bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinicopathologic analysis of follicular lymphoma occurring in children
Authors: Lorsbach Robert B. , Shay-Seymore Dominic , Moore Jennifer , Banks Peter M. , Hasserjian Robert P. , Sandlund John T. , Behm Frederick G. 
Published: October 2002

AbstractFollicular lymphoma is a rare lymphoid malignancy in pediatric patients and consequently remains poorly characterized, particularly with respect to its immunophenotype and molecular pathogenesis. A total of 23 pediatric patients with follicular lymphoma were identified, with a median age of 11 years and a male-to-female ratio of 2.3:1. Of the 19 patients for whom presenting clinical features were available, 15 patients had stage I, 1 had stage II, and 3 had stage III or IV disease. All tumors had a follicular architecture, and 74% of cases had grade 2 or 3 histologic features. All patients expressed CD20 and bcl-6, and 80% were positive for CD10. Bcl-2 expression was detected in only 5 of 16 cases. Consistent with this finding, bcl-2 gene rearrangements were detected in only 2 of 16 cases by polymerase chain reaction. These patients were treated primarily with cyclophosphamide, doxorubicin, vincristine, and prednisone–based chemotherapy; 4 patients also received involved-field irradiation. Of the 13 patients with available clinical follow-up, all but 2 achieved durable clinical remission. Importantly, all 4 patients with tumors diffusely positive for bcl-2 either presented with stage III/IV disease or had disease refractory to therapy, whereas patients with bcl-2–negative tumors uniformly had stage I disease, achieved complete remission, and experienced no relapses. These findings indicate that, in contrast to adult follicular lymphomas, dysregulated bcl-2 expression does not play a significant pathogenetic role in most pediatric follicular lymphomas. However, bcl-2 expression in pediatric follicular lymphoma identifies a subset of patients in whom disease is often disseminated at clinical presentation and is more refractory to combination chemotherapy.
Increased binding and defective migration across fibronectin of cycling hematopoietic progenitor cells
Authors: Giet Olivier , Van Bockstaele Dirk R. , Di Stefano Ivano , Huygen Sandra , Greimers Roland , Beguin Yves , Gothot André 
Published: October 2002

AbstractEngraftment of hematopoietic progenitor cells has been shown to decrease during cell cycle transit. We studied cell cycle–associated changes in adhesion and migration of mitotically activated cord blood CD34+ cells. Migration toward medium conditioned by the stromal-derived factor-1–producing cell line MS-5 was studied in bovine serum albumin– and fibronectin (Fn)–coated transwells. Migration was reduced in cycling CD34+ cells and long-term culture-initiating cells (LTC-ICs) compared with their noncycling counterparts across Fn but not across bovine serum albumin. Conversely, Fn binding was higher in cycling CD34+ cells and LTC-ICs compared with noncycling progenitor cells, while adhesion of both subsets to bovine serum albumin was undetectable. The contribution of α4 and α5 integrins in mediating adhesion and migration of activated CD34+ cells onto Fn was analyzed by neutralization experiments. While α4-mediated Fn binding decreased during G2/M, α5 integrin–mediated adhesion increased during transit from G0/G1 to S and G2/M phases. As for migration, the contribution of α4 integrin was similar in all phases, whereas α5-directed migration was lower in G2/M compared with G0/G1and S phases. Defective migration of cycling CD34+ cells was not due to differences in α5 integrin expression. In conclusion, chemotaxis across Fn is less efficient in cycling progenitor cells in correlation with an increased Fn binding capacity. In addition, α4 and α5 integrin functions are independently modulated during cell cycle transit.
Long-lasting memory-resting and memory-effector CD4+T cells in human X-linked agammaglobulinemia
Authors: Paroli Marino , Accapezzato Daniele , Francavilla Vittorio , Insalaco Antonella , Plebani Alessandro , Balsano Francesco , Barnaba Vincenzo 
Published: October 2002

AbstractConflicting results obtained from animal studies suggest that B cells play a role in maintaining long-term T-cell memory and in skewing T-cell response toward a T-helper 2 (TH2) phenotype. X-linked agammaglobulinemia (XLA) is a genetic human disease characterized by the lack of circulating B cells due to the mutation of Bruton tyrosine kinase. This disease thus represents a unique model for studying the role of B lymphocytes in regulating T-cell functions in humans. To this aim, we analyzed hepatitis B envelope antigen (HBenvAg)–specific T-cell memory in a series of XLA patients vaccinated against hepatitis B virus (HBV). We found HBenvAg-specific T lymphocytes producing interferon–γ, interleukin-4, or both in the peripheral blood of XLA patients up to at least 24 months after completing the standard anti-HBV immunization protocol. The HBenvAg-specific T-cell frequencies and the percentage of patients with these responses were not significantly different from healthy vaccinated controls. By combining cell purification and enzyme-linked immunospot assay, we found that effector CD27− T cells, which promptly produced cytokines in response to antigen (Ag), and memory-resting CD27+ T cells, which required Ag restimulation to perform their functions, were maintained in both XLA patients and controls for up to 24 months after the last vaccination boost. These data strongly suggest that B cells are not an absolute requirement for the generation of effective T-cell memory in humans, nor do they seem to influence TH1/TH2 balance.
Requirements of src family kinase activity associated with CD45 for myeloma cell proliferation by interleukin-6
Authors: Ishikawa Hideaki , Tsuyama Naohiro , Abroun Saeid , Liu Shangqin , Li Fu-Jun , Taniguchi Osamu , Kawano Michio M. 
Published: October 2002

AbstractSpecific intracellular signals mediated by interleukin-6 (IL-6) receptor complexes, such as signal transducer and activator of transcription 3 (STAT 3) and extracellular signal–regulated kinase (ERK) 1/2, are considered to be responsible for inducing a variety of cellular responses. In multiple myeloma, IL-6 only enhanced the proliferation of CD45+ tumor cells that harbored the IL-6–independent activation of src family kinases even though STAT3 and ERK1/2 could be activated in response to IL-6 in both CD45+ and CD45− cells. Furthermore, the IL-6–induced proliferation of CD45+ U266 myeloma cells was significantly suppressed by Lyn-specific antisense oligodeoxynucleotides or a selective src kinase inhibitor. These results indicate that the activation of both STAT3 and ERK1/2 is not enough for IL-6–induced proliferation of myeloma cell lines that require src family kinase activation independent of IL-6 stimulation. Thus, the activation of the src family kinases associated with CD45 expression is a prerequisite for the proliferation of myeloma cell lines by IL-6. We propose a mechanism for IL-6–induced cell proliferation that is strictly dependent upon the cellular context in myelomas.
Nasal peak inspiratory flow at altitude
Authors: Barry P.W. , Mason N.P. , Richalet J-P. 
Published: October 2002

The present study investigated whether there are changes in nasal peak inspiratory flow (NPIF) during hypobaric hypoxia under controlled environmental conditions.During operation Everest III (COMEX '97), eight subjects ascended to a simulated altitude of 8,848 m in a hypobaric chamber. NPIF was recorded at simulated altitudes of 0 m, 5,000 m and 8,000 m. Oral peak inspiratory and expiratory flow (OPIF, OPEF) were also measured. Ambient air temperature and humidity were controlled.NPIF increased by a mean±sd of 16±12% from sea level to 8,000 m, whereas OPIF increased by 47±14%. NPIF rose by 0.085±0.03 L·s−1per kilometre of ascent (p<0.05), significantly less than the rise in OPIF and OPEF of 0.35±0.10 and 0.33±0.04 L·s−1per kilometre (p<0.0005).Nasal peak inspiratory flow rises with ascent to altitude. The rise in nasal peak inspiratory flow with altitude was far less than oral peak inspiratory flow and less than the predicted rise according to changes in air density. This suggests flow limitation at the nose, and occurs under controlled environmental conditions, refuting the hypothesis that nasal blockage at altitude is due to the inhalation of cold, dry air. Further work is needed to determine if nasal blockage limits activity at altitude.
Occupational asthma in France: a 1-yr report of the Observatoire National de Asthmes Professionnels project
Authors: Kopferschmitt-Kubler M.C. , Ameille J. , Popin E. , Calastreng-Crinquand A. , Vervloet D. , Bayeux-Dunglas M.C. , Pauli G. ,   members of Observatoire National de Asthmes Professionnels Group
Published: October 2002

Observatoire National des Asthmes Professionnels (ONAP) was created in 1996 by two French professional societies to estimate the incidence of occupational asthma and to promote preventive measures against it.Occupational and chest physicians were asked to report newly diagnosed cases of work-related asthma and reactive airway dysfunction syndrome (RADS), the information collected included age, sex, occupation, suspected causal agents and diagnostic methods.In 1997, 82.3% of 559 cases reported (64% males, mean age 36±13 yrs) involved occupational asthma, 4.7% RADS and 12.7% atypical asthma syndromes. Incidence rates (expressed as number of cases per million workers) showed a regional variation that ranged from 4 to 73 (national mean: 25.7). The most frequently suspected agents were flour (23.3%), followed by isocyanates (16.6%), latex (7.5%), aldehydes (5.5%), and persulphates (4.1%). Occupations at risk were bakers (23.9%), healthcare workers (12%), painters (9.1%), hairdressers (5.2%), wood industry workers (4.8%) and cleaners (3.5%). These results are compared to those of other systems set up in Europe and North America.Because of the considerable bias inherent in a surveillance system based on voluntary, reporting, the number of occupational asthma cases reported is probably lower than the real incidence. Nevertheless, the French National Observatory for Occupational Asthma encourages physician awareness of occupational asthma and provides an estimate of its incidence and aetiologies in France.
Evaluation of alveolar surfactant aggregatesin vitroandin vivo
Authors: Brackenbury A.M. , Malloy J.L. , McCaig L.A. , Yao L-J. , Veldhuizen R.A.W. , Lewis J.F. 
Published: October 2002

In acute lung injury, a decrease in surface-active large aggregates and an increase in the less surface-active small surfactant aggregates are observed. The objective of the current study was to determine if the increase in small aggregates interfered with the function of large aggregates, thereby independently contributing to lung dysfunction.Isolated large aggregates, small aggregates, and large aggregate+small aggregate combinations were analysed forin vitrosurface activity utilizing a pulsating bubble surfactometer. Subsequently, large aggregates, small aggregates, and large aggregate+small aggregate combinations were administered to surfactant-deficient, adult Sprague-Dawley rats. Physiological parameters were measured during 1 h of ventilation. After sacrifice, the whole lung lavage was analysed for protein concentration, and surface activity of the recovered large aggregates.The minimum surface tension of the large aggregate+small aggregate preparations (10 mN·m−1) was significantly higher than large aggregates alone (1 mN·m−1), but lower than small aggregates alone (21 mN·m−1) after 100 pulsations.In vivo, rats receiving large aggregates+small aggregates showed immediate increases in oxygenation, similar to animals given large aggregates, whereas animals given small aggregates and control animals maintained low oxygenation values.In conclusion, small aggregates interfered with large aggregates functionin vitro, but this was not observedin vivoin this experimental model.
Effect of hypobaric hypoxia on blood gases in patients with restrictive lung disease
Authors: Christensen C.C. , Ryg M.S. , Kåre Refvem O. , Henning Skjønsberg O. 
Published: October 2002

Several publications have reported effects of hypobaric conditions in patients with chronic obstructive pulmonary disease. To the current authors' knowledge, similar studies concerning patients with restrictive lung disease have not been published.The effect of simulated air travel in a hypobaric chamber on arterial blood gases, blood pressure, and cardiac frequency during rest and 20 W exercise, and the response to supplementary oxygen in 17 patients with chronic restrictive ventilatory impairment has been investigated.Resting oxygen tension in arterial blood (Pa,O2) decreased from 10.4±1.6 kPa at sea level to 6.5±1.1 kPa at 2,438 m simulated altitude, and decreased further during light exercise in all patients (5.1±0.9 kPa).Pa,O2at this altitude correlated positively with sea-levelPa,O2and transfer factor of the lung for carbon monoxide (TL,CO), and negatively with carbon dioxide tension in arterial blood (Pa,CO2).Pa,O2increased to acceptable levels with an O2supply of 2 L·min−1at rest and 4 L·min−1during 20 W exercise.In conclusion, most of the patients with restrictive ventilatory impairment developed hypoxaemia below the recommended levels of in-flight oxygen tension in arterial blood during simulated air travel. Light exercise aggravated the hypoxaemia. Acceptable levels of oxygen tension in arterial blood, with only a minor increase in carbon dioxide tension in arterial blood, were obtained by supplementary oxygen.
Neutrophil degranulation and cell lysis is associated with clinical severity in virus-induced asthma
Authors: Wark P.A.B. , Johnston S.L. , Moric I. , Simpson J.L. , Hensley M.J. , Gibson P.G. 
Published: October 2002

Acute exacerbations of asthma are frequently caused by viral infections, but the inflammatory mechanisms in virus-induced asthma are poorly understood. The aim of the present study was to determine whether viral infection in acute asthma was associated with increased sputum neutrophil degranulation and increased cellular lysis and whether these changes are related to clinical severity.Adults (n=49) presenting to the emergency department with acute asthma were examined for infection by means of sputum direct-fluorescence antigen detection, sputum culture, and sputum polymerase chain reaction for Mycoplasma, Chlamydia andLegionella pneumophila, and all common respiratory viruses. Subjects infected with one of these agents were classed as having an infective exacerbation. Spirometry and sputum induction were performed on presentation and 4–5 weeks later.Thirty-seven subjects (76%) had virus infection and acute asthma. Those with virus infection had increased sputum neutrophils (p<0.05) and increased neutrophil elastase (p<0.05), this was related to increased elevated sputum lactate dehydrogenase (LDH). Subjects with noninfective asthma had an increase in the proportion of sputum eosinophils. Both groups had elevated sputum eosinophil cationic protein (ECP) concentrations. Higher levels of sputum LDH and ECP were associated with a longer hospital stay.Virus infection and acute asthma is associated with neutrophilic inflammation, cell lysis and more severe clinical disease.
Host determinants for the development of allergy in apprentices exposed to laboratory animals
Authors: Gautrin D. , Ghezzo H. , Infante-Rivard C. , Malo J-L. 
Published: October 2002

The aim of this study was to evaluate whether determinants of work-related symptoms, skin sensitization and diseases differ between atopic and nonatopic subjects starting a career with exposure to laboratory animals (LA).A cohort of 417 apprentices in animal-health technology was prospectively followed during 32 or 44 months. The effect on the study outcomes of variables derived from questionnaire, skin reactivity, and lung function assessments at baseline were compared in atopic (n=212) and nonatopic (n=183) subjects.Eighty-five incident cases of sensitization to a LA-derived allergen were identified, 67 among atopic and 18 among nonatopic subjects. Baseline rhinitis symptoms in contact with pets and skin sensitization to pets were associated with the development of work-related rhinoconjunctivitis (RC) symptoms in atopic subjects, whereas perannual rhinitis symptoms and having a PC20(provocative concentration causing a 20% fall in forced expiratory volume in one second) ≤32 mg·mL−1were associated in nonatopic subjects. Baseline rhinitis symptoms on contact with pets and a PC20value ≤32 mg·mL−1were significant determinants for developing sensitization to a specific allergen in atopic subjects only. Finally, baseline rhinitis symptoms in contact with pets and perannual rhinitis symptoms were associated with the development of occupational RC in atopic subjects, whereas in nonatopic subjects this was associated with having a PC20value ≤32 mg·mL−1.In conclusion, the determinants for the development of specific skin sensitization, symptoms and disease are different between atopic and nonatopic apprentices starting occupational exposure to laboratory-animal-derived allergens.
Lymphocyte activation after exposure to swine dust: a role of humoral mediators and phagocytic cells
Authors: Müller-Suur C. , Larsson P.H. , Larsson K. , Grunewald J. 
Published: October 2002

Exposure to swine dust causes intense airway inflammation with multifold increase in inflammatory cells and secretion of pro-inflammatory cytokines. Thisin vitrostudy focuses on the swine-dust activation of lymphocytes in whole blood, in phagocyte-depleted whole blood and in peripheral blood mononuclear cells (PBMC), in order to investigate whether phagocytic cells and/or soluble mediators are involved in the activation of T-cells following exposure to organic dust from a swine confinement house.T-cell activation was analysed by flow cytometry with double staining for CD3 and the activation marker CD69.Swine dust (50 µg) incubated (24 h) with heparinized whole blood was shown to activate 27.6% of the T-cells, while swine dust incubated with whole blood depleted from phagocytic cells or PBMC only activated 4.5% and 4.8% of the T-cells, respectively. Plasma separated from whole blood preincubated with swine dust for 24 h stimulated as much as 32.4% of PBMC T-cells and contained high levels of interleukin (IL)-12 (14 pg·mL) and interferon (IFN)-γ (2284 pg·mL−1), while plasma from PBMC incubated with swine dust contained low levels of IL-12 (2 pg·mL−1) and IFN-γ (196 pg·mL−1).This study demonstrates that activation of T-cells by organic dust from a swine confinement building seems to require phagocytic cells, most likely acting through the release of soluble mediators. Also, conditioned plasma from swine-dust exposed whole blood, which was capable of activating T-cells, contained high concentrations of interleukin-12 and interferon-γ.
Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes
Authors: Jiang B.H. , Maruyama J. , Yokochi A. , Amano H. , Mitani Y. , Maruyama K. 
Published: October 2002

The purpose of the present study was to determine the relationship between hypertensive pulmonary vascular remodelling and the changes in mean pulmonary artery pressure (mPAP) during low-dose nitric oxide (NO) inhalation.Rats were exposed to chronic hypobaric hypoxia (air at 50.5 kPa (380 mmHg), 10% oxygen, for 5–29 days) to induce chronic pulmonary hypertension (PH) with pulmonary vascular structural changes. After the chronic hypoxic exposure, the rats had an indwelling pulmonary artery catheter inserted and changes in mPAP with NO were correlated to morphometrical analysis of pulmonary vascular changes.All concentrations of inhaled NO (0.1–2.0 parts per million) reduced mPAP with a similar per cent reduction from baseline mPAP in PH rats, while no changes were observed in control rats. During NO inhalation in PH rats, the absolute value of the decrease in mPAP, but not per cent reduction in mPAP, significantly correlated with baseline mPAP, the percentage of muscularised arteries at the alveolar wall level and at the alveolar duct level, and the per cent medial wall thickness of muscularised arteries.In the chronic hypoxic pulmonary hypertension model, the severity of pulmonary vascular remodelling did not alter the reactivity of the pulmonary arteries to nitric oxide and might, in part, determine the magnitude of nitric-oxide induced absolute reduction in mean pulmonary artery pressure.
Repeated allergen exposure changes collagen composition in airways of sensitised Brown Norway rats
Authors: Palmans E. , Pauwels R.A. , Kips J.C. 
Published: October 2002

Increased or altered collagen deposition in the airway wall is one of the characteristics of airway remodelling in asthma. The mechanisms underlying this increase, and its functional consequences remain to be established further. Representativein vivoanimal models might be useful in this respect.In the present study, collagen deposition after prolonged allergen exposure was characterised in the airway wall of Brown Norway rats. Sensitised rats were repeatedly exposed to ovalbumin (OA) or phosphate-buffered saline during 2 and 12 weeks.The deposition of collagen type I, III, IV, V and VI was not altered in animals exposed to OA for 2 weeks. After 12 weeks of OA exposure, more collagen type I was deposited in the inner and outer airway wall and more type V and VI collagen was observed in the outer airway wall. At 12 weeks the number of vessels, identifiedviatype IV collagen staining was not increased, but the total vessel area was.In conclusion, prolonged allergen exposure in sensitised rats is associated with enhanced deposition of type I, V and VI collagens and increased vascularity. This suggests that some aspects of airway remodelling in asthma could be driven by long-term allergen exposure.
Pulmonary arterial hypertension and type-I glycogen-storage disease: the serotonin hypothesis
Authors: Humbert M. , Labrune P. , Sitbon O. , Le Gall C. , Callebert J. , Hervé P. , Samuel D. , Machado R. , Trembath R. , Drouet L. , Launay J-M. , Simonneau G. 
Published: October 2002

A case of pulmonary arterial hypertension in a patient with type-Ia glycogen-storage disease, a rare autosomal recessive disorder caused by a deficiency of glucose-6-phosphatase is reported in this study. It has been suggested that the occurrence of pulmonary arterial hypertension in type-Ia glycogen-storage disease could be due to an abnormal production of vasoconstrictive amines such as serotonin.To test this hypothesis, plasma serotonin concentrations were prospectively measured in 13 patients with type-Ia glycogen-storage disease, one patient with severe pulmonary hypertension and type-Ia glycogen-storage disease, 16 patients displaying severe pulmonary arterial hypertension, and 26 normal healthy controls.Elevated plasma serotonin concentrations were found in patients with either severe pulmonary arterial hypertension (38.8±7.3 nmol·L−1) or type-Ia glycogen-storage disease (36.8±11.5 nmol·L−1), as compared with controls (8.8±0.6 nmol·L−1, p<0.001). Plasma serotonin was dramatically elevated in the patient with type-Ia glycogen-storage disease and pulmonary arterial hypertension (113.4 nmol·L−1).It is concluded that type-Ia glycogen-storage disease may be another condition in which abnormal handling of serotonin is one event in a multistep process leading to severe pulmonary arterial hypertension.