bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitro and in vivo anti-malarial activity of Boerhavia elegans and Solanum surattense
Authors: Ramazani Ali , Zakeri Sedigheh , Sardari Soroush , Khodakarim Nastaran , Djadidt Navid Dinparas 
Published: May 2010

Abstract

Background
There is an urgent need to identify new anti-malarial drug targets for both prophylaxis and chemotherapy, due to the increasing problem of drug resistance to malaria parasites. In the present study, the aim was to discover novel, effective plant-based extracts for the activity against malaria.

Methods
Ten plants found in Iran were selected by ethnobotanical survey of medicinal plants. The crude ethanolic extracts were tested for in vitro anti-plasmodial activity against two strains of Plasmodium falciparum: K1 (chloroquine-resistant strain) and CY27 (chloroquine-sensitive strain), using the parasite lactate dehydrogenase (pLDH) assay. The anti-plasmodial activity of the extracts was also assessed in the 4-day suppressive anti-malarial assay in mice inoculated with Plasmodium berghei (ANKA strain). Crude ethanolic extracts showed good anti-plasmodial activity were further fractionated by partitioning in water and dichloromethane.

Results
Of 10 plant species assayed, three species: Boerhavia elegans (Choisy), Solanum surattense (Burm.f.) and Prosopis juliflora (Sw.) showed promising anti-plasmodial activity in vitro (IC50 ≤ 50 μg/ml) and in vivo with no toxicity. The dichloromethane fraction of three extracts revealed stronger anti-plasmodial activity than the total extracts.

Conclusion
Anti-plasmodial activities of extracts of B. elegans and S. surattense are reported for the first time.
Gene-based outcome prediction in multiple cohorts of pediatric T-cell acute lymphoblastic leukemia: a Children's Oncology Group study
Authors: Cleaver Amanda L , Beesley Alex H , Firth Martin J , Sturges Nina C , O'Leary Rebecca A , Hunger Stephen P , Baker David L , Kees Ursula R 
Published: May 2010

Abstract

Background
Continuous complete clinical remission in T-cell acute lymphoblastic leukemia (T-ALL) is now approaching 80% due to the implementation of aggressive chemotherapy protocols but patients that relapse continue to have a poor prognosis. Such patients could benefit from augmented therapy if their clinical outcome could be more accurately predicted at the time of diagnosis. Gene expression profiling offers the potential to identify additional prognostic markers but has had limited success in generating robust signatures that predict outcome across multiple patient cohorts. This study aimed to identify robust gene classifiers that could be used for the accurate prediction of relapse in independent cohorts and across different experimental platforms.

Results
Using HG-U133Plus2 microarrays we modeled a five-gene classifier (5-GC) that accurately predicted clinical outcome in a cohort of 50 T-ALL patients. The 5-GC was further tested against three independent cohorts of T-ALL patients, using either qRT-PCR or microarray gene expression, and could predict patients with significantly adverse clinical outcome in each. The 5-GC featured the interleukin-7 receptor (IL-7R), low-expression of which was independently predictive of relapse in T-ALL patients. In T-ALL cell lines, low IL-7R expression was correlated with diminished growth response to IL-7 and enhanced glucocorticoid resistance. Analysis of biological pathways identified the NF-κB and Wnt pathways, and the cell adhesion receptor family (particularly integrins) as being predictive of relapse. Outcome modeling using genes from these pathways identified patients with significantly worse relapse-free survival in each T-ALL cohort.

Conclusions
We have used two different approaches to identify, for the first time, robust gene signatures that can successfully discriminate relapse and CCR patients at the time of diagnosis across multiple patient cohorts and platforms. Such genes and pathways represent markers for improved patient risk stratification and potential targets for novel T-ALL therapies.
Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB
Authors: Miguel-Carrasco José L , Zambrano Sonia , Blanca Antonio J , Mate Alfonso , Vázquez Carmen M 
Published: May 2010

AbstractBackgroundCaptopril is an angiotensin-converting enzyme (ACE) inhibitor widely used in the treatment of arterial hypertension and cardiovascular diseases. Our objective was to study whether captopril is able to attenuate the cardiac inflammatory process associated with arterial hypertension.MethodsLeft ventricle mRNA expression and plasma levels of pro-inflammatory (interleukin-1β (IL-1β) and IL-6) and anti-inflammatory (IL-10) cytokines, were measured in spontaneously hypertensive rats (SHR) and their control normotensive, Wistar-Kyoto (WKY) rats, with or without a 12-week treatment with captopril (80 mg/Kg/day; n = six animals per group). To understand the mechanisms involved in the effect of captopril, mRNA expression of ACE, angiotensin II type I receptor (AT1R) and p22phox (a subunit of NADPH oxidase), as well as NF-κB activation and expression, were measured in the left ventricle of these animals.ResultsIn SHR, the observed increases in blood pressures, heart rate, left ventricle relative weight, plasma levels and cardiac mRNA expression of IL-1β and IL-6, as well as the reductions in the plasma levels and in the cardiac mRNA expression of IL-10, were reversed after the treatment with captopril. Moreover, the mRNA expressions of ACE, AT1R and p22phox, which were enhanced in the left ventricle of SHR, were reduced to normal values after captopril treatment. Finally, SHR presented an elevated cardiac mRNA expression and activation of the transcription nuclear factor, NF-κB, accompanied by a reduced expression of its inhibitor, IκB; captopril administration corrected the observed changes in all these parameters.ConclusionThese findings show that captopril decreases the inflammation process in the left ventricle of hypertensive rats and suggest that NF-κB-driven inflammatory reactivity might be responsible for this effect through an inactivation of NF-κB-dependent pro-inflammatory factors.
Binary polypeptide system for permanent and oriented protein immobilization
Authors: Ferrari Enrico , Darios Frédéric , Zhang Fan , Niranjan Dhevahi , Bailes Julian , Soloviev Mikhail , Davletov Bazbek 
Published: May 2010

Abstract

Background
Many techniques in molecular biology, clinical diagnostics and biotechnology rely on binary affinity tags. The existing tags are based on either small molecules (e.g., biotin/streptavidin or glutathione/GST) or peptide tags (FLAG, Myc, HA, Strep-tag and His-tag). Among these, the biotin-streptavidin system is most popular due to the nearly irreversible interaction of biotin with the tetrameric protein, streptavidin. The major drawback of the stable biotin-streptavidin system, however, is that neither of the two tags can be added to a protein of interest via recombinant means (except for the Strep-tag case) leading to the requirement for chemical coupling.

Results
Here we report a new immobilization system which utilizes two monomeric polypeptides which self-assemble to produce non-covalent yet nearly irreversible complex which is stable in strong detergents, chaotropic agents, as well as in acids and alkali. Our system is based on the core region of the tetra-helical bundle known as the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex. This irreversible protein attachment system (IPAS) uses either a shortened syntaxin helix and fused SNAP25-synaptobrevin or a fused syntaxin-synaptobrevin and SNAP25 allowing a two-component system suitable for recombinant protein tagging, capture and immobilization. We also show that IPAS is suitable for use with traditional beads and chromatography, planar surfaces and Biacore, gold nanoparticles and for protein-protein interaction in solution.

Conclusions
IPAS offers an alternative to chemical cross-linking, streptavidin-biotin system and to traditional peptide affinity tags and can be used for a wide range of applications in nanotechnology and molecular sciences.
Is Obesity Associated with an Increased Risk for Airway Hyperresponsiveness and Development of Asthma?
Authors: Sharma Sat , Tailor Adarsh , Warrington Richard , Cheang Mary 
Published: May 2010

Abstract
We investigated the association between airway hyperresponsiveness (AHR) and obesity in adults referred for confirmation of asthma diagnosis. Data were analyzed for obesity class I (body mass index [BMI] 30-34.9 kg/m2), class II (BMI ≥ 35-39.9 kg/m2), and class III (BMI ≥ 40 kg/m2). Of 861 subjects, 401 demonstrated AHR; the mean dose of methacholine was 4.16 ± 2.55 mg/mL. A significant association between obesity and AHR was evident for all subjects: the odds ratio was 1.37 (95% CI 1.02-1.82; p = .0317). One unit of increased BMI (1 kg/m2) was associated with a 3.1% increase in AHR risk (95% CI 1.01-1.05, p < .005). The odds ratio increased from 1.86 (95% CI 1.27-1.76; p = .0012) for class I to 2.61 (95% CI 1.48-4.60; p = .0006) for class III. Obesity was found to be associated with AHR and appears to be a risk factor for asthma.
Occupational Contact Dermatitis
Authors: Sasseville Denis 
Published: May 2010

Abstract
Occupational contact dermatitis accounts for 90% of all cases of work-related cutaneous disorders. It can be divided into irritant contact dermatitis, which occurs in 80% of cases, and allergic contact dermatitis. In most cases, both types will present as eczematous lesions on exposed parts of the body, notably the hands. Accurate diagnosis relies on meticulous history taking, thorough physical examination, careful reading of Material Safety Data Sheets to distinguish between irritants and allergens, and comprehensive patch testing to confirm or rule out allergic sensitization. This article reviews the pathogenesis and clinical manifestations of occupational contact dermatitis and provides diagnostic guidelines and a rational approach to management of these often frustrating cases.
Atypical Bacteria and Macrolides in Asthma
Authors: Xepapadaki Paraskevi , Koutsoumpari Ioanna , Papaevagelou Vasiliki , Karagianni Christina , Papadopoulos Nikolaos G. 
Published: May 2010

AbstractChlamydophila pneumoniaeandMycoplasma pneumoniaeare common pathogens causing acute illness in both the upper and lower airways. Several observations are supportive of a possible causative role of these pathogens in asthma; however, more evidence is required before this becomes meaningful in clinical practice. Atypical bacteria can enhance airway hyperresponsiveness and inflammation, both of which have been associated with exacerbations in patients with preexisting asthma. It is less clear whether the above mechanisms might also be responsible for the development of asthma. Difficulties in accurately diagnosing these infections contribute to such uncertainty. In the present report, evidence of the involvement ofChlamydophilaandMycoplasmainfection in the development and the progression of asthma are reviewed.
Should Younger Siblings of Peanut-Allergic Children Be Assessed by an Allergist before Being Fed Peanut?
Authors: Liem Joel J. , Huq Saiful , Kozyrskyj Anita L. , Becker Allan B. 
Published: May 2010

Abstract
The objective of this study was to determine the risk of peanut allergy in siblings of peanut-allergic children. In 2005-2006, 560 households of children born in 1995 in the province of Manitoba, Canada, were surveyed. The index children (8-to 10-year-olds) were assessed by a pediatric allergist and had skin-prick testing and/or capRAST for peanut allergy. Surveys were completed by parents for siblings to determine the presence of peanut allergy. Of 560 surveys, 514 (92%) were completed. Twenty-nine (5.6%) index children were peanut allergic. Fifteen of 900 (1.7%) siblings had peanut allergy. Four of 47 (8.5%) were siblings of peanut-allergic children and 11 of 853 (1.3%) were siblings of non-peanut-allergic children. The risk of peanut allergy was markedly increased in siblings of a peanut-allergic child (odds ratio 6.72, 95% confidence interval 2.04-22.12). Siblings of peanut-allergic children are much more likely to be allergic to peanut. An allergy assessment by a qualified allergist should be routinely recommended before feeding peanut to these children.
Patterns of Expression of Vaginal T-Cell Activation Markers during Estrogen-Maintained Vaginal Candidiasis
Authors: Al-Sadeq Ameera , Hamad Mawieh , Abu-Elteen Khaled 
Published: May 2010

AbstractThe immunosuppressive activity of estrogen was further investigated by assessing the pattern of expression of CD25, CD28, CD69, and CD152 on vaginal T cells during estrogen-maintained vaginal candidiasis. A precipitous and significant decrease in vaginal fungal burden toward the end of week 3 postinfection was concurrent with a significant increase in vaginal lymphocyte numbers. During this period, the percentage of CD3+, CD3+CD4+, CD152+, and CD28+vaginal T cells gradually and significantly increased. The percentage of CD3+and CD3+CD4+cells increased from 43% and 15% at day 0 to 77% and 40% at day 28 postinfection. Compared with 29% CD152+vaginal T cells in naive mice, > 70% of vaginal T cells were CD152+at day 28 postinfection. In conclusion, estrogen-maintained vaginal candidiasis results in postinfection time-dependent changes in the pattern of expression of CD152, CD28, and other T-cell markers, suggesting that T cells are subject to mixed suppression and activation signals.
Prenatal allergen and diesel exhaust exposure and their effects on allergy in adult offspring mice
Authors: Corson Lin , Zhu Huaijie , Quan Chunli , Grunig Gabriele , Ballaney Manisha , Jin Ximei , Perera Frederica P , Factor Phillip H , Chen Lung-Chi , Miller Rachel L 
Published: May 2010

AbstractBackgroundMultiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring. However, the effects of prenatal environmental exposures on adult offspring have not been well-studied. We hypothesized that combined prenatal exposure to Aspergillus fumigatus (A. fumigatus) allergen and diesel exhaust particles will be associated with altered IgE production, airway inflammation, airway hyperreactivity (AHR), and airway remodeling of adult offspring.MethodsFollowing sensitization via the airway route toA. fumigatusand mating, pregnant BALB/c mice were exposed to additionalA. fumigatusand/or diesel exhaust particles. At age 9-10 weeks, their offspring were sensitized and challenged withA. fumigatus.ResultsWe found that adult offspring from mice that were exposed toA. fumigatusor diesel exhaust particles during pregnancy experienced decreases in IgE production. Adult offspring of mice that were exposed to bothA. fumigatusand diesel exhaust particles during pregnancy experienced decreases in airway eosinophilia.ConclusionThese results suggest that, in this model, allergen and/or diesel administration during pregnancy may be associated with protection from developing systemic and airway allergic immune responses in the adult offspring.
Rapid sympatric ecological differentiation of crater lake cichlid fishes within historic times
Authors: Elmer Kathryn R , Lehtonen Topi K , Kautt Andreas F , Harrod Chris , Meyer Axel 
Published: May 2010

AbstractBackgroundAfter a volcano erupts, a lake may form in the cooled crater and become an isolated aquatic ecosystem. This makes fishes in crater lakes informative for understanding sympatric evolution and ecological diversification in barren environments. From a geological and limnological perspective, such research offers insight about the process of crater lake ecosystem establishment and speciation. In the present study we use genetic and coalescence approaches to infer the colonization history of Midas cichlid fishes (Amphilophuscf.citrinellus) that inhabit a very young crater lake in Nicaragua-theca. 1800 year-old Lake Apoyeque. This lake holds two sympatric, endemic morphs of Midas cichlid: one with large, hypertrophied lips (~20% of the total population) and another with thin lips. Here we test the associated ecological, morphological and genetic diversification of these two morphs and their potential to represent incipient speciation.ResultsGene coalescence analyses [11 microsatellite loci and mitochondrial DNA (mtDNA) sequences] suggest that crater lake Apoyeque was colonized in a single event from the large neighbouring great lake Managua only about 100 years ago. This founding in historic times is also reflected in the extremely low nuclear and mitochondrial genetic diversity in Apoyeque. We found that sympatric adult thin- and thick-lipped fishes occupy distinct ecological trophic niches. Diet, body shape, head width, pharyngeal jaw size and shape and stable isotope values all differ significantly between the two lip-morphs. The eco-morphological features pharyngeal jaw shape, body shape, stomach contents and stable isotopes (δ15N) all show a bimodal distribution of traits, which is compatible with the expectations of an initial stage of ecological speciation under disruptive selection. Genetic differentiation between the thin- and thick-lipped population is weak at mtDNA sequence (FST= 0.018) and absent at nuclear microsatellite loci (FST< 0.001).ConclusionsThis study provides empirical evidence of eco-morphological differentiation occurring very quickly after the colonization of a new and vacant habitat. Exceptionally low levels of neutral genetic diversity and inference from coalescence indicates that the Midas cichlid population in Apoyeque is much younger (ca. 100 years or generations old) than the crater itself (ca. 1 800 years old). This suggests either that the crater remained empty for many hundreds of years after its formation or that remnant volcanic activity prevented the establishment of a stable fish population during the early life of the crater lake. Based on our findings of eco-morphological variation in the Apoyeque Midas cichlids, and known patterns of adaptation in Midas cichlids in general, we suggest that this population may be in a very early stage of speciation (incipient species), promoted by disruptive selection and ecological diversification.
Role of the C-terminal domain of the HIV-1 glycoprotein in cell-to-cell viral transmission between T lymphocytes
Authors: Emerson Vanessa , Haller Claudia , Pfeiffer Tanya , Fackler Oliver T , Bosch Valerie 
Published: May 2010

Abstract

Background
Mutant HIV (HIV-Env-Tr712) lacking the cytoplasmic tail of the viral glycoprotein (Env-CT) exhibits a cell-type specific replication phenotype such that replicative spread occurs in some T-cell lines (referred to as permissive cells) but fails to do so in most T-cell lines or in PBMCs (referred to as non-permissive cells). We aim to gain insight on the underlying requirement for the Env-CT for viral spread in non-permissive cells.

Results
We established that in comparison to HIV-Wt, both cell-free and cell-to-cell transmission of mutant HIV-Env-Tr712 from non-permissive cells were severely impaired under naturally low infection conditions. This requirement for Env-CT could be largely overcome by using saturating amounts of virus for infection. We further observed that in permissive cells, which supported both routes of mutant virus transmission, viral gene expression levels, Gag processing and particle release were inherently higher than in non-permissive cells, a factor which may be significantly contributing to their permissivity phenotype. Additionally, and correlating with viral transfer efficiencies in these cell types, HIV-Gag accumulation at the virological synapse (VS) was reduced to background levels in the absence of the Env-CT in conjugates of non-permissive cells but not in permissive cells.

Conclusions
During natural infection conditions, the HIV-Env-CT is critically required for viral transmission in cultures of non-permissive cells by both cell-free and cell-to-cell routes and is instrumental for Gag accumulation to the VS. The requirement of the Env-CT for these related processes is abrogated in permissive cells, which exhibit higher HIV gene expression levels.
Biomechanical modulation of collagen fragment-induced anabolic and catabolic activities in chondrocyte/agarose constructs
Authors: Chowdhury Tina T , Schulz Ronny M , Rai Sonpreet S , Thuemmler Christian B , Wuestneck Nico , Bader Augustinus , Homandberg Gene A 
Published: May 2010

Abstract
Introduction
The present study examined the effect of collagen fragments on anabolic and catabolic activities by chondrocyte/agarose constructs subjected to dynamic compression.

Methods
Constructs were cultured under free-swelling conditions or subjected to continuous and intermittent compression regimes, in the presence of the N-terminal (NT) and C-terminal (CT) telopeptides derived from collagen type II and/or 1400 W (inhibits inducible nitric oxide synthase (iNOS)). The anabolic and catabolic activities were compared to the amino-terminal fibronectin fragment (NH2-FN-f) and assessed as follows: nitric oxide (NO) release and sulphated glycosaminoglycan (sGAG) content were quantified using biochemical assays. Tumour necrosis factor-α (TNFα) and interleukin-1β (IL-1β) release were measured by ELISA. Gene expression of matrix metalloproteinase-3 (MMP-3), matrix metalloproteinase-13 (MMP-13), collagen type II and fibronectin were assessed by real-time quantitative polymerase chain reaction (qPCR). Two-way ANOVA and the post hoc Bonferroni-corrected t-test was used to examine data.

Results
The presence of the NT or CT peptides caused a moderate to strong dose-dependent stimulation of NO, TNFα and IL-1β production and inhibition of sGAG content. In some instances, high concentrations of telopeptides were just as potent in stimulating catabolic activities when compared to NH2-FN-f. Depending on the concentration and type of fragment, the increased levels of NO and cytokines were inhibited with 1400 W, resulting in the restoration of sGAG content. Depending on the duration and type of compression regime employed, stimulation with compression or incubation with 1400 W or a combination of both, inhibited telopeptide or NH2-FN-f induced NO release and cytokine production and enhanced sGAG content. All fragments induced MMP-3 and MMP-13 expression in a time-dependent manner. This effect was reversed with compression and/or 1400 W resulting in the restoration of sGAG content and induction of collagen type II and fibronectin expression.

Conclusions
Collagen fragments containing the N- and C-terminal telopeptides have dose-dependent catabolic activities similar to fibronectin fragments and increase the production of NO, cytokines and MMPs. Catabolic activities were downregulated by dynamic compression or by the presence of the iNOS inhibitor, linking reparative activities by both types of stimuli. Future investigations which examine the signalling cascades of chondrocytes in response to matrix fragments with mechanical influences may provide useful information for early osteoarthritis treatments.