That pays for a lot of wheezes and dodges.
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Books Winning the war with wheezers Andro Linklater. Fighter pilots under instruction, June Andro Linklater 9 February 9: The Engineers of Victory: Most Popular Read Recent Read. The nine lessons of Brexit Ivan Rogers. The myth of the Brexit cliff edge Matthew Lynn.
Corbyn tables a motion of no confidence in May — will it backfire? Why business and the City should speak out against a second referendum Matthew Lynn. What to read next. The raid was immortalized in the film "Cockleshell Heroes". During the years after the war, Ex-Servicemen would be encouraged to wear their uniforms and medals at Remembrance Day Services.
John would wear his Commander, RN uniform but not his medals. One day my mother found them in the wastepaper basket. When asked why, he said he did not believe in medals as for every medal awarded there were many people who went unrecognized, both military and civilian. They were retrieved and I now have them, along with my father's, encased and framed.
Find out how you can use this. These messages were added to this story by site members between June and January It is no longer possible to leave messages here. Find out more about the site contributors. Graeme, I have to admit my interest in naval guns and armour is probably unusual but do you have any more info on what John's Military OBE work was for i.
At the time of publication its real purpose was uncertain but the book points out that Panjandrum was not kept very secret. It suggests the bomb was part of the very important deception plan to fool the Germans into thinking the invasion was to be in the Pas De Calaise. Had that been true, it or something similar, would definitely have been required.
Panjandrum therefore played its part. Do you know if the deception has been officially admitted? I wonder how expendable the military personnel there were! One final point re Westminster Bridge. I did some work recently looking at shipping accidents. Hitting bridges, warfs etc. Did the control system actually fail or was it just inadequate for the conditions? His service record for includes "Expression of T. L's appreciation of zeal and abiolity displayed in working at proposal for system of fire control now under investigation.
L's appreciation of zeal and ability in development of firing through smokescreen". Royal Sovereign", 1st Battle Squadron". He did some further work "in connection with development of Fire Control Table. He finally took the Admiralty to Court regarding his inventions. The file on John Dove was sealed and "not to be opened for 50 years. Under separate cover I can email you an attachment of what I have written about his part in Naval Gunnery at the time of the "Great Gunnery Scandal". I remember him telling me that the Panjandrum was originally designed to blow a hole in the Altantic Wall.
Children in the northeastern USA with greater levels of mouse allergen exposure in inner city schools have been found to have more asthma-related missed school days. Cockroach exposure is considered to be a significant factor related to the high prevalence of asthma in inner city children.
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It was postulated that the level of these allergens in the houses sampled was low, making the assessment less accurate. It appears that there is a dose-response relationship between dust mite exposure and sensitization. Mold exposure in the home is frequently linked to exacerbations of asthma. The Pollution and the Young study obtained data on exposure and health parameters in 57, children aged 6—12 years in 12 countries. However, these results were based on self-reported questionnaires, limiting their accuracy.
The concentration of bacterial endotoxins lipopolysac-charides found in the outer membranes of Gram-negative bacteria in house dust correlates with the presence of pets in the house, in particular that of dogs. Infants may spend 20 hours per day in their homes. Crowding may increase the levels of exposure to indoor pollutants, so may be associated with an increased risk of developing asthma and increased severity of asthma. Studies examining the effect of daycare attendance on the development of asthma have demonstrated inconsistent results.
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A recent publication on the presence of an asthma diagnosis at age 7 years in children in Cincinnati reported that having attended daycare can increase or decrease the risk of having asthma, depending on the duration of attendance during the first 12 months of life. Viral infections during infancy are common and frequently present prior to the development of asthma.
Despite significant research efforts to identify the role of specific viral infections in the development of asthma, it remains unclear if specific viral infections during early childhood can lead to having asthma later in life. In a prospective study of children from birth to 6 years of age, investigators attempted to identify a relationship between early childhood asthma development and viral infections. The study reported an increased risk of developing asthma at age 6 years in those patients who had wheezing triggered by respiratory syncytial virus infection, rhinovirus infection, or both.
Rhinovirus infection-related wheezing during the first year of life was associated with an increased risk of asthma at age 6 years. The results from this study lead to the conclusion that infant wheezing with rhinovirus infection is a significant predictor for later development of clinical asthma. Another study evaluated infants who presented with upper respiratory tract infection or bronchiolitis. This study showed that human rhinovirus infection frequently triggered bronchiolitis and upper respiratory illnesses in previously healthy infants and frequently was the cause of hospitalization or sick outpatient visits.
The study described a higher severity in illness in children whose mothers had a history of atopy. In a community-based cohort study of children at risk of atopy, followed from birth to the age 5 of years, aspirates for viral identification were collected during respiratory illnesses. At the end of the study, The association was present in those children with early sensitization and not in those without a history of atopy.
The results of this study led to the conclusion that development of asthma is multifactorial and that viral infections early in life likely play a role in the development of asthma. Evidence has shown that double-stranded RNA from respiratory viruses cause significant airway hyperresponsiveness and pulmonary inflammation in a mouse model. Another pathogen that has been related to the pathophysiology of asthma is Chlamydia pneumonia. In a study by Zaitsu et al, infection with Chlamydia pneumonia was identified by looking at the serum of infants presenting with wheezing. The children were followed for 1 year to determine if asthma could be associated with this type of infection.
The investigators reported that infants with Chlamydia pneumonia and wheezing progressed to asthma more frequently than those who were not infected, and concluded that Chlamydia infection during infancy can be involved in the later development of asthma. Breastfeeding is almost universally recommended and has been proposed as a way to prevent atopic disease. However, a recent large study, ie, the Promotion of Breastfeeding Intervention Trial, found no reduction in risk of asthma or other atopic diseases at the age of 6 and a half years in breastfed children.
However, it is clear that lack of breastfeeding is associated with a fold increased risk of pneumonia in children. Another topic of importance in the development of childhood atopic diseases, including asthma, is dietary exposures in early life. Data for the same cohort focused on children with parental allergy, and demonstrated no protective effect of delayed food exposure on atopic outcomes. The only outcome that demonstrated some protection from delayed exposure was food allergen sensitization.
Food allergen sensitization was 3. One of the existing limitations in studying and diagnosing asthma in young children is that the pathological hallmarks of asthma, ie, airflow limitation and chronic airway inflammation, are difficult to measure objectively in young children. Many studies have tried to find a tool to predict asthma in early childhood wheezers, but this goal remains elusive. In a study by Castro Rodriguez el al, an attempt was made to create a tool, ie, the asthma predictive index, to help in identifying the likelihood of later development of asthma in children with wheezing early in childhood.
Investigators have also explored airway inflammatory markers as measured in exhaled breath condensates. Measurement of airway inflammatory markers in preschoolers with a history of persistent wheezing showed elevated airway inflammation markers, ie, IL-2, IL-4, IL-8, IL, and soluble intercellular adhesion molecules when compared with children without wheezing.
The fraction of exhaled nitric oxide FeNO has been proposed as a marker of eosinophilic-predominant inflammation in the airways. Several studies have reported higher levels of FeNO in preschoolers with recurrent wheezing and atopy when compared with other preschoolers who have wheezing without atopy. A prospective study compared the predictive values of single-breath FeNO, tidal breathing mixed FeNO, clinical response to bronchodilators, and the asthma predictive index devised by Castro Rodriguez et al in infants and toddlers with a history of recurrent wheezing over 3 years.
The single-breath FeNO measure had better sensitivity, specificity, and positive and negative predictive values for the prediction of a later diagnosis of asthma when compared with tidal FeNO, clinical response to bronchodilator, and the asthma predictive index. A new index to help identify future risk of wheezing in infants with a first episode of wheezing has been proposed by Zhang et al. Their personal and family history of atopic diseases was recorded.
Wheezing severity was evaluated using the Preschool Respiratory Assessment Measure. Sputum samples were collected from patients, stained with hematoxylin and eosin, and studied by optical microscopy. The number of shed exfoliated airway epithelial cells was counted. The predictive value of exfoliated airway epithelial cells counted, family or personal history of atopic disease, and severity of wheezing for subsequent development of wheezing were analyzed. A sensitivity of In a retrospective study designed to establish predictive factors for persistence of asthma during adolescence in a population of recurrent wheezing infants, infants younger than 36 months of age who had a history of at least three doctor-diagnosed wheezing episodes were evaluated.
At 13 years, active asthma was assessed by questionnaire. The results indicated that risk factors for asthma persisting into adolescence were: The conclusion of the study was that atopy is a major risk factor for persistence of asthma. Investigators have conducted interventional and observational studies to explore the potential of reducing the odds of development of asthma among children at higher risk. Interventions have included breastfeeding, probiotics, and reduction of exposure.
Childhood wheeze is common and is the cause of a large burden for the affected child, their family, and society at large. Clinicians are in need of simple-to-use, well-validated tools to determine which children who wheeze will progress to develop asthma. Over the last few decades, progress has been made in determining risk factors for the development of wheeze and asthma; however, efforts are hampered by the multiple phenotypes of asthma and the complexity of the disease.
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Investigators have attempted to identify clusters or phenotypes of childhood wheeze. Unfortunately, there is no simple consensus classification system for children with wheeze that would enhance research efforts. The most widely used classification system for childhood asthma is that proposed by the National Institutes of Health asthma management guidelines, but this system applies to children with asthma not infant wheeze.
A system for early classification of early childhood wheezers might help inform research of treatment options for different phenotypes. There are no genetic tests to identify which children who wheeze will develop asthma, and many of the genetic studies have not been replicated. Moreover, genetics only explain a small portion of the risk for development of asthma.
Many environmental factors contribute to the development of asthma. No single exposure has been associated with an increase in prevalence of asthma, so it is likely that the changes in asthma prevalence are likely related to a combination of environmental exposures and genetic susceptibility Figure 2. Clinicians are also hampered by a paucity of objective testing options that can be used to predict which children with wheeze will develop asthma.
Current predictive indices often can only be applied after many wheezing episodes, were developed solely based on expert opinion, or are of limited clinical applicability. Other objective tools involve maneuvers that are difficult for young children to perform or are of limited predictive value beyond specific individual asthma phenotypes.
Another challenge in the field is that early intervention studies among children who wheeze have demonstrated limited influence on the course of the disease or development of asthma. If efforts to intervene early in pathogenesis are of limited value, families may have less motivation to seek early treatment beyond acute episodes. Childhood wheeze is common and a substantial burden. Tools to identify children who will develop asthma are limited, and early intervention options have not proven efficacious. Additional research is needed to clarify childhood wheeze phenotypes, to develop tools that can determine which children will develop asthma, and to determine how and when to intervene.
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