bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced Biofilm Formation and Increased Resistance to Antimicrobial Agents and Bacterial Invasion Are Caused by Synergistic Interactions in Multispecies Biofilms
Authors: Burmølle Mette , Webb Jeremy S. , Rao Dhana , Hansen Lars H. , Sørensen Søren J. , Kjelleberg Staffan 
Published: June 2006

ABSTRACT

Most biofilms in their natural environments are likely to consist of consortia of species that influence each other in synergistic and antagonistic manners. However, few reports specifically address interactions within multispecies biofilms. In this study, 17 epiphytic bacterial strains, isolated from the surface of the marine alga
Ulva australis
, were screened for synergistic interactions within biofilms when present together in different combinations. Four isolates,
Microbacterium phyllosphaerae
,
Shewanella japonica
,
Dokdonia donghaensis
, and
Acinetobacter lwoffii
, were found to interact synergistically in biofilms formed in 96-well microtiter plates: biofilm biomass was observed to increase by >167% in biofilms formed by the four strains compared to biofilms composed of single strains. When exposed to the antibacterial agent hydrogen peroxide or tetracycline, the relative activity (exposed versus nonexposed biofilms) of the four-species biofilm was markedly higher than that in any of the single-species biofilms. Moreover, in biofilms established on glass surfaces in flow cells and subjected to invasion by the antibacterial protein-producing
Pseudoalteromonas tunicata
, the four-species biofilms resisted invasion to a greater extent than did the biofilms formed by the single species. Replacement of each strain by its cell-free culture supernatant suggested that synergy was dependent both on species-specific physical interactions between cells and on extracellular secreted factors or less specific interactions. In summary, our data strongly indicate that synergistic effects promote biofilm biomass and resistance of the biofilm to antimicrobial agents and bacterial invasion in multispecies biofilms.
Construction of a Large Signature-Tagged Mini-Tn
5
Transposon Library and Its Application to Mutagenesis of
Sinorhizobium meliloti
Authors: Pobigaylo Nataliya , Wetter Danijel , Szymczak Silke , Schiller Ulf , Kurtz Stefan , Meyer Folker , Nattkemper Tim W. , Becker Anke 
Published: June 2006

ABSTRACT

Sinorhizobium meliloti
genome sequence determination has provided the basis for different approaches of functional genomics for this symbiotic nitrogen-fixing alpha-proteobacterium. One of these approaches is gene disruption with subsequent analysis of mutant phenotypes. This method is efficient for single genes; however, it is laborious and time-consuming if it is used on a large scale. Here, we used a signature-tagged transposon mutagenesis method that allowed analysis of the survival and competitiveness of many mutants in a single experiment. A novel set of signature tags characterized by similar melting temperatures and G+C contents of the tag sequences was developed. The efficiencies of amplification of all tags were expected to be similar. Thus, no preselection of the tags was necessary to create a library of 412 signature-tagged transposons. To achieve high specificity of tag detection, each transposon was bar coded by two signature tags. In order to generate defined, nonredundant sets of signature-tagged
S. meliloti
mutants for subsequent experiments, 12,000 mutants were constructed, and insertion sites for more than 5,000 mutants were determined. One set consisting of 378 mutants was used in a validation experiment to identify mutants showing altered growth patterns.
Completeness of cause of injury coding in healthcare administrative databases in the United States, 2001
Authors: Coben J H , Steiner C A , Barrett M , Merrill C T , Adamson D 
Published: June 2006

Objectives:To determine the completeness of external cause of injury coding (E-coding) within healthcare administrative databases in the United States and to identify factors that contribute to variations in E-code reporting across states.Design:Cross sectional analysis of the 2001 Healthcare Cost and Utilization Project (HCUP), including 33 State Inpatient Databases (SID), a Nationwide Inpatient Sample (NIS), and nine State Emergency Department Databases (SEDD). To assess state reporting practices, structured telephone interviews were conducted with the data organizations that participate in HCUP.Results:The percent of injury records with an injury E-code was 86% in HCUP’s nationally representative database, the NIS. For the 33 states represented in the SID, completeness averaged 87%, with more than half of the states reporting E-codes on at least 90% of injuries. In the nine states also represented in the SEDD, completeness averaged 93%. Twenty two states had mandates for E-code reporting, but only eight had provisions for enforcing the mandates. These eight states had the highest rates of E-code completeness.Conclusions:E-code reporting in administrative databases is relatively complete, but there is significant variation in completeness across the states. States with mandates for the collection of E-codes and with a mechanism to enforce those mandates had the highest rates of E-code reporting. Nine statewide ED data systems demonstrate consistently high E-coding completeness.
Trends in childhood injury mortality in Canada, 1979–2002
Authors: Pan S Y , Ugnat A-M , Semenciw R , Desmeules M , Mao Y , MacLeod M 
Published: June 2006

Objective:To examine national trends in mortality rates for injuries among Canadian children younger than 15 years in 1979–2002.Methods:Data on injury deaths were obtained from the Canadian Vital Statistics system at Statistics Canada. Injuries were classified using the codes for external cause of injury and poisoning (E-codes) by intent and by mechanism. Mortality rates were age adjusted to the 1990 world standard population. Negative binomial regression was used to estimate the secular trends.Results:Annual mortality rates for total and unintentional injuries declined substantially (from 23.8 and 21.7 in 1979 to 7.2 and 5.8 in 2002, respectively), whereas suicide deaths among children aged 10–14 showed an increasing trend. All Canadian provinces and territories showed a decreasing trend in mortality rates of total injuries. Motor vehicle related injuries were the most common cause of injury deaths (accounted for an average of 36.4% of total injury deaths), followed by suffocation (14.3%), drowning (13.5%), and burning (11.1%); however, suffocation was the leading cause for infants. The number of potential years of life lost due to injury before age 75 decreased from 89 343 in 1979 to 27 948 in 2002 for children aged 0–14 years.Conclusions:During the period 1979–2002, there were dramatic decreases in childhood mortality for total injuries and unintentional injuries as well as various degrees of reduction for all causes of injury except suffocation in children aged 10–14 years and drowning in infants. The reason for the reduction in injury mortality might be multifactoral.
Depressive symptoms as a risk factor for unintentional injury: a cohort study in a rural county
Authors: Tiesman H M , Peek-Asa C , Whitten P , Sprince N L , Stromquist A , Zwerling C 
Published: June 2006

Objective:The authors used data from a population based prospective cohort study to determine if depressive symptoms predicted incidence of unintentional injury.Methods:The Keokuk County Rural Health Study, based in Iowa, is a prospective cohort study of health status that includes injury outcomes. Depressive symptoms were measured using the 11-item Center for Epidemiologic Studies Depression Scale at the beginning of the study on 1493 participants. Quarterly follow up phone calls were made to measure injury incidence.Results:471 injuries were reported for an overall injury rate of 9.8 per 100 person-years. Crude injury rates were significantly higher for those with depressive symptoms (p = 0.0003). Those with depressive symptoms had a 41% increased risk for injury after controlling for antidepressant medication use, gender, prior injury, income, and sleepiness (RR = 1.41, 95% CI 1.10 to 1.80). Depressive symptoms remained a risk factor for injury regardless of current antidepressant medication use (no medication use, RR = 1.43, 95% CI 1.09 to 1.88; medication use, RR = 1.31, 95% CI 0.76 to 2.26).Conclusions:Depressive symptoms were found to be risk factors for unintentional injury. Medical practitioners should consider talking about safety with their patients, especially those reporting symptoms of depression, and recognize that an increased risk for injury remains until the depressive symptoms subside.
Developing valid indicators of injury incidence for “all injury”
Authors: Cryer C , Langley J D 
Published: June 2006

Background/aims:This paper focuses on the methods used to develop indicators for “all injury” incidence for the New Zealand Injury Prevention Strategy (NZIPS), launched in June 2003. Existing and previously proposed New Zealand national non-fatal injury indicators exhibited threats to validity.Population/setting:The total population of New Zealand.Methods:The authors proposed fatal and new non-fatal injury indicators for “all injury” based on national mortality and hospitalizations data. All of the candidate indicators were subjected to a systematic assessment of validity, using the International Collaborative Effort on Injury Statistics (ICE) criteria. Based on the results of that validation, the authors identified four proposed NZIPS indicators.Results:The proposed “all injury” indicators were as follows: age standardized injury mortality rate per 100 000 person-years at risk; number of injury deaths; age standardized serious non-fatal injury rate per 100 000 person-years at risk; and number of cases of serious non-fatal injury. The authors identified no threat-to-validity when assessed against the ICE criteria. The estimated numbers and rates of serious non-fatal injury increased over the period, in contrast to the numbers and rates of fatal injury.Conclusion:The authors have proposed serious non-fatal injury indicators that they judge suffer substantially less bias than traditional non-fatal injury indicators. This approach to indicator development is consistent with the view that before newly proposed indicators are promulgated, they should be subjected to formal validation. The authors are encouraged that the New Zealand Government has accepted these arguments and proposed indicators, and are starting to act on some of their recommendations, including the development of complementary indicators.
Parthenolide Modulates the NF-κB–Mediated Inflammatory Responses in Experimental Atherosclerosis
Authors: López-Franco Oscar , Hernández-Vargas Purificación , Ortiz-Muñoz Guadalupe , Sanjuán Guillermo , Suzuki Yusuke , Ortega Luis , Blanco Julia , Egido Jesús , Gómez-Guerrero Carmen 
Published: June 2006

Objective—Activation of transcription factor NF-κB is an important step in the development of vascular damage, because it controls inducible genes, including many inflammatory mediators. The pharmacological modulation of this process is the main objective in the design of new therapies for atherosclerosis. In this work we analyzed the effects of the natural compound parthenolide (PTN), an NF-κB inhibitor.Methods and Results—In vascular smooth muscle cells (VSMCs) and monocytes stimulated with lipopolysaccharide (LPS), nontoxic doses of PTN reduced IκBα degradation, NF-κB activation, and MCP-1 expression, without inhibiting AP-1 and MAPK. In apoE mice, treatment with low (2 mg/kg, 20 weeks), medium (4 mg/kg, 10 weeks), and high (10 mg/kg, 10 weeks) dose of PTN reduced the size of aortic lesion, decreased macrophage, and increased VSMC content in the lesions. Treated mice showed reduced serum levels of MCP-1 and attenuated NF-κB activity, but not AP-1, in the lesions. Moreover, PTN affects neither apoptotic cell death nor oxidative stress in cultured cells and mice.Conclusion—NF-κB inhibition by PTN retards atherosclerotic lesions in apoE mice, by reducing lesion size and changing plaque composition. This natural compound could represent a novel therapeutic approach to inflammation during vascular damage.
CD154 induces p73 to overcome the resistance to apoptosis of chronic lymphocytic leukemia cells lacking functional p53
Authors: Dicker Frank , Kater Arnon P. , Prada Carlos E. , Fukuda Tetsuya , Castro Januario E. , Sun Guizhen , Wang Jean Y. , Kipps Thomas J. 
Published: June 2006

AbstractIntravenous infusion of autologous chronic lymphocytic leukemia (CLL) cells transduced with an adenovirus encoding CD40-ligand (CD154) caused rapid reductions in leukemia-cell counts and lymphnode size. We hypothesized that CD40-ligation via CD154 sensitized CLL cells to death-receptor-mediated apoptosis. We found that CD154-expressing cells induced expression of CD95 and the BH3-interacting-domain death agonist (Bid) in CLL, regardless of whether the leukemia cells had functional p53. Such treatment also induced p73, a p53-related transcription factor regulated by c-Abl kinase, and enhanced the sensitivity to fludarabine (F-ara-A) of CLL cells lacking functional p53. Transduction of CLL cells with an adenovirus encoding p73 also induced Bid and CD95 and enhanced the sensitivity to F-ara-A of p53-deficient CLL cells. However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis. Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib. These results indicate that CD154 can sensitize leukemia cells to apoptosis via the c-Abl-dependent activation of p73 and mitigate the resistance of p53-deficient CLL cells to anticancer drug therapy.
A mosaic genetic screen for novel mutations affecting Drosophila neuroblast divisions
Authors: Slack Cathy , Somers W Gregory , Sousa-Nunes Rita , Chia William , Overton Paul M 
Published: June 2006

AbstractBackgroundThe asymmetric segregation of determinants during cell division is a fundamental mechanism for generating cell fate diversity during development. InDrosophila, neural precursors (neuroblasts) divide in a stem cell-like manner generating a larger apical neuroblast and a smaller basal ganglion mother cell. The cell fate determinant Prospero and its adapter protein Miranda are asymmetrically localized to the basal cortex of the dividing neuroblast and segregated into the GMC upon cytokinesis. Previous screens to identify components of the asymmetric division machinery have concentrated on embryonic phenotypes. However, such screens are reaching saturation and are limited in that the maternal contribution of many genes can mask the effects of zygotic loss of function, and other approaches will be necessary to identify further genes involved in neuroblast asymmetric division.ResultsWe have performed a genetic screen in the third instar larval brain using the basal localization of Miranda as a marker for neuroblast asymmetry. In addition to the examination of pupal lethal mutations, we have employed the MARCM (MosaicAnalysis with aRepressibleCellMarker) system to generate postembryonic clones of mutations with an early lethal phase. We have screened a total of 2,300 mutagenized chromosomes and isolated alleles affecting cell fate, the localization of basal determinants or the orientation of the mitotic spindle. We have also identified a number of complementation groups exhibiting defects in cell cycle progression and cytokinesis, including both novel genes and new alleles of known components of these processes.ConclusionWe have identified four mutations which affect the process of neuroblast asymmetric division. One of these, mapping to theimaginal discs arrestedlocus, suggests a novel role for the anaphase promoting complex/cyclosome (APC/C) in the targeting of determinants to the basal cortex. The identification and analysis of the remaining mutations will further advance our understanding of the process of asymmetric cell division. We have also isolated a number of mutations affecting cell division which will complement the functional genomics approaches to this process being employed by other laboratories. Taken together, these results demonstrate the value of mosaic screens in the identification of genes involved in neuroblast division.
Lymph node retrieval in abdominoperineal surgical specimen is radiation time-dependent
Authors: Sermier Alain , Gervaz Pascal , Egger Jean F , Dao My , Allal Abdelkarim S , Bonet Marta , Morel Philippe 
Published: June 2006

Abstract

Background
A low yield of lymph nodes (LN) in abdominoperineal resection (APR) specimen has been associated with preoperative radiation therapy (XRT) in population-based studies, which may preclude adequate staging of anorectal carcinomas. We hypothesized that the number of LN retrieved in APR specimen was correlated with the dose and the timing of pelvic irradiation.

Patients and methods
We performed a retrospective study of 102 patients who underwent APR in a single institution between 1980 and 2004. Pathological reports were reviewed and the number of lymph nodes retrieved in APR specimens was correlated with: 1) Preoperative radiation; 2) Dose of pelvic irradiation; and 3) Time interval between the end of XRT and surgery.

Results
There were 61 men and 41 women, with a median age of 66 (range 25–89) years. There were 12 patients operated for squamous cell carcinoma of the anal canal (SCCA) and 90 for rectal cancer. 83% and 46% of patients with anal and rectal cancer respectively underwent radical/neoadjuvant radiotherapy. The mean ± SD number of LN in APR specimen was 9.2 ± 5.9. The mean number of LN in APR specimen was significantly lower in patients who underwent preoperative XRT (8 ± 5.5 vs. 10.5 ± 6.1, Mann-Whitney U test, p = 0.02). The mean number of LN was not significantly different after XRT in patients with SCCA than in patients with rectal cancer (6.2 ± 5.3 vs. 7.8 ± 5.3, p = 0.33). Finally, there was an inverse correlation between the yield of LN and the time elapsed between XRT and surgery (linear regression coefficient r = -0.32, p = 0.03).

Conclusion
Our data indicate that: 1) radiation therapy affects the yield of LN retrieval in APR specimen; 2) this impact is time-dependent. These findings have important implications with regard to anatomic-pathological staging of anal and rectal cancers and subsequent decision-making regarding adjuvant chemotherapy.
Coordinated elevation of membrane type 1-matrix metalloproteinase and matrix metalloproteinase-2 expression in rat uterus during postpartum involution
Authors: Manase Kengo , Endo Toshiaki , Chida Mitunobu , Nagasawa Kunihiko , Honnma Hiroyuki , Yamazaki Kiyohiro , Kitajima Yoshimitu , Goto Taeko , Kanaya Mika , Hayashi Takuhiro , Mitaka Toshihiro , Saito Tsuyoshi 
Published: June 2006

Abstract

Background
The changes occurring in the rodent uterus after parturition can be used as a model of extensive tissue remodeling. As the uterus returns to its prepregnancy state, the involuting uterus undergoes a rapid reduction in size primarily due to the degradation of the extracellular matrix, particularly collagen. Membrane type-I matrix metalloproteinase (MT1-MMP) is one of the major proteinases that degrades collagen and is the most abundant MMP form in the uterus. Matrix metalloproteinase-2(MMP-2) can degrade type I collagen, although its main function is to degrade type IV collagen found in the basement membrane. To understand the expression patterns of matrix metalloproteinases (MMPs) in the rat uterus, we analyzed their activities in postpartum uterine involution.

Methods
We performed gelatin zymography, northern blot analysis and immunohistochemistry to compare the expression levels of MT1-MMP, MMP-2, matrix metalloproteinase-9 (MMP-9) and the tissue inhibitors of MMPs-1 and 2 (TIMP-1 and TIMP-2) in the rat uterus 18 h, 36 h and 5 days after parturition with their expression levels during pregnancy (day 20).

Results
We found that both MT1-MMP and MMP-2 localized mainly in the cytoplasm of uterine interstitial cells. The expression levels of MT1-MMP and MMP-2 mRNAs and the catalytic activities of the expressed proteins significantly increased 18 h and 36 h after parturition, but at postpartum day 5, their mRNA expression levels and catalytic activities decreased markedly. The expression levels of MMP-9 increased 18 h and 36 h after parturition as determined by gelatin zymography including the expression levels of TIMP-1 and TIMP-2.

Conclusion
These expression patterns indicate that MT1-MMP, MMP-2, MMP-9, TIMP-1 and TIMP-2 may play key roles in uterine postpartum involution and subsequent functional regenerative processes.
Analysis of gene expression in operons of Streptomyces coelicolor
Authors: Laing Emma , Mersinias Vassilis , Smith Colin P , Hubbard Simon J 
Published: June 2006

Abstract
Background
Recent studies have shown that microarray-derived gene-expression data are useful for operon prediction. However, it is apparent that genes within an operon do not conform to the simple notion that they have equal levels of expression.

Results
To investigate the relative transcript levels of intra-operonic genes, we have used a Z-score approach to normalize the expression levels of all genes within an operon to expression of the first gene of that operon. Here we demonstrate that there is a general downward trend in expression from the first to the last gene in Streptomyces coelicolor operons, in contrast to what we observe in Escherichia coli. Combining transcription-factor binding-site prediction with the identification of operonic genes that exhibited higher transcript levels than the first gene of the same operon enabled the discovery of putative internal promoters. The presence of transcription terminators and abundance of putative transcriptional control sequences in S. coelicolor operons are also described.

Conclusion
Here we have demonstrated a polarity of expression in operons of S. coelicolor not seen in E. coli, bringing caution to those that apply operon prediction strategies based on E. coli 'equal-expression' to divergent species. We speculate that this general difference in transcription behavior could reflect the contrasting lifestyles of the two organisms and, in the case of Streptomyces, might also be influenced by its high G+C content genome. Identification of putative internal promoters, previously thought to cause problems in operon prediction strategies, has also been enabled.