bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hemorrhage After Coronary Artery Bypass Graft Procedures
Authors: Herwaldt Loreen A , Swartzendruber Sheri K. , Zimmerman M. Bridget , Scholz David A. , Franklin Jo Ann , Caldarone Christopher A. 
Published: February 2006

AbstractObjectives:To identify risk factors for excessive bleeding after coronary artery bypass graft (CABG) procedures and to quantify the outcomes related to this complication.Design:We conducted a case–control study to identify risk factors for hemorrhage following CABG surgery and a historical cohort study to quantify outcomes of hemorrhage.Setting:The cardiothoracic surgery service of a university hospital.Results:Factors associated with excessive blood loss were recent catheterization (odds ratio [OR] = 0.44; 95% confidence interval [CI95], 0.21 to 0.91); age older than 65 years (OR = 1.94; CI95, 0.96 to 3.93); bypass time of 150 minutes or more (OR = 2.91; CI95, 1.09 to 7.81); and postoperative platelet count of 160,000/mm3 or less (OR = 2.36; CI95, 1.06 to 5.22). The attributable cost of a postoperative hemorrhage was $3,866 (P= .0002) overall, $9,912 (P= .0001) for patients who required reoperation, and $3,316 (P= .03) for those treated medically. The median attributable postoperative length of stay was 1 day longer for cases than for controls (P= .011). Postoperatively, patients who hemorrhaged received significantly larger volumes of packed red blood cells (P< .0001), fresh frozen plasma (P< .0001), platelets (P< .0001), plasminate (P= .007), protamine sulfate (P< .0001), desmopressin acetate (P< .0001), and epsilon-aminocaproic acid (P< .0001) than did controls.Conclusions:Age, duration of bypass, and postoperative platelet count were associated with excessive bleeding. Hemorrhage after CABG surgery significantly increased the length of stay and cost of care.
Resource Utilization Among Patients With Sepsis Syndrome
Authors: Bates David W. , Yu D. Tony , Black Edgar , Sands Kenneth E. , Schwartz J. Sanford , Hibberd Patricia L. , Graman Paul S. , Lanken Paul N. , Kahn Katherine L. , Snydman David R. , Parsonnet Jeffrey , Moore Richard , Platt Richard 
Published: February 2006

AbstractObjective:To assess the resource utilization associated with sepsis syndrome in academic medical centers.Design:Prospective cohort study.Setting:Eight academic, tertiary-care centers.Patients:Stratified random sample of 1,028 adult admissions with sepsis syndrome and all 248,761 other adult admissions between January 1993 and April 1994. The main outcome measures were length of stay (LOS) in total and after onset of sepsis syndrome (post-onset LOS) and total hospital charges.Results:The mean LOS for patients with sepsis was 27.7 ± 0.9 days (median, 20 days), with sepsis onset occurring after a mean of 8.1 ± 0.4 days (median, 3 days). For all patients without sepsis, the LOS was 7.2 ± 0.03 days (median, 4 days). In multiple linear regression models, the mean for patients with sepsis syndrome was 18.2 days, which was 11.0 days longer than the mean for all other patients (P< .0001), whereas the mean difference in total charges was $43,000 (bothP< .0001). These differences were greater for patients with nosocomial as compared with community-acquired sepsis, although the groups were similar after adjusting for pre-onset LOS. Eight independent correlates of increased post-onset LOS and 12 correlates of total charges were identified.Conclusions:These data quantify the resource utilization associated with sepsis syndrome, and demonstrate that resource utilization is high in this group. Additional investigation is required to determine how much of the excess post-onset LOS and charges are attributable to sepsis syndrome rather than the underlying medical conditions.
Autoimmune lymphoproliferative syndrome: molecular basis of disease and clinical phenotype
Authors: Worth Austen , Thrasher Adrian J. , Bobby Gaspar H. 
Published: February 2006

SummaryAutoimmune lymphoproliferative syndrome (ALPS) is a variable clinical condition manifest by lymphoproliferative disease, autoimmune cytopenias and susceptibility to malignancy. Central to the cellular pathogenesis is defective FAS‐induced apoptosis, which in turn leads to dysregulation of lymphocyte homeostasis. The majority of patients have heterozygous mutations in the FAS (TNFRSF6) gene, but the condition is genetically heterogeneous and mutations in FAS ligand and caspase‐8 and caspase‐10, all of which are involved in Fas mediated signalling, have also been identified. This review provides a detailed insight into the pathophysiology of lymphocyte apoptosis and how this relates to the variable and complex clinical manifestations of ALPS.
Effect of glucocorticoids on stem cell factor expression in human asthmatic bronchi
Authors: Da Silva C. A. , de Blay F. , Israel‐Biet D. , Laval A.‐M. , Glasser N. , Pauli G. , Frossard N. 
Published: February 2006

SummaryBackground
Stem cell factor (SCF) is a major mast cell growth factor promoting differentiation, chemotaxis as well as inhibition of apoptosis of mast cells. Regulation of SCF expression by glucocorticoids has not yet been reported in human asthmatic bronchi.Objective
To evaluate SCF mRNA and protein expression in biopsy specimen and bronchoalveolar lavage fluid, respectively, and to determine the mast cell numbers in biopsy sections from control and asthmatic subjects treated or not with glucocorticoids.Methods
Volunteers were recruited out of pollen season. Asthmatic patients were allergic to common allergen extracts including grass and tree pollen, cat, dog or mite; three volunteers had non‐allergic asthma. Mast cell numbers were counted after anti‐human tryptase immunolabelling. SCF mRNA was quantified by real‐time fluorescent PCR (LightCycler™) after reverse transcription, and SCF protein was measured by ELISA.Results
Asthmatic patients not treated with glucocorticoids showed a 5.8‐, 1.8‐ and 3.1‐fold significant increase in SCF mRNA, protein levels and mast cell numbers, respectively, compared with healthy volunteers of the control group (7.8 and 1.3 pg/μg SCF mRNA/GAPDH; 99.8±11.5 and 56.0±11.0 pg/mL SCF protein; 103±21 and 33±8 mast cells/mm2, respectively; P<0.05). In asthmatic patients treated with glucocorticoids, a significant decrease of SCF mRNA, protein levels and mast cell numbers was observed as compared with untreated asthmatic patients (1.1 pg/μg mRNA; 62.0±10.3 pg/mL SCF protein and 39±13 mast cells/mm2; P<0.05), reaching levels comparable to those of the control group.Conclusion
Our study shows that SCF is expressed in the bronchus in humans in vivo. This expression is increased in asthma, and is parallel to the increased mast cell numbers in the airways. Both increases were normalized in glucocorticoid‐treated patients, strongly suggesting an involvement of SCF in the mast cell‐associated asthmatic disease.
Sensitization to Empynase®(pronase B) in exposed hospital personnel and identification of the Empynase® allergen
Authors: Bahn J.‐W. , Lee J.‐Y. , Jang S.‐H. , Kim S.‐H. , Kim H.‐M. , Park H.‐S. 
Published: February 2006

SummaryBackground
Empynase® is a proteolytic enzyme that is widely used as an anti‐inflammatory drug in Korea. We evaluated the prevalence of sensitization to Empynase® in association with respiratory allergy symptoms in exposed hospital personnel, and identified the IgE‐binding components in the Empynase® extract, using sera with high levels of specific IgE antibodies.Methods
A total of 154 hospital personnel (135 nurses and 19 pharmacists) who worked in a university hospital and 123 unexposed healthy control subjects were enrolled. A questionnaire was administered that addressed demographics, job category, history of atopic diseases, diverse symptoms including nasal and lower respiratory symptoms, and the association of symptoms with work. Skin prick tests (SPTs) to common aeroallergens and Empynase® extract were performed. Empynase®‐specific IgE antibody was detected by ELISA, and ELISA inhibition tests were conducted. IgE‐binding components were identified by SDS‐PAGE and IgE immunoblotting.Results
Forty‐two subjects (27.3%) complained of work‐related respiratory symptoms (WRRS). Five nurses (3.7%) and one pharmacist (5.3%) had work‐related asthma symptoms, and 34 nurses (25.2%) and six pharmacists (31.6%) had work‐related rhinitis symptoms. The prevalence of sensitization to Empynase® on SPTs was 20.1%, and tended to be higher in pharmacists (31.6%) than in nurses (18.5%). It was estimated that 3.9–8.4% of hospital personnel had WRRS attributable to Empynase®. The duration of exposure was longer in positive SPT responders than in negative responders (51.9±27.5 vs. 39.2±27.3 months, respectively; P<0.05), and the prevalence of Empynase®‐positive SPTs was significantly higher in subjects with asthma than in those without asthma (57.1% vs. 18.4%, respectively; P<0.05). The levels of Empynase®‐specific IgE antibodies were significantly higher in pharmacists (76.1±83.4 OD units) and nurses (56.3±103.0 OD units) than in normal controls (39.8±12.7 OD units; P<0.05). Seven subjects (two pharmacists and five nurses) had high serum levels of Empynase®‐specific IgE antibodies; six of these subjects had WRRS. ELISA inhibition tests were performed with the sera of these six subjects, revealing significant inhibition only with the addition of Empynase®. Four strongly staining protein bands (sizes: 36, 33, 16, and 10 kDa) from Empynase® extract were observed to bind to the IgE antibodies of sensitized subjects.Conclusion
Exposure to Empynase® powder may cause rhinitis and asthma in hospital personnel, and the pathogenic mechanism appears to be IgE mediated.
Natural and recombinant molecules of the cherry allergen Pru av 2 show diverse structural and B cell characteristics but similar T cell reactivity
Authors: Fuchs H. C. , Bohle B. , Dall'Antonia Y. , Radauer C. , Hoffmann‐Sommergruber K. , Mari A. , Scheiner O. , Keller W. , Breiteneder H. 
Published: February 2006

SummaryBackground
Cherry allergy is often reported in the context of allergy to other fruits of the Rosaceae family and pollinosis to trees because of cross‐reactive allergens. Allergic reactions to cherry are reported by 19–29% of birch pollen‐allergic patients. Pru av 2, identified as a thaumatin‐like protein (TLP) from sweet cherry, was recognized by the majority of cherry‐allergic patients in immunoblotting.Objectives
In order to investigate the structural characteristics and the immunoglobulin (Ig)E‐ and T cell reactivity of cherry‐derived TLP, recombinant Pru av 2 was expressed in Escherichia coli and natural Pru av 2 was purified.Methods
Parallel‐His and FLAG expression vectors were used for recombinant production of Pru av 2 in the cytoplasm and the periplasm of E. coli. Natural Pru av 2 was purified from fresh cherries and verified by N‐terminal sequencing. Structural characterization was performed using circular dichroism (CD) measurements, and the biologic activity was measured in a glucanase assay. Using cherry‐specific sera, the IgE‐binding ability of recombinant and natural Pru av 2 was investigated in IgE‐ELISA and the T cell reactivity was studied in proliferation assays.Results
Natural Pru av 2 revealed thaumatin‐like structural features and bound IgE of 50% of cherry‐allergic patients. It was demonstrated to be enzymatically active. Recombinant Pru av 2 expressed in the cytoplasm of E. coli exhibited a slightly different folding compared with the natural protein. It was not recognized by IgE from cherry‐allergic subjects, but retained the ability to stimulate T lymphocytes. Periplasmic recombinant Pru av 2 was able to bind an anti‐grape TLP antibody and cherry‐specific IgE.Conclusions
We prepared two recombinant model TLPs from cherry, and compared their molecular characteristics as well as their IgE‐binding activity and T cell interactions in relation to the natural counterpart. The cytoplasmic recombinant Pru av 2 can be used as a hypoallergenic variant in allergen‐specific immunotherapy, whereas the periplasmic protein can be included in a component‐resolved diagnosis.
Inhibition of rBet v 1‐induced basophil histamine release with specific immunotherapy ‐induced serum immunoglobulin G: no evidence that FcγRIIB signalling is important
Authors: Ejrnaes A. M. , Svenson M. , Lund G. , Larsen J. N. , Jacobi H. 
Published: February 2006

SummaryBackground
Human basophils and mast cells express the low‐affinity immunoglobulin (Ig)G receptor FcγRIIB. It has previously been shown in artificial model systems that cross‐linking of the high‐affinity IgE receptor FcɛRI and FcγRIIB leads to inhibition of FcɛRI signalling.Objective
The aim of the present study was to investigate whether cross‐linking of FcɛRI and FcγRIIB contributes to IgG‐mediated inhibition of histamine release in human basophils in a system using the sera from specific immunotherapy (SIT) patients and the major allergen from birch pollen, Bet v 1. As IgG4 furthermore has been proposed to have special blocking properties, we investigated the significance of IgG subclass specificity for this inhibition.Methods
Binding of recombinant Bet v 1–IgG complexes to FcγRII and IgG‐binding activities in the sera from 25 birch pollen‐allergic patients treated with SIT were measured using 125I‐rBet v 1. Inhibition of basophil histamine release was assessed by incubating washed leucocytes with complexes of rBet v 1–IgG with or without blocking of FcγRII.Results
We observed low binding of rBet v 1–IgG complexes to FcγRII, which was negatively correlated with the relative IgG4‐binding activities. Blocking of FcγRII did not reverse the SIT–IgG‐induced inhibition of basophil histamine release. However, IgG‐binding activities correlated significantly with the ability of the SIT sera to inhibit basophil histamine release.Conclusion
We suggest that at least in birch pollen SIT, the contribution of FcγRIIB‐mediated inhibitory signalling to SIT–IgG‐induced inhibition of human basophil histamine release is of minor importance. The main contributor to the inhibitory effect of SIT‐induced IgG seems to be blocking of the allergen–IgE interaction.
4‐1BB stimulation inhibits allergen‐specific immunoglobulin E production and airway hyper‐reactivity but partially suppresses bronchial eosinophilic inflammation in a mouse asthma model
Authors: Cho Y. S. , Kwon B. , Lee T.‐H. , Kim T.‐B. , Moon K.‐A. , La S. , Lee J. , Lee S. D. , Oh Y.‐M. , Moon H.‐B. 
Published: February 2006

SummaryBackground
4‐1BB, a member of the tumour necrosis factor receptor superfamily, functions as a co‐stimulatory molecule. Recently, stimulation of the 4‐1BB pathway was shown to suppress antigen‐specific CD4+ T cell and subsequent T cell‐dependent humoral immune responses.Objective
We examined the effect of agonistic anti‐4‐1BB monoclonal antibody (mAb) treatment on allergic asthma, in which allergen‐specific type 2 helper T cells (Th2) have been shown to play an important role.Methods
BALB/c mice were systemically sensitized with intraperitoneal injections of ovalbumin (OVA) and alum on days 0 and 14, and then challenged with inhaled OVA on days 28, 29 and 30. In test groups, the agonistic anti‐4‐1BB mAb was administered at the time of initial systemic sensitization with OVA. On day 31, mice were challenged with inhaled methacholine, and enhanced pause was measured as an index of airway hyper‐responsiveness (AHR). Levels of OVA‐specific IgE in serum, and levels of various cytokines in bronchoalveolar lavage (BAL) fluids were measured. The severity of airway inflammation was determined by differential cell counts in BAL fluids and histopathologic lung analysis. To evaluate local immunity, we cultured lymphocytes from draining perihilar lymph nodes and evaluated the proliferative response to OVA and the levels of IL‐5 in the culture supernatant. In addition, the functional mechanism of 4‐1BB stimulation was evaluated in splenocytes obtained at day 7 after systemic OVA sensitization.Results
We found that treatment with the anti‐4‐1BB mAb significantly decreased AHR and the production of allergen‐specific IgE. Bronchial inflammation, however, had only partially improved and the levels of IL‐4 and IL‐5 in BAL fluids showed only a small degree of reduction compared with the control Ig‐treated mice. Thoracic lymphocytes from anti‐4‐1BB‐treated mice showed significant suppression of OVA‐induced proliferation and IL‐5 production. In anti‐4‐1BB‐treated mice, splenocytes exhibited poor proliferation and marked apoptosis 7 days after systemic OVA challenge.Conclusion
These results suggest that stimulation of the 4‐1BB pathway effectively suppresses some features of allergic asthma, including allergen‐specific IgE production and AHR, through deletion of allergen‐specific Th2 cells. However, we found that bronchial allergic inflammation was not strictly mediated by suppression of the Th2 immune response in this murine model of asthma. Despite these somewhat contradictory effects, intervention in the 4‐1BB pathway might provide a potential novel immunotherapeutic approach for treatment of allergic asthma.
Characterization of glutathione S‐transferase from dust mite, Der p 8 and its immunoglobulin E cross‐reactivity with cockroach glutathione S‐transferase
Authors: Huang C. H. , Liew L. M. , Mah K. W. , Kuo I. C. , Lee B. W. , Chua K. Y. 
Published: February 2006

SummaryBackground
Sensitization to mite and cockroach allergens is common, and diagnosis and therapy of allergy can be further complicated by the presence of allergen isoforms and panallergens. Purified recombinant and native allergens are useful for studies to resolve such problems.Objective
To assess the allergenicity of native and recombinant mite glutathione S‐transferase (GST) (Der p 8) and study the IgE cross‐reactivity between Der p 8 and cockroach GST.Methods
Der p 8 cDNA encoding a new isoform was isolated and expressed in yeast. Native Der p 8 was affinity purified from mite extract. IgE reactivity to native and recombinant Der p 8 was assessed by ELISA using sera from allergic subjects from Taiwan, Singapore and Malaysia. IgE cross‐reactivity between Der p 8 and cockroach GST was examined by IgE inhibition assays.Results
Our Der p 8 cDNA encoded a basic isoform (pI=8.5) containing six polymorphic residues located at positions 46, 106, 149, 160, 167 and 184. At least 8 isoforms of native Der p 8 were detected by two‐dimensionalgel and immunoblot analyses. Sera from Taiwanese asthmatics showed 96% and 84% IgE reactivity to native Der p 8 and recombinant Der p 8, respectively. Native Der p 8 showed 75% and 65% IgE reactivity with sera from Malaysia and Singapore, respectively.Conclusions
A high frequency of sensitization to mite GST among allergic subjects was observed but the titres of IgE reactivity were low. The IgE cross‐reactivity between mite and cockroach GST suggests that GST is a panallergen.
Intranasal steroid reduces exhaled bronchial cysteinyl leukotrienes in allergic patients
Authors: Failla M. , Biondi G. , Provvidenza Pistorio M. , Gili E. , Mastruzzo C. , Vancheri C. , Crimi N. 
Published: February 2006

SummaryBackground
Allergic rhinitis (AR) precedes and is often associated with bronchial asthma. Indeed, local and systemic inflammations in both conditions are very similar. Cysteinyl‐leukotrienes (cys‐LTs) are generated during early‐ and late‐phase allergic reactions and induce smooth‐muscle contraction, microvascular leakage, and mucous hypersecretion. Cys‐LTs are detected in exhaled breath condensate (EBC) of asthmatics and regardless of bronchial symptoms, they are also found in EBC of rhinitic patients.Objective
To evaluate cys‐LTs in EBC of allergic patients and to assess the activity of nasal fluticasone propionate (FP) on EBC cys‐LTs levels.Methods
Cys‐LTs coefficient of variation (CV) was evaluated from different EBC in 5 healthy volunteers. Cys‐LTs levels from EBCs in 13 healthy controls and 56 allergic rhinitic (n=31) and rhinitic/asthmatic (n=25) patients were also evaluated at baseline. Subsequently patients were randomized to receive either FP 100 μg/day per nostril or placebo for 2 weeks and then re‐evaluated for EBC cys‐LTs.Results
The CV was 14.12%. EBC cys‐LTs in allergic patients were significantly higher than in healthy subjects (70.9  vs. 20.6 pg/mL (median), P<0.05), while it did not differ between asthmatic/rhinitic and purely rhinitic patients. Treatment significantly reduced cys‐LTs (from 93.6 to 19.9 pg/mL, P<0.001). This effect was evident both in asthmatic/rhinitic and in rhinitic patients.Conclusion
Treatment of AR with FP significantly reduces the levels of cys‐LTs, major noninvasive markers of lower airway inflammation, suggesting that upper and lower airway inflammation is present and should be thus treated as a whole in subjects with AR with and without asthma.
Impaired virus‐induced interferon‐α2 release in adult asthmatic patients
Authors: Gehlhar K. , Bilitewski C. , Reinitz‐Rademacher K. , Rohde G. , Bufe A. 
Published: February 2006

SummaryBackground
Interferon‐α (IFN‐α) not only serves as a first defence line of the immune system against viral attacks but also interacts with T‐helper type 1 (Th1)/ T‐helper type 2 (Th2) regulation and various other cell types like basophils and monocytes, thereby linking innate and acquired immunity. Recently, we demonstrated that children with allergic asthma produced significantly lower amounts of virus‐induced IFN‐α2 compared with healthy children or those with intrinsic asthma.Objective
In this study, we extend our analysis to examine in a cohort study whether IFN‐α2 is also reduced in allergic asthma of adults.Methods
Adults with allergic asthma and healthy controls were prospectively recruited. Blood cultures were stimulated with different viruses (respiratory syncytial virus (RSV), newcastle disease virus (NDV)) and analysed for IFN‐α2 protein release and gene transcription.Results
Virus‐induced IFN‐α2 release from blood cells of allergic asthmatic patients was significantly reduced compared with healthy controls, independent of the virus used (NDVasthma=221±134 pg/mL, NDVhealthy=555±341 pg/mL, P=0.003 and RSVasthma=46±27 pg/mL, RSVhealthy=108±90 pg/mL, P=0.014). Values=mean±standard deviation). It was not influenced by medication, especially cortico‐steroids. IFN‐α2 mRNA expression 5 h after NDV stimulation confirmed the ELISA results and correlated well with release data (r=0.397, P=0.033).Conclusion
Like children, adults with allergic asthma show impaired virus‐induced IFN‐α2 release in whole blood, indicating a systemic phenomenon in patients with bronchial asthma and atopic phenotype. Impaired virus‐induced IFN‐α release could be a marker of inflammation in chronic allergic asthma.
Intensity correction of fluorescent confocal laser scanning microscope images by mean‐weight filtering
Authors: LEE SANG‐CHUL , BAJCSY PETER 
Published: February 2006

SummaryThis paper addresses the problem of intensity correction of fluorescent confocal laser scanning microscope images. Confocal laser scanning microscope images are frequently used in medicine for obtaining 3D information about specimen structures by imaging a set of 2D cross sections and performing 3D volume reconstruction afterwards. However, 2D images acquired from fluorescent confocal laser scanning microscope images demonstrate significant intensity heterogeneity, for example, due to photo‐bleaching and fluorescent attenuation in depth. We developed an intensity heterogeneity correction technique that (a) adjusts the intensity heterogeneity of 2D images, (b) preserves fine structural details and (c) enhances image contrast, by performing spatially adaptive mean‐weight filtering. Our solution is obtained by formulating an optimization problem, followed by filter design and automated selection of filtering parameters. The proposed filtering method is experimentally compared with several existing techniques by using four quality metrics: contrast, intensity heterogeneity (entropy) in a low frequency domain, intensity distortion in a high frequency domain and saturation. Based on our experiments and the four quality metrics, the developed mean‐weight filtering outperforms other intensity correction methods by at least a factor of 1.5 when applied to fluorescent confocal laser scanning microscope images.