knowledge gap in research pdf

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Knowledge Gap: A Panacea for Conducting Research and Theory Building

• P. Alamina , Opudu Derek Okubokeme , +1 author Chijioke
• Published 2020
• Education, Psychology

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Antecedents of employees’ perception and attitude to risks: the experience of egyptian tourism and hospitality industry, 37 references, knowledge gap: history and development.

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A Framework for Rigorously Identifying Research Gaps in Qualitative Literature Reviews

Theory building in the human resource development profession, the elusive definition of knowledge, knowledge strategy: an integrated approach for managing uncertainty, research, research gap and the research problem, development of a framework to identify research gaps from systematic reviews., the general method of theory-building research in applied disciplines, a new perspective on knowledge metaphorical analysis: knowledge as a field, knowledge sharing: a review and directions for future research, related papers.

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Theories and Methods in Knowledge Gap Research

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Study of the knowledge gap focuses on inequalities in social power, the relative disparities in knowledge gain among socioeconomic strata, and the interconnections among information sources, mass media channels, and audience elements of the communication subsystem. This chapter describes four theoretical frameworks for approaching knowledge gap research. Two dimensions are cross-tabulated—the social unit of analysis (individual or collective) and social ontology, or nature of existence (naturally occurring or socially constructed). Each perspective permits scholars to pose questions that the others do not. These explanations are followed by descriptions of analyses of knowledge gap literature, multilevel linkages, causal processes, motivations, and types and measurement of knowledge. An example of a knowledge gap study with testable hypotheses is given. After reviewing these topics, researchers may be encouraged to break new ground.

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European Respiratory Society statement on preschool wheezing disorders: updated definitions, knowledge gaps and proposed future research directions

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Since the publication of the European Respiratory Society (ERS) task force reports on the management of preschool wheezing in 2008 and 2014, a large body of evidence has accumulated suggesting that the clinical phenotypes that were proposed (episodic (viral) wheezing and multiple-trigger wheezing) do not relate to underlying airway pathology and may not help determine response to treatment. Specifically, using clinical phenotypes alone may no longer be appropriate, and new approaches that can be used to inform clinical care are needed for future research. This ERS task force reviewed the literature published after 2008 related to preschool wheezing and has suggested that the criteria used to define wheezing disorders in preschool children should include age of diagnosis (0 to <6 years), confirmation of wheezing on at least one occasion, and more than one episode of wheezing ever. Furthermore, diagnosis and management may be improved by identifying treatable traits, including inflammatory biomarkers (blood eosinophils, aeroallergen sensitisation) associated with type-2 immunity and differential response to inhaled corticosteroids, lung function parameters and airway infection. However, more comprehensive use of biomarkers/treatable traits in predicting the response to treatment requires prospective validation. There is evidence that specific genetic traits may help guide management, but these must be adequately tested. In addition, the task force identified an absence of caregiver-reported outcomes, caregiver/self-management options and features that should prompt specialist referral for this age group. Priorities for future research include a focus on identifying 1) mechanisms driving preschool wheezing; 2) biomarkers of treatable traits and efficacy of interventions in those without allergic sensitisation/eosinophilia; 3) the need to include both objective outcomes and caregiver-reported outcomes in clinical trials; 4) the need for a suitable action plan for children with preschool wheezing; and 5) a definition of severe/difficult-to-treat preschool wheezing.

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Priorities for future research in preschool wheezing include a focus on identifying underlying mechanisms, biomarkers for treatable traits, patient-reported outcomes and suitable action plans https://bit.ly/4dScXGe

• Introduction

Wheezing disorders in children aged <6 years are heterogeneous, incorporating several clinical phenotypes, with distinct underlying pathophysiological mechanisms that result in similar clinical manifestations.

The European Respiratory Society (ERS) published a task force report entitled “Definition, assessment and treatment of wheezing disorders in preschool children: an evidence-based approach” in 2008 [ 1 ]. In 2014, this report was briefly updated [ 2 ]. Both documents proposed a pragmatic approach to classify and manage preschool wheezing based predominantly on the clinical history of symptom patterns. A body of evidence has accumulated since 2008, suggesting that the distinction between the proposed phenotypes of “episodic (viral) wheezing” (children who wheeze intermittently and are well between episodes) and “multiple-trigger wheezing” (children who wheeze both during and outside discrete episodes) is not sufficient to predict the response to therapy. These phenotypes are often not stable over time [ 3 – 5 ] and do not reflect underlying airway pathology [ 6 ]. The use of these phenotypes based solely on the clinical history of symptom patterns to guide treatment decisions, without additional objective tests, may no longer be appropriate. Therefore, new approaches and research are needed to guide clinical practice.

• Scope of the document

This task force aimed to summarise new evidence and gaps in knowledge about the diagnosis and management of preschool wheezing disorders since the last (ERS) task force in 2008 (partially updated in 2014). Given the new evidence, the task force committee 1) proposed revised definitions for preschool wheezing disorders; 2) identified knowledge gaps; and 3) prioritised directions for future research to improve clinical management. This task force did not focus on factors predicting the progression of preschool wheezing to asthma; the aim was to highlight knowledge gaps in management to improve symptom control and prevent wheezing episodes.

The task force agreed on three overarching aims to be addressed ( table 1 ).

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Task force aims and research questions

Subsequently, specific questions were framed to aid the literature search and enable a thorough evaluation of the evidence for each aim. In some cases where very little evidence was available, critical earlier studies were included as directed by the expertise of the task force members. A search of the published literature from 1 January 2008 until 1 December 2023 was performed via two databases (MEDLINE and the Cochrane Library) by using Boolean algorithms described in detail in the supplementary material . The screening and decision around the inclusion of relevant studies was performed by H. Makrinioti and V. Fainardi under the supervision of senior task force members. All task force members declared that they have no conflicts of interest relevant to the subject matter or materials discussed in this document. The relevant methodology, details of databases and composition of the task force are summarised in the supplementary material .

Task force aims and questions

The methodology (including search strategy and inclusion and exclusion criteria) is described in detail in the supplementary methods . The task force summarised the main findings from the literature review for each research question with concluding remarks for that question. Subsequently, based on an overall review of the available evidence, the task force agreed on summary statements and recommendations for future research for each aim.

Aim 1: summarise current definitions for preschool wheezing in clinical guidelines and definitions used in preschool wheezing research studies

Question 1a: what is the age range used to define preschool wheezing.

As described in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flowchart ( supplementary figure 1S ), following the application of the search algorithm, 37 relevant studies were identified.

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Biological pathways in a) peripheral blood and b) nasopharyngeal airway linked to biomarkers ( i.e. eosinophils, immunoglobulin E, type 2 cytokines and fractional exhaled nitric oxide ( F ENO )) for preschool wheeze incidence or severity. IL: interleukin; APC: antigen-presenting cell; Th: T helper cell; IFN: interferon; IRF: IFN regulatory factor; NO: nitric oxide; TLR: toll-like receptor; TSLP: thymic stromal lymphopoietin.

An agreed age range to define “preschool wheezing” is needed to enable consistency in diagnosis and uniform inclusion criteria for research studies. Studies have defined age cut-offs based on practicalities ( e.g. convenience and feasibility), the study aims, planned investigations and country-specific definitions of school entry age. Our literature search confirmed this heterogeneity in age definition in different countries and healthcare systems [ 7 ]. In summary, certain definitions, like that of the Centers for Disease Control and Prevention, align with the “preschool age” category ( i.e. the period between infancy and school age corresponding roughly to 3–5 years old) [ 8 ]. Other publications use the term “preschool” for all ages between birth and school age. The literature review revealed variable age ranges to define “preschool wheezing”, including 0–4 years [ 9 – 11 ], 1–4 years [ 12 , 13 ], 0–5 years [ 14 , 15 ] or 0–6 years [ 16 , 17 ]. The ERS task force on preschool wheezing in 2008 and the current ERS task force defined the cut-off at <6 years [ 1 , 2 ]. The supplementary material describes details of the age ranges used in different studies ( supplementary tables 1S and 3S ). Importantly, to distinguish preschool wheezing from bronchiolitis, the current task force agreed that more than one episode of wheezing was necessary in this age range, and that the term “recurrent preschool wheezing” provided clarity.

Question 1b: how is the presence of wheezing confirmed?

As described in the PRISMA flowchart ( supplementary figure 2S ), following the application of the search algorithm, we identified 30 relevant studies.

Summary statements. T2: type 2; Th: T helper; ICS: inhaled corticosteroid.

Objective confirmation of wheezing can be difficult if the child is not wheezing during consultation. In research studies focusing on preschool wheezing prevalence, wheezing episodes are usually ascertained retrospectively from parental report [ 18 ]. However, parents do not always adequately distinguish wheezing from other respiratory sounds [ 18 – 20 ]. When interviewed about a validated video clip showing wheezing, stridor, snoring and normal breathing, only 38.5% of parents correctly identified wheezing [ 21 ], and when questioned about their understanding of the term “wheezing”, only 31% recognised this condition [ 22 ].

Approaches to determine the presence of wheezing differ according to the type of study. Interventional trials which require wheezing confirmation frequently use “doctor-diagnosed wheezing”, involving a record of objectively confirmed wheezing by a clinician [ 23 – 25 ]. In contrast, large observational studies, which require longitudinal assessments, usually rely predominantly on parental reports. However, one study suggested that up to one-third of parentally reported wheezing could not be objectively confirmed by the doctor, and that children with doctor-confirmed wheezing had poorer lung function compared to those with parentally reported but unconfirmed wheezing [ 20 ]. The frequency of asking parents to report symptoms may also be important [ 26 ]. It is also of note that parental ability to recall wheezing episodes is related to number of wheezing events during the period of recall, timing of the last episode and parental history of asthma [ 27 ].

The prevalence of wheezing estimated from parental questionnaires tends to be higher compared to physician-confirmed wheezing [ 28 ], and a combination of parental report and confirmation in medical records has also been used to investigate preschool wheezing.

These differences in data sources have to be taken into account when making inference from observational studies to intervention trials and clinical practice. Finally, it may be important to consider other symptoms ( e.g. cough, shortness of breath, chest tightness, chest congestion) and not wheezing alone, as the pattern of different coexisting symptoms may better reflect the presence of respiratory disease [ 29 ].

Moving toward objective assessments of wheezing by caregivers, recent studies have described technologies that can be used to detect wheezing. Digital stethoscopes that use artificial intelligence can identify normal breath sounds, crackles and wheezing in children [ 30 , 31 ], even in a home setting [ 32 ]. Some studies have shown good concordance with clinician detection [ 33 ] and high sensitivity and specificity [ 34 , 35 ]. However, larger studies validating use of electronic wheeze detection devices are needed, and very few to date have included change after interventions or longitudinal assessments in large cohorts.

Objective confirmation of wheezing symptoms is helpful for caregivers and clinicians who cannot always confirm the presence of wheezing during the consultation and often rely on parental reports [ 36 , 37 ]. In the context of clinical decision-making, current evidence shows that evidence of objective confirmation of wheezing either during consultation, or from a recording, alongside parental reports can be useful [ 37 ].

Question 1c: which risk factors are currently used in preschool wheezing definitions?

As described in the PRISMA flowchart ( supplementary figure 3S ), following the application of the search algorithm, we identified 60 relevant studies.

Future directions for aim 1: research related to recurrent preschool wheeze phenotypes. T2: type 2; F ENO : fractional exhaled nitric oxide.

As the impact of recurrent preschool wheezing on the healthcare system and caregivers and families is immense, identifying avoidable risk factors for preschool wheezing is important [ 38 ]. Some studies have identified risk factors for specific wheezing phenotypes ( supplementary table 3S ) [ 39 , 40 ]. Broadly, these include behavioural ( e.g. maternal smoking during pregnancy, maternal nutrition), demographic ( e.g. sex, ethnicity, socioeconomic factors), environmental ( e.g. air pollution, climatic variables, respiratory viral infections, allergens) and genetic variables [ 41 – 48 ]. A concise overview of studies describing these risk factors is presented in table 2 , and studies are depicted in detail in supplementary tables 3S and 4S . Genetic risk factors are discussed separately in section 2e.

Summary of studies investigating risk factors for preschool wheezing

Summary of studies investigating biomarkers for preschool wheezing

Before considering any pharmacotherapy (discussed in section 2f), evidence shows that it is important to address relevant risk factors and triggers for recurrent preschool wheezing. For example, there is consistent evidence that passive exposure to tobacco smoke or vaping, indoor and outdoor pollutants and indoor allergens is associated with increased risk of recurrent symptoms and exacerbations [ 78 – 80 ]. Consequently, families are usually advised that exposure to air pollutants and allergens (when there is evidence of allergic sensitisation [ 81 ]) should be avoided where possible.

Question 1d: what are the currently described phenotypes of preschool wheezing?

As described in the PRISMA flowchart ( supplementary figure 1S ), following the application of the search algorithm, we have identified 37 relevant studies.

Various features have been used to group preschool children with wheezing [ 82 ]. These distinctions are mainly based on clinical observations, as follows.

1) Temporal patterns (such as transient early wheezing, disappearing around school-age, or early-onset persistent wheezing, developing in early life and persisting into school-age) [ 8 , 83 , 84 ].

2) Severity (such as mild or severe preschool wheezing); with severity having been defined variably either as severe (potentially life-threatening) attacks resulting in hospitalisation, oxygen need or intensive care unit use (independent of their frequency); or alternatively, as frequency of attacks [ 1 , 39 , 85 ].

3) Trigger factors, distinguishing children who wheeze only when they have an infection (viral or virus-induced wheezing, or wheezy bronchitis), from children who also wheeze between infections (multiple trigger wheezing, chronic wheezing) [ 82 ].

4) Atopy, distinguishing atopic wheezing and nonatopic wheezing [ 83 , 86 , 87 ].

Over the past 15 years, data-driven techniques that group individuals using unbiased approaches have been increasingly used to uncover the temporal patterns of wheezing (recently reviewed in [ 88 ]). Approaches have included latent class analysis [ 83 , 89 – 91 ], cluster analysis [ 92 ], latent trajectory analysis, etc . The classes/clusters identified in such analyses are not observable but latent ( i.e. hidden), and should ideally not be referred to as “phenotypes”. Such approaches are hypothesis-generating, and the results to some extent remain dependent on the study designs, sample size, frequency and timing of data collection [ 26 ], methods and choice of indicator variables used for modelling, and model selection [ 93 ]. Nevertheless, most cohorts have reported similar “phenotypes”, including never-wheezing, early-onset remitting (transient), late-onset wheezing and persistent wheezing [ 26 ]. Ultimately, the important question is whether different wheezing “phenotypes” derived by data-driven methods are underpinned by different mechanisms [ 94 ]. The largest study of this type to date, which used latent class analysis to investigate development of wheezing from birth to adolescence in >15 000 participants in five birth cohorts, recently suggested that genetic associates of different wheeze phenotypes are indeed phenotype-unique [ 48 ], highlighting the potential value of using data-driven analyses for deep phenotyping to disaggregate childhood wheezing, with follow-up genetic/mechanistic studies probing underlying mechanisms of discovered classes/clusters [ 88 ].

Irrespective of the uncertainties related to data-driven methods, one important finding must be emphasised: all clusters/phenotypes of preschool wheezing (including transient) are associated with impaired lung function trajectories from childhood through early adulthood. Since diminished lung function at physiological peak is associated with adverse health outcomes through the life-course, including higher risk of COPD, cardiovascular/cerebrovascular events and premature death of all causes [ 95 ], we have to pursue research to understand mechanisms of all preschool wheeze phenotypes.

Rather than using only the information on presence/absence of wheezing, some studies have used several symptoms assessed cross-sectionally or longitudinally, including measurable traits (such as allergic sensitisation, reversible airways obstruction, bronchial reactivity) [ 96 ]. There are also studies linking biological variables ( i.e. genetic variation) to derived phenotypes [ 47 , 48 , 97 ].

There are ongoing reports describing preschool wheezing phenotypes and their associations with school-age asthma and various risk factors [ 98 ]. However, assessments of their utility for predicting response to treatment (phenotype-based management) has not been reported, highlighting an unmet need of clinical community.

Studies related to aim 1d are tabulated in supplementary table 1S . For clinical practice, in the short-term, it may be more useful to describe preschool wheezing illness using treatable traits that reflect underlying disease processes (such as allergy, airway obstruction, inflammation and infection, or frequency of attacks) [ 99 ], rather than trying to classify patients into discrete groups (distinct phenotypes) of uncertain aetiology [ 100 ].

Question 1e: which objective biomarkers are used to phenotype patients?

As described in the PRISMA flowcharts ( supplementary figures 4S, 5S and 6S ), following the application of three search algorithms, we have identified 51 relevant studies [ 101 ]. This section discusses recent findings to understand the potential utility of objective biomarkers in patient classification.

Future directions for aim 2: research to investigate pathophysiology and mechanisms underpinning preschool wheezing. GWAS: genome-wide association studies.

Biomarkers for recurrent wheezing

Studies have identified biomarkers that may better address the heterogeneity of preschool wheezing, including 1) peripheral blood eosinophilia, 2) aeroallergen sensitisation, 3) fractional exhaled nitric oxide ( F ENO ) and 4) volatile organic compounds (VOCs). It should be noted that currently described biomarkers only help to identify children who are more likely to have type-2 preschool wheezing. Studies describing these biomarkers and their links to preschool wheezing are summarised in table 3 and are described in detail in supplementary tables 3S and 4S . Basic characteristics linking these biomarkers to preschool wheezing are described herein and in figure 1 .

Peripheral blood eosinophilia: although peripheral blood eosinophilia ≥4% has been used as a minor criterion in the Asthma Predictive Index [ 114 ], cut-offs for normal/elevated blood eosinophils are probably different between preschool and school-age children, and the optimal cut-off for elevated blood eosinophils remains uncertain in preschool wheezing [ 115 ]. In addition, data relating blood eosinophils to the number of wheezing episodes and clinical, symptom-based wheezing phenotypes remain inconclusive. For example, elevated blood eosinophil levels have been associated with increased odds of exacerbations in preschoolers with recurrent wheezing, but when stratifying treatment based on peripheral blood eosinophil count, there was no association between eosinophil count and reduction in exacerbations in children with either episodic viral wheeze or multiple-trigger wheeze [ 116 ]. In addition, changes over time and the impact of atopic comorbidities such as eczema on blood eosinophilia as a biomarker for recurrent wheezing are unknown.

The current evidence suggests blood eosinophils are most helpful as a biomarker of response to treatment, whereby elevated eosinophils identify those recurrent preschool wheezers most likely to respond to maintenance inhaled corticosteroids (ICS). This is discussed in more detail in question 2f.

Aeroallergen sensitisation: early-life sensitisation to aeroallergens such as pollen, dust mites and mould spores has been associated with an increased risk of preschool recurrent wheezing [ 16 , 67 , 117 ]. In addition, aeroallergen sensitisation has been identified as a possible biomarker of wheezing persistence and response to treatment. For example, in children enrolled in the Childhood Origins of Asthma study (COAST), early-life aeroallergen sensitisation and an elevated blood eosinophil count were robust predictors of the development of persistent wheezing [ 118 ]. However, recent data suggest that although early-life sensitisation increases the risk of wheezing persistence, >50% of children with infantile-onset atopic wheezing did not develop asthma 10 years later, while up to 40% of those with infantile wheezing and recurrent infections did have asthma at age 10 years [ 98 ].

Like blood eosinophils, data suggest that aeroallergen sensitisation in preschool recurrent wheezing may help to identify children most likely to respond to maintenance ICS (see question 2f).

F ENO : various methods have been used to measure F ENO in preschool children. Due to the lack of subject cooperation, standardisation is limited in this age group and there is high variability in the cut-offs for F ENO in preschool children. In most studies the offline method was used [ 109 , 110 ]. An online tidal breathing method, the single-breath method, allows measurements in natural sleep [ 119 , 120 ] and is performed by forced exhalation in addition to sedated sleep. The standard method with exhalation flows at 50 mL·s −1 is only successful in older preschoolers aged 4–6 years [ 121 , 122 ].

Studies describing associations between elevated F ENO , and preschool wheezing incidence and phenotypes are depicted in table 3 and supplementary table 4S .

Summary of genetic association studies in preschool wheezing

VOCs: analysis of exhaled breath condensate to measure VOCs is feasible and reproducible in young children [ 111 , 112 , 123 ]. It has been shown that a prediction model combining information about inflammatory gene expression, VOCs and airway resistance has increased predictive value for childhood asthma development [ 113 ]. However, limited data to date ( supplementary table 4S ) do not allow firm conclusions about using specific VOCs in preschoolers with recurrent wheezing for diagnosis or to distinguish phenotypes.

Summary statements aim 1

Future directions are presented in figures 2 and 3 .

Definition of preschool wheezing

This task force proposes the following clinical definition for preschool wheezing based on current evidence. The definition incorporates age, wheezing confirmation and wheezing recurrence as follows.

1) Children aged <6 years.

2) Current/prior documented objective confirmation of wheezing.

3) More than one episode of wheezing.

Proposed preschool wheezing phenotyping incorporating objective biomarkers

1) There is preliminary evidence to suggest that assessment of blood eosinophils and/or aeroallergen sensitisation identifies children who will preferentially respond to maintenance ICS in preschool recurrent wheezing.

2) Based on current evidence for the clinical utility of F ENO or VOCs in preschool children, it is not possible to justify their use in a diagnostic definition. Utility of lung function is discussed in question 2a.

3) Although different symptom patterns can be described, such as “infection-induced episodes” or “wheezing during and between episodes”, additional objective tests to define allergic status, eosinophil phenotype, lung function (question 2a) and airway infection (question 2d) may be helpful.

Aim 2: identify current evidence defining the physiology, pathology and mechanisms underpinning preschool wheezing

Question 2a: which lung function tests can be used in preschool children and which tests have been used to define preschool wheeze phenotypes.

As described in the PRISMA flowchart ( supplementary figure 7S ), following the application of the search algorithm, we have identified 99 relevant studies which have been summarised in supplementary tables 5S, 6S and 7S .

Summary of studies describing current treatments in preschool wheezing

Lung function techniques

A diverse range of lung function tests have been reported in preschool children with wheezing ( supplementary tables 5S, 6S and 7S ). The commonest techniques used are impulse oscillometry (IOS) and spirometry. For IOS, several parameters have been measured in preschool children including resistance and reactance [ 124 ]. IOS measures have been used to record changes with exercise [ 122 ], or to measure bronchodilator response [ 125 ] and bronchial provocation tests [ 126 ]. Studies have also reported the use of IOS to assess response to inhaled corticosteroids, as well as lung function trajectory over time [ 124 , 127 ].

Other tests are the forced oscillometry technique (FOT) [ 128 ], resistance interrupter technique [ 129 ], multiple breath washout [ 130 ], plethysmography [ 130 ], raised volume rapid thoracoabdominal compression technique (RVRTC) [ 131 ], tidal breathing flow and dynamics, impedance pneumology [ 132 ] and thoraco-abdominal synchrony.

Compared to healthy children, preschool children with persistent wheezing have reportedly lower infant flow measures such as maximum flow measured at functional residual capacity [ 133 ], higher specific airway resistance (s R aw ) by plethysmography [ 134 ], reduced forced expiratory volume in 0.5 s z-score and forced mid-expiratory flow using forced flow techniques (RVRTC manoeuvre) [ 135 ], higher baseline resistance measured by FOT [ 136 ], higher respiratory resistance at 5–20 Hz [ 137 ], higher respiratory resistance at the end of expiration [ 138 ] and lower spirometry values [ 139 ]. Higher values of Lung Clearance Index (LCI) [ 121 ] and Scond (conducting zone ventilation inhomogeneity) [ 130 ] have been found in studies conducted in preschool children with persistent or multiple trigger wheezing. LCI [ 140 ], plethysmography [ 141 ], spirometry [ 142 ], airway resistance measured by IOS [ 143 ] and s R aw [ 144 ] are significantly distinct among children with preschool wheezing experiencing exacerbations compared to healthy children.

Bronchodilator response has been demonstrated in preschool children with wheezing [ 143 ]. Children with uncontrolled symptoms show less reversibility compared to children with totally/partly controlled symptoms, mainly explained by the fact that young children with severe symptoms require a high dose of salbutamol to obtain/demonstrate airway bronchodilator response [ 144 ]. Although it is still unclear, demonstration of bronchodilator response may be helpful in selecting which wheezy preschool children are likely to benefit from inhaled steroids.

Importantly, it is noted that tests reported are diverse; the populations and ages of those studied differ; the context of the assessments (acute wheezing versus baseline versus bronchial challenge, etc .); and even the measurements reported from studies using the same tests are not consistent. Longitudinal studies ( supplementary tables 5S, 6S and 7S ) from infancy to school age demonstrate that reduced lung function identified in infancy often remains at school age. Consequently, preschool children with recurrent wheezing will be expected to show similar trajectories [ 117 ]. Studies in preschool children have demonstrated that poor lung function may correlate with wheezing (acute or reported recurrence), deteriorate over time with exacerbations [ 117 ] and predict a diagnosis of persistent asthma [ 145 ].

Question 2b: what is known about inflammation (airway and peripheral) and allergic sensitisation in preschool wheezing?

As described in the PRISMA flowchart ( supplementary figure 8S ), following the application of the search algorithm, we have identified 21 relevant studies.

Difficulties obtaining lower airway samples from preschool children mean very few direct assessments of inflammation are made. Blood sampling is used as an indirect assessment.

Nasal epithelial cell brushing or lavage, and other noninvasive sampling such as exhaled breath and exhaled breath condensate analysis are limited at present to research settings.

Studies investigating lower airway inflammation are limited to preschool children with severe recurrent wheezing episodes [ 146 , 147 ]. In a subgroup of these children, eosinophils contribute to pathogenesis. For example, increased numbers of eosinophils are present in the airway submucosa of children with severe recurrent wheezing episodes compared to control patients [ 148 ], irrespective of their atopic status [ 149 , 150 ]. However, the site and compartment may affect their relative abundance.

In addition to eosinophils, neutrophils likely play a role in the inflammatory process underlying recurrent preschool wheezing, and certain markers indicate their activation and involvement. For instance, the shedding of l -selectin from the neutrophil cell surface, suggesting that neutrophils become activated and move towards sites of inflammation, and the upregulation of macrophage-1 (Mac-1) expression, have been linked to the underlying pathology in preschool wheezing [ 151 ]. In another study including 350 children with moderate-to-severe preschool wheezing, distinct clusters of children based on peripheral blood and bronchoalveolar lavage (BAL) eosinophils, neutrophils and other clinical symptoms ( e.g. gastro-oesophageal reflux) have been identified [ 152 ]. The cluster with the highest BAL neutrophil count was distinct and linked to a steroid-refractory phenotype with an increased incidence of pneumonia and gastroesophageal reflux, while aeroallergen sensitisation was associated with a separate cluster whose symptoms were controlled on high-dose inhaled corticosteroids [ 152 ].

Other inflammatory mediators that have been identified by using upper airway samples ( e.g. nasopharyngeal aspirates) and serve as surrogates of increased inflammation and remodelling include the epidermal growth factor, vascular endothelial growth factor and transforming growth factor-β1 mediators [ 153 ]. Assessment of inflammation using other noninvasive samples such as nasal epithelial lining fluid has shown immune mediator levels of interferon (IFN)-γ, tumour necrosis factor-α, interleukin (IL)-1β and IL-10 from children aged 0–3 years with “asthma-like episodes” have been significantly higher during episodes than during stable disease, in a post hoc analysis [ 154 ]. Data on exhaled breath condensate and VOCs point towards different inflammatory mediators and are listed in supplementary table 4S .

The current data suggest important roles for both lower airway eosinophils and neutrophils in recurrent preschool wheezing. However, reliable inflammatory biomarkers easily measured and applied in the clinic are missing.

Question 2c: what is known about airway remodelling in recurrent preschool wheeze?

As described in the PRISMA flowchart ( supplementary figure 9S ), following the application of the search algorithm, we have identified 17 relevant studies.

Studies published prior to 2008 show evidence of increased reticular basement membrane thickness in severe preschool wheezing compared to nonwheezing patients, independent of atopic status [ 150 , 155 ]. Defective bronchial epithelial cell repair has also been described in recurrent preschool wheezing similar to school-age asthma [ 156 ]. Primary bronchial epithelial cells from children with preschool wheezing secrete high levels of pro-inflammatory cytokines (IFN-γ, IL-6 and IL-13), and show reduced proliferation capacity, thereby delaying wound healing and restoration of barrier function [ 157 ]. In addition, submucosal IL-33-positive cells are increased in treatment-nonresponsive preschool children with wheezing. This is also the case for ST2, the receptor of IL-33 [ 158 ]. Latent class analysis of several remodelling parameters (epithelial integrity, reticular basement membrane thickness, mucus glands, smooth muscle and vessels) show distinct remodelling patterns that are associated with more frequent and severe preschool wheezing exacerbations [ 158 ]. In summary, there is evidence supporting early airway remodelling in recurrent preschool wheezing, but there are currently no therapeutic targets to modulate these changes, and critically, there are no noninvasive tests to quantify remodelling.

Question 2d: what is known about infection in recurrent preschool wheeze?

As described in the PRISMA flowchart ( supplementary figure 10S ), following the application of the search algorithm, we have identified 43 relevant studies.

Infections during acute preschool wheezing episodes

Several observational studies have identified respiratory viral infections as the main triggers of preschool wheezing episodes [ 159 , 160 ]. Respiratory viruses are isolated from nasal airway secretions in 80–90% of children presenting with acute wheezing [ 161 ]. Respiratory syncytial virus and human rhinovirus are the most detected viral pathogens and account for more than half of all detected viruses within the first 3 years of life [ 162 ].

The Copenhagen Prospective Study on Asthma in Childhood (COPSAC) study is among the first to investigate the role of both respiratory viruses and bacteria in acute wheezing [ 163 ]. Children with Haemophilus influenzae and Moraxella catarrhalis , when detected in high abundance in hypopharyngeal aspirates, have three times higher odds for an acute wheezing episode than those with no bacteria detected [ 163 ]. The emerging understanding is that both respiratory viruses and bacteria are implicated in acute preschool wheezing pathogenesis. In preschool wheezing, airways are not sterile from bacteria during stable disease, and it is unclear whether airway microbial dysbiosis is associated with an increased risk for future wheezing attacks. Understanding whether respiratory viruses or bacteria are the triggering pathogens, or whether microbial dysbiosis represents an underlying dysfunctional innate immune system requires interventional study designs and mechanistic studies to improve our understanding of whether infections are a cause or trigger of recurrent wheezing.

Severe bronchiolitis cohort studies have shown that rhinovirus-induced bronchiolitis is associated with an increased risk of future recurrent wheezing, particularly in infants with allergic sensitisation [ 164 ]. In addition, interactions between respiratory viruses and bacteria detected in nasal airway samples from infants with severe bronchiolitis are linked to endotypes at high risk of recurrent wheezing development [ 165 ]. These data require validation, but suggest that nasal airway pathogens present during acute wheezing episodes could be used as biomarkers to identify children at risk of subsequent recurrent wheezing.

The role of viral and bacterial infection in recurrent preschool wheezing

There is evidence from several longitudinal studies that rhinovirus in nasopharyngeal samples acquired during acute wheezing episodes is associated with an increased risk of recurrent wheezing episodes [ 156 , 164 ]. Equally, 20% of children have asymptomatic rhinovirus in upper airway samples and this has also been associated with an increased risk of school-age asthma [ 166 , 167 ].

In stable diseases, there are variable rates of respiratory viruses detected [ 168 ]. H. influenzae , M. catarrhalis and Streptococcus pneumoniae are also cultured from lower airway samples in up to 50% of these children [ 6 , 168 ]. Moreover, there appears to be an association between specific bacterial species and allergic sensitisation. M. catarrhalis is the most commonly cultured pathogen (30% of children) in BAL from children with preschool wheezing and aeroallergen sensitisation and is linked to coexisting lower airway neutrophilia [ 6 , 169 ].

In summary, airway infection, both viral and bacterial, is associated with recurrent preschool wheezing. However, we need reliable noninvasive techniques to identify airway infections, to understand whether infections play a causal role in recurrent wheezing episodes and whether treatments targeting infection can improve outcomes in preschool wheezing. Interventional trials with targeted antibiotics, antivirals, bacterial lysates or vaccines may enable us to understand this better.

Question 2e: what is the role of genetic susceptibility in recurrent preschool wheeze?

Our search strategy aimed to identify research studies focusing on genetic determinants of preschool wheezing incidence and severity. We identified 31 publications with relevant information ( supplementary figure 11S ).

The studies investigating genetic susceptibility and recurrent preschool wheezing are summarised in table 4 . Overall, these studies focus on the investigation of gene ( i.e. GSDMB , ORMDL3 , IL33 , IL1R1 , ILRL1 , RAD50 , IL13 , CDHR3 , FUT2 , MAMSTR , IL10 , IL4RA , IL9R , VDR , GSTP1 , TLR2 , TNFRSF13B , ANXA1)– gene or gene–environment interactions in preschool children with recurrent wheezing. The strongest genetic effects were seen for more-severe disease. As different genes are likely to represent specific underlying mechanisms, genetics might in theory help guiding treatment, but the role of these genetic markers in stratifying patients in clinical trials and defining responsiveness to treatment approaches has not been investigated.

Question 2f: what is the evidence for treatments for preschool wheezing being determined by and impacting pathophysiology and mechanisms?

As described in the PRISMA flowchart ( supplementary figures 12S and 13S ), following the application of the search algorithm, we have identified 41 relevant studies. 20 out of 41 studies are randomised controlled trials (RCTs). Summaries of these studies are presented in table 5 and supplementary table 12S . In addition, the studies investigating the impact of treatments on biomarkers, lung function and clinical symptoms are summarised in table 6 . Key novel data relating to the efficacy of ICS and the use of mixed bacterial lysates in recurrent preschool wheezing without allergen sensitisation are highlighted herein.

Summary of studies describing impact of treatments in preschool wheezing on symptom score, biomarkers and lung function

Inhaled corticosteroids

Management with maintenance ICS remains the first line of treatment for preschool wheezing according to Global Initiative for Asthma guidelines [ 216 ]. A meta-analysis of studies comparing the effectiveness of daily versus intermittent treatment with ICS in preschool children shows no significant difference in the number of wheezing exacerbations between treatment groups [ 217 ]. Evidence from three RCTs shows that there is no effect of ICS on long-term respiratory sequelae ( i.e. asthma development) [ 23 – 25 ]. When choosing between ICS or leukotriene receptor antagonists (LTRAs) as the first line of management, the Individualized Therapy for Asthma in Toddlers (INFANT) trial [ 208 ] did not identify markers of differential responders to LTRAs. However, the trial did demonstrate that by using two easily detectable biomarkers (elevated blood eosinophils (≥300 cells·μL −1 ) and/or aeroallergen sensitisation) differential responders to daily ICS treatment could be identified [ 208 ]. Further prospective validation of this approach is needed; therefore, using blood eosinophils as a biomarker in preschool children is currently not an evidence-based recommended clinical approach [ 115 ]. The cut-off levels for elevated blood eosinophils recommended in the INFANT trial were within the normal range for children and, evidently, children with coexisting allergic diseases ( i.e. eczema) are expected to have higher blood eosinophils regardless of their recurrent wheezing diagnosis [ 115 ]. Differential treatment responses in the INFANT trial have provided evidence for the heterogeneity of recurrent preschool wheezing. A latent class analysis of five clinical trials, incorporating 1708 children with recurrent preschool wheezing also showed that aeroallergen sensitisation identified children most likely to respond to maintenance ICS [ 218 ]. The role of alternative biomarkers that may identify ICS responders, such as F ENO , still remains unknown. Results from both interventional and observational studies in preschool wheezing identifying characteristics of ICS responders are presented in tables 5 and 6 .

Macrolides, most commonly azithromycin, have only been investigated for treatment of acute preschool wheezing episodes [ 200 ]. Data show that if macrolides are started within 6 days of onset of “asthma-like episodes” in 1–3-year-old children, duration of symptoms is reduced by 83%, but with unclear mechanism of action, and in the absence of bacterial detection [ 200 ]. In contrast, there is no benefit of azithromycin in 1–5-year-old children presenting with acute wheezing in the emergency room either on the duration of the episode or time to re-occurrence of an episode [ 201 ]. In a third RCT testing the impact of azithromycin on progression to severe lower respiratory tract infection (LRTI) requiring oral corticosteroid prescription, azithromycin, when started at the onset of upper respiratory tract infection, was associated with a significantly reduced risk of progression to severe LRTI [ 219 ]. However, induction of azithromycin-resistant organisms was observed [ 219 ]. A systematic review of the three trials concluded limited evidence for efficacy of macrolides in acute preschool wheezing based on available data [ 220 ]. Importantly, no trials have assessed the efficacy of longer-term prophylactic azithromycin as a maintenance therapy to prevent recurrent preschool wheeze attacks.

Mixed bacterial lysates

There have been several clinical trials to determine the efficacy of mixed bacterial lysates as a treatment to prevent preschool wheezing episodes [ 221 ]. Bacterial lysates are orally or sublingually delivered inactivated bacterial extracts from a mix of pathogenic respiratory bacteria and are proposed to work by exhibiting immunomodulatory activity [ 222 ]. The mixed bacteria in the compounds include the three that have been most commonly cultured from lower airways in severe recurrent preschool wheezing ( M. catarrhalis , H. influenzae , S. pneumoniae ) [ 223 ]. The immunomodulatory activity is proposed to occur via NF-κB and mitogen-activated protein kinase pathways that activate dendritic cells. This activation is proposed to stimulate an antiviral response by its effect on the production of antiviral cytokines, including interferons, type1 T helper cytokines, and (local) immunoglobulins [ 224 ]. Their greatest benefit is thought to be in the group of children who have virus-induced episodes and are nonallergic. An initial double-blind randomised controlled trial of 75 children aged 1–6 years showed a significant reduction in rate and duration of wheezing attacks associated with acute respiratory infections [ 225 ]. Subsequently, a phase-3 double-blind randomised placebo-controlled trial which included 120 children aged <3 years with at least three wheeze attacks in the previous year, showed that 6 months treatment with the bacterial lysates MV130 resulted in fewer wheeze attacks at 1 year (even though the intervention was for only 6 months) [ 203 ]. A cost–utility analysis showed the use of bacterial lysates as add-on to standard care of preschool children with recurrent wheezing was an efficient treatment intervention that reduced the clinical and economic burden [ 226 ].

Impact of currently available pharmacological interventions on wheezing pathophysiology

Impact of treatments on lung function: Discordant results have been reported on the effect of ICS or montelukast on lung function in children with preschool wheeze. These results are summarised in table 7 .

Summary of studies describing characteristics of patients with preschool wheezing who respond to inhaled corticosteroid (ICS) treatment

Impact of treatments on type 2 biomarkers: There are two studies from the same group suggesting that systemic corticosteroids might impact eosinophil activation, especially in rhinovirus-induced episodes. Other than these studies, there is no evidence of impact of currently available treatments on blood biomarkers. The studies are summarised in table 6 .

In addition to blood biomarkers, studies have assessed the impact of ICS or montelukast on F ENO with conflicting results ( table 6 ).

Summary statements aim 2

Future directions are summarised in figures 2 and 4 .

1)  Lung function is feasible in specialist centres in preschool children and provides measures of bronchodilator response and response to treatment, and can be tracked from preschool to school age.

2)  There is emerging evidence that blood eosinophils and aeroallergen sensitisation may help to define the group of preschool children with recurrent wheezing who have a predominant lower airway type 2 eosinophilic inflammatory phenotype and who will have a differential response to ICS.

3)  The current understanding of the role of inflammation in preschool wheezing mainly derives from studies utilising lower airway samples from children with severe wheezing episodes. These studies show both airway eosinophils and neutrophils in preschool wheezing. However, understanding the relationships between blood, upper airway and lower airway inflammation, and in children with different wheezing severity remains limited.

4)  The current evidence does not clearly identify specific markers of reduced responsiveness to treatment with inhaled corticosteroids ( table 6 ). However, absence of both blood eosinophilia and aeroallergen sensitisation can indicate reduced steroid responsiveness.

5)  Respiratory viruses are involved in preschool wheezing pathogenesis. Based on current evidence, rhinoviruses are commonly detected in the upper and lower airways both during acute attacks and during stable disease.

6)  Three bacterial species are most identified in upper and lower airways using traditional culture and culture-independent techniques in preschool wheezing: M. catarrhalis , H. influenzae and S. pneumoniae.

7)  Whether infections play a role in driving recurrent preschool wheezing or simply uncover underlying susceptibility is unknown.

8)  There is emerging evidence that oral mixed bacterial lysates reduce number and duration of preschool wheezing attacks, especially in children without aeroallergen sensitisation.

9)  Airway remodelling is present in severe recurrent preschool wheezing; however, there are no noninvasive biomarkers, and presence of remodelling in low-severity preschool wheezing is unknown.

10) The most robust gene signals relate to ORMDL3 , GSDMB and IL33 genes. However, the role of these genetic markers in stratifying patients in clinical trials and defining responsiveness to treatment approaches is unknown.

Aim 3: important outcomes for patients, caregivers and clinicians following diagnosis and/or management of preschool wheezing

To help highlight some priorities for parents and caregivers, we interviewed parents of preschool children with wheezing in the United Kingdom and the Netherlands who highlighted several important issues which are summarised in table 8 . These patient and public involvement (PPI) colleagues were recruited via the European Lung Foundation in collaboration with the PPI platform of the Asthma UK Centre for Applied Research.

Priorities suggested by patient and public involvement colleagues

Question 3a: what is known about important outcomes for patients/parents/caregivers following diagnosis and management of recurrent preschool wheeze?

Our search strategy aimed to identify research studies focusing on important outcomes for patients/caregivers. Our search has identified 34 relevant publications ( supplementary figure 14S ).

Important outcomes for patients and caregivers

Improved understanding about recurrent preschool wheezing among caregivers: Educational programmes, including training about management and parental coaching for a wide age range of children have shown improvements in knowledge [ 230 ], symptom-free days [ 231 – 234 ], need for emergency consultation [ 231 , 232 , 235 ] and reduction in oral steroid courses [ 232 ]. Below we discuss the impact of educational programmes and important outcomes for caregivers of preschool children with recurrent wheezing.

Support with administering daily medications: Managing daily treatments can be a major issue for parents. Smart inhalers reveal that only half of children with preschool wheezing use ICS optimally [ 236 ], and adherence is influenced by parental beliefs regarding benefit and harms of daily ICS treatment [ 237 , 238 ]. Administering inhaler devices to their young children can be a source of distress for parents who describe feeling poorly prepared for the task [ 239 ]. A feedback mechanism attached to a spacer provided reassurance of correct inhalation technique [ 240 ]. Families reporting better overall management of wheezing had fewer oral corticosteroid courses and higher caregiver asthma-related quality of life [ 241 ].

Managing acute wheeze attacks: Acute wheeze attacks and the need for emergency care are relatively frequent in preschool children compared to older children [ 242 ] and most parents report that their decisions to attend an emergency department (ED) are driven by perceptions of urgency [ 243 ], with a third citing difficulty accessing timely advice from primary care [ 243 ]. When interviewed during emergency care (in the ED or primary care) about wheeze attacks, parents reported the need for a better understanding of their child's condition, need for more support from clinicians in terms of medication use, and supportive communication [ 38 ].

This information could be provided during discharge from a hospital setting. For example, a study showed that video discharge instructions following a wheeze attack rather than written instructions improved caregivers’ understanding of their child's diagnosis, treatment and follow-up care [ 244 ]. A written wheeze plan given to parents in the emergency department to explain the discharge medication improves adherence to medication [ 245 ].

Achieving a better family quality of life: Children with severe wheezing have reportedly lower quality of life [ 246 – 248 ]. Poor disease control impacts on caregivers [ 249 ]. This impact, that can be measured with a validated questionnaire (Effects of a Young Child's Asthma Flare-up on the Parents) [ 250 ] may be reflected in domains of sleep/activity disruption, emotions, concerns about medication and acute care, concerns about losing control, and concerns about leaving the child with another caregiver.

Question 3b: does supported self-management improve outcomes for children with preschool wheezing and what components of support are effective?

Our first objective was to establish the evidence for the effectiveness of supported self-management interventions. Our primary interests were clinical outcomes of acute attacks and symptom control, but also the impact on caregiver quality of life. Process and intermediate outcomes were noted as evidence of feasibility, fidelity or potential for improving outcomes (improved adherence, self-efficacy). Our second objective was to explore evidence for specific components of supported self-management to inform future development of interventions.

Objective 1: effectiveness of supported self-management interventions in children with preschool wheezing

Eight RCTs assessed effectiveness of a supported self-management intervention. Five studies were conducted >10 years ago [ 235 , 251 – 253 ] and thus do not reflect current understanding of heterogeneity of preschool wheezing. A diagnosis of “asthma” (as opposed to wheeze/asthma) was an eligibility criterion for six of the studies [ 233 , 251 – 255 ].

Interventions ranged in duration from two 20-min hospital-based educational sessions [ 256 ] to eight 90-min home visits [ 251 ]. One programme was delivered in preschool classes [ 233 ], and one was a tailored computer programme [ 196 ]. Most were led by respiratory-trained paediatric nurses [ 233 , 251 , 252 , 255 , 256 ] or general practitioners (GPs) [ 253 ], but one was delivered by a paediatrician, nurse and psychologist team [ 235 ]. Education was a core component of all the interventions, but one included a psychological component [ 235 ], one targeted self-efficacy [ 254 ] and two addressed the social challenges of low-income African American communities [ 251 , 255 ]. One observational study reporting data on preschool children referred to a diagnostic therapeutic educational pathway [ 257 ].

There is considerable heterogeneity of study design: individual RCTs [ 251 , 252 , 254 – 256 ], two cluster RCTs [ 233 , 235 ] and follow-on from an RCT [ 253 ]. The most common outcome was acute attacks, but there was great diversity in how this was measured (any unscheduled care, ED/admission either combined, or separately [ 235 , 253 , 256 ] and reported (proportion with the outcome [ 233 , 235 ], number of attacks per participant [ 255 , 256 ], total number of attacks from routine data [ 253 ]). A range of patient-reported outcomes were used, such as knowledge around preschool asthma and feeling of self-efficacy. A validated questionnaire for caregiver quality of life was used by four trials [ 251 , 254 – 256 ]; two used nonvalidated questionnaires [ 251 , 252 ].

Impact on clinical outcomes: The four trials that used emergency care visits as their primary outcome reported no significant between-group difference [ 233 , 251 , 255 , 256 ]. Emergency healthcare consultations [ 233 , 235 ] and hospitalisations [ 235 ] were similar in the psychoeducational intervention (Preschoolers’ and Parents’ Asthma Education Trial) and control groups. There was no difference in mean number of GP consultations, ED attendances or admissions experienced by participants in the intervention group compared to controls and no reduction in wheeze attacks [ 251 , 256 ]. The only trial to demonstrate a reduction in “emergency and nonemergency visits” was a cluster RCT from 1994 that used routine data to assess the impact of training GP [ 253 ].

A reduction in ED visits and hospitalisations was seen in preschool children before and after enrolment in the Diagnostic Therapeutic Educational Pathway [ 254 ], with a reduction in outpatient visits and oral steroid courses in children aged 3–5 years [ 254 ]. Three studies using unvalidated questions reported a reduction in asthma symptoms [ 233 , 251 , 252 ], but another three studies which used validated questionnaires reported no between-group difference in asthma control [ 235 , 255 , 256 ].

Impact on caregivers’ quality-of-life: The home-delivered Wee Wheezers programme improved caregivers’ quality of life in the subgroup of 0–3-year-olds, but not overall [ 251 ]. In contrast, neither the multifaceted HeadStart programme [ 255 ], nor a less-intensive educational intervention [ 256 ], or a computer-based educational programme [ 254 ] showed a beneficial effect.

Knowledge, self-efficacy and adherence: Improving knowledge was a key aim of seven of the interventions, and four reported improvement in knowledge [ 235 ], self-management skills [ 252 , 253 ], inhaler technique [ 233 ] and self-efficacy [ 253 , 254 ] as well as an improvement in confidence among preschool staff [ 254 ].

One of two Wee Wheezer trials reported improvement in adherence to preventer medication [ 254 ], but there was a large between-group difference at baseline; the other reported no effect [ 251 ]. The preschool-based intervention reported an increase in the number of children using inhaled corticosteroids [ 233 ].

Objective 2: effectiveness of components of supported self-management

We identified four RCTs which evaluated components of supported self-management; one each from France [ 258 ], USA [ 259 ], Hong Kong [ 260 ] and Australia [ 261 ]. In addition, we included a “before and after” feasibility study from Germany [ 32 ], and developmental work using routine data from Australia [ 262 ]. Although the earlier studies specified a diagnosis of “asthma” as an eligibility criterion [ 259 , 261 ], two of the more recent studies explicitly included recurrent wheeze as well as asthma [ 32 , 260 , 262 ]. The five studies investigated a range of potential components ( e.g. carefully designed asthma education resources, web-based asthma education programmes, use of “wheezing detectors” to support parental confidence) described in table 9 .

Components of supported self-management interventions

Question 3c: which strategies should clinicians use to highlight need for further investigation and referral from primary care or general paediatrician to secondary and tertiary care?

The results of the search for this question did not reveal any original research manuscripts. Only review articles which included authors’ opinions/consensus were available ( supplementary material discussion and supplementary figure 15S ).

Summary statements aim 3

Future directions are presented in figures 2 and 5 .

Future directions for aim 3: important outcomes for parent/caregiver-reported outcomes, caregiver-led self-management and specialist referral.

The need for additional research in the area of patient- and caregiver-related outcomes has been highlighted.

1) There is currently insufficient evidence about supported self-management interventions that are effective for parents/caregivers of preschool children who wheeze, and a suitable action plan for preschool wheezers is urgently needed.

2) The impact of self-management interventions should be assessed using outcomes that reflect acute attacks (such as unscheduled healthcare), symptom control and impact on the child, the caregiver, and their family quality of life (using control or quality-of-life questionnaires validated in this age group).

3) There is a need for evidence to underpin clear guidance about when preschool children with recurrent wheeze should be referred for further investigations and specialist tests.

• Conclusions and future directions

This ERS task force reviewed the literature related to recurrent preschool wheezing ( figure 2 ). We suggest that three criteria should be fulfilled to define wheezing disorders in preschool children, as follows. 1) Age (0–6 years); 2) confirmation of wheezing on at least one occasion; and 3) more than one episode of wheezing. Although children with recurrent preschool wheezing may have similar clinical manifestations including acute episodes with/without interval symptoms, the underlying pathophysiology and causal mechanisms are heterogeneous. Therefore, in a similar manner to the approach proposed for school-age asthma, diagnosis and management may be improved by identifying treatable traits, which include inflammatory markers and lung function parameters. The current evidence suggests that certain biomarkers may be helpful to define the wheeze phenotype and to identify children likely to respond to inhaled corticosteroids [ 99 ]. These include elevated blood eosinophils and aeroallergen sensitisation. They require validation in prospective, longitudinal interventional studies to understand their role in daily clinical practice. However, a big gap at present is biomarkers that may help to identify children unlikely to respond to ICS, and those who may have a “type-2 low” phenotype. There is evidence that airway infection (bacterial and viral) may play a role in recurrent preschool wheezing; however, nothing is known about the cause–effect relationship, impact of anti-infection treatment strategies and biomarkers of treatment response. There is also increasing evidence that testing genetic traits that have been identified by genome-wide association studies studies may be helpful to identify phenotypes and guide management, but has not yet been tested. Importantly, the efficacy of any intervention should be assessed with both objective outcomes ( e.g. reduction in the number of acute episodes and healthcare visits) and caregiver-reported outcomes. However, currently, there is little or no evidence from trials that have incorporated caregiver-reported outcomes or quality-of-life measures. In summary, to effectively manage recurrent preschool wheeze, we need to accept the need to objectively identify observable traits, treat this based on measurable traits, and efficiently follow this through based on observable, measured and caregiver-reported traits.

• Supplementary material

Supplementary Material

Please note: supplementary material is not edited by the Editorial Office, and is uploaded as it has been supplied by the author.

Supplementary material ERJ-00624-2024.SUPPLEMENT

Table S1 ERJ-00624-2024.SUPPLEMENT2

Table S2 ERJ-00624-2024.SUPPLEMENT3

Table S3 ERJ-00624-2024.SUPPLEMENT4

Table S4 ERJ-00624-2024.SUPPLEMENT5

Table S5 ERJ-00624-2024.SUPPLEMENT6

Table S6 ERJ-00624-2024.SUPPLEMENT7

Table S7 ERJ-00624-2024.SUPPLEMENT8

Table S8 ERJ-00624-2024.SUPPLEMENT9

Table S9 ERJ-00624-2024.SUPPLEMENT10

Table S10 ERJ-00624-2024.SUPPLEMENT11

Table S11 ERJ-00624-2024.SUPPLEMENT12

Table S12 ERJ-00624-2024.SUPPLEMENT13

Table S13 ERJ-00624-2024.SUPPLEMENT14

Table S14 ERJ-00624-2024.SUPPLEMENT15

• Shareable PDF

This one-page PDF can be shared freely online.

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• Acknowledgements

Infrastructure support for this research was provided by the NIHR Imperial Biomedical Research Centre.

This document was endorsed by the ERS Executive Committee on 22 May 2024.

Conflict of interest: A. Custovic reports personal fees from Novartis, Sanofi, Stallergenes Greer, AstraZeneca, GSK, La Roche-Posay and Reacta Healthcare, outside the submitted work.

Conflict of interest: C. Coleman is an employee of the European Lung Foundation.

Conflict of interest: T. Tonia acts as ERS methodologist.

Conflict of interest: The remaining authors have no potential conflicts of interest to disclose.

Support statement: This statement was funded by the ERS. Funding information for this article has been deposited with the Crossref Funder Registry .

• Received March 29, 2024.
• Accepted May 5, 2024.
• Copyright ©The authors 2024. For reproduction rights and permissions contact permissions{at}ersnet.org
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Knowledge Gap : The Magic behind Knowledge Expansion

As the world moves to a global knowledge based economy, the idea of knowledge expansion becomes cardinal to the growth and development of depressed economies and in expanding these knowledge frontiers individuals and organizations need to continually interact with each other to enhance knowledge. The study therefore, seeks to evaluate the concept of knowledge gap as the magic behind knowledge expansion. In meeting theoretical expectations and needs, the study interrogate the nature and concept of knowledge showing vividly the functionality of social interactions as a device for acknowledging epistemic authority where valuable information can be shared since social interactions provide enabling ground for the development of common identity. In identifying the factors hampering knowledge expansion among developing economies, the study came up with the pore model of knowledge gap which acknowledges the fact that political power and lack of access to financial resources has corrupted kn...

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SUBJECT AND OBJECTIVES: Awareness gap theory is one of the theories related to the sphere of influence of mass media. The design of the awareness gap theory initially included a simple relationship between the socio-economic status of individuals and the extent of the awareness gap between different groups. This means that the lower the socio-economic status of individuals, the less access they have to information, and vice versa; but later, it was not only the socio-economic base that determined people's access to information, but also their level of awareness of important issues related to social groups can be influenced by other variables such as people's interest or need for information. METHOD AND FINDING: A descriptive-analytical study of this issue shows that the gap knowledge theory does not mean the lower class is unaware of the available data and information, but claims that the growth of knowledge is relatively higher among high-ranking groups, and this information gap It will get deeper and deeper day by day. CONCLUSION: The basis of this theory is that the mass communication strengthens or increases the existing information inequalities. This research seeks to answer the question of what the theory of knowledge gap is and how its effects can be influenced by information inequalities.

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About the book: In a knowledge-based economy, knowledge alone sustains competitive advantage, whether at an organizational or at a national level. Four structural forces drive economic transformation globally—revolutionary changes in Information and Communication ...

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The term "Knowledge Society" refers to any society where knowledge is that the primary production resource rather than capital and labor. A Knowledge society "creates, shares, and uses knowledge for the prosperity and well-being of its people". Knowledge Society is characterized by the recognition of data as the main source of efficiency, competitiveness, and economic process. The seed of any invention was the knowledge that was cultivated, applied, and shared to advance human wellbeing. These days, governments that invest heavily within the education system, research, and development see themselves as creating a far better knowledge economy. Since the late 1990s, an outsized segment of economists and bureaucrats are hooked into the continued run of "Knowledge Economy" in OECD countries and its emergence within the developing countries. India too has its rendezvous with this idea.

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Purpose: In today's world, epistemology, like other disciplines, has undergone fundamental changes, so that we witness transition from the power creation of knowledge to the power creation of knowledge sharing. Therefore, the purpose of this study was to understand the transition of power creating of knowledge to power creating of knowledge sharing at the viewpoint of graduate students of Tabriz University. Methodology: This research was conducted using the grounded theory approach as a qualitative research method. The data were collected through interviews with 20 graduate students of Tabriz University selected through purposeful sampling method. Interviews continued to data saturation. The data were analyzed immediately after each interview based on open, axial and selective coding. Findings: Findings indicated that in the view of graduate students, four important themes were the basis for sharing knowledge in universities and higher education institutions including religiosity, academic social capital, the promotion of academic services quality, and motivational factors. These main themes also had sub-themes as follow: in religiosity (belief in religious beliefs, science zakat, science publishing) in academic social capital (interpersonal trust, scientific community formation), in improving the quality of academic services (provision of facilities and resources, technological infrastructure), in motivational factors (macro support, micro support). The central issue in this research was the concept of academic social capital. Conclusions: The result of this research showed that the majority of respondents expressed academic social capital as the main source of knowledge sharing but the impact of economic, cultural and motivational variables should also be regarded.

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We are now living in times of global business activity and the knowledge economy. Knowledge-based resources represent the organizational Know-how as the knowledge of employees, organizational production processes, and overall knowledge of one collective. Knowledge management has long been recognized as a factor necessary for the development of business organizations. Only those managers that embrace knowledge as the most important resource can expect to be better positioned than the competition. Know-how is very important segment of overall knowledge that is deposited within the organization. The value of knowledge is much more important than all other forms of assets that an organization possesses. But knowledge cannot be communicated without the interested employees. So, managers have to create the business environment which uses adequate business communication. Good communication stimulates ideas and creativity of employees. Management must be able to manage business information ...

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At the Jerusalem synagogue where Hersh Goldberg-Polin danced in life, grief and anger reign after his death

JERUSALEM — Three hundred and thirty-two days after Hersh Goldberg-Polin danced in the courtyard next to his Jerusalem synagogue on the holiday of Simchat Torah, more than a thousand people gathered there in grief and prayer to mourn his murder by Hamas terrorists in Gaza.

During the Sunday night vigil, the courtyard railings were lined with oversized yellow ribbons to symbolize advocacy for the hostages, Hapoel Jerusalem soccer flags — the 23-year-old’s favorite team — and posters that read, “We love you, stay strong, survive,” a mantra coined by his mother, Rachel Goldberg-Polin.

Just hours earlier, one of the posters had been hanging over the balcony of the home of Shira Ben-Sasson, a leader of Hakhel, the Goldberg-Polins’ egalitarian congregation in the Baka neighborhood of Jerusalem.

“We were sure we would take it down when he came home,” Ben-Sasson said.

The community wanted to unite while respecting the Goldberg-Polins’ desire for privacy, she said, prompting them to organize the prayer gathering.

“But it’s like a Band-Aid or giving first aid, it’s what you do in an emergency. I don’t know how we go on after this,” she said.

A covered courtyard at the Hakhel congregation was filled with mourners the day after Hersh Goldberg-Polin, whose family are prominent members, was found to have been killed in Gaza. Hundreds of other people crowded outside the gates, Sept. 1, 2024. (Deborah Danan)

She added that the community, which has a large contingent of English-speaking immigrants, was not prepared for the High Holidays, which begin in about a month. She said, “Seeing his empty seat is hard.”

For Ben-Sasson, who wore a T-shirt bearing the Talmudic dictum “There is no greater mitzvah than the redeeming of captives,” the tragedy is especially painful because, she said, it could have been avoided with a ceasefire agreement that freed hostages.

“Hersh was alive 48 hours ago. We think a deal could have saved him. There is no military solution to this,” she said.

That feeling of bereavement, often mixed with betrayal, pervaded gatherings across Israel on Sunday, as the country struggled with the news that six hostages who may have been freed in an agreement were now dead as negotiations continue to stall. Speakers at protests in Tel Aviv blamed Israeli Prime Minister Benjamin Netanyahu, who himself apologized for not getting the hostages out alive but blamed Hamas for obstructing a deal. The country’s labor union, the Histadrut, has called a national strike on Monday to demand a deal.

A rare early September rain lashed parts of Israel on Sunday, leading to a widespread interpretation: God, too, was weeping.

Some at the Jerusalem gathering, including the relative of another former hostage, said Netanyahu had chosen defeating Hamas over freeing the captives.

Josef Avi Yair Engel’s grandson Ofir was released from Hamas captivity in November. He paid tribute to Hersh Goldberg-Polin, murdered in captivity, in Jerusalem, Sept. 1, 2024. (Deborah Danan)

Josef Avi Yair Engel, whose grandson Ofir, 18, was released from Hamas captivity in November during that month’s ceasefire deal, expressed shock over Hersh’s murder but said he was not surprised, given the wartime policies of Netanyahu’s government.

“We knew months ago this was going to happen. Bibi’s formula, to dismantle Hamas and return the hostages, wasn’t logical. It’s an either/or situation,” Engel said, referring to Netanyahu by his nickname. “He’s tearing the country apart. I’m afraid that in the coming months there won’t be a state at all.”

Engel said he felt a close bond with Hersh’s father Jon Polin, not only because of their joint activism in the hostage families’ tent outside the Prime Minister’s Residence, but also because of their shared identity as Jerusalemites.

“There aren’t many of us in the hostage circle,” he said. “We’re like family.”

Sarah Mann, who did not know the family personally, said the weekend’s tragedy reminded her of Oct. 7.

“This day has sparks of the seventh, which created numbness and an inability to talk. Just complete shock,” she said.

Mourners left notes at a gathering at Hersh Goldberg-Polin’s family synagogue in Jerusalem. Many of the messages used the Hebrew word for “sorry.” (Deborah Danan)

Part of the reason for that, Mann said, was Rachel, who she described as a “force of faith.” Goldberg-Polin’s mother emerged as the most prominent advocate for the hostages globally and became a symbol in her own right as she crisscrossed the world calling for her son’s freedom.

“Millions of people around the world held onto her. Once that was cut, people’s ability to hold onto faith was knocked out today. But even though this has shattered us, we need to keep holding onto God,” Mann said.

For Susi Döring Preston, the day called to mind was not Oct. 7 but Yom Kippur, and its communal solemnity.

She said she usually steers clear of similar war-related events because they are too overwhelming for her.

“Before I avoided stuff like this because I guess I still had hope. But now is the time to just give in to needing to be around people because you can’t hold your own self up any more,” she said, tears rolling down her face. “You need to feel the humanity and hang onto that.”

Like so many others, Döring Preston paid tribute to the Goldberg-Polins’ tireless activism. “They needed everyone else’s strength but we drew so much strength from them and their efforts, “she said. “You felt it could change the outcome. But war is more evil than good. I think that’s the crushing thing. You can do everything right, but the outcome is still devastating.”

Guy Gordon, with his daughter Maya, added a broken heart to the piece of tape he has worn daily to mark the number of days since the hostage crisis began, Sept. 1, 2024. (Deborah Danan)

Guy Gordon, a member of Hakhel who moved to Israel from Dublin, Ireland, in the mid-1990s, said the efforts towards ensuring Hersh’s safe return have been an anchor for the community during the war. The community knew him as the family described him in its announcement of his funeral on Tuesday, as “a child of light, love and peace” who enjoyed exploring the world and coming home to his family, including his parents and younger sisters, Leebie and Orly.

“It gave us something to hope for, and pray for and to demonstrate for,” he said. “We had no choice but to be unreasonably optimistic. Tragically it transpired that he survived until the very end.”

Gordon, like many others in the crowd, wore a piece of duct tape marked with the number of days since Oct. 7 — a gesture initiated by Goldberg-Polin’s mother. Unlike on previous days, though, his tape also featured a broken red heart beside the number.

Nadia Levene, a family friend, also reflected on the improbability of Hersh’s survival.

“He did exactly what his parents begged him to do. He was strong. He did survive. And look what happened,” Levene said.

She hailed Rachel Goldberg-Polin’s “unwavering strength and belief in God,” adding, “There were times I lost faith. I suppose I was angry with God. But she just kept inspiring us all to pray, pray, pray.”

Leah Silver of Jerusalem examined stickers showing Rachel Goldberg-Polin’s mantra for her son Hersh, who was murdered in captivity in Gaza, at a gathering after Hersh’s death, Sept. 1, 2024. (Deborah Danan)

Jerusalem resident Leah Silver rejected politicizing the hostages’ deaths.

“Everything turns political so quickly. I came here because I felt that before all the protests, we need to just mourn for a moment and to pray. And show respect for each other,” she said. “We’ve become confused about who the enemy is. It’s very sad.”

But not everyone at the gathering joined in to sing Israel’s national anthem at the closing of the prayer gathering.

“I’m sorry, I can’t sing ‘Hatikvah,'” Reza Green, a Baka resident who did not know the Goldberg-Polins personally, said. “I’m too angry. We shouldn’t be here.”

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