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Besides environmental triggers, a family history of asthma is a strong risk factor for the development
of asthma in offspring. The pooled data from 13,963 interviews of randomly selected, 20 to 48 yr-old
participants from the 30 centers of the European Community Respiratory Health Survey (ECRHS)
were analyzed with conventional logistic regression and a Class A regressive model adapted for the
segregation of various transmission modes in families. The asthma prevalence in the interviewed index
generation was 6.9% (95% confidence interval [CI]: 6.5 to 7.3), and in the parent generation was
6.1% (5.8 to 6.4). As with asthma prevalence, the risk of a subject having asthma if a parent had
asthma also had a large geographic variation across the survey centers. The mean risk if a father had
asthma was 2.9 (2.4 to 3.5), and if the mother had asthma was 3.2 (2.6 to 3.9). The risk increased to
7.0 (3.9 to 12.7) if both parents were affected. For developing extrinsic asthma, extrinsic asthma in
any parent was a greater risk factor (4.9 [3.9 to 6.0]) than intrinsic asthma of the parent (1.5 [0.8 to
2.6]), and the risk for women was slightly higher than that for men (4.3 [3.3 to 5.5] versus 3.6 [2.6 to
5.0]). Applying different segregation models, only a model for a two-allele gene with a codominant
inheritance could not be rejected, assuming a major gene with a population frequency of 24.2%. Further
results make a multilocus/threshold model likely. In conclusion, a history of asthma in parents is
a strong risk factor for asthma in the offspring. Under the assumptions of the applied segregation analysis,
at least one major gene exists which could be a gene involved also in allergy. However, asthma is
not fully described by a single-gene model. The risk for asthma varies within the European countries,
and should be seen in the context of a complex genetic and environmental pathophysiology.
Genes for Asthma? An Analysis of the European Community Respiratory Health Survey
The European Community Respiratory Health Survey group : Co ordinating Center of : P. Burney;S. Chinn;C. Luczynska;D. Jarvis;E. L.a.i. Participating Centers: Algeria: N. Ait Khaled;Austria: W. Popp;Australia: M. Abramson, J. Kutin;Belgium: P. Vermeire, F. van Bastelaer;Denmark: R. Dahl, M. Iversen;Estonia: R. Jögi;France: J. Bousquet F. Neukirch;R. Liard I. Pin;C. Pison A. Taytard D. Teculescu;Germany: H. Magnussen, D. Nowak;J. Heinrich, H. E. Wichmann;Greece: N. Papageorgiou;P. Avarlis;M. Gaga;C. Marossis;Iceland: T. Gislason, D. Gislason;India: R. Chowgule;I.r.e.l.a.n.d.:.J. Prichard;S. Allwright;D. MacLeod;Italy: M. Bugiani;BUCCA, Caterina;ROMANO, Canzio;C. Campello A. Marinoni;I. Cerveri;L. Casali;Netherlands: B. Rijcken, A. Kremer;New Zealand: J. Crane, S. Lewis;Norway: A. Gulsvik, E. Omenaas;Portugal: R. Avila;R. Amaral Marques C. Loureiro;C. Chieira;R. Cordeiro J. A. Marques;J. Alves;Spain: J. Anto;J. Castellsague;J. Sunyer;J. Soriano;M. Galobardes;J. Roca N. Muniozguren;J. Ramos González;A. Capelastegui J. Castillo;J. Rodriguez Portal
1997-01-01
Abstract
Besides environmental triggers, a family history of asthma is a strong risk factor for the development
of asthma in offspring. The pooled data from 13,963 interviews of randomly selected, 20 to 48 yr-old
participants from the 30 centers of the European Community Respiratory Health Survey (ECRHS)
were analyzed with conventional logistic regression and a Class A regressive model adapted for the
segregation of various transmission modes in families. The asthma prevalence in the interviewed index
generation was 6.9% (95% confidence interval [CI]: 6.5 to 7.3), and in the parent generation was
6.1% (5.8 to 6.4). As with asthma prevalence, the risk of a subject having asthma if a parent had
asthma also had a large geographic variation across the survey centers. The mean risk if a father had
asthma was 2.9 (2.4 to 3.5), and if the mother had asthma was 3.2 (2.6 to 3.9). The risk increased to
7.0 (3.9 to 12.7) if both parents were affected. For developing extrinsic asthma, extrinsic asthma in
any parent was a greater risk factor (4.9 [3.9 to 6.0]) than intrinsic asthma of the parent (1.5 [0.8 to
2.6]), and the risk for women was slightly higher than that for men (4.3 [3.3 to 5.5] versus 3.6 [2.6 to
5.0]). Applying different segregation models, only a model for a two-allele gene with a codominant
inheritance could not be rejected, assuming a major gene with a population frequency of 24.2%. Further
results make a multilocus/threshold model likely. In conclusion, a history of asthma in parents is
a strong risk factor for asthma in the offspring. Under the assumptions of the applied segregation analysis,
at least one major gene exists which could be a gene involved also in allergy. However, asthma is
not fully described by a single-gene model. The risk for asthma varies within the European countries,
and should be seen in the context of a complex genetic and environmental pathophysiology.
The European Community Respiratory Health Survey (ECRHS) group : Co-ordinating Center of : P. Burney (project leader), S. Chinn, C. Luczynska, D. Jarvis, E. Lai (all London). Participating Centers: Algeria: N. Ait-Khaled (Algiers); Austria: W. Popp (Vienna); Australia: M. Abramson, J. Kutin (Melbourne); Belgium: P. Vermeire, F. van Bastelaer (Antwerp South, Antwerp Central); Denmark: R. Dahl, M. Iversen (Aarhus); Estonia: R. Jögi (Tartu); France: J. Bousquet (Montpellier) F. Neukirch, R. Liard (Paris) I. Pin, C. Pison (Grenoble) A. Taytard (Bordeaux) D. Teculescu (Nancy); Germany: H. Magnussen, D. Nowak (Hamburg); J. Heinrich, H. E. Wichmann (Erfurt); Greece: N. Papageorgiou, P. Avarlis, M. Gaga, C. Marossis (Athens); Iceland:
T. Gislason, D. Gislason (Reykjavik); India: R. Chowgule (Bombay); Ireland:J. Prichard, S. Allwright, D. MacLeod (Dublin, Kilkenny-Wexford); Italy: M. Bugiani, C. Bucca, C. Romano, (Turin) R. de Marco Lo Cascio, C. Campello (Verona) A. Marinoni, I. Cerveri, L. Casali (Pavia); Netherlands: B. Rijcken, A. Kremer
(Groningen, Bergen-op-Zoom, Geleen); New Zealand: J. Crane, S. Lewis (Wellington,Auckland, Christchurch, Hawkes Bay); Norway: A. Gulsvik, E. Omenaas (Bergen); Portugal: R. Avila, R. Amaral Marques (Lisbon) C. Loureiro, C. Chieira, R. Cordeiro (Coimbra) J. A. Marques, J. Alves (Oporto); Spain: J. Anto, J. Castellsague, J. Sunyer, J. Soriano, M. Galobardes, J. Roca (Barcelona) N. Muniozguren, J. Ramos González, A. Capelastegui (Galdakao) J. Castillo, J. Rodriguez Portal
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/124846
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simulazione ASN
Il report seguente simula gli indicatori relativi alla produzione scientifica in relazione alle soglie ASN 2023-2025 del proprio SC/SSD. Si ricorda che il superamento dei valori soglia (almeno 2 su 3) è requisito necessario ma non sufficiente al conseguimento dell'abilitazione.
La simulazione si basa sui dati IRIS e presenta gli indicatori calcolati alla data indicata sul report. Si ricorda che in sede di domanda ASN presso il MIUR gli indicatori saranno invece calcolati a partire dal 1° gennaio rispettivamente del quinto/decimo/quindicesimo anno precedente la scadenza del quadrimestre di presentazione della domanda (art 2 del DM 598/2018).
In questa simulazione pertanto il valore degli indicatori potrà differire da quello conteggiato all’atto della domanda ASN effettuata presso il MIUR a seguito di:
Correzioni imputabili a eventuali periodi di congedo obbligatorio, che in sede di domanda ASN danno diritto a incrementi percentuali dei valori.
Presenza di eventuali errori di catalogazione e/o dati mancanti in IRIS
Variabilità nel tempo dei valori citazionali (per i settori bibliometrici)
Variabilità della finestra temporale considerata in funzione della sessione di domanda ASN a cui si partecipa.
La presente simulazione è stata realizzata sulla base delle regole riportate nel DM 598/2018 e dell'allegata Tabella A e delle specifiche definite all'interno del Focus Group Cineca relativo al modulo IRIS ER. Il Cineca non si assume alcuna responsabilità in merito all'uso che il diretto interessato o terzi faranno della simulazione.