Every player wins a prize? Family provision applications and bequests to charity

This research deals with the interaction of family provision law and charitable bequests in wills, including qualitative research relating to the practical issues arising with both legal practitioners and charities’ bequest officers.

Daddies, assistants and foolsbdifferentiation of male representations in present-day advertising.

This paper explores the way men are represented in present-day advertising. Most gender related studies have concentrated in studying women in advertising and claim that men are still represented as the dominant gender and in more active, independent and functional roles than women. This paper asks whether this still holds for advertising in the beginning of 21st century. Many cultural changes may have broken the earlier stereotypes, for example changes in the family life, attitudes toward various sexual identities, concepts of masculinity and femininity, and changes in cultural style.

The relationship of loneliness and social anxiety with children’s and adolescents’ online communication

Children and adolescents now communicate online to form and/or maintain relationships with friends, family, and strangers. Relationships in “real life” are important for children’s and adolescents’ psychosocial development; however, they can be difficult for those who experience feelings of loneliness and/or social anxiety. The aim of this study was to investigate differences in usage of online communication patterns between children and adolescents with and without self-reported loneliness and social anxiety. Six hundred and twenty-six students aged between 10-16 years completed a survey on the amount of time they spent communicating online, the topics they discussed, the partners they engaged with, and their purposes for communicating over the Internet. Participants were administered a shortened version of the UCLA Loneliness Scale and an abbreviated sub-scale of the Social Anxiety Scale for Adolescents (SAS-A). Additionally, age and gender differences in usage of the aforementioned online communication patterns were examined across the entire sample. Findings revealed that children and adolescents who self-reported being lonely communicated online significantly more frequently about personal things and intimate topics than did those who did not self-report being lonely. The former were motivated to use online communication significantly more frequently to compensate for their weaker social skills to meet new people. Results suggest that Internet usage allows them to fulfill critical needs of social interactions, self-disclosure, and identity exploration. Future research, however, should explore whether or not the benefits derived from online communication may also facilitate lonely children’s and adolescents’ offline social relationships.

Listening, sharing understanding and facilitating consumer, family and community empowerment through a priority driven partnership in Far North Queensland

Objectives: This paper provides an example of a mental health research partnership underpinned by empowerment principles that seeks to foster strength among community organizations to support better outcomes for consumers, families and communities. It aims to raise awareness among researchers and service providers that empowerment approaches to assist communities to address mental health problems are not too difficult to be practical but require long-term commitment and appropriate support. Methods: A collaborative research strategy that has become known as the Priority Driven Research (PDR) Partnership emerged through literature review,consultations, Family Wellbeing Program delivery with community groups and activities in two discrete Indigenous communities. Progress to date on three of the four components of the strategy is described. Results: The following key needs were identified in a pilot study and are now being addressed in a research-based implementation phase: (i) gaining two-way understanding of perspectives on mental health and promoting universal awareness; (ii) supporting the empowerment of carers, families, consumers and at-risk groups through existing community organizations to gain greater understanding and control of their situation; (iii) developing pathways of care at the primary health centre level to enable support of social and emotional wellbeing as well as more integrated mental health care; (iv) accessing data to enable an ongoing process of analysis/sharing/planning and monitoring to inform future activity. Conclusion: One of the key learnings to emerge in this project so far is that empowerment through partnership becomes possible when there is a concerted effort to strengthen grassroots community organizations. These include social health teams and men’s and women’s groups that can engage local people in an action orientation. Key words: Aboriginal, empowerment, Indigenous, mental health.

AITPM Email Newsletter Volume 0902, February 2009: Presidents Message

President’s Report Hello fellow AITPM members, Welcome to the first edition of the AITPM National Newsletter for 2009! I trust we all had a relaxing break and managed to lose track of all things transport for just a little while. I know I had trouble doing so when hunting for a car space at the shopping centre, and experiencing new projects such as the Tugun Bypass – the new gateway between New South Wales and Queensland. Byron Bay is now as close as Noosa for those high profile beach goers of Brisbane. There was also my experience of the reduced posted speed of 90km/h on the Bruce Highway around the troublesome Gympie stretch, when returning from a short Fraser Coast holiday. I expect that this relatively inexpensive safety improvement will pay substantial dividends in terms of crash reduction. The Newsletter took its annual leave last month and is refreshed and ready for a new year to keep us all informed of the latest in traffic and transport engineering, planning and management. I would like to take this opportunity to acknowledge the ongoing significant contributions of many volunteers in the Newsletter’s production. Mr Andrew Hulse, AITPM’s Immediate Past National President, serves as the Editorial Coordinator on behalf of the Institute. Each Branch Committee also includes a Newsletter Coordinator and committee members frequently contribute as well. And the ongoing contributions of readers enable us to offer the Newsletter as a vehicle for dialogue and debate around our sector. If you would like to contribute please email AITPM’s administration officer Josephine Mitton at aitpm@aitpm.com or through your local Branch Committee. I would also like to welcome back on deck our Editor, Mr David Brown of Driven Media, who creates a fantastic package for us each month. Lastly, members would have received the Call for Papers for the AITPM 2009 National Conference, Traffic Beyond Tomorrow, to be held at the Adelaide Convention Centre between 5 – 7 August. Abstracts will be accepted up to 20 February 2009. We look forward to seeing everyone at this, our flagship event for the year. To all a good year ahead, Jon Bunker Post Script: We all will have seen through the media the enormous scale and nature of the two natural disasters Australia is experiencing at present. AITPM’s thoughts are with all of those members, family and friends who may be experiencing hardship as a result of the Victorian bushfires and North Queensland floods. AITPM is a not for profit organisation however the National Executive has taken the decision to donate in measure to the Red Cross Victorian Bushfire Disaster Relief fund and the Queensland Premier’s Disaster Relief fund as a gesture to support our fellow Australians in their time of need. Details about these funds can be found via the Victorian and Queensland Governments’ websites.

Investigating relationships between relationship quality, customer loyalty and cooperation : an empirical study of convenience stores' franchise chain systems in Taiwan

Franchising has been widely accepted as an effective way to conduct and expand businesses. However, a franchise system is not a guarantee of success in the market. A successful franchise system should rely on a close and strong franchising relationship. Franchising is an important relationship management business. Franchising arrangements normally last for a number of years, so the franchisor and franchisee in the arrangement relationship are usually motivated to cooperate with each other. In addition, highly loyal franchisees may be obtained through a successful long-term franchising relationship. Over the last few decades, there has been a tremendous wave of interest in franchising relationships. However, little research has been conducted to determine the reasons for long-term franchising relationships. As a result, this study focuses on the important elements that might lead to a successful long-term franchising relationship. This study attempts to examine empirically three essential constructs (relationship quality, cooperation and customer loyalty), which might lead to successful long-term franchising relationships between franchisees and franchisors among the convenience stores in Taiwan. Mailed questionnaires were utilised to collect the research data. A total of 500 surveys were mailed randomly to the manager/supervisor of convenience stores’ franchisees among the four main franchisors (7-ELEVEN, Family, Hi-Life and OK) in Taiwan. The final sample size is 120, yielding a response rate of 24 per cent. The results show that relationship quality positively influences the cooperative relationships between franchisors and franchisees. Relationship quality is also positively correlated with franchisees’ loyalty. Additionally, the results indicate that the cooperative relationships between franchisors and franchisees are significantly associated with franchisees’ loyalty.

AITPM Email Newsletter Volume 0905, May 2009: Presidents Message

President’s Message Hello fellow AITPM members, We’ve been offered a lot of press lately about the Federal Government’s plan for the multibillion dollar rollout of its high speed broadband network, which at the moment is being rated to a speed of 100Mb/s. This seems fantastic in comparison to the not atypical 250 to 500kb/s that I receive on my metropolitan cable broadband, which incidentally my service provider rates at theoretical speeds of up to 8 Mb/s. I have no doubt that such a scheme will generate significant advantages to business and consumers. However, I also have some reservations. Only a few of years ago I marvelled at my first 256Mb USB stick, which cost my employer about $90. Last month I purchased a 16Gb stick with a free computer carry bag for $80, which on the back of my envelope has given me about 72 times the value of my first USB stick not including the carry bag! I am pretty sure the technology industry will find a way to eventually push a lot more than 100Mb/s down the optic fibre network just as they have done with pushing several Mb/s ADSL2 down antique copper wire. This makes me wonder about the general problem of inbuilt obsolescence of all things high-tech due to rapid advances in the tech industry. As a transport professional I then think to myself that our industry has been moving forward at somewhat of a slower pace. We certainly have had major milestones having significant impacts, such as the move from horse and cart to the self propelled motor vehicle, sealing and formal geometric design of roads, development of motorways, signalisation of intersections, coordination of networks, to simulation modelling for real time adaptive control (perhaps major change has been at a frequency of 30 years or so?). But now with ITS truly penetrating the transport market, largely thanks to the in-car GPS navigator, smart phone, e-toll and e-ticket, I believe that to avoid our own obsolescence we’re going to need to “plan for ITS” rather than just what we seem to have been doing up until now, that is, to get it out there. And we’ll likely need to do it at a faster pace. It will involve understanding how to data mine enormous data sets, better understanding the human/machine interface, keeping pace with automotive technology more closely, resolving the ethical and privacy chestnuts, and in the main actually planning for ITS to make peoples’ lives easier rather than harder. And in amongst this we’ll need to keep pace with the types of technology advances similar to my USB stick example above. All the while we’ll be making a brand new set of friends in the disciplines that will morph into ITS along with us. Hopefully these will all be “good” problems for our profession to have. I should close in reminding everyone again that AITPM’s flagship event, the 2009 AITPM National Conference, Traffic Beyond Tomorrow, is being held in Adelaide from 5 to 7 August. www.aitpm.com has all of the details about how to register, sponsor a booth, session, etc. Best regards all, Jon Bunker

Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1

Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.

Modulation of the SHBG signalling axis

Sex hormone-binding globulin (SHBG) is a homodimeric plasma glycoprotein that is the major sex steroid carrier-protein in the bloodstream and functions also as a key regulator of steroid bioavailability within target tissues, such as the prostate. Additionally, SHBG binds to prostatic cell membranes via the putative and unidentified SHBG receptor (RSHBG), activating a signal transduction pathway implicated in stimulating both proliferation and expression of prostate specific antigen (PSA) in prostate cell lines in vitro. A yeast-two hybrid assay suggested an interaction between SHBG and kallikrein-related protease (KLK) 4, which is a serine protease implicated in the progression of prostate cancer. The potential interaction between these two proteins was investigated in this PhD thesis to determine whether SHBG is a proteolytic substrate of KLK4 and other members of the KLK family including KLK3/PSA, KLK7 and KLK14. Furthermore, the effects from SHBG proteolytic degradation on SHBG-regulated steroid bioavailability and the activation of the putative RSHBG signal transduction pathway were examined in the LNCaP prostate cancer cell line. SHBG was found to be a proteolytic substrate of the trypsin-like KLK4 and KLK14 in vitro, yielding several proteolysis fragments. Both chymotrypsin-like PSA and KLK7 displayed insignificant proteolytic activity against SHBG. The kinetic parameters of SHBG proteolysis by KLK4 and KLK14 demonstrate a strong enzyme-substrate binding capacity, possessing a Km of 1.2 ± 0.7 µM and 2.1 ± 0.6 µM respectively. The catalytic efficiencies (kcat/Km) of KLK4 and KLK14 proteolysis of SHBG were 1.6 x 104 M-1s-1 and 3.8 x 104 M-1s-1 respectively, which were comparable to parameters previously reported for peptide substrates. N-terminal sequencing of the fragments revealed cleavage near the junction of the N- and C-terminal laminin globulin-like (G-like) domains of SHBG, resulting in the division of the two globulins and ultimately the full degradation of these fragments by KLK4 and KLK14 over time. Proteolytic fragments that may retain steroid binding were rapidly degraded by both proteases, while fragments containing residues beyond the steroid binding pocket were less degraded over the same period of time. Degradation of SHBG was inhibited by the divalent metal cations calcium and zinc for KLK4, and calcium, zinc and magnesium for KLK14. The human secreted serine protease inhibitors (serpins), α1-antitrypsin and α2-antiplasmin, inhibited KLK4 and KLK14 proteolysis of SHBG; α1-antichymotrypsin inhibited KLK4 but not KLK14 activity. The inhibition by these serpins was comparable and in some cases more effective than general trypsin protease inhibitors such as aprotinin and phenylmethanesulfonyl fluoride (PMSF). The binding of 5α-dihydrotestosterone (DHT) to SHBG modulated interactions with KLK4 and KLK14. Steroid-free SHBG was more readily digested by both enzymes than DHT-bound SHBG. Moreover, a binding interaction exists between SHBG and pro-KLK4 and pro-KLK14, with DHT strengthening the binding to pro-KLK4 only. The inhibition of androgen uptake by cultured prostate cancer cells, mediated by SHBG steroid-binding, was examined to assess whether SHBG proteolysis by KLK4 and KLK14 modulated this process. Proteolytic digestion eliminated the ability of SHBG to inhibit the uptake of DHT from conditioned media into LNCaP cells. Therefore, the proteolysis of SHBG by KLK4 and KLK14 increased steroid bioavailability in vitro, leading to an increased uptake of androgens by prostate cancer cells. Interestingly, different transcriptional responses of PSA and KLK2, which are androgen-regulated genes, to DHT-bounsd SHBG treatment were observed between low and high passage number LNCaP cells (lpLNCaP and hpLNCaP respectively). HpLNCaP cells treated with DHT-bound SHBG demonstrated a significant synergistic upregulation of PSA and KLK2 above DHT or SHBG treatment alone, which is similar to previously reported downstream responses from RSHBG-mediated signaling activation. As this result was not seen in lpLNCaP cells, only hpLNCaP cells were further investigated to examine the modulation of potential RSHBG activity by KLK4 and KLK14 proteolysis of SHBG. Contrary to reported results, no increase in intracellular cAMP was observed in hpLNCaP cells when treated with SHBG in the presence and absence of either DHT or estradiol. As a result, the modulation of RSHBG-mediated signaling activation could not be determined. Finally, the identification of the RSHBG from both breast (MCF-7) and prostate cancer (LNCaP) cell lines was attempted. Fluorescently labeled peptides corresponding to the putative receptor binding domain (RBD) of SHBG were shown to be internalized by MCF-7 cells. Crosslinking of the RBD peptide to the cell surfaces of both MCF-7 and LNCaP cells, demonstrated the interaction of the peptide with several targets. These targets were then captured using RBD peptides synthesized onto a hydrophilic scaffold and analysed by mass spectrometry. The samples captured by the RBD peptide returned statistically significantly matches for cytokeratin 8, 18 and 19 as well as microtubule-actin crosslinking factor 1, which may indicate a novel interaction between SHBG and these proteins, but ultimately failed to detect a membrane receptor potentially responsible for the putative RSHBG-mediated signaling. This PhD project has reported the proteolytic processing of SHBG by two members of the kallikrein family, KLK4 and KLK14. The effect of SHBG proteolysis by KLK4 and KLK14 on RSHBG-mediated signaling activation was unable to be determined as the reported signal transduction pathway was not activated after treatment with SHBG, in combination with either DHT or estradiol. However, the digestion of SHBG by these two proteases positively regulated androgen bioavailability to prostate cancer cells in vitro. The increased uptake of androgens is deleterious in prostate cancer due to the promotion of proliferation, metastasis, invasion and the inhibition of apoptosis. The increased bioavailability of androgens, from SHBG proteolysis by KLK4 and KLK14, may therefore promote both carcinogenesis and progression of prostate cancer. Finally, this information may contribute to the development of therapeutic treatment strategies for prostate cancer by inhibiting the proteolysis of SHBG, by KLK4 and KLK14, to prevent the increased uptake of androgens by hormone-dependent cancerous tissues.

The family attitude scale : reliability and validity of a new scale for measuring the emotional climate of families

Research on outcomes from psychiatric disorders has highlighted the importance of expressed emotion (EE), but its cost-effective measurement remains a challenge. This article describes development of the Family Attitude Scale (FAS), a 30-item instrument that can be completed by any informant. Its psychometric characteristics are reported in parents of undergraduate students and in 70 families with a schizophrenic member. The total FAS had high internal consistency in all samples, and reports of angry behaviour in FAS items showed acceptable inter-rater agreement. The FAS was associated with the reported anger, anger expression and anxiety of respondents. Substantial associations between the parents' FAS and the anger and anger expression of students was also observed. Parents of schizophrenic patients had higher FAS scores than parents of students, and the FAS was higher if disorder duration was longer or patient functioning was poorer. Hostility, high criticism and low warmth on the Camberwell Family Interview (CFI) were associated with a more negative FAS. The highest FAS in the family was a good predictor of a highly critical environment on the CFI. The FAS is a reliable and valid indicator of relationship stress and expressed anger that has wide applicability.

Domestic violence in the urban fringe

Police call data for domestic violence incidents in the city of Brisbane were used to further explore the locational disadvantage thesis. it was hypothesised that the supposed additional burdens and stresses on disadvantaged families living in the outer suburbs may be reflected in significantly higher rates of reported domestic violence. Using an index of relative socioeconomic disadvantage and employing Analysis of variance (ANOVA) this research shows that significantly higher rates of reported domestic violence occur in the inner suburbs relative to the middle or outer suburbs of Brisbane. This finding adds further doubt to the magnitude of locational disadvantage impacts on outer suburban low income family households.

Entrepreneurship and family firms : growth and survival

Family businesses dominate in a majority of economies (Astrachan and Shanker, 2003; Chrisman, Chua, and Sharma, 2005; Morck and Yeung, 2004). As entrepreneurial activities have been shown to be central to economic growth it is essential that family businesses, irrespective of ownership patterns, not only survive but also grow thus growing the economy overall. While a great deal is known about entrepreneurial activities and a body of knowledge is being developed in relation to entrepreneurial processes in family firms, more needs to be understood in relation to the dynamics of entrepreneurial activities at the individual family firm level. One area of particular interest is the dynamics within the business and the family and how these dynamics impact upon entrepreneurial activities. Specifically how relationships between and among family members engaged in the business can interact with professional non-family member senior executives. The senior executives can actively use their positions in such ways that initiatives suggested by family members are less successful than they might be. This paper addresses how ‘family��� aspects of a business can assist or impede the entrepreneurial activities of individuals. It takes into account some of the unique features of family businesses – such as the importance of ‘familiness’ as a competitive advantage; the direct links between ownership and control of a business and the recognition (often implicit) that individuals in families do make a difference to how the business functions (Habbershon and Williams, 1999, Sharma, 2004; and Tokarczyk, Hansen Green, and Down, 2007). This emphasis on individuals in families fits well with the idea of entrepreneur as individual, as expressed by Schumpeter (1934), Baumol et al (2007). The theoretical approach that adopted to explore the dynamics of processes occurring within family firms is structuration theory combined with a theory of embeddeness (Dacin, Ventresca and Beal, 1999; Giddens, 1979, 1984, Jack and Anderson, 2002; and Sarason, Dean and Dillard, 2006).

Parent and child experiences of childhood cancer : an interpretative phenomenological analysis approach

A diagnosis of cancer represents a significant crisis for the child and their family. As the treatment for childhood cancer has improved dramatically over the past three decades, most children diagnosed with cancer today survive this illness. However, it is still an illness which severely disrupts the lifestyle and typical functioning of the family unit. Most treatments for cancer involve lengthy hospital stays, the endurance of painful procedures and harsh side effects. Research has confirmed that to manage and adapt to such a crisis, families must undertake measures which assist their adjustment. Variables such as level of family support, quality of parents’ marital relationship, coping of other family members, lack of other concurrent stresses and open communication within the family have been identified as influences on how well families adjust to a diagnosis of childhood cancer. Theoretical frameworks such as the Resiliency Model of Family Adjustment and Adaptation (McCubbin and McCubbin, 1993, 1996) and the Stress and Coping Model by Lazarus and Folkman (1984) have been used to explain how families and individuals adapt to crises or adverse circumstances. Developmental theories have also been posed to account for how children come to understand and learn about the concept of illness. However more descriptive information about how families and children in particular, experience and manage a diagnosis of cancer is still needed. There are still many unanswered questions surrounding how a child adapts to, understands and makes meaning from having a life-threatening illness. As a result, developing an understanding of the impact that such a serious illness has on the child and their family is crucial. A new approach to examining childhood illness such as cancer is currently underway which allows for a greater understanding of the experience of childhood cancer to be achieved. This new approach invites a phenomenological method to investigate the perspectives of those affected by childhood cancer. In the current study 9 families in which there was a diagnosis of childhood cancer were interviewed twice over a 12 month period. Using the qualitative methodology of Interpretative Phenomenological Analysis (IPA) a semi-structured interview was used to explicate the experience of childhood cancer from both the parent and child’s perspectives. A number of quantitative measures were also administered to gather specific information on the demographics of the sample population. The results of this study revealed a number of pertinent areas which need to be considered when treating such families. More importantly experiences were explicated which revealed vital phenomena that needs to be added to extend current theoretical frameworks. Parents identified the time of the diagnosis as the hardest part of their entire experience. Parents experienced an internal struggle when they were forced to come to the realization that they were not able to help their child get well. Families demonstrated an enormous ability to develop a new lifestyle which accommodated the needs of the sick child, as the sick child became the focus of their lives. Regarding the children, many of them accepted their diagnosis without complaint or question, and they were able to recognise and appreciate the support they received. Physical pain was definitely a component of the children’s experience however the emotional strain of loss of peer contact seemed just as severe. Changes over time were also noted as both parental and child experiences were often pertinent to the stage of treatment the child had reached. The approach used in this study allowed for rich and intimate detail about a sensitive issue to be revealed. Such an approach also allowed for the experience of childhood cancer on parents and the children to be more fully realised. Only now can a comprehensive and sensitive medical and psychosocial approach to the child and family be developed. For example, families may benefit from extra support at the time of diagnosis as this was identified as one of the most difficult periods. Parents may also require counselling support in coming to terms with their lack of ability to help their child heal. Given the ease at which children accepted their diagnosis, we need to question whether children are more receptive to adversity. Yet the emotional struggle children battled as a result of their illness also needs to be addressed.