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Search Results: 1 - 10 of 13834 matches for " Anna-Carin Enelund "
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The Heterogeneity of Asthma Phenotypes in Children and Young Adults
Bill Hesselmar,Anna-Carin Enelund,Bo Eriksson,Leonid Padyukov,Lars ?. Hanson,Nils ?berg
Journal of Allergy , 2012, DOI: 10.1155/2012/163089
Abstract: Objective. Genetic heterogeneity and risk factor distribution was analyzed in two previously proposed asthma phenotypes. Method. A sample of 412 subjects was investigated at 7-8, 12-13, and 21-22 years of age with questionnaires, skin prick tests, and genetic analysis of IL-4 receptor (IL4R) single-nucleotide polymorphisms. The sample was subdivided in one group with no asthma, and two groups with asthma separated by age of onset of symptoms, namely, early onset asthma (EOA) and late onset asthma (LOA). Risk factors and IL4R markers were analyzed in respect to asthma phenotypes. Results. EOA and LOA groups were both associated with atopy and a maternal history of asthma. Female gender was more common in LOA, whereas childhood eczema, frequent colds in infancy, and a paternal history of asthma were more common in EOA. The AA genotype of rs2057768 and the GG genotype of rs1805010 were more common in LOA, whereas the GG genotype of rs2107356 was less common in EOA. Conclusion. Our data suggest that early and late onset asthma may be of different endotypes and genotypes. 1. Introduction Asthma is a common disease, but it has been questioned if it is one single disease, or a group of asthmatic diseases. Such different “phenotypes” of asthma may vary in response to treatment [1], in prognosis [2], in inflammatory patterns [3], and in susceptibility to environmental exposure [4]. Identifying possible subphenotypes has therefore rendered increasing interest in recent years [5, 6]. But a reliable subgroup classification of asthma (or any other disease) can seldom include only clinical parameters, very often additional biomarkers have to be included [7] in order to find genetic or endotypic differences. In the 1990s, the Tucson group presented data on lung function of infants from a population-based birth-cohort study and they also retrospectively classified preschool wheeze into three subgroups or phenotypes, namely, transient wheeze, early persistent wheeze, and late onset asthma [8]. Interestingly, not only transient wheeze had a characteristic phenotype pattern, there were also differences between the two asthma subgroups, with eczema being more common among children with early persistent wheeze than among children with asthma onset after the age of 3 years. If the noticed difference in the prevalence of eczema in children with early versus late onset of respiratory symptoms is of any phenotypic significance is, however, not known. Our own data reveal that 12-13-year-old children with asthma and eczema differ regarding the interleukin-4 receptor genotype from
Canonical Wnt/β-Catenin Signalling Is Essential for Optic Cup Formation
Anna-Carin H?gglund, Anna Berghard, Leif Carlsson
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081158
Abstract: A multitude of signalling pathways are involved in the process of forming an eye. Here we demonstrate that β-catenin is essential for eye development as inactivation of β-catenin prior to cellular specification in the optic vesicle caused anophthalmia in mice. By achieving this early and tissue-specific β-catenin inactivation we find that retinal pigment epithelium (RPE) commitment was blocked and eye development was arrested prior to optic cup formation due to a loss of canonical Wnt signalling in the dorsal optic vesicle. Thus, these results show that Wnt/β-catenin signalling is required earlier and play a more central role in eye development than previous studies have indicated. In our genetic model system a few RPE cells could escape β-catenin inactivation leading to the formation of a small optic rudiment. The optic rudiment contained several neural retinal cell classes surrounded by an RPE. Unlike the RPE cells, the neural retinal cells could be β-catenin-negative revealing that differentiation of the neural retinal cell classes is β-catenin-independent. Moreover, although dorsoventral patterning is initiated in the mutant optic vesicle, the neural retinal cells in the optic rudiment displayed almost exclusively ventral identity. Thus, β-catenin is required for optic cup formation, commitment to RPE cells and maintenance of dorsal identity of the retina.
Lhx2 Is Required for Patterning and Expansion of a Distinct Progenitor Cell Population Committed to Eye Development
Anna-Carin H?gglund, Lina Dahl, Leif Carlsson
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023387
Abstract: Progenitor cells committed to eye development become specified in the prospective forebrain and develop subsequently into the optic vesicle and the optic cup. The optic vesicle induces formation of the lens placode in surface ectoderm from which the lens develops. Numerous transcription factors are involved in this process, including the eye-field transcription factors. However, many of these transcription factors also regulate the patterning of the anterior neural plate and their specific role in eye development is difficult to discern since eye-committed progenitor cells are poorly defined. By using a specific part of the Lhx2 promoter to regulate Cre recombinase expression in transgenic mice we have been able to define a distinct progenitor cell population in the forebrain solely committed to eye development. Conditional inactivation of Lhx2 in these progenitor cells causes an arrest in eye development at the stage when the optic vesicle induces lens placode formation in the surface ectoderm. The eye-committed progenitor cell population is present in the Lhx2?/? embryonic forebrain suggesting that commitment to eye development is Lhx2-independent. However, re-expression of Lhx2 in Lhx2?/? progenitor cells only promotes development of retinal pigment epithelium cells, indicating that Lhx2 promotes the acquisition of the oligopotent fate of these progenitor cells. This approach also allowed us to identify genes that distinguish Lhx2 function in eye development from that in the forebrain. Thus, we have defined a distinct progenitor cell population in the forebrain committed to eye development and identified genes linked to Lhx2's function in the expansion and patterning of these progenitor cells.
Cyclic Expression of Lhx2 Regulates Hair Formation
Gunilla T?rnqvist equal contributor,Anna Sandberg equal contributor,Anna-Carin H?gglund,Leif Carlsson
PLOS Genetics , 2010, DOI: 10.1371/journal.pgen.1000904
Abstract: Hair is important for thermoregulation, physical protection, sensory activity, seasonal camouflage, and social interactions. Hair is generated in hair follicles (HFs) and, following morphogenesis, HFs undergo cyclic phases of active growth (anagen), regression (catagen), and inactivity (telogen) throughout life. The transcriptional regulation of this process is not well understood. We show that the transcription factor Lhx2 is expressed in cells of the outer root sheath and a subpopulation of matrix cells during both morphogenesis and anagen. As the HFs enter telogen, expression becomes undetectable and reappears prior to initiation of anagen in the secondary hair germ. In contrast to previously published results, we find that Lhx2 is primarily expressed by precursor cells outside of the bulge region where the HF stem cells are located. This developmental, stage- and cell-specific expression suggests that Lhx2 regulates the generation and regeneration of hair. In support of this hypothesis, we show that Lhx2 is required for anagen progression and HF morphogenesis. Moreover, transgenic expression of Lhx2 in postnatal HFs is sufficient to induce anagen. Thus, our results reveal an alternative interpretation of Lhx2 function in HFs compared to previously published results, since Lhx2 is periodically expressed, primarily in precursor cells distinct from those in the bulge region, and is an essential positive regulator of hair formation.
Lhx2 Expression Promotes Self-Renewal of a Distinct Multipotential Hematopoietic Progenitor Cell in Embryonic Stem Cell-Derived Embryoid Bodies
Lina Dahl, Karin Richter, Anna-Carin H?gglund, Leif Carlsson
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002025
Abstract: The molecular mechanisms regulating the expansion of the hematopoietic system including hematopoietic stem cells (HSCs) in the fetal liver during embryonic development are largely unknown. The LIM-homeobox gene Lhx2 is a candidate regulator of fetal hematopoiesis since it is expressed in the fetal liver and Lhx2?/? mice die in utero due to severe anemia. Moreover, expression of Lhx2 in embryonic stem (ES) cell-derived embryoid bodies (EBs) can lead to the generation of HSC-like cell lines. To further define the role of this transcription factor in hematopoietic regulation, we generated ES cell lines that enabled tet-inducible expression of Lhx2. Using this approach we observed that Lhx2 expression synergises with specific signalling pathways, resulting in increased frequency of colony forming cells in developing EB cells. The increase in growth factor-responsive progenitor cells directly correlates to the efficiency in generating HSC-like cell lines, suggesting that Lhx2 expression induce self-renewal of a distinct multipotential hematopoietic progenitor cell in EBs. Signalling via the c-kit tyrosine kinase receptor and the gp130 signal transducer by IL-6 is necessary and sufficient for the Lhx2 induced self-renewal. While inducing self-renewal of multipotential progenitor cells, expression of Lhx2 inhibited proliferation of primitive erythroid precursor cells and interfered with early ES cell commitment, indicating striking lineage specificity of this effect.
Exhaled nitric oxide and urinary EPX levels in infants: a pilot study
Fredrik Carlstedt, Dagmara Lazowska, Carl-Gustaf Bornehag, Anna-Carin Olin, Mikael Hasselgren
Clinical and Molecular Allergy , 2011, DOI: 10.1186/1476-7961-9-8
Abstract: To investigate the feasibility of measuring FeNO and uEPX in infants and their mothers and to determine if any relations between these two variables and environmental factors can be seen in a small sample size. This was conducted as a pilot study for the ongoing Swedish Environmental Longitudinal Mother and child Asthma and allergy study (SELMA).Consecutive infants between two and six months old and their mothers at children's health care centres were invited, and 110 mother-infant pairs participated. FeNO and uEPX were analysed in both mothers and infants. FeNO was analyzed in the mothers online by the use of the handheld Niox Mino device and in the infants offline from exhaled air sampled during tidal breathing. A 33-question multiple-choice questionnaire that dealt with symptoms of allergic disease, heredity, and housing characteristics was used.FeNO levels were reduced in infants with a history of upper respiratory symptoms during the previous two weeks (p < 0.002). There was a trend towards higher FeNO levels in infants with windowpane condensation in the home (p < 0.05). There was no association between uEPX in the infants and the other studied variables.The use of uEPX as a marker of early inflammation was not supported. FeNO levels in infants were associated to windowpane condensation. Measuring FeNO by the present method may be an interesting way of evaluating early airway inflammation. In a major population study, however, the method is difficult to use, for practical reasons.Asthma and allergic diseases in children are important public health problems, but they are not fully understood from an aetiological point of view. Allergic diseases usually start in early childhood with food allergies and atopic dermatitis, followed by asthma and rhinitis. These conditions are usually diagnosed in a clinical setting when they are manifest. However, there is a strong need for early and objective markers of preclinical disease, as eosinophilic inflammation, both in cl
Subjects in a Population Study with High Levels of FENO Have Associated Eosinophil Airway Inflammation
Gerdt C. Riise,Kjell Torén,Anna-Carin Olin
ISRN Allergy , 2011, DOI: 10.5402/2011/792613
Interaction Effects of Long-Term Air Pollution Exposure and Variants in the GSTP1, GSTT1 and GSTCD Genes on Risk of Acute Myocardial Infarction and Hypertension: A Case-Control Study
Anna Levinsson, Anna-Carin Olin, Lars Modig, Santosh Dahgam, Lena Bj?rck, Annika Rosengren, Fredrik Nyberg
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099043
Abstract: Introduction Experimental and epidemiological studies have reported associations between air pollution exposure, in particular related to vehicle exhaust, and cardiovascular disease. A potential pathophysiological pathway is pollution-induced pulmonary oxidative stress, with secondary systemic inflammation. Genetic polymorphisms in genes implicated in oxidative stress, such as GSTP1, GSTT1 and GSTCD, may contribute to determining individual susceptibility to air pollution as a promoter of coronary vulnerability. Aims We aimed to investigate effects of long-term traffic-related air pollution exposure, as well as variants in GSTP1, GSTT1 and GSTCD, on risk of acute myocardial infarction (AMI) and hypertension. In addition, we studied whether air pollution effects were modified by the investigated genetic variants. Methods Genotype data at 7 single nucleotide polymorphisms (SNPs) in the GSTP1 gene, and one in each of the GSTT1 and GSTCD genes, as well as air pollution exposure estimates, were available for 119 AMI cases and 1310 randomly selected population controls. Population control individuals with systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg or on daily antihypertensive medication were defined as hypertensive (n = 468). Individual air pollution exposure levels were modeled as annual means of NO2 (marker of vehicle exhaust pollutants) using central monitoring data and dispersion models, linking to participants' home addresses. Results Air pollution was significantly associated with risk of AMI: OR 1.78 (95%CI 1.04–3.03) per 10 μg/m3 of long-term NO2 exposure. Three GSTP1 SNPs were significantly associated with hypertension. The effect of air pollution on risk of AMI varied by genotype strata, although the suggested interaction was not significant. We saw no obvious interaction between genetic variants in the GST genes and air pollution exposure for hypertension. Conclusion Air pollution exposure entails an increased risk of AMI, and this risk differed over genotype strata for variants in the GSTP1, GSTT1 and GSTCD genes, albeit not statistically-significantly.
Bronchial Responsiveness Is Related to Increased Exhaled NO (FENO) in Non-Smokers and Decreased FENO in Smokers
Andrei Malinovschi, Christer Janson, Marieann H?gman, Giovanni Rolla, Kjell Torén, Dan Norb?ck, Anna-Carin Olin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035725
Abstract: Rationale Both atopy and smoking are known to be associated with increased bronchial responsiveness. Fraction of nitric oxide (NO) in the exhaled air (FENO), a marker of airways inflammation, is decreased by smoking and increased by atopy. NO has also a physiological bronchodilating and bronchoprotective role. Objectives To investigate how the relation between FENO and bronchial responsiveness is modulated by atopy and smoking habits. Methods Exhaled NO measurements and methacholine challenge were performed in 468 subjects from the random sample of three European Community Respiratory Health Survey II centers: Turin (Italy), Gothenburg and Uppsala (both Sweden). Atopy status was defined by using specific IgE measurements while smoking status was questionnaire-assessed. Main Results Increased bronchial responsiveness was associated with increased FENO levels in non-smokers (p = 0.02) and decreased FENO levels in current smokers (p = 0.03). The negative association between bronchial responsiveness and FENO was seen only in the group smoking less <10 cigarettes/day (p = 0.008). Increased bronchial responsiveness was associated with increased FENO in atopic subjects (p = 0.04) while no significant association was found in non-atopic participants. The reported interaction between FENO and smoking and atopy, respectively were maintained after adjusting for possible confounders (p-values<0.05). Conclusions The present study highlights the interactions of the relationship between FENO and bronchial responsiveness with smoking and atopy, suggesting different mechanisms behind atopy- and smoking-related increases of bronchial responsiveness.
Effects of wood smoke particles from wood-burning stoves on the respiratory health of atopic humans
Ingunn S. Riddervold, Jakob Hjort B?nl?kke, Anna-Carin Olin, Therese Koops Gr?nborg, Vivi Schlünssen, Kristin Skogstrand, David M. Hougaard, Andreas Massling, Torben Sigsgaard
Particle and Fibre Toxicology , 2012, DOI: 10.1186/1743-8977-9-12
Abstract: No statistically significant effect of wood smoke exposure was found for lung function, for FENO, for NAL or for the nasal patency. Limited signs of airway inflammation were found in EBC.In conclusion, short term exposure with wood smoke at a concentration normally found in a residential area with a high density of burning wood stoves causes only mild inflammatory response.
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