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1.  Housing Shortages in Urban Regions: Aggressive Interactions at Tree Hollows in Forest Remnants 
PLoS ONE  2013;8(3):e59332.
Urbanisation typically results in a reduction of hollow-bearing trees and an increase in the density of particularly species, potentially resulting in an increased level of competition as cavity-nesting species compete for a limited resource. To improve understanding of hollow usage between urban cavity-nesting species in Australia, particularly parrots, we investigated how the hollow-using assemblage, visitation rate, diversity and number of interactions varied between hollows within urban remnant forest and continuous forest. Motion-activated video cameras were installed, via roped access to the canopy, and hollow usage was monitored at 61 hollows over a two-year period. Tree hollows within urban remnants had a significantly different assemblage of visitors to those in continuous forest as well as a higher rate of visitation than hollows within continuous forest, with the rainbow lorikeet making significantly more visitations than any other taxa. Hollows within urban remnants were characterised by significantly higher usage rates and significantly more aggressive interactions than hollows within continuous forest, with parrots responsible for almost all interactions. Within urban remnants, high rates of hollow visitation and both interspecific and intraspecific interactions observed at tree hollows suggest the number of available optimal hollows may be limiting. Understanding the usage of urban remnant hollows by wildlife, as well as the role of parrots as a potential flagship for the conservation of tree-hollows, is vital to prevent a decrease in the diversity of urban fauna, particularly as other less competitive species risk being outcompeted by abundant native species.
PMCID: PMC3605434  PMID: 23555657
2.  Diagnosing Patients with Age-Related Hearing Loss and Tinnitus: Supporting GP Clinical Engagement through Innovation and Pathway Redesign in Audiology Services 
The public health challenge of hearing impairment is growing, as age is the major determinant of hearing loss. Almost one in four (22.6%) over 75-year olds reports moderate or severe worry because of hearing problems. There is a 40% comorbidity of tinnitus and balance disorders. Good outcomes depend on early presentation and appropriate referral. This paper describes how the NHS Improvement Programme in England used service improvement methodologies to identify referral pathways and tools which were most likely to make significant improvements in diagnosing hearing loss, effective referrals and better patient outcomes. An audiometric screening device was used in GP surgeries to enable thresholds for effective referrals to be measured in the surgery. Revised referral criteria, the use of this device, new “assess and fit” technology in the audiology clinic, and direct access pathways can transform audiology service delivery so that patient outcomes are measurably better. This, in turn, changes the experience of GPs, so they are more likely to refer patients who can benefit from treatment. At the end of 2011, 51 GP practices in one of the audiology pilot areas had bought HearCheck screeners, a substantial development from the 4 practices who first engaged with the pilot.
PMCID: PMC3399359  PMID: 22829836
3.  Hearing in 44–45 year olds with m.1555A>G, a genetic mutation predisposing to aminoglycoside-induced deafness: a population based cohort study 
BMJ Open  2012;2(1):e000411.
The mitochondrial DNA mutation m.1555A>G predisposes to permanent idiosyncratic aminoglycoside-induced deafness that is independent of dose. Research suggests that in some families, m.1555A>G may cause non-syndromic deafness, without aminoglycoside exposure, as well as reduced hearing thresholds with age (age-related hearing loss).
To determine whether adults with m.1555A>G have impaired hearing, a factor that would inform the cost–benefit argument for genetic testing prior to aminoglycoside administration.
Population-based cohort study.
Individuals from the British 1958 birth cohort.
Hearing thresholds at 1 and 4 kHz at age 44–45 years; m.1555A>G genotyping.
19 of 7350 individuals successfully genotyped had the m.1555A>G mutation, giving a prevalence of 0.26% (95% CI 0.14% to 0.38%) or 1 in 385 (95% CI 1 in 714 to 1 in 263). There was no significant difference in hearing thresholds between those with and without the mutation. Single-nucleotide polymorphism analysis indicated that the mutation has arisen on a number of different mitochondrial haplogroups.
No data were collected on aminoglycoside exposure. For three subjects, hearing thresholds could not be predicted because information required for modelling was missing.
In this cohort, hearing in those with m.1555A>G is not significantly different from the general population and appears to be preserved at least until 44–45 years of age. Unbiased ascertainment of mutation carriers provides no evidence that this mutation alone causes non-syndromic hearing impairment in the UK. The findings lend weight to arguments for genetic testing for this mutation prior to aminoglycoside administration, as hearing in susceptible individuals is expected to be preserved well into adult life. Since global use of aminoglycosides is likely to increase, development of a rapid test is a priority.
Article summary
Article focus
Individuals who have the m.1555A>G mutation are exquisitely sensitive to rapid-onset hearing loss after receiving aminoglycosides at normal therapeutic levels.
We sought to determine whether a cohort of mature individuals with the m.1555A>G mutation have hearing loss by their mid-40s because the mutation has been reported to cause later-onset less severe hearing loss in people who have never been exposed to aminoglycosides. We wished to determine whether genetic screening prior to aminoglycoside administration is justified.
Key messages
This study demonstrates the prevalence of m.1555A>G to be 1 in 385 (95% CI 1 in 714 to 1 in 263) in the 1958 British birth cohort, confirming that this mutation occurs frequently in Caucasian populations.
The hearing of individuals with the m.1555A>G mutation is no different to that of the general population at age 44–45 years, in contrast to previous reports which suggested that hearing decreases with age in people with m.1555A>G; any such effect is not large and likely to be subject to previous ascertainment bias.
These findings lend weight to the argument for genetic testing for the m.1555A>G mutation prior to aminoglycoside administration in order to prevent avoidable hearing loss.
Strengths and limitations of this study
Hearing data have been collected prospectively, which avoids some of the biases inherent in studies related to deafness and hearing loss.
A potential limitation of the study was that data on aminoglycoside exposure were not collected.
PMCID: PMC3253422  PMID: 22223843
4.  Elements of statistical treatment of speech and hearing science data 
Many of the statistical issues involved in speech and hearing research are shared with other areas of medicine. This article is the first in a series intended to stimulate examination of research data in speech and hearing areas using a wide variety of techniques. This article specifically deals with two essential, but elementary, issues. The first is concerned with experimental design and choice of test data. The second, defines and explains statistical terms, concentrating particularly on the inference to the population mean from the sample mean.
PMCID: PMC2231513  PMID: 18259586
Statistics; experimental design; choice of data; inferential statistics
5.  Sexual dimorphism in immune response genes as a function of puberty 
BMC Immunology  2006;7:2.
Autoimmune diseases are more prevalent in females than in males, whereas males have higher mortality associated with infectious diseases. To increase our understanding of this sexual dimorphism in the immune system, we sought to identify and characterize inherent differences in immune response programs in the spleens of male and female mice before, during and after puberty.
After the onset of puberty, female mice showed a higher expression of adaptive immune response genes, while males had a higher expression of innate immune genes. This result suggested a requirement for sex hormones. Using in vivo and in vitro assays in normal and mutant mouse strains, we found that reverse signaling through FasL was directly influenced by estrogen, with downstream consequences of increased CD8+ T cell-derived B cell help (via cytokines) and enhanced immunoglobulin production.
These results demonstrate that sexual dimorphism in innate and adaptive immune genes is dependent on puberty. This study also revealed that estrogen influences immunoglobulin levels in post-pubertal female mice via the Fas-FasL pathway.
PMCID: PMC1402325  PMID: 16504066
6.  Fighting obesity 
BMJ : British Medical Journal  2004;329(7456):53.
PMCID: PMC443493  PMID: 15231635
8.  Prevalence of permanent childhood hearing impairment in the United Kingdom and implications for universal neonatal hearing screening: questionnaire based ascertainment study 
BMJ : British Medical Journal  2001;323(7312):536.
To estimate the prevalence of confirmed permanent childhood hearing impairment and its profile across age and degree of impairment in the United Kingdom.
Retrospective total ascertainment through sources in the health and education sectors by postal questionnaire.
Hospital based otology and audiology departments, community health clinics, education services for hearing impaired children.
Children born from 1980 to 1995, resident in United Kingdom in 1998, with severe permanent childhood hearing impairment (hearing level in the better ear >40 dB averaged over 0.5, 1, 2, and 4 kHz).
Main outcome measures
Numbers of cases with date of birth and severity of impairment converted to prevalences for each annual birth cohort (cases/1000 live births) and adjusted for underascertainment.
26 000 notifications ascertained 17 160 individual children. Prevalence rose from 0.91 (95% confidence interval 0.85 to 0.98) for 3 year olds to 1.65 (1.62 to 1.68) for children aged 9-16 years. Adjustment for underascertainment increased estimates to 1.07 (1.03 to 1.12) and 2.05 (2.02 to 2.08). Comparison with previous studies showed that prevalence increases with age, rather than declining with year of birth.
Prevalence of confirmed permanent childhood hearing impairment increases until the age of 9 years to a level higher than previously estimated. Relative to current yields of universal neonatal hearing screening in the United Kingdom, which are close to 1/1000 live births, 50-90% more children are diagnosed with permanent childhood hearing impairment by the age of 9 years. Paediatric audiology services must have the capacity to achieve early identification and confirmation of these additional cases.
What is already known on this topicThe prevalence of confirmed permanent childhood hearing impairment (>40 dB HL) in the United Kingdom has been estimated to rise with age to 1.33/1000 live births among children aged 5 years and olderIt has been predicted that only an additional 16% of children will remain to be detected in the postnatal years, given current yields from universal neonatal hearing screeningWhat this study addsThe prevalence of confirmed permanent childhood hearing impairment (>40 dB HL) in the United Kingdom has risen with age to at least 1.65/1000 live births (and may be as high as 2.05/1000 live births) among children 9 years of age and olderIf the current yield from screening is sustained, then an additional 50-90% of children will remain to be detected in the postnatal years
PMCID: PMC48157  PMID: 11546698
11.  The future role of genetic screening to detect newborns at risk of childhood-onset hearing loss 
To explore the future potential of genetic screening to detect newborns at risk of childhood-onset hearing loss.
An expert led discussion of current and future developments in genetic technology and the knowledge base of genetic hearing loss to determine the viability of genetic screening and the implications for screening policy.
Results and Discussion:
Despite increasing pressure to adopt genetic technologies, a major barrier for genetic screening in hearing loss is the uncertain clinical significance of the identified mutations and their interactions. Only when a reliable estimate of the future risk of hearing loss can be made at a reasonable cost, will genetic screening become viable. Given the speed of technological advancement this may be within the next 10 years. Decision-makers should start to consider how genetic screening could augment current screening programmes as well as the associated data processing and storage requirements.
In the interim, we suggest that decision makers consider the benefits of (1) genetically testing all newborns and children with hearing loss, to determine aetiology and to increase knowledge of the genetic causes of hearing loss, and (2) consider screening pregnant women for the m.1555A> G mutation to reduce the risk of aminoglycoside antibiotic-associated hearing loss.
PMCID: PMC3545543  PMID: 23131088
Horizon scanning; genetic screening; genetic testing; hearing loss; innovation

Results 1-11 (11)