bluuebunny/crossref_metadata_2025_split huggingface dataset:
Respiratory symptoms, bronchial hyper‐responsiveness, and eosinophilic airway inflammation in patients with moderate‐to‐severe atopic dermatitis
Authors: Kyllönen H. , Malmberg P. , Remitz A. , Rytilä P. , Metso T. , Helenius I. , Haahtela T. , Reitamo S. 
Published: January 2006

SummaryBackgroundPatients with atopic dermatitis (AD) often have symptoms suggestive of asthma or rhinitis. The prevalence and signs of respiratory disease in AD patients have been studied to a limited extent.ObjectivesTo assess the prevalence and clustering of respiratory symptoms, bronchial hyper‐responsiveness (BHR), and eosinophilic airway inflammation in patients with moderate‐to‐severe AD.MethodsEighty‐six consecutive patients with moderate‐to‐severe AD and 49 randomly selected control subjects without AD were studied by questionnaire, flow volume spirometry, histamine challenge to detect BHR, induced sputum test to detect eosinophilic airway inflammation, and skin prick tests (SPTs) and total serum immunoglobulin (Ig)E measurements to detect atopy.ResultsThe patients with AD showed increased risk of physician‐diagnosed asthma (36% vs. 2%, odds ratio (OR) 10.1, confidence interval (CI) 1.3–79.7,P=0.03), physician‐diagnosed allergic rhinitis (AR) (45% vs. 6%, OR 4.5, CI 1.2–16.7,P=0.02), BHR (51% vs. 10%, OR 5.5, CI 1.5–20.1,P=0.01), and sputum eosinophilia (81% vs. 11%, OR 76.1, CI 9.3‐623.5,P<0.0001) compared with the control subjects. In AD patients, elevated s‐IgE and positive SPTs were associated with the occurrence of physician‐diagnosed asthma and AR, BHR, and the presence of sputum eosinophilia.ConclusionsBHR and eosinophilic airway inflammation are more common in patients with AD than in control subjects. The highest prevalences were seen in patients with AD who were SPT positive and had high IgE levels. Longitudinal studies are needed to assess the outcome of patients with signs of airway disease, in order to identify those who need early initiation of asthma treatment.
Recurrent childhood upper respiratory tract infections do not reduce the risk of adult atopic disease
Authors: Balemans W. A. F. , Rovers M. M. , Schilder A. G. M. , Sanders E. A. M. , Kimpen J. L. L. , Zielhuis G. A. , van der Ent C. K. 
Published: January 2006

SummaryBackground
Children of large families and those attending day care are at increased risk of respiratory tract infections, which in turn may protect against the development of allergic disease. Longitudinal studies investigating these associations beyond childhood are, however, scarce.Objective
To investigate the association between childhood recurrent upper respiratory tract infections (URTI) and asthma, allergic rhinitis (AR) and eczema in adulthood.Methods
A birth cohort of 1055 members followed prospectively from the ages of 2 to 21 years. Detailed information on URTI between the ages of 2 and 4 years was collected at 3 monthly intervals in a standardized interview. At the age of 8 years, a parental questionnaire regarding URTI between the ages of 4 and 8 years was used. The incidence of asthma and atopic disease at the age of 21 years was determined using a standardized questionnaire.Results
Of the original cohort, 693 (66%) members completed the questionnaire. Children who experienced recurrent URTI before the age of 2 years, between the ages of 2–4 years and between ages of 4 and 8 years were not less likely to have asthma at 21 years of age than children who did not experience recurrent URTI, relative risk (RR) 0.97 (95% confidence interval (CI) 0.65–1.46), RR 1.45 (CI 0.95–2.21) and RR 1.51 (CI 0.97–2.36), respectively. Neither were recurrent URTI associated with a decreased risk of AR, nor eczema at the age of 21 years.Conclusions
Recurrent URTI in childhood did not reduce the risk of atopic disease in young adulthood.
The common G‐allele of interleukin‐18 single‐nucleotide polymorphism is a genetic risk factor for atopic asthma. The SAPALDIA Cohort Study
Authors: Imboden M. , Nicod L. , Nieters A. , Glaus E. , Matyas G. , Bircher A. J. , Ackermann‐Liebrich U. , Berger W. , Probst‐Hensch N. M. ,   SAPALDIA Team
Published: January 2006

SummaryBackground
IL‐18 is a pleiotrophic cytokine involved in both, T‐helper type 1 (Th1) and Th2 differentiation. Recently genetic variants in the IL‐18 gene have been associated with increased risk of atopy and asthma.Objective
To examine the relationship of a genetic, haplotype‐tagging promotor variant −137G/C in the IL‐18 gene with atopic asthma in a large, well‐characterized and population‐based study of adults.Methods
Prospective cohort study design was used to collect interview and biological measurement data at two examination time‐points 11 years apart. Multivariate logistic regression analysis was used to assess the association of genotype with asthma and atopy.Results
The G‐allele of the IL‐18 promotor variant (−137G/C) was associated with a markedly increased risk for the prevalence of physician‐diagnosed asthma with concomitant skin reactivity to common allergens. Stratification of the asthma cases by skin reactivity to common allergens revealed an exclusive association of IL‐18 −137 G‐allele with an increased prevalence of atopic asthma (adjusted odds ratio (OR): 3.63; 95% confidence interval: (1.64–8.02) for GC or GG carriers vs. CC carriers), and no according association with asthma and concomitant negative skin reactivity (adjusted OR: 1.13; 0.66–1.94). The interaction between IL‐18 −137G/C genotype and positive skin prick test was statistically significant (P=0.029). None of 74 incident asthma cases with atopy at baseline exhibited the CC genotype.Conclusion
Our results strongly suggest that this variant of the IL‐18 gene is an important genetic determinant involved in the development of atopic asthma.
Indomethacin disrupts the protective effect of phosphatidylcholine against bile salt‐induced ileal mucosa injury
Authors: Venneman N. G. , Petruzzelli M. , van Dijk J. E. , Verheem A. , Akkermans L. M. A. , Kroese A. B. A. , van Erpecum K. J. 
Published: January 2006

AbstractBackground  Indomethacin (Indo) exerts local toxic effects on small intestinal mucosa, possibly in association with hydrophobic bile salts. We investigated the potential toxic effects of Indo on ileal mucosa and the role of phosphatidylcholine (PC).Materials and methods  Transmucosal resistance and Na‐fluorescein permeability of ileal mucosa segments from female Wistar rats were determined in Ussing chambers during a 30‐min incubation with model systems containing: control‐buffer, taurodeoxycholate (TDC), Indo, TDC‐Indo, TDC‐PC, or TDC‐PC‐Indo. Decrease of resistance and increase of permeability were considered as parameters for mucosal injury. After incubation in Ussing chambers, the histopathology was examined to quantify the extent of mucosal injury. Also, in CaCo‐2 cells, LDH‐release was determined as a measure of cytotoxicity, after incubation with various model systems.Results  Decrease of resistance and increase of permeability were highest in systems containing TDC‐Indo (P < 0·01). Phosphatidylcholine protected against the cytotoxic effects of TDC in absence of Indo only. Extent of mucosal injury by histological examination was also highest in systems containing TDC‐Indo (P = 0·006). Again, PC exhibited protective effects in absence of Indo only. The LDH‐release by CaCo2‐cells was strongest in TDC‐Indo systems (P < 0·001).Conclusions  Indomethacin disrupts protective effects of PC against bile salt‐induced ileal mucosa injury. This finding is relevant for small intestinal injury induced by non‐steroidal anti‐inflammatory drugs.
Effects of simvastatin withdrawal on serum matrix metalloproteinases in hypercholesterolaemic patients
Authors: Huang C. Y. , Wu T. C. , Lin W. T. , Leu H. B. , Lin C. P. , Lin S. J. , Chen J. W. 
Published: January 2006

AbstractBackground  Serum matrix metalloproteinase (MMP) levels have been related to clinical outcomes in patients with coronary artery disease. Though statin treatment might reduce serum MMPs the change of levels after statin withdrawal remains obscure.Materials and method  Sixty‐one consecutive hypercholesterolaemic patients whose lipid profiles had been well controlled by regular simvastatin (20 mg day−1) treatment for more than 6 months were enrolled. Statin was discontinued after their lipid profiles reached the treatment goal of the ATP‐III guideline. The lipid profiles, serum MMP‐2, MMP‐3 and MMP‐9, tissue inhibitor of MMP and highly sensitive C‐reactive protein (hsCRP) levels were measured on the day of simvastatin withdrawal and 120 days later. A further 50 hyperlipidaemia patients who had never received statin treatment (positive control group) and 28 healthy patients with normal lipid profiles (negative control group) were also studied as control groups.Results  While the lipid profiles had been normalized, the levels of serum inflammatory markers were still higher in hypercholesterolaemic patients than in the healthy subjects. Up to 120 days after statin withdrawal there was no coronary event, but the lipid profiles and serum hsCRP levels had significantly rebounded in study patients. However, serum MMP‐2 and MMP‐9 levels remained unchanged and the MMP‐3 level was even further reduced after statin withdrawal (115·04 ± 84·54 vs. 92·71 ± 66·71 ng mL−1, P = 0·022). Moreover, the amplitudes of variation (%) of each parameter including MMPs, TIMP, hsCRP and lipid profiles after statin withdrawal were inversely correlated to their respective baseline levels before withdrawal (r = −0·702 to −0·284; P < 0·005).Conclusions  The effects of short‐term discontinuation of statin were different on serum hsCRP and MMPs levels in hypercholesterolaemic patients. While lipid profiles and serum hsCRP level had rebounded the serum MMPs levels were still unchanged, or even reduced, suggesting the prolonged effect of statin treatment, especially on serum MMP‐3 level up to 120 days after simvastatin withdrawal. Further work is required to clarify the situation both in terms of these serum markers and clinical effects.
Is carbon within the global terrestrial biosphere becoming more oxidized? Implications for trends in atmospheric O2
Authors: RANDERSON J. T. , MASIELLO C. A. , STILL C. J. , RAHN T. , POORTER H. , FIELD C. B. 
Published: January 2006

AbstractMeasurements of atmospheric O2 and CO2 concentrations serve as a widely used means to partition global land and ocean carbon sinks. Interpretation of these measurements has assumed that the terrestrial biosphere contributes to changing O2 levels by either expanding or contracting in size, and thus serving as either a carbon sink or source (and conversely as either an oxygen source or sink). Here, we show how changes in atmospheric O2 can also occur if carbon within the terrestrial biosphere becomes more reduced or more oxidized, even with a constant carbon pool. At a global scale, we hypothesize that increasing levels of disturbance within many biomes has favored plant functional types with lower oxidative ratios and that this has caused carbon within the terrestrial biosphere to become increasingly more oxidized over a period of decades. Accounting for this mechanism in the global atmospheric O2 budget may require a small increase in the size of the land carbon sink. In a scenario based on the Carnegie–Ames–Stanford Approach model, a cumulative decrease in the oxidative ratio of net primary production (NPP) (moles of O2 produced per mole of CO2 fixed in NPP) by 0.01 over a period of 100 years would create an O2 disequilibrium of 0.0017 and require an increased land carbon sink of 0.1 Pg C yr−1 to balance global atmospheric O2 and CO2 budgets. At present, however, it is challenging to directly measure the oxidative ratio of terrestrial ecosystem exchange and even more difficult to detect a disequilibrium caused by a changing oxidative ratio of NPP. Information on plant and soil chemical composition complement gas exchange approaches for measuring the oxidative ratio, particularly for understanding how this quantity may respond to various global change processes over annual to decadal timescales.
Comparative dynamics of avian communities across edges and interiors of North American ecoregions
Authors: Karanth Krithi K. , Nichols James D. , Sauer John R. , Hines James E. 
Published: January 2006

AbstractAim Based ona priorihypotheses, we developed predictions about how avian communities might differ at the edges vs. interiors of ecoregions. Specifically, we predicted lower species richness and greater local turnover and extinction probabilities for regional edges. We tested these predictions using North American Breeding Bird Survey (BBS) data across nine ecoregions over a 20‐year time period.Location Data from 2238 BBS routes within nine ecoregions of the United States were used.Methods The estimation methods used accounted for species detection probabilities < 1. Parameter estimates for species richness, local turnover and extinction probabilities were obtained using the program COMDYN. We examined the difference in community‐level parameters estimated from within exterior edges (the habitat interface between ecoregions), interior edges (the habitat interface between two bird conservation regions within the same ecoregion) and interior (habitat excluding interfaces). General linear models were constructed to examine sources of variation in community parameters for five ecoregions (containing all three habitat types) and all nine ecoregions (containing two habitat types).Results Analyses provided evidence that interior habitats and interior edges had on average higher bird species richness than exterior edges, providing some evidence of reduced species richness near habitat edges. Lower average extinction probabilities and turnover rates in interior habitats (five‐region analysis) provided some support for our predictions about these quantities. However, analyses directed at all three response variables, i.e. species richness, local turnover, and local extinction probability, provided evidence of an interaction between habitat and region, indicating that the relationships did not hold in all regions.Main conclusions The overall predictions of lower species richness, higher local turnover and extinction probabilities in regional edge habitats, as opposed to interior habitats, were generally supported. However, these predicted tendencies did not hold in all regions.
Pathology of Edwardsiella tarda infection in turbot, Scophthalmus maximus (L.)
Authors: Padrós F , Zarza C , Dopazo L , Cuadrado M , Crespo S 
Published: January 2006

AbstractMacroscopic and histopathological changes in cultured turbot, Scophthalmus maximus (L.), in Spain caused by infection with Edwardsiella tarda are described. Eye tumefaction, inflammation, haemorrhages, ascites and the presence of a purulent fluid were the main macroscopic lesions observed. Histopathological lesions were found in the kidney, spleen and liver. In the kidney and spleen these were characterized by a severe apostematous inflammatory reaction, with a large number of abscesses. The liver was affected to a lesser degree and only some phagocytes loaded with bacteria were observed. Ultrastructural observations indicated that macrophages were the main cell type implicated in the inflammatory response. Most of the bacteria observed within the phagocyte cytoplasm showed no degenerative changes and some were dividing. Degenerative changes observed in macrophages indicate their failure in preventing the infection.
Dietary β‐1,3 glucan potentiates innate immunity and disease resistance of Asian catfish, Clarias batrachus (L.)
Authors: Kumari J , Sahoo P K 
Published: January 2006

AbstractThis study investigated the effects of short and prolonged administration of a yeast β‐glucan on non‐specific immune parameters, growth rate and the disease resistance of Asian catfish, Clarias batrachus. Fish fed with a basal diet (control) and test diet (basal diet supplemented with 0.1% glucan) for 1, 2 and 3 weeks were assayed for superoxide production, serum myeloperoxidase (MPO) content, natural haemagglutinin level, complement and lysozyme activities. Fish were weighed at weekly intervals and specific growth rate (SGR, % increase in body weight per day) was determined. After each week, fish were challenged with Aeromonas hydrophila to measure the level of protection. Results showed that glucan administration at 0.1% in feed, significantly (P < 0.05) enhanced MPO and lysozyme levels, superoxide production, haemagglutination titre and level of protection against A. hydrophila challenge, irrespective of length of exposure. The alternative complement activity and SGR were not affected by the dietary supplementation of yeast glucan. As glucan feeding at 0.1% for 1 week is able to enhance the non‐specific immunity and disease resistance of catfish efficiently, short‐term feeding might be used in farmed catfish diets to enhance disease resistance.
Structure of the Mycobacterium tuberculosis proteasome and mechanism of inhibition by a peptidyl boronate
Authors: Hu Guiqing , Lin Gang , Wang Ming , Dick Lawrence , Xu Rui‐Ming , Nathan Carl , Li Huilin 
Published: January 2006

SummaryMycobacterium tuberculosis (Mtb) has the remarkable ability to resist killing by human macrophages. The 750 kDa proteasome, not available in most eubacteria except Actinomycetes, appears to contribute to Mtb's resistance. The crystal structure of the Mtb proteasome at 3.0 Å resolution reveals a substrate‐binding pocket with composite features of the distinct β1, β2 and β5 substrate binding sites of eukaryotic proteasomes, accounting for the broad specificity of the Mtb proteasome towards oligopeptides described in the companion article [Lin et al. (2006), Mol Microbiol doi:10.1111/j.1365‐2958.2005.05035.x]. The substrate entrance at the end of the cylindrical proteasome appears open in the crystal structure due to partial disorder of the α‐subunit N‐terminal residues. However, cryo‐electron microscopy of the core particle reveals a closed end, compatible with the density observed in negative‐staining electron microscopy that depended on the presence of the N‐terminal octapetides of the α‐subunits in the companion article, suggesting that the Mtb proteasome has a gated structure. We determine for the first time the proteasomal inhibition mechanism of the dipeptidyl boronate N‐(4‐morpholine)carbonyl‐β‐(1‐naphthyl)‐l‐alanine‐l‐leucine boronic acid (MLN‐273), an analogue of the antimyeloma drug bortezomib. The structure improves prospects for designing Mtb‐specific proteasomal inhibitors as a novel approach to chemotherapy of tuberculosis.
Kimura's disease and angiolymphoid hyperplasia with eosinophilia: two disease entities in the same patient. Case report and review of the literature
Authors: Chong Wei‐Sheng , Thomas Anjula , Goh Chee‐Leok 
Published: January 2006

AbstractBackground  Much controversy has existed with regard to the relationship between Kimura's disease and angiolymphoid hyperplasia with eosinophilia. They were initially thought to represent the same disease spectrum, but it has now been widely accepted that they are two separate disease entities. To our knowledge, there have been no reports to date describing a case of both Kimura's disease and angiolymphoid hyperplasia with eosinophilia coexisting in the same patient.Methods  We describe a patient presenting initially with a right postauricular subcutaneous swelling and subsequently developing multiple erythematous facial papules and nodules. The medical literature is reviewed.Results  Clinical features of the right postauricular subcutaneous swelling and multiple erythematous facial papules/nodules suggest Kimura's disease in the former and angiolymphoid hyperplasia with eosinophilia in the latter. Histopathological examinations of these lesions helped to confirm the diagnosis of Kimura's disease and angiolymphoid hyperplasia with eosinophilia, respectively.Conclusions  Kimura's disease and angiolymphoid hyperplasia with eosinophilia can coexist in the same patient. Coexistence of the two types of lesions in one patient may also be considered evidence that Kimura's disease and angiolymphoid hyperplasia with eosinophilia form a spectrum in one disease.
Clinico‐epidemiological features of primary hereditary ichthyoses in the Eastern province of Saudi Arabia
Authors: Al‐Zayir Ahmad A. , Al‐Amro Al‐Alakloby Omar M. 
Published: January 2006

AbstractBackground  A total of 10 455 new dermatology patients were seen in the dermatology clinics of King Fahad Hospital of the University (KFHU), Al‐Khobar, Saudi Arabia, between January 1990 and December 1995. We identified 71 patients with a histopathologically confirmed diagnosis of specific forms of primary hereditary ichthyoses (PHI). We have reviewed the epidemiological and clinical features of these patients.Objective  To document the epidemiological and clinical features of patients with PHI in the Eastern Province of Saudi Arabia.Methods  We used the dermatology out‐patient department (OPD) logbooks to identify cases of PHI from new patients presenting with different dermatological problems over a 6‐year period. We used specifically designed protocol forms to extract epidemiological and clinical data from the study patients’ medical records. These were entered into a computer database and analyzed using standard statistical software.Results  A total of 71 patients, 44 males and 27 females (male : female sex ratio of 1.63 : 1), were identified from a total of 10 455 new patients seen in our dermatology clinics between January 1990 and December 1995. The occurrence rate of PHI, in our clinics, was 0.67% or 7 per 1000 new dermatology cases. The clinical pattern of PHI showed that Icthyosis Vulgaris was the most common form seen, followed by Nonbullous Ichthyosiform Erythroderma. Thirty‐one patients (44.7%) with Ichthyosis Vulgaris (IV) were seen: 12 patients (16.9%) with X‐linked Recessive Ichthyosis (XLRI), four patients (5.6%) with Lamellar Ichthyosis (LI), three patients (4.2%) with Bullous Ichthyosiform Erythroderma (BIE) and 21 patients (29.6%) with Nonbullous Ichthyosiform Erythroderma (NBIE). There was a significantly high consanguinity rate in our patients (85%), and the family history was positive in 53 cases out of the 71 (75%).Conclusions  This preliminary study is the first report of its kind from Saudi Arabia and documents the clinico‐epidemiological features of PHI patients in the Eastern Province. The high rate of parental consanguinity among our Saudi patients may account for the high proportion of patients with a positive family history. Consanguinity also probably explains why the most severe forms of PHI were seen in a significant number of new patients’ siblings. These severe forms of PHI (Nonbullous Ichthyosiform Erythroderma, Bullous Ichthyosiform Erythroderma and Lamellar Ichthyosis) together constituted nearly 40% of all cases.
A case of hydroxyurea‐induced transverse melanonychia
Authors: Teo Rachael Yu Lin , Tan Eileen 
Published: January 2006

A 33‐year‐old Malay female presented to our clinic for the evaluation of nail pigmentation. She had been diagnosed with essential thrombocytosis 2 years previously, but had failed to return for follow‐up. She presented again to the hematology department with symptoms of giddiness, blurring of vision, and left‐sided weakness and was started on hydroxyurea 3 g/day.Hydroxyurea was stopped after 1 month of administration because of pancytopenia. Concurrent medications taken included anagrelide, buscopan, allopurinol, omeprazole, and sangobion. None of these medications are known to cause nail pigmentation.She first presented to our department when she noticed nail pigmentation 7 weeks after starting hydroxyurea, but was otherwise well. There were no other cutaneous features of hyperpigmentation. Clinical examination revealed transverse bands which were seen on all 20 nails. These involved the proximal half of the fingernails and the proximal third of the toenails and were colored brown (seeFig. 1).Transverse bands on all 10 fingernails 9 weeks after the commencement of hydroxyurea therapyimage