus aureus
are of crucial importance, as one major role of lactic acid bacteria (LAB) in fermented foods is to inhibit undesirable and pathogenic flora. It was never questioned if the presence of a pathogen can actively modify the gene expression patterns of LAB in a shared environment. In this study, transcriptome and biochemical analyses were combined to assess the dynamic response of
L. lactis
in a mixed culture with
S. aureus
. The presence of
S. aureus
hardly affected the growth of
L. lactis
but dramatically modified its gene expression profile. The main effect was related to earlier carbon limitation and a concomitantly lower growth rate in the mixed culture due to the consumption of glucose by both species. More specific responses involved diverse cellular functions. Genes associated with amino acid metabolism, ion transport, oxygen response, menaquinone metabolism, and cell surface and phage expression were differentially expressed in the mixed culture. This study led to new insights into possible mechanisms of interaction between
L. lactis
and
S. aureus
. Moreover, new and unexpected effects of
L. lactis
on the virulence of
S. aureus
were discovered, as described elsewhere (S. Even, C. Charlier, S. Nouaille, N. L. Ben Zakour, M. Cretenet, F. J. Cousin, M. Gautier, M. Cocaign-Bousquet, P. Loubière, and Y. Le Loir, Appl. Environ. Microbiol. 75:4459-4472, 2009).
Dominant Negative Autoregulation Limits Steady-State Repression Levels in Gene Networks
Authors: Semsey Szabolcs , Krishna Sandeep , Erdőssy János , Horváth Péter , Orosz László , Sneppen Kim , Adhya Sankar 
Published: May 2009

ABSTRACT

Many transcription factors repress transcription of their own genes. Negative autoregulation has been shown to reduce cell-cell variation in regulatory protein levels and speed up the response time in gene networks. In this work we examined transcription regulation of the
galS
gene and the function of its product, the GalS protein. We observed a unique operator preference of the GalS protein characterized by dominant negative autoregulation. We show that this pattern of regulation limits the repression level of the target genes in steady states. We suggest that transcription factors with dominant negative autoregulation are designed for regulating gene expression during environmental transitions.
Wall Teichoic Acid Protects
Staphylococcus aureus
against Antimicrobial Fatty Acids from Human Skin
Authors: Kohler Thomas , Weidenmaier Christopher , Peschel Andreas 
Published: May 2009

ABSTRACT

Skin-colonizing gram-positive bacteria produce wall teichoic acids (WTAs) or related glycopolymers for unclear reasons. Using a WTA-deficient
Staphylococcus aureus
mutant, we demonstrated that WTA confers resistance to antimicrobial fatty acids from human sebaceous glands by preventing fatty acid binding. Thus, WTA is probably important for bacterial skin colonization.
Correct Timing ofdnaATranscription and Initiation of DNA Replication RequirestransTranslation
Authors: Cheng Lin , Keiler Kenneth C. 
Published: May 2009

ABSTRACTThetranstranslation pathway for protein tagging and ribosome release has been found in all bacteria and is required for proliferation and differentiation in many systems.Caulobacter crescentusmutants that lack thetranstranslation pathway have a defect in the cell cycle and do not initiate DNA replication at the correct time. To determine the molecular basis for this phenotype, effects on events known to be important for initiation of DNA replication were investigated. In the absence oftranstranslation, transcription from thednaApromoter and an origin-proximal promoter involved in replication initiation is delayed. Characterization of thednaApromoter revealed twocis-acting elements that have dramatic effects ondnaAgene expression. A 5′ leader sequence indnaAmRNA represses gene expression by >15-fold but does not affect the timing ofdnaAexpression. The secondcis-acting element, a sequence upstream of the −35 region, affects both the amount ofdnaAtranscription and the timing of transcription in response totranstranslation. Mutations in this promoter element eliminate the transcription delay and partially suppress the DNA replication phenotype in mutants lackingtranstranslation activity. These results suggest that thetranstranslation capacity of the cell is sensed through thednaApromoter to control the timing of DNA replication initiation.
Rapamycin Prevents Early Onset of Tumorigenesis in an Oral-Specific K-ras and p53 Two-Hit Carcinogenesis Model
Authors: Raimondi Ana R. , Molinolo Alfredo , Gutkind J. Silvio 
Published: May 2009

Abstract
Head and neck squamous cell carcinomas (HNSCC), the majority of which occur in the oral cavity, remain a significant cause of morbidity and mortality worldwide. A major limitation in HNSCC research has been the paucity of animal models to test the validity of current genetic paradigms of tumorigenesis and to explore the effectiveness of new treatment modalities and chemopreventive strategies. Here, we have developed an inducible oral-specific animal tumor model system, which consists in the expression of a tamoxifen-inducible Cre recombinase (CreERtam) under the control of the cytokeratin 14 (K14) promoter (K14-CreERtam) and mice in which the endogenous K-ras locus is targeted (LSL-K-rasG12D), thereby causing the expression of endogenous levels of oncogenic K-rasG12D following removal of a stop element. Surprisingly, whereas K14-CreERtam can also target the skin, K14-CreERtam/LSL-K-rasG12D mice developed papillomas exclusively in the oral mucosa within 1 month after tamoxifen treatment. These lesions were highly proliferative but never progressed to carcinoma. However, when crossed with p53 conditional knockout (p53flox/flox) mice, mice developed SCCs exclusively on the tongue as early as 2 weeks after tamoxifen induction, concomitant with a remarkable activation of the mammalian target of rapamycin (mTOR) signaling pathway. The availability of this ras and p53 two-hit animal model system recapitulating HNSCC progression may provide a suitable platform for exploring novel molecular targeted approaches for the treatment of this devastating disease. Indeed, we show here that mTOR inhibition by the use of rapamycin is sufficient to halt tumor progression in this genetically defined oral cancer model system, thereby prolonging animal survival. [Cancer Res 2009;69(10):4159–66]
Targeting DNA Repair in Chronic Lymphocytic Leukemia Cells with a Novel Acyclic Nucleotide Analogue, GS-9219
Authors: Tsai Cheng-Yu , Ray Adrian S. , Tumas Daniel B. , Keating Michael J. , Reiser Hans , Plunkett William 
Published: May 2009

AbstractPurpose: GS-9219 is a cell-permeable prodrug of the acyclic nucleotide analogue 9-(2-phosphonylmethoxyethyl)guanine (PMEG); the incorporation of the active metabolite PMEG diphosphate (PMEGpp) into DNA results in DNA chain termination due to the lack of a 3′-hydroxyl moiety. We hypothesized that the incorporation of PMEGpp into DNA during repair resynthesis would result in the inhibition of DNA repair and the accumulation of DNA breaks in chronic lymphocytic leukemia (CLL) cells that would activate signaling pathways to cell death.Experimental Design: To test this hypothesis, CLL cells were irradiated with UV light to stimulate nucleotide excision repair pathways, enabling the incorporation of PMEGpp into DNA. The combination effects of GS-9219 and DNA-damaging agents and the signaling mechanisms activated in response to DNA repair inhibition by GS-9219, as well as changes in CLL cell viability, were investigated.Results: PMEGpp was incorporated into DNA in CLL cells when nucleotide excision repair was activated by UV. Following PMEGpp incorporation, DNA repair was inhibited, which led to the accumulation of DNA strand breaks. The presence of DNA strand breaks activated the phosphatidylinositol 3-kinase–like protein kinase family members ataxia-telangiectasia mutated and DNA-dependent protein kinase. P53 was phosphorylated and stabilized in response to the inhibition of DNA repair. P53 targeted proteins, Puma and Bax, were up-regulated and activated. The combination of GS-9219 and DNA-damaging agents resulted in more cell death than the sum of the single agents alone.Conclusion: GS-9219 inhibits DNA repair in CLL cells, an action that stimulates signaling pathways for apoptosis induction.
Histone Deacetylase Inhibitor Induction of P-Glycoprotein Transcription Requires Both Histone Deacetylase 1 Dissociation and Recruitment of CAAT/Enhancer Binding Protein β and pCAF to the Promoter Region
Authors: Kim Su-Nam , Kim Nam Hyun , Lee Woojung , Seo Dong-Wan , Kim Yong Kee 
Published: May 2009

Abstract
Although histone deacetylase (HDAC) inhibitors are appreciated as a promising class of anticancer drugs, recent reports show that P-glycoprotein (P-gp) is induced by HDAC inhibitor treatment in cancer cells, resulting in multidrug resistance of cancer cells to other chemotherapeutic agents. In this study, we investigated the molecular mechanism of HDAC inhibitor induction of P-gp expression. HDAC inhibitor treatment causes cell type–specific induction of P-gp expression without changes in the CpG methylation status of the promoter region. In addition, our data show that HDAC inhibitor does not alter the DNA binding activity of Sp1 but facilitates both the recruitment of a coactivator complex that includes CAAT/enhancer binding protein β and pCAF and the dissociation of the repressive complex, HDAC1, to the Sp1 binding region. Subsequently, the hyperacetylated histone H3 becomes enriched in the promoter region, leading to RNA polymerase II recruitment to activate P-gp gene transcription. Furthermore, specific down-regulation of HDAC1, but not HDAC2, by RNA silencing was enough to induce P-gp expression in HeLa cells, strongly supporting the essential role of HDAC1 in HDAC inhibitor induction of P-gp. Concomitantly, cell type–specific induction of P-gp expression seems to be dependent on phosphatidylinositol 3-kinase activity. Taken together, our findings show that HDAC inhibitor treatment leads to an increase in P-gp expression through dynamic changes in chromatin structure and transcription factor association within the promoter region. (Mol Cancer Res 2009;7(5):735–44)
Conceptualizing Occupational Prestige: An Empirical Case Study from Iran
Authors: Abdollahyan Hamid , Nayebi Hooshang 
Published: May 2009

Abstract
This paper attempts to present a theoretically justified methodological
concept of occupational prestige as one of the common indexes of social
stratification. In order to do that, we first critically review Davis and
Moor's theory of social stratification and argue that social stratification,
defined as “systematically unequal distribution of symbolic and material
rewards among social positions”, is conceptually distinct from Marx's
conception of social class. Davis and Moor's concept of social
stratification has a functional necessity in any complex society, in the
sense that no position is expected to remain vacant, and that qualified
people are conditioned into positions. The determinants for ranking
positions in such a context are the degree of specialty required to perform
duties related to positions, or the level of the authority related to each
position. Secondly, we claim that the prestige structure of the social
positions, which is the stable symbolic dimension of stratification and is
correlated closely with its material dimension, is indeed the representative
of the whole social stratification and that the structure of occupational
prestige is the index of the former. In conclusion, we verify our claims by
providing empirical evidence that has resulted from our own research in Iran
or that comes from similar research carried out by other scholars across the
world.
Comparison of the in vitro and in vivo susceptibilities of Burkholderia mallei to Ceftazidime and Levofloxacin
Authors: Judy Barbara M , Whitlock Gregory C , Torres Alfredo G , Estes D Mark 
Published: May 2009

Abstract

Background

Burkholderia mallei is a zoonotic Gram negative bacterium which primarily infects solipeds but can cause lethal disease in humans if left untreated. The effect of two antibiotics with different modes of action on Burkholderia mallei strain ATCC23344 was investigated by using in vitro and in vivo studies.

Results
Determination of minimal inhibitory concentrations (MICs) in vitro was done by the agar diffusion method and the dilution method. The MICs of levofloxacin and ceftazidime were in the similar range, 2.5 and 5.0 μg/ml, respectively. Intracellular susceptibility of the bacterium to these two antibiotics in J774A.1 mouse macrophages in vitro was also investigated. Macrophages treated with antibiotics demonstrated uptake of the drugs and reduced bacterial loads in vitro. The efficacy of ceftazidime and levofloxacin were studied in BALB/c mice as post-exposure treatment following intranasal B. mallei infection. Intranasal infection with 5 × 105 CFUs of B. mallei resulted in 90% death in non-treated control mice. Antibiotic treatments 10 days post-infection proved to be effective in vivo with all antibiotic treated mice surviving to day 34 post-infection. The antibiotics did not result in complete clearance of the bacterial infection and presence of the bacteria was found in lungs and spleens of the survivors, although bacterial burden recovered from levofloxacin treated animals appeared reduced compared to ceftazidime.

Conclusion
Both antibiotics demonstrated utility for the treatment of glanders, including the ability for intracellular penetration and clearance of organisms in vitro.
The genetic control of neocortex volume and covariation with neocortical gene expression in mice
Authors: Gaglani Shiv M , Lu Lu , Williams Robert W , Rosen Glenn D 
Published: May 2009

Abstract

Background
The size of the cerebral cortex varies widely within human populations, and a large portion of this variance is modulated by genetic factors. The discovery and characterization of these genes and their variants can contribute to an understanding of individual differences in brain development, behavior, and disease susceptibility. Here we use unbiased stereological techniques to map quantitative trait loci (QTLs) that modulate the volume of neocortex.

Results
We estimated volumes bilaterally in an expanded set of BXD recombinant inbred strains (n = 56 strains and 223 animals) taken from the Mouse Brain Library http://www.mbl.org. We generated matched microarray data for the cerebral cortex in the same large panel of strains and in parental neonates to efficiently nominate and evaluate candidate genes. Volume of the neocortex varies widely, and is a heritable trait. Genome-wide mapping of this trait revealed two QTLs – one on chromosome (Chr) 6 at 88 ± 5 Mb and another at Chr 11 (41 ± 8 Mb). We generated both neonatal and adult neocortical gene expression databases using microarray technology. Using these databases in combination with other bioinformatic tools we have identified positional candidates on these QTL intervals.

Conclusion
This study is the first to use the expanded set of BXD strains to map neocortical volume, and we found that normal variation of this trait is, at least in part, genetically modulated. These results provide a baseline from which to assess the genetic contribution to regional variation in neocortical volume, as well as other neuroanatomic phenotypes that may contribute to variation in regional volume, such as proliferation, death, and number and packing density of neurons
Suggestion for linkage of chromosome 1p35.2 and 3q28 to plasma adiponectin concentrations in the GOLDN Study
Authors: Rasmussen-Torvik Laura J , Pankow James S , Peacock James M , Borecki Ingrid B , Hixson James E , Tsai Michael Y , Kabagambe Edmond K , Arnett Donna K 
Published: May 2009

AbstractBackgroundAdiponectin is inversely associated with obesity, insulin resistance, and atherosclerosis, but little is known about the genetic pathways that regulate the plasma level of this protein. To find novel genes that influence circulating levels of adiponectin, a genome-wide linkage scan was performed on plasma adiponectin concentrations before and after 3 weeks of treatment with fenofibrate (160 mg daily) in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study. We studied Caucasian individuals (n = 1121) from 190 families in Utah and Minnesota. Of these, 859 individuals from 175 families had both baseline and post-fenofibrate treatment measurements for adiponectin. Plasma adiponectin concentrations were measured with an ELISA assay. All participants were typed for microsatellite markers included in the Marshfield Mammalian Genotyping Service marker set 12, which includes 407 markers spaced at approximately 10 cM regions across the genome. Variance components analysis was used to estimate heritability and to perform genome-wide scans. Adiponectin was adjusted for age, sex, and field center. Additional models also included BMI adjustment.ResultsBaseline and post-fenofibrate adiponectin measurements were highly correlated (r = 0.95). Suggestive (LOD > 2) peaks were found on chromosomes 1p35.2 and 3q28 (near the location of the adiponectin gene).ConclusionTwo candidate genes,IL22RA1andIL28RA, lie under the chromosome 1 peak; further analyses are needed to identify the specific genetic variants in this region that influence circulating adiponectin concentrations.
Sleep quality in middle-aged and elderly Chinese: distribution, associated factors and associations with cardio-metabolic risk factors
Authors: Haseli-Mashhadi Nazanin , Dadd Tony , Pan An , Yu Zhijie , Lin Xu , Franco Oscar H 
Published: May 2009

Abstract

Background
Poor sleep quality has been associated with increased risk of heart disease, diabetes and mortality. However, limited information exists on the distribution and determinants of sleep quality and its associations with cardio-metabolic risk factors in Chinese populations. We aimed to evaluate this in the current study.

Methods
A cross-sectional survey conducted in 2005 of 1,458 men and 1,831 women aged 50–70 years from urban and rural areas of Beijing and Shanghai. Using a questionnaire, sleep quality was measured in levels of well, common and poor. Comprehensive measures of socio-demographical and health factors and biomarkers of cardio-metabolic disease were recorded. These were evaluated in association with sleep quality using logistic regression models.

Results
Half of the population reported good sleep quality. After adjusting for potential confounders, women and Beijing residents had almost half the probability to report good sleep quality. Good physical and mental health (good levels of self-rated health (OR 2.48; 95%CI 2.08 to 2.96) and no depression (OR 4.05; 95%CI 3.12 to 5.26)) related to an increased chance of reporting good sleep quality, whereas short sleep duration (<7 hrs OR 0.10; 95%CI 0.07 to 0.14)) decreased it substantially. There were significant associations between levels of sleep quality and concentrations of plasma insulin, total and LDL cholesterol, and index of insulin resistance.

Conclusion
Levels of good sleep quality in middle-age and elderly Chinese were low. Gender, geographical location, self-rated health, depression and sleep quantity were major factors associated with sleep quality. Prospective studies are required to distil the factors that determine sleep quality and the effects that sleep patterns exert on cardio-metabolic health.