bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stratospheric Vacillations and the Major Warming over Antarctica in 2002
Authors: Scaife A. A. , Jackson D. R. , Swinbank R. , Butchart N. , Thornton H. E. , Keil M. , Henderson L. 
Published: April 2005

Abstract
The conditions that lead to the major warming over Antarctica in late September 2002 are examined. In many respects, the warming resembled wave-2 warmings seen in the Northern Hemisphere; the winter cyclonic circulation was split into two smaller cyclones by a large amplitude planetary wave disturbance that appeared to propagate upward from the troposphere. However, in addition to this classic warming mechanism, distinctive stratospheric vacillations occurred throughout the preceding winter months. These vacillations in wave amplitude, Eliassen–Palm fluxes, and zonal-mean zonal winds are examined. By comparison with a numerical model experiment, it is shown that the vacillation is accompanied by a systematic weakening of the westerly winds over the season. This preconditions the Antarctic circulation, and it is argued that it allows anomalously strong vertical propagation of planetary waves from the troposphere into the stratosphere. By contrast, a survey of previous winters shows that stratospheric westerlies usually vary much more gradually, with vacillations only occurring for short periods of time, if at all, in a given winter.
Similar vacillations in a numerical model of the stratosphere only occur if the forcing amplitude is above a certain value. However, the level of winter-mean wave activity entering the stratosphere during 2002 is not unprecedented, and there is still some uncertainty over the cause of the onset and persistence of the vacillation and, ultimately, the major warming.
Reconstruction and Simulation of Stratospheric Ozone Distributions during the 2002 Austral Winter
Authors: Randall C. E. , Manney G. L. , Allen D. R. , Bevilacqua R. M. , Hornstein J. , Trepte C. , Lahoz W. , Ajtic J. , Bodeker G. 
Published: April 2005

Abstract
Satellite-based solar occultation measurements during the 2002 austral winter have been used to reconstruct global, three-dimensional ozone distributions. The reconstruction method uses correlations between potential vorticity and ozone to derive “proxy” distributions from the geographically limited occultation observations. Ozone profiles from the Halogen Occultation Experiment (HALOE), the Polar Ozone and Aerosol Measurement III (POAM III), and the Stratospheric Aerosol and Gas Experiment II and III (SAGE II and III) are incorporated into the analysis. Because this is one of the first uses of SAGE III data in a scientific analysis, preliminary validation results are shown. The reconstruction method is described, with particular emphasis on uncertainties caused by noisy and/or multivalued correlations. The evolution of the solar occultation data and proxy ozone fields throughout the winter is described, and differences with respect to previous winters are characterized. The results support the idea that dynamical forcing early in the 2002 winter influenced the morphology of the stratosphere in a significant and unusual manner, possibly setting the stage for the unprecedented major stratospheric warming in late September. The proxy is compared with ozone from mechanistic, primitive equation model simulations of passive ozone tracer fields during the time of the warming. In regions where chemistry is negligible compared to transport, the model and proxy ozone fields agree well. The agreement between, and changes in, the large-scale ozone fields in the model and proxy indicate that transport processes, particularly enhanced poleward transport and mixing, are the primary cause of ozone changes through most of the stratosphere during this unprecedented event. The analysis culminates with the calculation of globally distributed column ozone during the major warming, showing quantitatively how transport of low-latitude air to the polar region in the middle stratosphere led to the diminished ozone hole in 2002.
A clinically relevant SCID-hu in vivo model of human multiple myeloma
Authors: Tassone Pierfrancesco , Neri Paola , Carrasco Daniel R. , Burger Renate , Goldmacher Victor S. , Fram Robert , Munshi Vidit , Shammas Masood A. , Catley Laurence , Jacob Gary S. , Venuta Salvatore , Anderson Kenneth C. , Munshi Nikhil C. 
Published: April 2005

Abstract
We developed a novel in vivo multiple myeloma (MM) model by engrafting the interleukin 6 (IL-6)-dependent human MM cell line INA-6 into severe combined immunodeficiency (SCID) mice previously given implants of a human fetal bone chip (SCID-hu mice). INA-6 cells require either exogenous human IL-6 (huIL-6) or bone marrow stromal cells (BMSCs) to proliferate in vitro. In this model, we monitored the in vivo growth of INA-6 cells stably transduced with a green fluorescent protein (GFP) gene (INA-6GFP+ cells). INA-6 MM cells engrafted in SCID-hu mice but not in SCID mice that had not been given implants of human fetal bone. The level of soluble human IL-6 receptor (shuIL-6R) in murine serum and fluorescence imaging of host animals were sensitive indicators of tumor growth. Dexamethasone as well as experimental drugs, such as Atiprimod and B-B4-DM1, were used to confirm the utility of the model for evaluation of anti-MM agents. We report that this model is highly reproducible and allows for evaluation of investigational drugs targeting IL-6-dependent MM cells in the human bone marrow (huBM) milieu. (Blood. 2005;106:713-716)
Quantification of collagen and proteoglycan deposition in a murine model of airway remodelling
Authors: Reinhardt Alistair K , Bottoms Stephen E , Laurent Geoffrey J , McAnulty Robin J 
Published: April 2005

Abstract
Background
Sub-epithelial extracellular matrix deposition is a feature of asthmatic airway remodelling associated with severity of disease, decline in lung function and airway hyperresponsiveness. The composition of, and mechanisms leading to, this increase in subepithelial matrix, and its importance in the pathogenesis of asthma are unclear. This is partly due to limitations of the current models and techniques to assess airway remodelling.

Methods
In this study we used a modified murine model of ovalbumin sensitisation and challenge to reproduce features of airway remodelling, including a sustained increase in sub-epithelial matrix deposition. In addition, we have established techniques to accurately and specifically measure changes in sub-epithelial matrix deposition, using histochemical and immunohistochemical staining in conjunction with digital image analysis, and applied these to the measurement of collagen and proteoglycans.

Results
24 hours after final ovalbumin challenge, changes similar to those associated with acute asthma were observed, including inflammatory cell infiltration, epithelial cell shedding and goblet cell hyperplasia. Effects were restricted to the bronchial and peribronchial regions with parenchymal lung of ovalbumin sensitised and challenged mice appearing histologically normal. By 12 days, the acute inflammatory changes had largely resolved and increased sub-epithelial staining for collagen and proteoglycans was observed. Quantitative digital image analysis confirmed the increased deposition of sub-epithelial collagen (33%, p < 0.01) and proteoglycans (32%, p < 0.05), including decorin (66%, p < 0.01). In addition, the increase in sub-epithelial collagen deposition was maintained for at least 28 days (48%, p < 0.001).

Conclusion
This animal model reproduces many of the features of airway remodelling found in asthma and allows accurate and reproducible measurement of sub-epithelial extra-cellular matrix deposition. As far as we are aware, this is the first demonstration of increased sub-epithelial proteoglycan deposition in an animal model of airway remodelling. This model will be useful for measurement of other matrix components, as well as for assessment of the molecular mechanisms contributing to, and agents to modulate airway remodelling.
Individual sequences in large sets of gene sequences may be distinguished efficiently by combinations of shared sub-sequences
Authors: Gibbs Mark J , Armstrong John S , Gibbs Adrian J 
Published: April 2005

Abstract
Background
Most current DNA diagnostic tests for identifying organisms use specific oligonucleotide probes that are complementary in sequence to, and hence only hybridise with the DNA of one target species. By contrast, in traditional taxonomy, specimens are usually identified by 'dichotomous keys' that use combinations of characters shared by different members of the target set. Using one specific character for each target is the least efficient strategy for identification. Using combinations of shared bisectionally-distributed characters is much more efficient, and this strategy is most efficient when they separate the targets in a progressively binary way.

Results
We have developed a practical method for finding minimal sets of sub-sequences that identify individual sequences, and could be targeted by combinations of probes, so that the efficient strategy of traditional taxonomic identification could be used in DNA diagnosis. The sizes of minimal sub-sequence sets depended mostly on sequence diversity and sub-sequence length and interactions between these parameters. We found that 201 distinct cytochrome oxidase subunit-1 (CO1) genes from moths (Lepidoptera) were distinguished using only 15 sub-sequences 20 nucleotides long, whereas only 8–10 sub-sequences 6–10 nucleotides long were required to distinguish the CO1 genes of 92 species from the 9 largest orders of insects.

Conclusion
The presence/absence of sub-sequences in a set of gene sequences can be used like the questions in a traditional dichotomous taxonomic key; hybridisation probes complementary to such sub-sequences should provide a very efficient means for identifying individual species, subtypes or genotypes. Sequence diversity and sub-sequence length are the major factors that determine the numbers of distinguishing sub-sequences in any set of sequences.
Power and sample size calculations in the presence of phenotype errors for case/control genetic association studies
Authors: Edwards Brian J , Haynes Chad , Levenstien Mark A , Finch Stephen J , Gordon Derek 
Published: April 2005

Abstract
Background
Phenotype error causes reduction in power to detect genetic association. We present a quantification of phenotype error, also known as diagnostic error, on power and sample size calculations for case-control genetic association studies between a marker locus and a disease phenotype. We consider the classic Pearson chi-square test for independence as our test of genetic association. To determine asymptotic power analytically, we compute the distribution's non-centrality parameter, which is a function of the case and control sample sizes, genotype frequencies, disease prevalence, and phenotype misclassification probabilities. We derive the non-centrality parameter in the presence of phenotype errors and equivalent formulas for misclassification cost (the percentage increase in minimum sample size needed to maintain constant asymptotic power at a fixed significance level for each percentage increase in a given misclassification parameter). We use a linear Taylor Series approximation for the cost of phenotype misclassification to determine lower bounds for the relative costs of misclassifying a true affected (respectively, unaffected) as a control (respectively, case). Power is verified by computer simulation.

Results
Our major findings are that: (i) the median absolute difference between analytic power with our method and simulation power was 0.001 and the absolute difference was no larger than 0.011; (ii) as the disease prevalence approaches 0, the cost of misclassifying a unaffected as a case becomes infinitely large while the cost of misclassifying an affected as a control approaches 0.

Conclusion
Our work enables researchers to specifically quantify power loss and minimum sample size requirements in the presence of phenotype errors, thereby allowing for more realistic study design. For most diseases of current interest, verifying that cases are correctly classified is of paramount importance.
Outcome of infections due to pandrug-resistant (PDR) Gram-negative bacteria
Authors: Falagas Matthew E , Bliziotis Ioannis A , Kasiakou Sofia K , Samonis George , Athanassopoulou Panayiota , Michalopoulos Argyris 
Published: April 2005

Abstract

Background
The increasing problem of infections due to multidrug-resistant Gram-negative bacteria has led to re-use of polymyxins in several countries. However, there are already clinical isolates of Gram-negative bacteria that are resistant to all available antibiotics, including polymyxins.

Methods
We present a case series of patients with infections due to pathogens resistant to all antimicrobial agents tested, including polymyxins. An isolate was defined as pandrug-resistant (PDR) if it exhibited resistance to all 7 anti-pseudomonal antimicrobial agents, i.e. antipseudomonal penicillins, cephalosporins, carbapenems, monobactams, quinolones, aminoglycosides, and polymyxins.

Results
Clinical cure of the infection due to pandrug-resistant (PDR) Gram-negative bacteria, namely Pseudomonas aeruginosa or Klebsiella pneumoniae was observed in 4 out of 6 patients with combination of colistin and beta lactam antibiotics.

Conclusion
Colistin, in combination with beta lactam antibiotics, may be a useful agent for the management of pandrug-resistant Gram-negative bacterial infections. The re-use of polymyxins, an old class of antibiotics, should be done with caution in an attempt to delay the rate of development of pandrug-resistant Gram-negative bacterial infections.
Effective antiprotease-antibiotic treatment of experimental anthrax
Authors: Popov Serguei G , Popova Taissia G , Hopkins Svetlana , Weinstein Raymond S , MacAfee Rebecca , Fryxell Karl J , Chandhoke Vikas , Bailey Charles , Alibek Ken 
Published: April 2005

AbstractBackgroundInhalation anthrax is characterized by a systemic spread of the challenge agent,Bacillus anthracis. It causes severe damage, including multiple hemorrhagic lesions, to host tissues and organs. It is widely believed that anthrax lethal toxin secreted by proliferating bacteria is a major cause of death, however, the pathology of intoxication in experimental animals is drastically different from that found during the infectious process. In order to close a gap between our understanding of anthrax molecular pathology and the most prominent clinical features of the infectious process we undertook bioinformatic and experimental analyses of potential proteolytic virulence factors ofB. anthracisdistinct from lethal toxin.MethodsSecreted proteins (other than lethal and edema toxins) produced byB. anthraciswere tested for tissue-damaging activity and toxicity in mice. Chemical protease inhibitors and rabbit immune sera raised againstB. anthracisproteases were used to treat mice challenged withB. anthracis(Sterne) spores.ResultsB. anthracisstrain delta Ames (pXO1-, pXO2-) producing no lethal and edema toxins secrets a number of metalloprotease virulence factors upon cultivation under aerobic conditions, including those with hemorrhagic, caseinolytic and collagenolytic activities, belonging to M4 and M9 thermolysin and bacterial collagenase families, respectively.These factors are directly toxic to DBA/2 mice upon intratracheal administration at 0.5 mg/kg and higher doses. Chemical protease inhibitors (phosphoramidon and 1, 10-phenanthroline), as well as immune sera against M4 and M9 proteases ofB. anthracis, were used to treat mice challenged withB. anthracis(Sterne) spores. These substances demonstrate a substantial protective efficacy in combination with ciprofloxacin therapy initiated as late as 48 h post spore challenge, compared to the antibiotic alone.ConclusionSecreted proteolytic enzymes are important pathogenic factors ofB. anthrasis, which can be considered as effective therapeutic targets in the development of anthrax treatment and prophylactic approaches complementing anti-lethal toxin therapy.
Diffusion and dissemination of evidence-based dietary srategies for the prevention of cancer
Authors: Ciliska Donna , Robinson Paula , Armour Tanya , Ellis Peter , Brouwers Melissa , Gauld Mary , Baldassarre Fulvia , Raina Parminder 
Published: April 2005

Abstract
Objective
The purpose was to determine what strategies have been evaluated to disseminate cancer control interventions that promote the uptake of adult healthy diet?

Methods
A systematic review was conducted. Studies were identified by searching MEDLINE, PREMEDLINE, Cancer LIT, EMBASE/Excerpta Medica, PsycINFO, CINAHL, the Cochrane Database of Systematic Reviews, and reference lists and by contacting technical experts. English-language primary studies were selected if they evaluated the dissemination of healthy diet interventions in individuals, healthcare providers, or institutions. Studies of children or adolescents only were excluded.

Results
One hundred one articles were retrieved for full text screening. Nine reports of seven distinct studies were included; four were randomized trials, one was a cohort design and three were descriptive studies. Six studies were rated as methodologically weak, and one was rated as moderate. Studies were not meta-analyzed because of heterogeneity, low methodological quality, and incomplete data reporting. No beneficial dissemination strategies were found except one that looks promising, the use of peer educators in the worksite, which led to a short-term increase in fruit and vegetable intake.

Conclusions and Implications
Overall, the quality of the evidence is not strong and is primarily descriptive rather than evaluative. No clear conclusions can be drawn from these data. Controlled studies are needed to evaluate dissemination strategies, and to compare dissemination and diffusion strategies with different messages and different target audiences.
Location of DNA damage by charge exchanging repair enzymes: effects of cooperativity on location time
Authors: Eriksen Kasper Astrup 
Published: April 2005

Abstract
Background
How DNA repair enzymes find the relatively rare sites of damage is not known in great detail. Recent experiments and molecular data suggest that individual repair enzymes do not work independently of each other, but interact with each other through charges exchanged along the DNA. A damaged site in the DNA hinders this exchange. The hypothesis is that the charge exchange quickly liberates the repair enzymes from error-free stretches of DNA. In this way, the sites of damage are located more quickly; but how much more quickly is not known, nor is it known whether the charge exchange mechanism has other observable consequences.

Results
Here the size of the speed-up gained from this charge exchange mechanism is calculated and the characteristic length and time scales are identified. In particular, for Escherichia coli, I estimate the speed-up is 50000/N, where N is the number of repair enzymes participating in the charge exchange mechanism. Even though N is not exactly known, a speed-up of order 10 is not entirely unreasonable. Furthermore, upon over expression of all the repair enzymes, the location time only varies as N-1/2 and not as 1/N.

Conclusion
The revolutionary hypothesis that DNA repair enzymes use charge exchange along DNA to locate damaged sites more efficiently is actually sound from a purely theoretical point of view. Furthermore, the predicted collective behavior of the location time is important in assessing the impact of stress-ful and radioactive environments on individual cell mutation rates.
Differential effect of obesity on bone mineral density in White, Hispanic and African American women: a cross sectional study
Authors: Castro Jonathan P , Joseph Linda A , Shin John J , Arora Surender K , Nicasio John , Shatzkes Joshua , Raklyar Irina , Erlikh Irina , Pantone Vincent , Bahtiyar Gul , Chandler Leon , Pabon Lina , Choudhry Sara , Ghadiri Nilofar , Gosukonda Pramodini , Muniyappa Rangnath , von-Gicyzki Hans , McFarlane Samy I 
Published: April 2005

Abstract
Osteoporosis is a major public health problem with low bone mass affecting nearly half the women aged 50 years or older. Evidence from various studies has shown that higher body mass index (BMI) is a protective factor for bone mineral density (BMD). Most of the evidence, however, is from studies with Caucasian women and it is unclear to what extent ethnicity plays a role in modifying the effect of BMI on BMD.
A cross sectional study was performed in which records of postmenopausal women who presented for screening for osteoporosis at 2 urban medical centres were reviewed. Using logistic regression, we examined the interaction of race and BMI after adjusting for age, family history of osteoporosis, maternal fracture, smoking, and sedentary lifestyle on BMD. Low BMD was defined as T-score at the lumbar spine < -1.
Among 3,206 patients identified, the mean age of the study population was 58.3 ± 0.24 (Years ± SEM) and the BMI was 30.6 kg/m2. 2,417 (75.4%) were African Americans (AA), 441(13.6%) were Whites and 348 (10.9%) were Hispanics. The AA women had lower odds of having low BMD compared to Whites [Odds ratio (OR) = 0.079 (0.03–0.24) (95% CI), p < 0.01]. The odds ratio of low BMD was not statistically significant between White and Hispanic women. We examined the interaction between race and BMD. For White women; as the BMI increases by unity, the odds of low BMD decreases [OR = 0.9 (0.87–0.94), p < 0.01; for every unit increase in BMI]. AA women had slightly but significantly higher odds of low BMD compared to Whites [OR 1.015 (1.007–1.14), p <0.01 for every unit increase in BMI]. This effect was not observed when Hispanic women were compared to Whites.
There is thus a race-dependent effect of BMI on BMD. With each unit increase in BMI, BMD increases for White women, while a slight but significant decrease in BMD occurs in African American women.