bluuebunny/crossref_metadata_2025_split huggingface dataset:
Peroxisome proliferator‐activated receptor‐gamma Pro12Ala polymorphism, Helicobacter pylori infection and non‐cardia gastric carcinoma in Chinese
Authors: LIAO S.‐Y. , ZENG Z.‐R. , LEUNG W. K. , ZHOU S.‐Z. , CHEN B. , SUNG J. J. Y. , HU P.‐J. 
Published: December 2005

SummaryBackground  Peroxisome proliferator‐activated receptor γ inhibits the growth and induces apoptosis of gastric cancer cells. A common polymorphism at codon 12 of this gene (Pro12Ala) has been shown to confer protection against diabetes and colorectal cancer.Aim  To study the association between peroxisome proliferator‐activated receptor γ gene polymorphism, Helicobacter pylori infection and gastric cancer in Chinese.Methods  One hundred and four consecutive patients with non‐cardia gastric adenocarcinoma and 104 matched controls were examined. Peroxisome proliferator‐activated receptor γ Pro12Ala polymorphism was analysed by polymerase chain reaction‐restriction fragment length polymorphism.Results  The frequency of peroxisome proliferator‐activated receptor γ G (Ala12) allele was significantly higher among cancer patients (19.2%) than in control (8.7%; OR 2.5, 95% CI 1.1–5.8). While H. pylori infection was more prevalent in gastric cancer patients (OR 3.0; 95% CI 1.6–5.7), the combination of peroxisome proliferator‐activated receptor γ G allele and H. pylori infection further increased the risk of gastric cancer (OR 12.8, 95% CI 3.2–50.5). The presence of the Ala12 did not increase the risk of gastric cancer in H. pylori‐negative subjects.Conclusion  Our study suggests the potential association between peroxisome proliferator‐activated receptor γ polymorphism and H. pylori infection in the development of non‐cardia gastric cancer.
Long‐term follow‐up of 13C‐urea breath test results after Helicobacter pylori eradication: frequency and significance of borderline δ13CO2 values
Authors: GISBERT J. P. , OLIVARES D. , JIMENEZ I. , PAJARES J. M. 
Published: December 2005

SummaryBackground  The precise choice of cut‐off point for the 13C‐urea breath test to define whether it is positive or negative represents a controversial issue.Aim  To quantify the 13C‐urea breath test result for several years following Helicobacter pylori eradication, and to evaluate the frequency and the significance of borderline δ13CO2 values.Methods  Two‐hundred H. pylori eradicated patients confirmed by 13C‐urea breath test (100 mg of urea, citric acid), and having had repeated this test yearly up to 5 years, were studied. δ13CO2 values between 2 and 5‰ were considered as borderline results.Results  Eight H. pylori recurrences were observed during 406 patient‐years of follow‐up (1.97% yearly). In two of eight reinfected patients, the reinfection was preceded by a negative δ13CO2 value >2‰. Borderline δ13CO2 values were detected in 4% of the 606 urea breath tests performed, and in 25% when only patients in whom H. pylori recurrence was detected in subsequent urea breath tests were included (P < 0.05). The negative‐predictive value of a post‐treatment δ13CO2 >2‰ for the diagnosis of H. pylori recurrence was 99%.Conclusions  Positive and negative urea breath test results tend to cluster outside the range between 2‰ and 5‰. Nevertheless, a borderline urea breath test δ value (e.g. very close to the selected cut‐off point) should be interpreted cautiously, and the result should probably be confirmed either by repeating the urea breath test or by other diagnostic methods. On the contrary, a δ13CO2 value <2‰ very confidently confirms H. pylori eradication.
Budesonide foam versus budesonide enema in active ulcerative proctitis and proctosigmoiditis
Authors: GROSS V. , BAR‐MEIR S. , LAVY A. , MICKISCH O. , TULASSAY Z. , PRONAI L. , KUPCINSKAS L. , KIUDELIS G. , POKROTNIEKS J. , KOVÁCS Á. , FASZCZYK M. , RAZBADAUSKAS A. , MARGUS B. , STOLTE M. , MÜLLER R. , GREINWALD R. ,   THE INTERNATIONAL BUDESONIDE FOAM STUDY GROUP
Published: December 2005

SummaryBackground  Rectal budesonide is an effective treatment of active ulcerative proctitis or proctosigmoiditis.Aim  To compare the therapeutic efficacy, tolerability and safety, and patient's preference of budesonide foam vs. budesonide enema.Methods  Patients with active ulcerative proctitis or proctosigmoiditis (clinical activity index >4 and endoscopic index ≥4) were eligible for this double‐blind, double‐dummy, randomized, multicentre study. They received 2 mg/25 mL budesonide foam and placebo enema (n = 265), or 2 mg/100 mL budesonide enema and placebo foam (n = 268) for 4 weeks. Primary endpoint was clinical remission (clinical activity index ≤4) at the final/withdrawal visit (per protocol).Results  A total of 541 patients were randomized – 533 were evaluable for intention‐to‐treat analysis and 449 for per protocol analysis. Clinical remission rates (per protocol) were 60% for budesonide foam and 66% for budesonide enema (P = 0.02362 for non‐inferiority of foam vs. enema within a predefined non‐inferiority margin of 15%). Both formulations were safe and no drug‐related serious adverse events were observed. Because of better tolerability and easier application most patients preferred foam (84%).Conclusion  Budesonide foam is as effective as budesonide enema in the treatment of active ulcerative proctitis or proctosigmoiditis. Both budesonide formulations are safe, and most patients prefer foam.
The extent of oesophageal acid exposure overlap among the different gastro‐oesophageal reflux disease groups
Authors: SHAPIRO M. , GREEN C. , FAYBUSH E. M. , ESQUIVEL R. F. , FASS R. 
Published: December 2005

SummaryBackground  Studies have demonstrated that patients with Barrett's oesophagus have the highest oesophageal acid exposure profile, followed by erosive oesophagitis and non‐erosive reflux disease patients, but the exact extent of overlap remains unknown.Aim  To determine the extent of overlap in oesophageal acid exposure among the different gastro‐oesophageal reflux disease groups.Methods  A total of 121 patients with gastro‐oesophageal reflux disease underwent an upper endoscopy and were classified as having Barrett's oesophagus, erosive oesophagitis and non‐erosive reflux disease‐all (non‐erosive reflux disease‐positive and functional heartburn). Subsequently, patients underwent pH testing and overlap in oesophageal acid exposure among the different gastro‐oesophageal reflux disease groups was determined.Results  Of those enrolled, 24 had Barrett's oesophagus, 30 erosive oesophagitis and 28 were non‐erosive reflux disease‐positive. Mean oesophageal acid exposure time was 224.8 ± 35, 134.3 ± 21.9 and 141.3 ± 19.8 min for Barrett's oesophagus, erosive oesophagitis and non‐erosive reflux disease‐positive respectively. Per cent overlap for total, upright and supine time between non‐erosive reflux disease‐positive and erosive oesophagitis was 47.4%, 64.7% and 81.8%, between Barrett's oesophagus and erosive oesophagitis was 47.8%, 40.7% and 24%, and between Barrett's oesophagus and non‐erosive reflux disease‐positive was 31.6%, 37.5% and 20.8% respectively.Conclusions  Our study demonstrated a high oesophageal acid exposure overlap between patients with non‐erosive reflux disease‐positive and erosive oesophagitis, Barrett's oesophagus and erosive oesophagitis, as well as Barrett's oesophagus and non‐erosive reflux disease‐positive patients.
Histological effects of esomeprazole therapy on the squamous epithelium of the distal oesophagus
Authors: VIETH M. , KULIG M. , LEODOLTER A. , NAUCLÉR E. , JASPERSEN D. , LABENZ J. , MEYER‐SABELLEK W. , LIND T. , WILLICH S. , MALFERTHEINER P. , STOLTE M. 
Published: December 2005

SummaryBackground  Proton pump inhibitor therapy has been reported to reduce proliferative changes of the oesophagus significantly in gastro‐oesophageal reflux disease (GERD).Aim  To assess the histological effects of esomeprazole treatment on the oesophagus.Methods  Data were derived from a subgroup of patients participating in the proGERD study, who had either erosive reflux disease (n = 720) or non‐erosive reflux disease (n = 35) and who had biopsy data from two sites [(i) 2 cm above the z‐line and (ii) at the z‐line], obtained at baseline and following treatment with esomeprazole. Proliferative changes of the squamous epithelium were assessed histologically by measuring thickness of the basal cell layer and elongation of the papillae as a percentage of the whole epithelial thickness.Results  In erosive reflux disease patients, the thickness of the basal cell layer and length of the papillae pretreatment were associated with the severity of oesophagitis (P < 0.05), at both biopsy sites. After esomeprazole treatment, baseline thickness and length of papillae were significantly reduced (P < 0.05) at both biopsy sites in non‐erosive reflux disease and erosive reflux disease patients (particularly those with Los Angeles grades C and D).Conclusion  This demonstrates a strong correlation between severity of GERD and histological parameters. Esomeprazole therapy resulted in clear reversal of proliferative changes observed prior to treatment in the squamous epithelium at both biopsy locations.
Rabeprazole containing triple therapy to eradicate Helicobacter pylori infection on the Texas‐Mexican border
Authors: CARDENAS V. M. , GRAHAM D. Y. , EL‐ZIMAITY H. M. T. , OPEKUN A. R. , CAMPOS A. , CHAVEZ A. , GUERRERO L. 
Published: December 2005

SummaryBackground  Antibiotic resistance and duration of therapy influence the success of proton‐pump inhibitor‐containing Helicobacter pylori eradication therapy. Clarithromycin resistance is associated with treatment failure.Aim  To examine the success of a 7‐day rabeprazole‐clarithromycin‐amoxicillin therapy in the study population.Methods  Adults from Ciudad Juarez with H. pylori infections identified by culture or histology received rabeprazole 20 mg, clarithromycin 0.5 g and amoxicillin 1 g, each b.d. for 7 days. Outcome was assessed by 13C‐urea breath test carried out 4+ weeks after treatment.Results  A total of 111 patients were enrolled and evaluated by urea breath test; 102 completed the full 7 days therapy. Two deviated from protocol, and five stopped because of adverse events. The cure rate (intention‐to‐treat) was 85% (95% CI: 78–91%); the per‐protocol cure rate was 85% (95% CI: 78–91%). Side‐effects were not serious and only 6.6% of those with adverse events stopped medication. Only three isolates were clarithromycin‐resistant and none was cured. Compliance explained most of the successes.Conclusions  In the study population a 7‐day rabeprazole triple eradication therapy was both effective and well‐tolerated. Clarithromycin resistance was uncommon. We observed a slightly better outcome but consistent with results from recent large studies in US populations.
Oral administration of pulverized Konjac glucomannan prevents the increase of plasma immunoglobulin E and immunoglobulin G levels induced by the injection of syngeneic keratinocyte extracts in BALB/c mice
Authors: Oomizu S. , Onishi N. , Suzuki H. , Ueda K. , Mochizuki M. , Morimoto K. , Kawamoto S. , Ono K. , Kameyoshi Y. , Hide M. 
Published: December 2005

SummaryBackground
Immunoglobulin (Ig) E plays a key role in the pathogenesis of atopic diseases, such as asthma, atopic dermatitis and allergic rhinitis. Oral administration of pulverized Konjac glucomannan (PKGM) has recently been demonstrated to prevent both plasma IgE elevation and developing dermatitis in NC/Nga mice, a model of atopic dermatitis.Objective
To clarify the direct effect of PKGM on the increase of plasma IgE, we employed the system of BALB/c mouse that increases IgE level without developing dermatitis in response to continuous injection of the extract of syngeneic keratinocytes, PAM 212 cells (PAM extract).Methods
Three weeks after the start of feeding with either control or PKGM diet, mice were injected subcutaneously with PAM extract bi‐weekly for 10 weeks. The levels of plasma Igs were measured by enzyme‐linked immunosorbent assay every 2 weeks after the injection. The levels of ɛ germline transcription and the amounts of mRNA for IL‐4, IFN‐γ, GATA‐3 and T bet gene in the spleen were evaluated by real‐time RT‐PCR at the end of the experiment.Results
On the one hand, PKGM prevented the increase of plasma IgE and IgG (IgG1, IgG2b) induced by PAM extract, and on the other hand, it enhanced the levels of plasma IgG3. However, it did not affect the level of plasma IgM. PKGM also reduced the levels of plasma ovalbumin (OVA)‐specific IgE in OVA‐sensitized mice. Moreover, PKGM attenuated the induction of ɛ germline transcription and expression levels of mRNA for IL‐4, IFN‐γ and GATA‐3 in the spleen of PAM extract‐injected mice. PKGM also attenuated the induction of ɛ germline transcription and mRNA for IFN‐γ and T bet in the spleen of phosphate‐buffered saline‐injected control mice.Conclusions
These results suggested that oral administration of PKGM prevents the elevation of plasma IgE by suppressing IgE class switching in B cells and/or the commitment development of naive lymphocytes to both T‐helper type 1 (Th1) and Th2.
Anti‐tumor necrosis factor‐α antibody treatment reduces pulmonary inflammation and methacholine hyper‐responsiveness in a murine asthma model induced by house dust
Authors: Kim J. , McKinley L. , Natarajan S. , Bolgos G.L. , Siddiqui J. , Copeland S. , Remick D. G. 
Published: December 2005

SummaryBackground/Aims
Recent studies documented that sensitization and exposure to cockroach allergens significantly increase children's asthma morbidity as well as severity, especially among inner city children. TNF‐α has been postulated to be a critical mediator directly contributing to the bronchopulmonary inflammation and airway hyper‐responsiveness in asthma. This study investigated whether an anti‐TNF‐α antibody would inhibit pulmonary inflammation and methacholine (Mch) hyper‐responsiveness in a mouse model of asthma induced by a house dust extract containing both endotoxin and cockroach allergens.Methods
A house dust sample was extracted with phosphate‐buffered saline and then used for immunization and two additional pulmonary challenges of BALB/c mice. Mice were treated with an intravenous injection of anti‐TNF‐α antibody or control antibody 1  h before each pulmonary challenge.Results
In a kinetic study, TNF‐α levels within the bronchoalveolar lavage (BAL) fluid increased quickly peaking at 2 h while BAL levels of IL‐4, IL‐5, and IL‐13 peaked at later time‐points. Mch hyper‐responsiveness was measured 24 h after the last challenge, and mice were killed 24 h later. TNF inhibition resulted in an augmentation of these Th2 cytokines. However, the allergic pulmonary inflammation was significantly reduced by anti‐TNF‐α antibody treatment as demonstrated by a substantial reduction in the number of BAL eosinophils, lymphocytes, macrophages, and neutrophils compared with rat IgG‐treated mice. Mch hyper‐responsiveness was also significantly reduced in anti‐TNF‐α antibody‐treated mice and the pulmonary histology was also significantly improved. Inhibition of TNF significantly reduced eotaxin levels within the lung, suggesting a potential mechanism for the beneficial effects.These data indicate that anti‐TNF‐α antibody can reduce the inflammation and pathophysiology of asthma in a murine model of asthma induced by a house dust extract.
Mycobacterium tuberculosis infection may protect against allergy in a tuberculosis endemic area
Authors: Obihara C. C. , Kimpen J. L. L. , Gie R. P. , van Lill S. W. , Hoekstra M. O. , Marais B. J. , Schaaf H. S. , Lawrence K. , Potter P. C. , Bateman E. D. , Lombard C. J. , Beyers N. 
Published: December 2005

SummaryBackground
Epidemiological studies have shown an inverse relation of mycobacterial infection and the frequency of allergic diseases and asthma. Recent evidence suggests that allergic inflammation may be inhibited in the presence of chronic and persistent infections, such as that by Mycobacterium tuberculosis (MTB). The relation of tuberculin skin test (TST) size, an accepted marker of MTB infection and the frequency of allergic disease symptoms has not been reported from an area where MTB infection is endemic.Objective
To investigate the association of TST and allergic disease symptoms, in children living in a tuberculosis (TB) endemic area.Methods
In this cross‐sectional study, 841 children aged 6–14 years from randomly selected household addresses in two poor communities of Cape Town, South Africa, were investigated with TST and standardized International Study on Asthma and Allergies in Childhood‐based questionnaire on allergic disease symptoms.Results
Children with positive TST (10 mm) were significantly less likely to have allergic disease symptoms, in particular allergic rhinitis (AR) (adjusted odds ratio 0.43; 95% confidence interval 0.24–0.79) than those with negative TST. This association remained significant after adjusting for possible confounders and correcting for the effect of clustering (>1 child per household address) in the sample. There was a significant inverse linear trend in the relation of TST size in millimetre and the frequency of allergic disease symptoms, in particular AR (P<0.001).Conclusions
These results of inverse association of strong TST reaction and allergic disease symptoms in children from a TB endemic area are in support of the hypotheses that allergic inflammation may be inhibited by chronic infections, such as MTB.
Stronger nasal responsiveness to cold air in individuals with rhinitis and asthma, compared with rhinitis alone
Authors: Hanes L. S. , Issa E. , Proud D. , Togias A. 
Published: December 2005

SummaryBackground
We have previously proposed that, compared with rhinitis alone, theconstellation of upper and lower airway allergic disease is a manifestation of a more severe form of a syndrome affecting the entire airway. If this is correct, not only the lower, but also the upper airways of patients with asthma and rhinitis should demonstrate more abnormalities compared with patients with rhinitis alone, including higher sensitivity to irritant factors.Objective
To test the hypothesis that, a previously well‐studied natural nasal stimulus, cold, dry air (CDA), produces a stronger response in subjects with allergic rhinitis (AR) and asthma compared with subjects with AR alone.Methods
We performed nasal provocation with CDA on 24 individuals with asthma and rhinitis and 17 with rhinitis alone. Prior to and after the challenge, nasal symptoms were recorded using visual analogue scales and nasal lavages were performed to determine histamine and lysozyme levels.Results
The two groups reacted differently to CDA: after the challenge, patients with rhinitis and asthma reported significantly higher scores for nasal congestion, rhinorrhea and lacrimation. Also in this group, significant increases in histamine and in lysozyme levels in nasal lavage fluids were induced by CDA. In subjects with rhinitis alone, CDA failed to increase histamine or lysozyme levels above baseline. The CDA‐induced change from baseline in histamine was significantly higher in the patients with rhinitis and asthma, compared with the rhinitis‐only group.Conclusion
Patients with AR and asthma have stronger nasal responsiveness to CDA compared with patients with rhinitis alone. This observation is consistent with the notion that compared with rhinitis alone, the presence of asthma and rhinitis signifies a higher degree of functional abnormality of the entire airway.
Effects of steroid treatment on lung CC chemokines, apoptosis and transepithelial cell clearance during development and resolution of allergic airway inflammation
Authors: Uller L. , Lloyd C. M. , Rydell‐Törmänen K. , Persson C. G. A. , Erjefält J. S. 
Published: December 2005

SummaryBackground
Steroid treatment of allergic eosinophilic airway diseases is considered to attenuate cell recruitment by inhibiting several chemokines and to cause eosinophil clearance through inducement of apoptosis of these cells. However, roles of these mechanisms in the actions of steroids in vivo have not been fully established. Also, as regards clearance of tissue eosinophils other mechanisms than apoptosis may operate in vivo.Objective
This study explores anti‐inflammatory effects of steroids instituted during either development or resolution of airway allergic inflammation.Methods
Immunized mice were subjected to week‐long daily allergen challenges (ovalbumin). Steroid treatment was instituted either amidst the challenges or exclusively post‐allergen challenge. CC chemokines, goblet cell hyperplasia, occurrence of eosinophil apoptosis, and airway tissue as well as lumen eosinophilia were examined at different time‐points.Results
Daily steroids instituted amid the allergen challenges non‐selectively attenuated a range of chemokines, permitted egression of tissue eosinophils into airway lumen to increase, and reduced development of lung tissue eosinophilia. Steroid treatment instituted post‐challenge selectively inhibited the CC‐chemokine regulation upon activation, normal T cell expressed and secrted (RANTES), permitted continued egression of eosinophils into airway lumen, and resolved the tissue eosinophilia. Eosinophil apoptosis rarely occurred at development and resolution of the allergic eosinophilic inflammation whether the animals were steroid treated or not. However, anti‐Fas monoclonal antibodies given to mice with established eosinophilia post‐challenge produced apoptosis of the tissue eosinophils indicating that apoptotic eosinophils, if they occur, are well detectible in vivo.Conclusion
Airway tissue eosinophils are likely eliminated through egression into airway lumen with little involvement of apoptosis and phagocytosis. Our data further suggest that therapeutic steroids may resolve airway inflammation by permitting clearance of tissue eosinophils through egression and inhibiting RANTES‐dependent cell recruitment to lung tissues.
Cloning, expression and immunological characterization of full‐length timothy grass pollen allergen Phl p 4, a berberine bridge enzyme‐like protein with homology to celery allergen Api g 5
Authors: DeWitt Å. Marknell , Andersson K. , Peltre G. , Lidholm J. 
Published: December 2005

SummaryBackground
Timothy grass pollen is a common cause of respiratory allergy in the temperate regions. The major group 4 allergen, Phl p 4, has previously been purified and studied biochemically and immunologically, but has so far not been produced and characterized as a recombinant protein.Objective
To clone and characterize timothy grass pollen allergen Phl p 4.Methods
Full‐length Phl p 4 cDNA was cloned using a PCR‐based strategy including 3′‐and 5′‐RACE. Recombinant Phl p 4 was expressed in Escherichia coli and purified by immobilized metal ion affinity chromatography. Its immunological activity was investigated using experimental ImmunoCAP tests, sera from Phl p 4 sensitized individuals and Phl p 4 reactive polyclonal and monoclonal animal antibodies.Results
Five full‐length Phl p 4 cDNA clones were analysed. Sequence deviations between the clones were present at nine amino acid positions, and the consensus sequence comprised an open reading frame of 525 amino acids, including a predicted 25‐residue signal peptide. The calculated molecular weight of the deduced mature protein was 55.6 kDa and the isoelectric point 9.9, both consistent with previously observed properties of purified nPhl p 4. Close sequence similarity was found to genomic clones from several other Pooideae grass species and to Bermuda grass pollen allergen BG60. Further, similarity was found to members of the berberine bridge enzyme (BBE) family, including celery allergen Api g 5. Recombinant Phl p 4 bound specific immunoglobulin (Ig)E from 31 of 32 nPhl p 4‐reactive sera, and the IgE binding to rPhl p 4 could be inhibited by nPhl p 4 in a dose‐dependent manner.Conclusions
Full‐length Phl p 4 cDNA was cloned and showed sequence similarity to members of the BBE family. Recombinant Phl p 4 was produced and shared epitopes with natural Phl p 4.