User satisfaction with train fares: A comparative analysis in five Australian cities.

In the public transport industry, travellers' perceived satisfaction is a key element in understanding their evaluation of, and loyalty to ridership. Despite its notable importance, studies of customer satisfaction are under-represented in the literature, and most previous studies are based on survey data collected from a single city only. This does not allow a comparison across different transport systems. To address this underrepresentation, this paper reports on a study of train passengers' satisfaction with the fare paid for their most recent home-based train trip in five Australian capital cities: Sydney, Melbourne, Brisbane, Adelaide, and Perth. Two data sources are used: a nation-wide survey, and objective information on the train fare structure in each of the targeted cities. In particular, satisfaction with train fares is modelled as a function of socio-economic factors and train trip characteristics, using a random parameters ordered Logit model that accounts for unobserved heterogeneity in the population. Results indicate that gender, city of origin, transport mode from home to the train station, eligibility for either student or senior concession fare, one-way cost, and waiting time as well as five diverse interaction variables between city of origin and socio-economic factors are the key determinants of passenger satisfaction with train fares. In particular, this study reveals that female respondents tend to be less satisfied with their train fare than their male counterparts. Interestingly, respondents who take the bus to the train station tend to feel more satisfied with their fare compared with the rest of the respondents. In addition, notable heterogeneity is detected across respondents' perceived satisfaction with train fare, specifically with regard to the one-way cost and the waiting time incurred. An intercity comparison reveals that a city's train fare structure also affects a traveller's perceived satisfaction with their train fare. The findings of this research are significant for both policy makers and transport operators, allowing them to understand traveller behaviours, and to subsequently formulate effective transit policies.

A direct-to-patient telemedicine abortion service in Australia: Retrospective analysis of the first 18 months.

BACKGROUND: In 2015, the Tabbot Foundation launched a nationwide direct-to-patient telemedicine service to enable women to obtain medical abortion without visiting an abortion provider. AIMS: We aimed to describe results from the first 18 months of this service. MATERIALS AND METHODS: To have an abortion through the Foundation, a woman obtained screening tests locally and had a telephone consultation with a Foundation doctor. If she was eligible, mifepristone, misoprostol and other medications were sent to her by mail. After taking the drugs, the woman obtained follow-up tests at local facilities and had a consultation with Foundation professionals. The Foundation charged $250 to patients with Medicare eligibility and $600 otherwise. We summarised clinical data collected by the service. RESULTS: Between June 2015 and December 2016, 1010 women received medications, of whom 56% lived outside of major cities. Ninety-five percent of packages were sent within 15 days after registration. Of the 965 women who took misoprostol, outcomes were definitively documented for 754 (78%), of whom 96% had a complete abortion without surgical intervention, and 95% had no face-to-face clinical encounter after treatment. Of women with Medicare cards, 72% paid no out-of-pocket charges other than to the Foundation. Nearly all women (781/802; 97%) were highly satisfied. CONCLUSIONS: The direct-to-patient telemedicine medical abortion service was effective, safe, inexpensive and satisfactory. It disproportionately served women in parts of Australia with limited access to abortion facilities. This experience may be instructive for others desiring to use telemedicine to enhance access to abortion.

An investigation of the effects of the antioxidants, ebselen or N-acetyl cysteine on human peripheral blood mononuclear cells and T cells.

BACKGROUND: The research literature has documented age-related increases in genetic damage, including oxidative DNA damage, in human T lymphocytes, in vitro and ex vivo. Such damage has the potential to interfere with the ability of the T cells to proliferate at times when they need to, such as when antigen challenged. The consequence of this could be a sub-optimal immune response in vivo. CONTEXT AND PURPOSE: The purpose of the research reported in this paper was to investigate the impact of two antioxidants, which can be administered in vivo, Ebselen and N-acetyl L-cysteine, on the age-related increase in genetic damage, and on T cell proliferation and lifespan. In vitro human T cell clones, ex vivo peripheral blood mononuclear cells or T cells were supplemented with different concentrations of antioxidants, under standard conditions and for different periods of time. A range of assays were then applied in order to determine any impact of the antioxidants. RESULTS: 30 µM ebselen or 7.5 mM N-acetyl L-cysteine supplementation resulted in a significantly higher intracellular GSH: GSSG ratio. This increased ratio was accompanied by reduced levels of oxidative DNA damage in established CD4+ human T cell clones, from a young or a middle-aged donor. Additionally, cultures of primary human peripheral blood mononuclear cells and CD4+ T cells from donors aged 25-30 or 55-60 years were also supplemented with these agents. Cells from all sources exhibited increased proliferation, and in the case of the T cell clones, an increase in cumulative population doublings. Neither ebselen nor N-acetyl L-cysteine had such effects on clones supplemented from the midpoint of their in vitro lifespan. CONCLUSIONS: Ebselen and N-acetyl L-cysteine, under certain conditions, may have anti-immunosenescent potential in T cells in in vitro clonal and ex vivo polyclonal culture models.

Flow-cytometric assessment of cellular poly(ADP-ribosyl)ation capacity in peripheral blood lymphocytes.

BACKGROUND: Poly(ADP-ribosyl)ation is a posttranslational modification of nuclear proteins catalysed by poly(ADP-ribose) polymerases (PARPs), using NAD+ as a substrate. Activation of PARP-1 is in immediate response to DNA damage generated by endogenous and exogenous damaging agents. It has been implicated in several crucial cellular processes including DNA repair and maintenance of genomic stability, which are both intimately linked with the ageing process. The measurement of cellular poly(ADP-ribosyl)ation capacity, defined as the amount of poly(ADP-ribose) produced under maximal stimulation, is therefore relevant for research on ageing, as well as for a variety of other scientific questions. RESULTS: This paper reports a new, robust protocol for the measurement of cellular poly(ADP-ribosyl)ation capacity in PBMC or Jurkat T-cells using flow cytometry, based on a previously established immuno-dot-blot assay. In order to validate the new assay, we determined the dose-response curve of 3-aminobenzamide, a well-known competitive PARP inhibitor, and we derived an IC50 that is very close to the published value. When testing a set of PBMC samples taken from fifteen healthy young human donors, we could confirm the presence of a substantial interindividual variation, as previously observed using a radiometric assay. CONCLUSION: The methodology described in this paper should be generally useful for the determination of cellular poly(ADP-ribosyl)ation capacity in a wide variety of settings, especially for the comparison of large sets of samples, such as population studies. In contrast to previously published radiometric or immuno-dot-blot assays, the new FACS-based method allows (i) selective analysis of mononuclear cells by gating and (ii) detection of a possible heterogeneity in poly(ADP-ribosyl)ation capacity between cells of the same type.

An investigation of DNA mismatch repair capacity under normal culture conditions and under conditions of supra-physiological challenge in human CD4+T cell clones from donors of different ages.

T cells undergo rapid clonal expansion upon antigenic stimulation to produce an effective immune response. Any defect in the DNA mismatch repair (MMR) system may have a detrimental effect on T cell proliferation. This study employed an in vitro model of human CD4+T cell ageing to investigate MMR capacity at various stages of T cell lifespan. A novel modification of the alkaline comet assay, which utilised T4 endonuclease VII to detect single base DNA mismatches, was used to assess DNA mismatch frequency. No clear pattern in DNA mismatch frequency with increasing culture age was observed. However, the ability to repair induced DNA mismatches (following treatment with acridine mutagen ICR-191) revealed an age-related decline in the efficiency of the MMR system in clones derived from a 26 and a 45-year-old donor, but not from an 80-year-old very healthy SENIEUR donor. This study suggests that unchallenged, dividing human T cell clones have variable levels of DNA mismatches throughout their lifespan, not affecting proliferation. However, when challenged with supra-physiological levels of DNA mismatches, deficiencies were found in ageing T cell clones in MMR capacity, with the exception of T cell clones from a SENIEUR donor previously shown to maintain effective DNA excision repair.

An investigation of DNA excision repair capacity in human CD4+ T cell clones as a function of age in vitro.

DNA damage has been shown to increase with age in lymphocytes of healthy humans and in human CD4+ T cell clones. Such genetic damage, if unrepaired, may have a detrimental effect on lymphocyte-mediated immune responses. This study investigated DNA excision repair capacity of human CD4+ T cell clones as a function of age in vitro. Cultures of T cell clones were treated with a range of DNA damaging agents; hydrogen peroxide, N-methyl-N'-nitro-N-nitrosoguanidine or 254 nm ultraviolet irradiation. Following treatment, the amount of DNA damage in the clones was determined over a time course using modified comet assays. The results obtained revealed a decline related to in vitro age in the DNA repair capacity of clones derived from a 26 and a 45 year old donor. This decline may represent at least a partial explanation for the age related increase in DNA damage in these clones when cultured in vitro. In contrast, there was no evidence for a decline related to in vitro age in repair capacity in the clones derived from an 80 year old SENIEUR donor. An alternative mechanism must underlie the age related increased in DNA damage in these clones when cultured in vitro.

Effects of a reduced oxygen tension culture system on human T cell clones as a function of in vitro age.

Oxidative DNA damage has been suggested to contribute to the decline in T cell clone (TCC) function with increased age in vitro. To test this hypothesis the effect of a reduced oxygen tension culture system (6% O(2)) on TCCs was examined. Specifically, the effects of the altered culture conditions on DNA damage levels, in vitro lifespan and proliferative capacity were assessed in five independently derived human CD4+ TCCs. DNA damage levels over the entire lifespan were significantly lowered by reducing oxygen tension. Lifespan (total population doublings (PDs) achieved) and proliferative capacity (PDs/week) were reduced for all clones under reduced oxygen tension when compared to standard culture conditions. This observed tendency warrants further investigation using a greater number of clones from donors of all age groups before definitive conclusions regarding the effect of low oxygen tension on the lifespan and proliferative capacity of TCC can be made. However, these results may suggest that the reduced oxygen tension culture system has interfered with some aspect of T cell biology not yet examined within the remit of this study.

HLA haplotypes and TNF polymorphism do not associate with longevity in the Irish.

Polymorphism of the human leukocyte antigen has been implicated in a number of autoimmune disorders including ageing. In the course of the present study, no association of the human leukocyte antigen (HLA)-A1, B8, DR3 haplotype with a male Irish aged population, as previously reported, was observed. Two polymorphic nucleotides in the TNF cluster (G-308A TNF-alpha and G+252A TNF-beta), associated with increased TNF-alpha production, were shown to be in tight linkage disequilibrium with the class I and II HLA loci, generating HLA haplotypes with extended linkage disequilibrium. However, no age-related allele or genotype frequencies were observed for either polymorphic nucleotide.

Linking team competences to organisational capacities in health care.

Palliative care is a complex environment in which teams of healthcare professionals are constantly challenged to match the configuration of care delivery to suit the dynamics of the patient's bio-medical, social and spiritual situations as they change during the end-of-life process. In such an environment these teams need to engage in ongoing interaction between different professional disciplines, incremental improvement in care delivery, learning and radical innovation. This is aimed at combining operational effectiveness, strategic flexibility, exploitation and exploration, in a way that ensures the best possible care for the patient. This paper examines previous research on the management competences and the organisational capabilities necessary for continuous innovation, and analyses evidence emerging from a study of palliative care. Work on the relationships between innovation capacities, organisational capabilities and team-based competence is drawn together. Evidence is presented from research into the management of innovation in palliative care.

Mitochondrial DNA damage in lymphocytes: a role in immunosenescence?

An age-related increase of DNA damage/mutation has been previously reported in human lymphocytes. The high copy number and mutation rate make the mtDNA genome an ideal candidate for assessing damage and to act as a potential biomarker of ageing. In the present study, two assays were developed to evaluate the level of mtDNA(4977) and the accumulation of point mutations with age. A competitive polymerase chain reaction (PCR) methodology incorporating three primers was used to detect and quantify the levels of mtDNA(4977) and a novel heteroduplex reference strand conformational analysis (RSCA) technique was used to analyse the accumulation of point mutations. The assays were applied to an in vitro model of T cell ageing and ex vivo DNA samples from an elderly cohort of subjects and a younger control group. The mtDNA(4977) was detected in all the DNA samples examined but only a very low concentration was observed and no age-related increase or accumulation was observed. No accumulation of point mutations was identified using RSCA within the T cell clones as they were aged or the ex vivo lymphocytes from the elderly cohort. A higher level of variation was observed within the ex vivo DNA samples, verifying the high resolution of RSCA and its ability to identify different mtDNA species, although no correlation with age was observed. The low level of mtDNA damage observed with respect to the ex vivo lymphocyte DNA samples within this study may be due in part to the high turnover of blood cells/mtDNA, which may inhibit the accumulation of genetically abnormal mtDNA that may play a role in immunosenescence. A similar explanation may also apply to the in vitro model of T cell ageing if the vast majority of the cells are replicating rather than entering senescence.

Nonagenarians from the Swedish NONA Immune Study have increased plasma antioxidant capacity and similar levels of DNA damage in peripheral blood mononuclear cells compared to younger control subjects.

The results of previous work from our laboratories have suggested that free radical damage to T cells as they age may contribute to the age-related decline in the T cell-mediated immune response. The aims of this investigation were to assess the efficiency of in vivo antioxidant capacity through determining the antioxidant capacity of plasma using the ferric reducing ability of plasma assay, and to assess the levels and types of DNA damage (as a measure of in vivo antioxidant efficiency) using the alkaline comet assay and two enzymatic modifications of the comet assay, in peripheral blood mononuclear cells (PBMCs) from nonagenarian subjects drawn from the Swedish NONA Immune Study. The results obtained were compared with those from middle-aged (40-60 years) controls to identify potential anti-immunosenescent effects of in vivo antioxidants. The results revealed a significantly higher plasma antioxidant capacity in NONA subjects compared to controls, and these results support a relationship between longevity and intact immune function, which may be underpinned by antioxidant defences which reduce free radical damage to PBMC, thus helping to maintain cell function. The NONA subjects were found to have similar levels of DNA damage in their PBMCs to those found in middle aged controls.