bluuebunny/crossref_metadata_2025_split huggingface dataset:
Murine models of chronic lymphocytic leukaemia: role of microRNA‐16 in the New Zealand Black mouse model
Authors: Scaglione Brian J. , Salerno Erica , Balan Murugabaskar , Coffman Frederick , Landgraf Pablo , Abbasi Fatima , Kotenko Sergei , Marti Gerald E. , Raveche Elizabeth S. 
Published: October 2007

SummaryMouse models are valuable tools in the study of human chronic lymphocytic leukaemia (CLL). The New Zealand Black (NZB) strain is a naturally occurring model of late‐onset CLL characterized by B‐cell hyperproliferation and autoimmunity early in life, followed by progression to CLL. Other genetically engineered models of CLL that have been developed include (NZB × NZW) F1 mice engineered to expressIL5, mice expressing humanTCL1A, and mice overexpressing bothBCL2and a tumour necrosis factor receptor‐associated factor. The applicability to human CLL varies with each model, suggesting that CLL is a multifactorial disease. Our work with thede novoNZB model has revealed many similarities to the human situation, particularly familial CLL. In NZB, the malignant clones express CD5, zap‐70, and have chromosomal instability and germline Ig sequence. We also identified a point mutation in the 3′‐flanking sequence ofMirn16‐1, which resulted in decreased levels of the microRNA, miR‐16 in lymphoid tissue. Exogenous restoration of miR‐16 to an NZB malignant B‐1 cell line resulted in cell cycle alterations, suggesting that the altered expression ofMirn15a/16‐1is an important molecular lesion in CLL. Future studies utilizing the NZB mouse could ascertain the role of environmental triggers, such as low dose radiation and organic chemicals in the augmentation of a pre‐existing propensity to develop CLL.
The Victoria Climbié case: social work education for practice in children and families' work before and since
Authors: Balen Rachel , Masson Helen 
Published: October 2007

ABSTRACTBased on their research into the Victoria Climbié Inquiry, the authors outline an analysis they undertook of literature which had made substantial comment on either the inquiry itself and/or the subsequent inquiry report. An overview of 18 publications is provided, with four categories of themes emerging. These themes are outlined and then connected with concerns the authors of the current paper identified in journal papers written 10 years or more ago. It is argued that the gap between recognition that society needs competent, well‐trained and skilled social work and other professionals to safeguard the lives of children and families and understanding of what education, training and employment support mechanisms are necessary in order for workers to become and remain well‐trained, skilled and effective, remains as wide as ever. The paper concludes with an outline of teaching approaches the current authors have adopted in pursuit of the kinds of learning opportunities they believe need to be put in place to improve professional practice in children and families' work. These include creative use of child abuse inquiry reports themselves, role plays and simulations and workshops designed to enhance critical reflection skills.
Getting the complete picture: combining parental and child data to identify the barriers to social inclusion for children living in low socio‐economic areas
Authors: Davies B. , Davis E. , Cook K. , Waters E. 
Published: October 2007

AbstractBackground Childhood mental health problems are prevalent in Australian children (14–20%). Social exclusion is a risk factor for mental health problems, whereas being socially included can have protective effects. This study aims to identify the barriers to social inclusion for children aged 9–12 years living in low socio‐economic status (SES) areas, using both child‐report and parent‐report interviews.Methods Australian‐born English‐speaking parents and children aged 9–12 years were sampled from a low SES area to participate in semi‐structured interviews. Parents and children were asked questions around three prominent themes of social exclusion; exclusion from school, social activities and social networks.Results Many children experienced social exclusion at school, from social activities or within social networks. Overall, nine key barriers to social inclusion were identified through parent and child interviews, such as inability to attend school camps and participate in school activities, bullying and being left out, time and transport constraints, financial constraints and safety and traffic concerns. Parents and children often identified different barriers.Discussion There are several barriers to social inclusion for children living in low SES communities, many of which can be used to facilitate mental health promotion programmes. Given that parents and children may report different barriers, it is important to seek both perspectives.Conclusion This study strengthens the evidence base for the investments and action required to bring about the conditions for social inclusion for children living in low SES communities.
The involvement of type 1a angiotensin II receptors in the regulation of airway inflammation in a murine model of allergic asthma
Authors: Ohwada K. , Watanabe K. , Okuyama K. , Ohkawara Y. , Sugaya T. , Takayanagi M. , Ohno I. 
Published: October 2007

SummaryBackgroundThere has been increasing evidence suggesting the involvement of angiotensin II (Ang II) and type 1 Ang II receptors (AT1) in the pathogenesis of bronchial asthma. However, whether such an involvement would promote or suppress the pathophysiology of asthma is controversial.ObjectiveThe aim of this study was to investigate the role of AT1 in the development of allergic airway inflammation.MethodsAgtr1a+/+[wild‐type C57BL/6 mice (WT)] andAgtr1a−/−mice [AT1a knockout mice (AT1aKO)] with a genetic background of C57BL/6 were systemically sensitized to ovalbumin (OVA), followed by OVA inhalation. OVA‐specific IgE in serum obtained just before the inhalation was measured. Bronchoalveolar lavage (BAL) fluid and lung tissues were obtained at various time‐points. Cell numbers and differentiation, and cytokine contents in BAL fluids were determined. Peribronchial accumulation of eosinophils and mucus inclusions in the bronchial epithelium were evaluated in lung tissues stained histochemically. Cell numbers and differentiation in BAL fluids of the mice were also determined after lipopolysaccharide (LPS) inhalation.ResultsThe levels of OVA‐specific IgE in AT1aKO were significantly higher than those in WT. The numbers of total cell, eosinophils and lymphocytes in BAL fluids 7 days after OVA inhalation in AT1aKO were significantly higher than those in WT. Airway inflammation in bronchial tissues in terms of eosinophil accumulation and mucus hypersecretion in AT1aKO was also stronger than in WT. The contents of IL‐4, IL‐5 and IL‐13, but not IFN‐γ, in BAL fluids of AT1aKO were significantly higher than those of WT. In contrast, neutrophil accumulation in BAL fluids after LPS inhalation was significantly higher in WT than in AT1aKO.ConclusionAT1a might be involved in the negative regulation of the development of allergic airway inflammation through polarizing the T‐helper (Th) balance towards Th1 predominance. Therefore, it would be of clinical importance to investigate the effects of long‐term administration of AT1 blockers on the Th1/Th2 balance in hypertensive patients with bronchial asthma.
Relationship of fish and cod oil intake with adult asthma
Authors: Laerum B. N. , Wentzel‐Larsen T. , Gulsvik A. , Omenaas E. , Gíslason T. , Janson C. , Svanes C. 
Published: October 2007

SummaryBackground
A diet rich in fish or cod oil might possibly reduce the risk for asthma and atopic diseases. However, previous studies show conflicting results and no studies have assessed the potential long‐term effects of childhood fish intake on adult asthma.Objective
To investigate whether childhood and adult fish and cod oil intake was related to adult asthma.Methods
In a large population‐based study, Respiratory Health in Northern Europe (RHINE), 16 187 subjects aged 23–54 years answered a postal questionnaire. The relations of fish and cod oil intake with asthma symptoms and asthma were analysed using multiple logistic and Cox regression analyses, with adjustment for gender, adult hayfever, smoking, age, body mass index, household size, dwelling, parental education and centre, and for maternal smoking and family history of hayfever and asthma in a subsample (n=2459).Results
Subjects from Iceland and Norway reported much more frequent intake of fish both in childhood and adulthood as compared with subjects from Sweden, Estonia and Denmark. Current fish intake less than weekly in adults was associated with more asthma symptoms, while more frequent fish intake did not appear to decrease the risk further. No dose–response association was found between childhood fish intake and adult asthma, but those who never ate fish in childhood had an increased risk for asthma and earlier asthma onset. Adult consumption of cod oil had a u‐shaped association with asthma, with the highest risks in those taking cod oil never and daily.Conclusion
A minimum level of weekly fish intake in adulthood was associated with protection against asthma symptoms in this large North‐European multi‐centre study. Subjects who never ate fish in childhood were at an increased risk for asthma. Both indicate a possible threshold effect of fish on asthma.
Skin prick test can identify eczematous infants at risk of asthma and allergic rhinitis
Authors: Lowe A. J. , Hosking C. S. , Bennett C. M. , Carlin J. B. , Abramson M. J. , Hill D. J. , Dharmage S. C. 
Published: October 2007

SummaryBackground
Assessment of allergic sensitization is not routinely performed in infants and young children with eczema.Objective
To determine whether infants who have atopic eczema (with sensitization) are at a greater risk of developing asthma and allergic rhinitis (AR) than those with non‐atopic eczema (without concurrent sensitization).Methods
The presence of eczema was prospectively documented until 2 years of age in a birth cohort of 620 infants with a family history of atopic disease. Sensitization status was determined by skin prick tests (SPTs) at 6, 12, and 24 months using six common allergens. Interviews were conducted at 6 and 7 years to determine the presence of asthma and AR.Results
Within the first 2 years of life, 28.7% of the 443 children who could be classified had atopic eczema: 20.5% had non‐atopic eczema, 19.0% were asymptomatic but sensitized and 31.8% were asymptomatic and not sensitized. When compared with children with non‐atopic eczema in the first 2 years of life, children with atopic eczema had a substantially greater risk of asthma [odds ratio (OR)=3.52, 95% confidence interval=1.88–6.59] and AR (OR=2.91, 1.48–5.71). The increased risk of asthma was even greater if the infant had a large SPT (OR=4.61, 2.34–9.09) indicative of food allergy. There was no strong evidence that children with non‐atopic eczema had an increased risk of asthma or AR compared with asymptomatic children.Conclusion
In children with eczema within the first 2 years of life, SPT can provide valuable information on the risk of childhood asthma and AR.
Residential outdoor air pollution and allergen sensitization in schoolchildren in Oslo, Norway
Authors: Oftedal B. , Brunekreef B. , Nystad W. , Nafstad P. 
Published: October 2007

SummaryBackground
Epidemiological studies that have investigated the association between air pollution and atopy have found inconsistent results. Furthermore, often exposure to outdoor air pollution has had limited quality, and more individual exposure is needed.Objective
To investigate the relations between early and lifetime exposure to residential outdoor air pollution and allergen sensitization in 9–10‐year‐old children in Oslo, Norway.Methods
Sensitization to common allergens was measured by skin prick tests (SPTs), which were performed in 2244 children who had lived in Oslo since birth. Several definitions of positive SPT were used. Information on potential confounding variables was collected by a parental questionnaire. Exposure to outdoor air pollution was assessed by the EPISODE dispersion model, which calculates hourly concentrations of nitrogen dioxide (NO2), particulate matter (PM) with aerodynamic diameter <10 μm (PM10) and <2.5 μm (PM2.5), respectively.Results
We found no associations between long‐term air pollution exposure and sensitization to any allergen, any indoor or any pollen allergen. However, lifetime air pollution exposure was associated with sensitization to the house dust mite Dermatophagoides farinae. One interquartile increase of lifetime exposure to NO2, PM10 and PM2.5 was associated with 1.88 (adjusted odds ratio) (1.02, 3.47) [95% confidence interval (CI)], 1.61 (0.96, 2.72) and 1.46 (0.96, 2.22), respectively, for D. farinae. Lifetime exposure was also associated with sensitization to cat in a subpopulation. Both associations diminished after adjusting for a contextual socio‐economic factor.Conclusion
Long‐term exposure to traffic‐related pollutants was generally not associated with allergen sensitization in 9–10‐year‐old Oslo children. However, lifetime exposure was associated with sensitization to D. farinae, and with sensitization to cat in a subpopulation, which may be explained by socio‐economic confounding or multiple comparisons. The air pollution levels in Oslo may be too low to reveal associations with sensitization.
Increased release of histamine in patients with respiratory symptoms related to perfume
Authors: Elberling J. , Skov P. S. , Mosbech H. , Holst H. , Dirksen A. , Johansen J. D. 
Published: October 2007

SummaryBackground
Environmental perfume exposure may cause respiratory symptoms. Individuals with asthma and perfume contact allergy report such symptoms more frequently than others. However, immunologic mechanisms have not been demonstrated and the symptoms are not associated with IgE‐mediated allergy. The study aimed to investigate whether basophils from patients with respiratory symptoms related to perfume released more histamine in the presence of perfume as compared with healthy volunteers.Methods
Histamine release was measured by the glass fibre method. Blood was obtained from healthy volunteers (n=20) and patients with respiratory symptoms related to perfume (n=17) attending a dermatological outpatient clinic for patch testing. The effect of an international brand perfume was investigated using the basophil histamine release test with perfume. Furthermore, basophils from a healthy non‐atopic donor were incubated with participant's sera and histamine release induced by perfume was measured.Results
In both groups incremental perfume concentrations showed a positive and significant (P<0.001) dose‐response effect on the release of histamine. At the highest perfume concentration, the basophils released significantly (P<0.05) more histamine in patients as compared with healthy volunteers. No difference was found between the groups when sera were incubated with basophils from a healthy non‐atopic donor.Conclusion
Perfume induces a dose‐dependent non‐IgE‐mediated release of histamine from human peripheral blood basophils. Increased basophil reactivity to perfume was found in patients with respiratory symptoms related to perfume.
Human γδ T cells modulate the mite allergen‐specific T‐helper type 2‐skewed immunity
Authors: Korematsu S. , Tanaka Y. , Nagakura T. , Minato N. , Izumi T. 
Published: October 2007

SummaryBackground
γδ T cells have been described as one of immune regulators in patients with infection, malignancy, and allergy.Objective
To elucidate the ability of γδ T cells as an allergen immunotherapy candidate, the effectiveness of human γδ T cells in allergen‐specific T‐helper type 2 (Th2)‐type T cells was evaluated in vitro.Methods
House dust mite‐specific Th2‐type T cell clones, Bacillus Calmette–Guerin (BCG)‐specific Th1‐type T cell clones, and γδ T cell lines were established from the peripheral blood mononuclear cells of two patients with allergic rhinitis. The effectiveness of γδ T cells and BCG‐specific Th1‐type T cell clones in the modulation of allergen‐specific Th2 cells in terms of their cytokine productions was evaluated.Results
In response to cognate antigens, the γδ T cell lines demonstrated a proliferation and production of IFN‐γ that exceeded that of BCG‐specific Th1‐type T cell clones (mean stimulation index: 14.5 vs. 2.8, mean IFN‐γ: 130.5 vs. 10.0 pg/mL). When the γδ T cell lines and mite‐allergen‐specific Th2 clones were co‐cultured with each other, only the levels of IL‐4 (mean, −87%) decreased, but not the levels of IL‐5 and IL‐13, with an increasing concentration of γδ T cell antigen and IFN‐γ production (mean, +730%).Conclusion
These results demonstrated that γδ T cells derived from allergic patients might thus have a partial ability to modulate allergen‐specific Th2‐skewed immunity.
Fibrin formation by wounded bronchial epithelial cell layers in vitro is essential for normal epithelial repair and independent of plasma proteins
Authors: Perrio M. J. , Ewen D. , Trevethick M. A. , Salmon G. P. , Shute J. K. 
Published: October 2007

SummaryBackground
The bronchial epithelium is in contact with, and continually damaged by, the environment. Animal models have indicated that normal epithelial repair is rapid and supported by the formation of a provisional fibrin matrix that is exclusively plasma‐derived.Objectives
Our objectives were to demonstrate the ability of normal human bronchial epithelial (NHBE) cells to produce coagulation cascade proteins and form fibrin in response to damage, independently of plasma proteins, and to show that formation of a cross‐linked fibrin matrix is essential for normal epithelial repair in vitro.Methods
Primary NHBE cells and cells of the 16HBE 14o‐ bronchial epithelial cell line were grown and maintained in vitro prior to mechanical wounding of confluent monolayers in serum‐free media. Tissue factor (TF) and factor XIII (FXIII) were visualized on 16HBE 14o‐ monolayers using immunohistochemistry. The time‐dependent expression of TF, factor VII (FVII), factor X (FX), fibrinogen, soluble fibrin, FXIII subunit A (FXIIIA) and D‐dimers following wounding of confluent 16HBE 14o‐ monolayers was investigated using immunoassays. TF and FVII expression at the mRNA level was investigated by RT‐PCR. The role of coagulation cascade proteins in the repair response of NHBE and 16HBE 14o‐ monolayers was investigated using neutralizing antibodies.Results
Active TF was constitutively expressed in 16HBE 14o‐ cells. Levels of FVII, FX, fibrinogen, soluble fibrin, FXIIIA and D‐dimers in culture supernatants increased rapidly and were maximal 20 min after wounding the monolayers. Expression of TF and FVII mRNA was significantly increased 10 and 4 h, respectively, after wounding. Neutralizing antibodies to TF, fibrinogen and FXIIIA significantly inhibited repair of NHBE and 16HBE 14o‐ cell layers.Conclusions
The bronchial epithelium has the potential to respond rapidly to mechanical damage by forming a cross‐linked fibrin matrix that is essential for normal epithelial repair, independently of plasma proteins.
Differential activation of dendritic cells by nerve growth factor and brain‐derived neurotrophic factor
Authors: Noga O. , Peiser M. , Altenähr M. , Knieling H. , Wanner R. , Hanf G. , Grosse R. , Suttorp N. 
Published: October 2007

SummaryBackground
Neurotrophins are involved in inflammatory reactions influencing several cells in health and disease including allergy and asthma. Dendritic cells (DCs) play a major role in the induction of inflammatory processes with an increasing role in allergic diseases as well.Objective
The aim of this study was to investigate the influence of neurotrophins on DC function.Methods
Monocyte‐derived dendritic cells were generated from allergic and non‐allergic donors. Neurotrophin receptors were demonstrated by western blotting, flow cytometry and fluorescence microscopy. Activation of small GTPases was evaluated by pull‐down assays. DCs were incubated with nerve growth factor (NGF) and brain‐derived neurotrophic factor (BDNF) and supernatants were collected for measurement of IL‐4, IL‐6, IL‐10, IL‐12p70, TNF‐α and TGF‐β.Results
Receptor proteins were detectable by western blot, fluorescence activated cell sorting analysis and fluorescence microscopy. Signalling after neurotrophin stimulation occurred in a ligand‐specific pattern. NGF led to decreased RhoA and increased Rac activation, while BDNF affected RhoA and Rac activity in a reciprocal fashion. Cells of allergics released a significantly increased amount of IL‐6, while for healthy subjects a significantly higher amount of IL‐10 was found.Conclusion
These data indicate that DCs are activated by the neurotrophins NGF and BDNF by different pathways in a receptor‐dependant manner. These cells then may initiate inflammatory responses based on allergic sensitization releasing preferred cytokines inducing tolerance or a T‐helper type 2 response.
A general population from Thailand: incidence of common allergens with emphasis on para‐phenylenediamine
Authors: White J. M. L. , Gilmour N. J. , Jeffries D. , Duangdeeden I. , Kullavanijaya P. , Basketter D. A. , McFadden J. P. 
Published: October 2007

SummaryBackground
Most studies on the prevalence of allergy to the permanent hair dye chemical para‐phenylenediamine (PPD) are reported from populations of eczema patients attending patch‐test clinics, and are assumed to be much higher than in the normal population. No data exist on incidence of senitization to PPD resulting from the use of commercial hair dye preparations over a defined time period.Method
A total of 2545 healthy adult volunteers (Bangkok) were screened for PPD allergy through standard patch testing. Volunteers not allergic to PPD were then recruited into two groups: one group applying a commercial hair dye brand as instructed on a monthly basis for 6 months (n=548) and the other group (controls) (n=516) was instructed not to dye their hair for 6 months. Sensitization to PPD resulting from the use of hair dye over this period was then detected by repeat patch testing.Results
The prevalence of PPD allergy in a normal adult population was 2.7% (m=2.4%, f=3.2%). Projected to the adult Thai population, at least 1 000 000 Thai individuals could be allergic to PPD. The incidence of sensitization through the monthly application of standard commercial hair dye preparations over a 6‐month period was 1.3%, substantially higher than in controls (0.4%), although numbers were small and not statistically significant.Interpretation
There is a higher prevalence of hair dye allergy among the normal population than previously thought. The incidence of new cases of PPD allergy would indicate that current regulations and practice of hair dye exposure lead to PPD sensitization and allergy, which is a public health problem.