bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oral nicorandil‐induced lesions are not aphthous ulcers
Authors: Boulinguez S. , Sommet A. , Bédane C. , Viraben R. , Bonnetblanc J. M. 
Published: August 2003

AbstractObjectives:  (i) To accurately define these lesions determining whether oral nicorandil‐induced lesions are aphthous ulcers; (ii) To determine clinical characteristics of oral nicorandil‐induced lesions.Materials and methods:  Two slide conferences were held. A total of 60 dermatologists assigned diagnosis and clinical criteria to 11 photographs of oral nicorandil‐induced lesions. Two slides were randomly selected and duplicated to be used as control. The panel of slides included independent lesions and photographs of different lesions of the same patient. Statistical analysis used χ2‐test, estimation of the percentage interobserver agreement, and kappa‐values.Results:  The diagnosis of non‐aphthous ulcer (71.8%) was significantly held in comparison with the diagnosis of oral aphthous ulcer (28.2%; P < 0.001). To differentiate aphthous ulcer from non‐aphthous ulcer, physicians significantly used three clinical criteria. The diagnosis of non‐aphthous ulcer were significantly associated with the absence of yellow‐based ulceration (P < 0.001), with the linear shape (P = 0.006) and the absence of inflammatory halo (P = 0.003).Conclusion:  Oral nicorandil‐induced lesions are not aphthous ulcers. We propose that at this stage of our knowledge, oral nicorandil‐induced ulcer is the most suitable terminology.
Expression of vascular endothelial growth factor‐C correlates with the lymphatic microvessel density and the nodal status in oral squamous cell cancer
Authors: Sedivy Roland , Beck‐Mannagetta Johann , Haverkampf C. , Battistutti Walter , Hönigschnabl Selma 
Published: August 2003

AbstractBackground:  The cause of preferential metastatic spreading to cervical lymph nodes in oral squamous cell cancer (SCC) is not quite clear. As the density of microvessels may influence the metastatic behaviour, we were interested in how the density of blood/lymphatic microvessels are related to primary SCC and the clinical course of the disease.Methods:  Lymphatic and blood microvessels of 28 patients with oral SCC were identified immunohistochemically by antibodies against podoplanin and CD34, respectively. Lymphatic microvessel density (LVD) and blood microvessel density (MVD), and the expression of VEGF‐C were determined. These findings were compared with the long‐term clinicopathological data of the patients.Results:  LVD and MVD were significantly higher than in control tissues. The amount of lymphatic microvessels correlated positively with the expression of VEGF‐C, the tumour grade, the nodal status and with later appearing metastasis. The latter three parameters, however, did not influence the clinical course of the disease.Conclusions:  VEGF‐C expression in oral SCC triggers lymphatic angiogenesis, which may result in a higher risk for cervical lymph node metastasis. The angiogenetic effect of VEGF‐C may also favour the onset of late lymphatic and haematogenous metastases.
Multiple primary tumours following head and neck cancer in southern England during 1961–98
Authors: Warnakulasuriya K. A. A. S. , Robinson D. , Evans H. 
Published: August 2003

AbstractBackground:  Successful initial treatment of oral and oro‐phayngeal cancer has led to the emergence of second primary tumours (SPTs). Population data are meagre.Methods:  Occurrence of multiple primary cancers following a malignancy in a head and neck site was computed using data from a population‐based cancer registry covering a population of 14 million.Results:  Among 59,958 subjects reported to the registry, 5.5% males and 3.6% females developed a second primary cancer. At the sites studied, a total of 2771 second primary cancers were found, compared with an expected number of 2341. The standardised incidence ratio (SIR) for contracting a new primary cancer was 1.14 (95% CI = 1.09–1.19) for men and 1.34 (95% CI = 1.24–1.44) for women. There was a significantly increased risk for a second cancer in most of the upper aerodigestive tract sites that are generally regarded as tobacco associated, with an SIR for subsequent oral cancer of 5.56 in men and 15.31 in women. Subjects first detected with a pharyngeal cancer experienced the highest SIR for a subsequent tumour. Excluding tobacco‐associated sites, the risk of a subsequent cancer was not significantly raised in either sex (SIR 0.87 (95% CI 0.81–0.93) for men; SIR 0.99 (95% CI 0.90–1.09) for women).Conclusions:  The relative risk for multiple primary cancer was higher in younger subjects, those detected with a head and neck cancer during the 1990s as compared with earlier decades of the study, and among patients who received radiotherapy for their first tumour. By 20 years from the time of the first head and neck cancer, we estimate that approximately 30% of male patients and 20% of female patients will have developed an SPT.
The biphasic differential expression of the cellular membrane protein, caveolin‐1, in oral carcinogenesis
Authors: Hung Kai‐Feng , Lin Shu‐Chun , Liu Chung‐Ji , Chang Che‐Shoa , Chang Kuo‐Wei , Kao Shou‐Yen 
Published: August 2003

AbstractBackground:  The increased expression of Cav‐1 is seen in various cancers from prostate, esophagus, colon, breast and pancreas yet the information regarding the correlation between the expression of Cav‐1 and oral cancer is blind. Thus, the expression profile of caveolin‐1 (Cav‐1) in oral carcinogenesis and the correlation to the clinicopathologic covariates are examined in this study.Methods:  Immunohistochemistry was used to detect Cav‐1 expression in non‐cancerous matched tissues (NCMT; n = 12), and tissue from normal oral mucosa (NOM; n = 12), oral pre‐cancer lesions (OPL; n= 17), primary oral squamous cell carcinoma (POSCC; n = 47) and metastatic OSCC (MOSCC; n = 8). The Cav‐1 expression was correlated to the age, site, areca use, stage, size, nodal involvement, and differentiation stage. Western blot was used to confirm the specificity of antibody and to follow changes in Cav‐1 expression.Results:  The Cav‐1 immunoreactivity increased significantly from 8% in NOM and 17% in NCMT to 53% in OPL and 79% in POSCC. In addition, lymph node metastasis (LNM) was present in 62% of Cav‐1(+) POSCCs, but only in 10% of Cav‐1(–) POSCCs. Remarkably, only 38% of MOSCCs had Cav‐1 immunoreactivity.Conclusion:  An increased Cav‐1 expression is seen in the stepwise carcinogenesis from NOM, NCMT, OPL to POSCC. The decrease in expression from the POSCC to MOSCC indicates the value to explore its biphasic functions in oral carcinogenesis. Whether Cav‐1 is an important predictor or prognosis for survival still awaits the extension of clinical follow‐up.
Anaphylaxis: risk factors for recurrence
Authors: Mullins R. J. 
Published: August 2003

SummaryBackground  There are few studies on the incidence or recurrence of anaphylaxis.Objective  To examine the incidence of anaphylaxis and risk factors for recurrence.Methods  A prospective study of 432 patients referred to a community‐based specialist practice in the Australian Capital Territory with anaphylaxis, followed by a survey to obtain information on recurrence.Results  Of 432 patients (48% male, 73% atopic, mean 27.4 years, SD 19.5, median 26) with anaphylaxis, 260 patients were seen after their first episode; 172 experienced 584 previous reactions. fifty‐four percent of index episodes were treated in hospital. Aetiology was identified in 91.6% patients: food (61%), stinging insects (20.4%) or medication (8.3%). The minimum occurrence and incidence of new cases of anaphylaxis was estimated at 12.6 and 9.9 episodes/100,000 patient‐years, respectively. Follow‐up data were obtained from 304 patients (674 patient‐years). One hundred and thirty experienced further symptoms (45 serious), 35 required hospitalization and 19 administered adrenaline. Accidental ingestion of peanut/tree nut caused the largest number of relapses, but the highest risk of recurrence was associated with sensitivity to wheat and/or exercise. Rates of overall and serious recurrence were 57 and 10 episodes/100 patient‐years, respectively. Of those prescribed adrenaline, 3/4 carried it, 2/3 were in date, and only 1/2 patients faced with serious symptoms administered adrenaline. Five patients each developed new triggers for anaphylaxis, or re‐presented with significant psychiatric symptoms.Conclusion  In any 1 year, 1/12 patients who have suffered anaphylaxis will experience recurrence, and 1/50 will require hospital treatment or use adrenaline. Compliance with carrying and using adrenaline is poor. Occasional patients develop new triggers or suffer psychiatric morbidity.
Increased expression of surface activation markers on neutrophils following migration into the nasal lumen
Authors: Kinhult J. , Egesten A. , Benson M. , Uddman R. , Cardell L. O. 
Published: August 2003

SummaryBackground  The sequence of events following the recruitment of a free‐flowing neutrophil in the peripheral circulation, via adhesion, migration and release of mediators, to a neutrophil on the surface of the nasal epithelium is a co‐ordinated process. Little is known about the state of neutrophil activation following this course of events.Objectives  To investigate the expression of surface activation markers on neutrophils, reflecting activation during their recruitment to the nose, and to see whether the inflammatory process during allergic rhinitis influences this process.Method  Nine healthy controls and 12 patients with grass pollen‐induced intermittent allergic rhinitis were investigated during the peak of the pollen season. The expression of CD11b, CD66b and CD63 on the neutrophil cell surface, as a reflection of activation, was analysed using flow cytometry. Neutrophils were derived from peripheral blood and nasal lavage fluid. In addition, eosinophil cationic protein (ECP) and myeloperoxidase (MPO) as well as L‐, P‐ and E‐selectins in the nasal lavage fluid were analysed using RIA and ELISA, respectively.Results  A marked increase in the expression of all three CD markers on the neutrophil cell surface was noticed following migration from the bloodstream to the surface of the nasal mucosa. At the peak of the grass pollen season, the MPO levels increased, reflecting an increase in the total number of nasal fluid neutrophils. In parallel, the expression of CD11b was further augmented. The expression of the CDb11b was reduced on neutrophils remaining in the circulation. In addition, the level of L‐selectin was reduced on neutrophils derived from the blood during allergic inflammation.Conclusion  Neutrophils might become activated during their transfer from the blood to the surface of the nasal mucosa, but these changes may also be due to depletion of activated neutrophils in the blood via activated endothelial/epithelial adhesion and chemoattractant measures. The increased expression of surface activation markers during allergic rhinitis suggests roles for neutrophils in the inflammatory process.
Expression of CS‐1 fibronectin precedes monocyte chemoattractant protein‐1 production during elicitation of allergic contact dermatitis
Authors: Martín A. P. , Gagliardi J. , Baena‐Cagnani C. E. , Eberhard Y. , Uguccioni M. , Gallino N. , Mariani A. L. , Serra H. M. 
Published: August 2003

SummaryBackground
Leucocyte migration within inflammatory skin compartments in allergic contact dermatitis (ACD) is the result of a sophisticated multi‐step event where multiple molecules are involved.Objective
Since non‐antigen‐specific mechanisms have been described as an early participant in elicitation of ACD, we investigated the kinetics of the expression of monocyte chemoattractant protein‐1 (MCP‐1/CCL2) and the type of infiltrating cells. We compared the time course production of MCP‐1/CCL2 with connecting segment‐1 (CS‐1) fibronectin and thymus and activation‐regulated chemokine (TARC/ CCL17) expression.Methods
Biopsies from 10 individuals challenged in their back with the antigen responsible for their contact dermatitis and an irrelevant antigen were taken at different times and histology, immunohistochemistry for CS‐1 fibronectin, TARC/CCL17, CD3, CD68, CXCR3, CCR4 and in situ hybridization for MCP‐1/CCL2 were performed.Results
At positive antigen stimulated sites expression of MCP‐1/CCL2 by basal keratinocytes and isolated cells in dermis started at 10 h. CS‐1 fibronectin and TARC/CCL17 expression by blood endothelial cells was found at 2 and 10 h, respectively. This was followed by dermal accumulation of mononuclear cells with a significant increase of CD3+ and CD68+cells. At 48 h, approximately 58% of infiltrating cells were CXCR3+, and 35% CCR4+.Conclusions
We showed evidence of the fact that CS‐1 fibronectin expression precedes the production of MCP‐1/CCL2 and TARC/CCL17 in the skin of patients with ACD, suggesting that these molecules participate in the early complex process of migrating mononuclear cells during elicitation of ACD.
Proteolytic activity of the house dust mite allergen Der p 1 enhances allergenicity in a mouse inhalation model
Authors: Gough L. , Campbell E. , Bayley D. , Van Heeke G. , Shakib F. 
Published: August 2003

SummaryBackground
We have recently demonstrated that intraperitoneal immunization of mice with proteolytically active Der p 1, the major house dust mite allergen, results in a significant and selective enhancement of total and Der p 1‐specific IgE synthesis compared to mice immunized with proteolytically inactive Der p 1.Objective
To investigate whether the proteolytic activity of Der p 1 would lead to enhanced inflammatory cellular infiltration of the lungs and systemic IgE production when administered through the respiratory system, which is the natural route of entry for this allergen.Methods
Groups of mice were initially sensitized with proteolytically active Der p 1 through the intraperitoneal and the subcutaneous routes and subsequently exposed intranasally to either proteolytically active Der p 1, inactive Der p 1 or PBS. The extent of cellular infiltration of the lungs and systemic IgE production in the three animal groups were then compared.Results
Here, we show for the first time that the administration of proteolytically active Der p 1 to mice through the intranasal route leads to significant inflammatory cellular infiltration of the lungs and systemic production of IgE.Conclusions
These data underline the important role of the proteolytic activity of Der p 1 in driving the allergic response in the lungs.
In vitro and in vivo allergenicity of recombinant Bet v 1 compared to the reactivity of natural birch pollen extract
Authors: Tresch S. , Holzmann D. , Baumann S. , Blaser K. , Wüthrich B. , Crameri R. , Schmid‐Grendelmeier P. 
Published: August 2003

SummaryBackground
Diagnostic procedures using natural extracts show only limited quantitative correlation between in vivo and in vitro results. Highly pure recombinant allergens might show more predictive findings.Objective
The aim of this study was to compare natural birch pollen extract (BPE) and recombinant Betula verrucosa (rBet v 1) for their diagnostic value comparing skin prick tests (SPTS) and nasal provocation tests (NPTS) with specific IgE in the serum.Methods
Thirty‐four patients allergic to birch pollen and five healthy controls were investigated. SPT and NPT were performed with BPE and rBet v 1 at different concentrations. Specific serum IgE was measured by the Pharmacia CAP system.ResultsCommercial BPE and rBet v 1 (10 μg/mL) were able to elicit similar allergenic reactions in vivo and IgE binding in vitro. SPT reflects immediate‐type allergy as determined by NPT to a higher degree than specific IgE, for both reagents. To cause allergic reactions in NPT, higher amounts of rBet v 1 were needed than for skin tests and the sensitivity was lower than with BPE.ConclusionrBet v 1 alone is sufficient for a reliable diagnosis of birch pollen allergy in most patients and induces comparable skin test reactivity as BPE, but less allergic reactions in nasal provocations.
Epicutaneous exposure to protein antigen and food allergy
Authors: Hsieh K.‐Y. , Tsai C.‐C. , Herbert Wu C. H. , Lin R.‐H. 
Published: August 2003

SummaryBackground
The aetiology of food allergy remains unclear. Although failure to develop or breakdown in oral tolerance has been proposed, the existence of physiologic sensitization routes other than the gastrointestinal tract cannot be excluded.Objective
The purpose of this study is to clarify whether or not exposure to allergen through the skin can promote food allergy.Methods
BALB/c mice were shaved on the back, and a patch impregnated with 100 μg of ovalbumin (OVA) was applied to the dorsal skin for a 1‐week period and then removed. After three courses of sensitization, OVA‐specific antibodies in sera were measured, and then mice were orally challenged with 50 mg of OVA. Anaphylactic symptoms, plasma histamine levels, and histology of intestines and lungs after oral challenge were examined.Results
Epicutaneous (EC) sensitization of mice to OVA induced a high level of OVA‐specific IgE. Subsequent oral challenge with OVA resulted in symptoms of systemic anaphylaxis with elevated levels of plasma histamine as well as histological changes in both intestines and lungs. In the presence of anti‐IL‐4 antibodies, EC sensitization failed to provoke an IgE response, but still induced a Th2‐predominant cellular immune response in lungs after oral challenge.Conclusion
We demonstrated for the first time that food allergy can be induced by allergen exposure through the skin. Our results identify a novel role of EC sensitization in the pathogenesis of food allergy.
A kinetic study in adults with food hypersensitivity assessed as eosinophil activation in fecal samples
Authors: Magnusson J. , Gellerstedt M. , Ahlstedt S. , Andersson B. , Bengtsson U. , Telemo E. , Hansson T. , Peterson C. G. B. 
Published: August 2003

SummaryBackground
Immune‐mediated food hypersensitivity affecting the gut is difficult to evaluate, and objective tools to diagnose local gastrointestinal (GI) inflammatory reactions are lacking.Objectives
To determine whether allergic manifestations in adults with a history of food‐related GI symptoms could be assessed in feces during symptomatic and non‐symptomatic periods, using the surrogate markers, eosinophil cationic protein (ECP), eosinophil protein X (EPX) and myeloperoxidase (MPO).Methods
Thirteen subjects with food hypersensitivity‐related GI symptoms, confirmed by a positive double‐blind placebo‐controlled food challenge (DBPCFC), were subjected to an open kinetic food challenge design for 6 weeks. Symptoms were recorded and scored during the 3‐week study period and stool samples were obtained every day. The surrogate markers ECP, EPX and MPO were measured in the supernatants from feces samples.Results
A significant increase in abdominal pain, distension and flatulence was observed during challenge, with a gradual decrease during elimination diet. Both between days and subjects, EPX levels were more frequently increased compared to ECP and MPO. Individuals with a history of a short duration of symptoms had significantly higher mean levels of EPX and MPO than those with a longer duration of symptoms.Conclusions
An overall increase in levels of eosinophil markers, in particular EPX, was observed in feces from patients with food‐related GI symptoms. However, rather than being a tool to differentiate symptomatic from non‐symptomatic periods, EPX might be used for detecting an ongoing clinical or subclinical chronic inflammation, that may have an impact on the patient's clinical course of GI symptoms.
Regulation and kinetics of platelet‐activating factor and leukotriene C4 synthesis by activated human basophils
Authors: Lie W. J. , Homburg C. H. E. , Kuijpers T. W. , Knol E. F. , Mul F. P. J. , Roos D. , Tool A. T. J. 
Published: August 2003

SummaryBackground
Allergic disease is the result of an interplay of many different cell types, including basophils and mast cells, in combination with various inflammatory lipid mediators, such as platelet‐activating factor (PAF) and leukotrienes (LT). LTC4 synthesis by human basophils has been studied quite extensively. However, not much is known about the synthesis of PAF by human basophils.Objective
In this study, we have made a comprehensive comparison between the kinetics of PAF and LTC4 synthesis, in highly purified basophils, activated with different stimuli or with combinations of stimuli.Methods
Synthesis of PAF and LTC4 by human basophils was determined with commercially available assay kits. The basophils were activated with C5a, fMLP, PMA, allergen or anti‐IgE, in the absence and presence of IL‐3 and/or in combination with elevation of cytosolic free Ca2+ by the sarcoplasmic reticulum Ca2+‐ATPase inhibitor thapsigargin.Results
Most stimuli were found to induce both PAF and LTC4 synthesis. PAF synthesis and LTC4 release were enhanced by preincubation of the basophils with IL‐3 or by elevation of cytosolic free Ca2+ by thapsigargin. Incubation of human basophils with IL‐3 alone or thapsigargin alone did not result in detectable synthesis of PAF and LTC4, whereas the combination of the two resulted in high amounts of PAF and LTC4 synthesis. Depending on the stimulus used, LTC4 release was 5–100‐fold higher than PAF synthesis. In addition, PAF, but not LTC4, was transiently detected, probably due to PAF degradation.LTC4 and PAF synthesis was strongly blocked by inhibitors of cytosolic phospholipase A2, indicating that this enzyme is involved in PAF and LTC4 synthesis by activated human basophils.Conclusion
This study provides a first comprehensive comparison of PAF and LTC4 synthesis in highly purified human basophils, stimulated with a variety of stimuli.
Activation of mast cells by immunoglobulin E‐receptor cross‐linkage, but not through adenosine receptors, induces A1 expression and promotes survival
Authors: Möller C. , Xiang Z. , Nilsson G. 
Published: August 2003

SummaryBackground
Mast cells are a potent source of mediators that regulate the inflammatory response in allergy and asthma. Mast cells can be activated through different receptors, for example, via cross‐linkage of the high‐affinity IgE receptor (FcɛRI) and by adenosine acting on specific receptors. We have recently described mast cell survival of an IgE receptor activation by up‐regulation of the anti‐apoptotic gene A1.Objective
To compare mast cell survival and expression of A1 after activation through the FcɛRI and by an adenosine agonist.Methods
Bone marrow‐derived, cultured mouse mast cells (BMCMC) were activated either with IgE+antigen or with the adenosine receptor agonist 5′‐N‐ethylcarboxamido adenosine (NECA). Release of β‐hexosaminidase, cell viability, phosphorylation of Akt and IkB‐α, and expression of pro‐survival and pro‐apoptotic genes were measured after activation.Results
Activation of BMCMC with NECA caused the release of β‐hexosaminidase, although to a lesser extent than after FcɛRI activation (33% and 98%, respectively). Activation by both NECA and FcɛRI stimulated phosphorylation of Akt (Ser473 and Thr308) and IkB‐α (Ser32), both of which are implicated in the regulation of cell survival. However, only cells that were activated through FcɛRI, but not by NECA, expressed A1 and exhibited an increased survival rate compared to the control.Conclusion
These results show that adenosine receptor activation of BMCMC does not induce the same survival programme in mast cells as does activation through FcɛRI. These findings may be important for understanding the role that mast cells play in asthma provoked by different stimuli.