University of Tasmania, Australia

The TAHS study was born in 1968, when all 8583 Tasmanian school children born in 1961 were surveyed for asthma and respiratory disorders with a questionnaire filled out by their parents. These children, referred to as the 1961 birth group, also had a medical examination and breathing tests. Their 16,266 parents and 21,043 of their brothers and sisters were also asked about their respiratory health using separate questionnaires.

Since 2002, a major follow-up program of all the participants has been undertaken, including a 40-year follow-up of the 1961 birth group (called probands), Sibling follow-up, Parents follow-up, a bronchial hyperreactivity (BHR) study and a Breast Density Study.

Tasmanian Longitudinal Health Study (TAHS)

The BOLD study is a very important international research survey looking at lung health in the community. The study has been conducted in 15 countries around the world.

In Australia, the study has been undertaken in:

• Sydney NSW
• Busselton WA
• The Kimberley WA
• Hobart and Launceston TAS
• Melbourne VIC
• Orange and Wagga Wagga NSW

This study will give us a better understanding of lung health in Australia. Experienced respiratory researchers will carry out an interview, and a number of lung function tests, with some sites also conducting an allergy test.

Burden of Lung Disease (BOLD) Study

Little is known about the frequency or severity of Idiopathic Pulmonary Fibrosis (IPF) in Australia. The National Australian IPF Registry will help researchers to better understand the nature of IPF and assist in developing future research into this disorder. Relevant information for people suffering with IPF will be obtained and entered into a national database located in New South Wales. This database will be used to further medical knowledge and to improve treatment of IPF in the future.

Idiopathic Pulmonary Fibrosis (IPF) Registry

The Australian Cochrane Airways Group Network was established in 2001 by a number of Australian review authors and editors associated with the Cochrane Airways Group as a collaborative to support Cochrane activities. The Network was established through funding from the Department of Health and Ageing. The Network is well represented around Australia, and now comprises clinical researchers in five centres including:


• 
Professors Michael Hensley and Peter Gibson, Newcastle, New South Wales

• Associate Professor Brian Smith, Adelaide, South Australia

• 
Professor E Haydn Walters, Werribee, Victoria

• 
Associate Professor Richard Wood-Baker, Hobart, Tasmania

• 
Professor Anne Chang, Brisbane, Queensland and Darwin, NT


The Network meets annually in conjunction with the Annual Scientific Meeting of the Thoracic Society of Australia & New Zealand. The ACAGN often holds a review completion workshop in association with this meeting, where senior members of the Collaboration are available to assist review authors to progress individual Cochrane reviews.

Since 2001 the Network has provided an annual postgraduate scholarship to support the development or updating of Cochrane Systematic Reviews and their dissemination though presentations at local or national meetings. In 2004 annual scholarships supporting students in their first health-related degree were added to the scholarship programme, to further support the training of new authors and the completion or updating of Cochrane reviews.

Australian Cochrane Airways Group Network (ACAGN)

Chronic Obstructive Pulmonary Disease (COPD) has a profound impact on the health-related quality of life (HRQoL) in sufferers, is a major contributor to the burden of disease in Australia, and is ranked amongst the top causes of hospitalisation. We have developed a new model for COPD care involving community health nurse mentoring to increase self-efficacy, and have performed a cluster-randomised study design of participants with COPD recruited from general practices to compare our model with usual care provided in the community. Participants recruited to the active arm had an individual management plan and worked in partnership with participants to achieve behavioural change through a cycle of goal setting and action planning.

A total of 34 mentors were trained, of which 29 were community health nurses. A total of 182 patients with COPD were recruited to the study, 90 allocated to mentoring and 92 to the telephone call control group. The study has been completed and is subsequently being analysed. We aso interviewed a sub-group of patients who have completed the study to identify reasons for perseverance or discontinuation of the mentoring process.

The PCCC is a randomised controlled clinical trial, the Participant-CENTREd Continuum of Care (PCCC) in COPD. This study compares health-mentoring for self-management support via telephone with a home-based walking action plan plus pulmonary rehabilitation, compared to pulmonary rehabilitation alone. Delivery of health-mentoring is by community-based nurses trained in the ‘CENTREd’ Model for Self-Management Support which comprises the elements:

• Commit to partnership
• Engage and establish a mutually agreed agenda
• Negotiate goals
• Take action to address goals
• Repeat back decisions and information
• Establish planned proactive follow-up

Embedded in the Model is the ‘SNAPPS’ Health-Management Framework (Smoking, Nutrition, Alcohol, Physical activity, Psychosocial well-being and Symptom management), which has been endorsed by the Department of Health in Tasmania and provides a holistic focus on health.

This study will collect on health-related quality of life using the COPD Assessment Test, physical capacity measured by distance walked in the 6-minute walk test and hospital admissions.

A high proportion of smokers want to stop smoking and make attempts to quit but most attempts are not successful. We are studying new methods to support motivated smokers to quit and improve success rates. This research will help improve quit smoking education. Using a mobile device, we want to find out more about the situations and moods that make smoking more likely, so that we can provide help for smokers when they need it most.

COBS Study on UMORE

Research suggests that starting to use nicotine patches in the two weeks before a quit attempt can be more effective than only using patches after the quit date. In this project, we want to learn more about the mechanisms behind this effect.

PQP Study on UMORE

Cue-induced cravings have been shown to be one of the main influences in relapsing during a quit attempt. At present, there are few effective treatments available for treating cue-induced cravings. Acute administration of nicotine via gum and lozenge has been shown to have efficacy in reducing the duration of cue-induced cravings, however, such treatments are not a feasible option for all quitters. This study aims to evaluate whether cognitive coping techniques can speed the recovery from such craving episodes, which would indicate that the technique is useful for the treatment of cue-induced cravings. The results of this research will inform future smoking cessation interventions about effective techniques to deal with cravings and prevent relapses.

The PRIME project examines how far smokers who are uninterested in quitting can be encouraged to quit by providing advice and treatment.

This project will examine the effects of vitamin D in vitro on immune responses in asthmatics, people with chronic obstructive pulmonary disease (COPD), and healthy controls. Asthma and COPD show some seasonality, and it may be that fluctuating yearly vitamin D levels affect these diseases. Asthma is a disease mediated by T helper 2 cells (Th2), which control antibody responses. COPD, on the other hand, is mediated by T helper 1 cells (Th1), which are responsible for cellular responses.

Persons with diseases such as asthma have an over-exuberant Th2 response when challenged, whilst people with COPD are Th1 biased. There is evidence that low vitamin D drives Th1 activation, whereas high vitamin D drives Th2. Thus in summer, when vitamin D is high, asthma may be worse. In winter, when vitamin D is low, COPD may be worse.

We hypothesise that adding vitamin D in vitro to cells from healthy controls, asthma and COPD persons will have different results. In comparison to healthy controls, people with asthma will produce high levels of the Th2 cytokines (chemical messengers) Interleukins-4, -5, -6 and -13. In those with COPD, vitamin D will swing their immune response from Th1 towards Th2, resulting in a decrease in the Th1 cytokines IFNγ and TNFα and a more normal response. Further, we hypothesise that vitamin D will promote T regulatory cells, an important subset of cells responsible for controlling autoimmunity and normal immune reactions.

Data on airway changes in COPD are more extensive than in relatively physiological unimpaired smokers. The predominant picture in established COPD is of an inflammatory disease consisting of largely mononuclear cell infiltrate, with predominance of CD8+ T lymphocytes and macrophages, and some increase in neutrophils. In addition, information on airway wall remodelling is limited, but suggests a general increase in volume in both small and large airways.

We have recruited 80 smoking subjects to the current smoking cessation study. Of these, 64 had normal lung function, 9 small airways disease and 7 COPD. We have identified novel splitting of the basement membrane in COPD compared to normal subjects and that the surface area of vessels in the lamina propria is higher in normal than smoking COPD subjects. Endobronchial biopsies stained for S100A4 (a fibroblast epitope), epidermal growth factor receptors (EGFR), and matrix metalloproteinase-9 (MMP-9) have identified marked fragmentation of the respiratory basement membrane in all smoking groups. We have established that markers of EMT are evident in biopsies from all current smokers but are most consistently striking where there is physiological airway obstruction.

Chronic Obstructive Pulmonary Disease (COPD) is characterised by progressive fixed airflow limitation and is associated with chronic airway inflammation, usually due to inhalation of tobacco smoke. A new component of remodelling in inflammatory respiratory diseases, that may especially be applicable to COPD, involves differentiation of airway epithelial cells to a mesenchymal phenotype, with subsequent migration through the reticular basement membrane (Rbm) to the subepithelial lamina propria, a process termed epithelial mesenchymal transition (EMT). Of particular interest and importance is that EMT is closely related to the development of invasive malignancy, which is a major hazard in COPD.

The aim this project is to further examine the inflammatory and transcription factor processes underlying EMT in the airways of smokers compared to control non-smokers and their relationship to the continuing self-propagating nature of COPD once it has begun despite quitting smoking. Control of EMT is unclear. However, in-vitro studies have shown there are several inflammatory mechanisms that bear scrutiny, including the receptor for advanced glycation end products (RAGE), the transforming growth factor ß (TGF-ß) and TWIST, regarded as a "master" gene transcription regulator in embryogenesis and cancer. The changes to the extracellular matrix (ECM) that occur as a consequence of EMT will also be investigated and related to physiological change.

We intend to examine these factors in biopsies and primary epithelial cell cultures (PBECs) derived from airway brushings, and will use a variety of techniques including immunohistochemistry (IH), ELISA, in-situ hybridization (ISH) and reverse transcriptase polymerase chain reaction (RT-PCR).