Clinical outcomes associated with screening and referral for depression in an acute cardiac ward

Aim.  The aim of this paper is to describe the implementation of a depression screening and referral tool in two cardiac wards of a major metropolitan public hospital. The tool consisted of two sections: (1) screening for depression risk (Cardiac Depression Scale-5) and (2) consequential referral actions.

Background.  Prior research has shown that depression in patients with heart disease is associated with significantly impaired quality of life, decreased medication adherence, increased morbidity and increased use of healthcare services.

Design.  A prospective in-patient study design.

Method.  A consecutive sample of 202 patients admitted to either the cardiac medical (n = 145) or surgical (n = 57) wards of a major Melbourne metropolitan hospital were recruited into the study over an 18-week period.

Results.  Just over half (54%) of the patients were identified as ‘at risk’ of depression. Of these, 19% were assessed as moderate risk and 35% high risk. Of those patients, 91% had the risk score documented in their medical history, 90% had engaged in discussions with clinicians regarding their risk score, 85% had their risk score communicated formally to the medical team and 25% were formally referred for appropriate follow-up – significantly more than prior to implementation of the screening and referral tool.

Conclusions.  By providing a formalised mechanism for detecting depression, documented screening and referral rates improved for those with comorbid depression and heart disease affording an opportunity for early intervention. These findings support a move towards integrated approaches to screening of depression to become standard practice in the acute cardiac setting.

Relevance to clinical practice.  Such mechanisms also have the potential to initiate the development of new models of care that acknowledge the complexity of comorbid depression and heart disease and provide pathways from speciality to primary care which integrate the physical and psychosocial domains inclusive of screening, referral, systematic monitoring and streamlined behavioural and physical care.

Help-seeking pathways in early psychosis

INTRODUCTION: Understanding the help-seeking pathways of patients with a putative risk of developing psychosis helps improving development of specialised care services. This study aimed at obtaining information about: type of health professionals contacted by patients at putative risk for psychosis on their help-seeking pathways; number of contacts; type of symptoms leading to contacts with health professionals; interval between initial contact and referral to a specialised outpatient service. METHOD: The help-seeking pathways were assessed as part of a prospective study in 104 patients with suspected at-risk states for psychosis. RESULTS: The mean number of contacts prior to referral was 2.38. Patients with psychotic symptoms more often contacted mental health professionals, whereas patients with insidious and more unspecific features more frequently contacted general practitioners (GPs). CONCLUSIONS: GPs have been found to under-identify the insidious features of emerging psychosis (Simon et al. (2005) Br J Psychiatry 187:274-281). The fact that they were most often contacted by patients with exactly these features calls for focussed and specialised help for primary care physicians. Thus, delays along the help-seeking pathways may be shortened. This may be of particular relevance for patients with the deficit syndrome of schizophrenia.

Delays in diagnosis and referral and treatment for hematologic malignancies

The purpose of this thesis project was to identify factors that may contribute to a delay in the diagnosis, referral or treatment of the hematologic malignancies. This thesis is a secondary data analysis of both qualitative and quantitative data collected during a pilot study for a parent CDC study to determine factors related to time to diagnosis, referral, and treatment of chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), multiple myeloma (MM), and myelodisplastic syndrome (MDS). To identify patterns for referral, as well as explore referral, treatment, and follow-up patterns, MDACC performed a pathways analysis, and conducted semi-structured interviews with hematologic cancer patients to help identify factors related to delays. Interviews were also conducted with primary care physicians and community hematologists/oncologists to help identify factors associated with optimal and sub-optimal patterns of diagnosis and referral. The results of these analyses suggest a set of factors that may be related to a fairly smooth and rapid trajectory to treatment, and factors that may be related to a slower, more disrupted trajectory. Factors that may be especially important to facilitating rapid treatment include the presence of cues to seek diagnosis in the patient's environment and the patient recognizing and acting upon these cues to seek immediate medical attention. Furthermore, providers who perform behaviors including recognizing cues as indicators of hematologic malignancies and conducting appropriate diagnostic testing effectively and efficiently indicate that these behaviors may also contribute to shorter times to diagnosis. In regards to referrals, direct and effective communication between providers and patients, as well between providers themselves helped facilitate speedier referrals. A patient's insurance status as well as the presence or absence of social support in his environment served as factors that may increase or decrease time to diagnosis, referral, and treatment for a hematologic malignancy. Further research is needed to define delay to diagnosis, referral and treatment in order to improve early diagnosis, referral, and treatment of hematologic malignancies.^

Depression screening and referral in cardiac wards: A 12-month patient trajectory

Background: Depression is common among patients with coronary heart disease (CHD) and has a major impact on their quality of life, morbidity and mortality. Aim: The aim of this study was to map the 12-month psychosocial outcomes of patients with CHD who were screened positive for depression in an acute cardiac ward.

Methods: A prospective cohort study was conducted of the psychosocial trajectory (depression, anxiety, wellbeing, social support, mental health service access) of 212 patients with CHD who were screened for depression after being admitted to acute cardiac wards of a major metropolitan hospital. Outcomes were assessed before hospital discharge and at one, three, six and 12 months post-discharge.

Results: Linear mixed models identified that those patients screened at ‘moderate to high’ risk of depression at baseline had higher levels of depression (F(1,173)=53.93, p<0.0001) and anxiety (F(1,180)=67.01, p<0.001), and lower levels of wellbeing (F(1,186)=42.47, p<0.001) and social support (F(1,177)=25.40, p<0.0001), compared to those at ‘no to low’ risk of depression. Levels of depression and wellbeing remained fairly constant over the 12-month trajectory. Surgical and medical treatment groups were of similar psychological composition over the 12-month period.

Conclusions: These findings attest to the effectiveness and predictive validity of a simple nurse-administered screening tool designed to identify depression in hospital patients with CHD and also indicate that a screening and referral tool alone is not sufficient to achieve optimal disease management. A collaborative care model involving family members and integrated pathways to primary care is recommended.

Contrast sensitivity changes due to glaucoma and normal aging: low-spatial-frequency losses in both magnocellular and parvocellular pathways

PURPOSE: To explore the effects of glaucoma and aging on low-spatial-frequency contrast sensitivity by using tests designed to assess performance of either the magnocellular (M) or parvocellular (P) visual pathways. METHODS: Contrast sensitivity was measured for spatial frequencies of 0.25 to 2 cyc/deg by using a published steady- and pulsed-pedestal approach. Sixteen patients with glaucoma and 16 approximately age-matched control subjects participated. Patients with glaucoma were tested foveally and at two midperipheral locations: (1) an area of early visual field loss, and (2) an area of normal visual field. Control subjects were assessed in matched locations. An additional group of 12 younger control subjects (aged 20-35 years) were also tested. RESULTS: Older control subjects demonstrated reduced sensitivity relative to the younger group for the steady (presumed M)- and pulsed (presumed P)-pedestal conditions. Sensitivity was reduced foveally and in the midperiphery across the spatial frequency range. In the area of early visual field loss, the glaucoma group demonstrated further sensitivity reduction relative to older control subjects across the spatial frequency range for both the steady- and pulsed-pedestal tasks. Sensitivity was also reduced in the midperipheral location of "normal" visual field for the pulsed condition. CONCLUSIONS: Normal aging results in a reduction of contrast sensitivity for the low-spatial-frequency-sensitive components of both the M and P pathways. Glaucoma results in a further reduction of sensitivity that is not selective for M or P function. The low-spatial-frequency-sensitive channels of both pathways, which are presumably mediated by cells with larger receptive fields, are approximately equivalently impaired in early glaucoma.

Australia : The Challenges of Poverty, Pedagogy, and Pathways

A discussion of 2008/2009 developments in Australian educational policy, with specific reference to the adoption of US and UK trends in accountability, testing and school reform.

End-of-life care pathways for improving outcomes in caring for the dying (Protocol)

We aim to assess the effects of end-of-life care pathways, compared with usual care or with care guided by another end-of-life care pathway across all healthcare settings (hospitals, residential aged care facilities, community). In particular, we aim to assess the effects on symptom severity and quality of life of people who are dying and/or those related to the care such as families, caregivers and health professionals.

End-of-life care pathways for improving outcomes in caring for the dying (Review)

Background In many clinical areas, integrated care pathways are utilised as structured multidisciplinary care plans which detail essential steps in caring for patients with specific clinical problems. Particularly, care pathways for the dying have been developed as a model to improve the end-of-life care of all patients. They aim to ensure that the most appropriate management occurs at the most appropriate time and that it is provided by the most appropriate health professional. Clinical pathways for end-of-life care management are used widely around the world and have been regarded as the gold standard. Therefore, there is a significant need for clinicians to be informed about the utilisation of end-of-life care pathways with a systematic review. Objectives To assess the effects of end-of-life care pathways, compared with usual care (no pathway) or with care guided by another end-of-life care pathway across all healthcare settings (e.g. hospitals, residential aged care facilities, community). Search strategy The Cochrane Register of controlled Trials (CENTRAL), the Pain, Palliative and Supportive Care Review group specialised register,MEDLINE, EMBASE, review articles and reference lists of relevant articles were searched. The search was carried out in September 2009. Selection criteria All randomised controlled trials (RCTs), quasi-randomised trial or high quality controlled before and after studies comparing use versus non-use of an end-of-life care pathway in caring for the dying. Data collection and analysis Results of searches were reviewed against the pre-determined criteria for inclusion by two review authors. Main results The search identified 920 potentially relevant titles, but no studies met criteria for inclusion in the review. Authors’ conclusions Without further available evidence, recommendations for the use of end-of-life pathways in caring for the dying cannot be made. RCTs or other well designed controlled studies are needed for evaluating the use of end-of-life care pathways in caring for dying people.

Paving pathways : shaping the public health workforce through tertiary education

Public health educational pathways in Australia have traditionally been the province of Universities, with the Master of Public Health (MPH) recognised as the flagship professional entry program. Public health education also occurs within the fellowship training of the Faculty of Public Health Medicine, but within Australia this remains confined to medical graduates. In recent years, however, we have seen a proliferation of undergraduate degrees as well as an increasing public health presence in the Vocational Education and Training (VET) sector. ----- Following the 2007 Australian Federal election, the new Labour government brought with it a refreshing commitment to a more inclusive and strategic style of government. An important example of this was the 2020 visioning process that identified key issues of public health concern, including an acknowledgment that it was unacceptable to allocate less than 2% of the health budget towards disease prevention. This led to the recommendation for the establishment of a national preventive health agency (Australia: the healthiest country by 2020 National Preventative Health Strategy, Prepared by the Preventative Health Taskforce 2009). ----- The focus on disease prevention places a spotlight on the workforce that will be required to deliver the new investment in health prevention, and also on the role of public health education in developing and upskilling the workforce. It is therefore timely to reflect on trends, challenges and opportunities from a tertiary sector perspective. Is it more desirable to focus education efforts on selected lead issues such as the “obesity epidemic”, climate change, Indigenous health and so on, or on the underlying theory and skills that build a flexible workforce capable of responding to a range of health challenges? Or should we aspire to both? ----- This paper presents some of the key discussion points from 2008 – 2009 of the Public Health Educational Pathways workshops and working group of the Australian Network of Public Health Institutions. We highlight some of the competing tensions in public health tertiary education, their impact on public health training programs, and the educational pathways that are needed to grow, shape and prepare the public health workforce for future challenges.

Crosstalk between developmental and tumour-specific signalling pathways : kallikrein-related serine peptidases and nodal in prostrate cancer

Prostate cancer is an important male health issue. The strategies used to diagnose and treat prostate cancer underscore the cell and molecular interactions that promote disease progression. Prostate cancer is histologically defined by increasingly undifferentiated tumour cells and therapeutically targeted by androgen ablation. Even as the normal glandular architecture of the adult prostate is lost, prostate cancer cells remain dependent on the androgen receptor (AR) for growth and survival. This project focused on androgen-regulated gene expression, altered cellular differentiation, and the nexus between these two concepts. The AR controls prostate development, homeostasis and cancer progression by regulating the expression of downstream genes. Kallikrein-related serine peptidases are prominent transcriptional targets of AR in the adult prostate. Kallikrein 3 (KLK3), which is commonly referred to as prostate-specific antigen, is the current serum biomarker for prostate cancer. Other kallikreins are potential adjunct biomarkers. As secreted proteases, kallikreins act through enzyme cascades that may modulate the prostate cancer microenvironment. Both as a panel of biomarkers and cascade of proteases, the roles of kallikreins are interconnected. Yet the expression and regulation of different kallikreins in prostate cancer has not been compared. In this study, a spectrum of prostate cell lines was used to evaluate the expression profile of all 15 members of the kallikrein family. A cluster of genes was co-ordinately expressed in androgenresponsive cell lines. This group of kallikreins included KLK2, 3, 4 and 15, which are located adjacent to one another at the centromeric end of the kallikrein locus. KLK14 was also of interest, because it was ubiquitously expressed among the prostate cell lines. Immunohistochemistry showed that these 5 kallikreins are co-expressed in benign and malignant prostate tissue. The androgen-regulated expression of KLK2 and KLK3 is well-characterised, but has not been compared with other kallikreins. Therefore, KLK2, 3, 4, 14 and 15 expression were all measured in time course and dose response experiments with androgens, AR-antagonist treatments, hormone deprivation experiments and cells transfected with AR siRNA. Collectively, these experiments demonstrated that prostatic kallikreins are specifically and directly regulated by the AR. The data also revealed that kallikrein genes are differentially regulated by androgens; KLK2 and KLK3 were strongly up-regulated, KLK4 and KLK15 were modestly up-regulated, and KLK14 was repressed. Notably, KLK14 is located at the telomeric end of the kallikrein locus, far away from the centromeric cluster of kallikreins that are stimulated by androgens. These results show that the expression of KLK2, 3, 4, 14 and 15 is maintained in prostate cancer, but that these genes exhibit different responses to androgens. This makes the kallikrein locus an ideal model to investigate AR signalling. The increasingly dedifferentiated phenotype of aggressive prostate cancer cells is accompanied by the re-expression of signalling molecules that are usually expressed during embryogenesis and foetal tissue development. The Wnt pathway is one developmental cascade that is reactivated in prostate cancer. The canonical Wnt cascade regulates the intracellular levels of β-catenin, a potent transcriptional co-activator of T-cell factor (TCF) transcription factors. Notably, β-catenin can also bind to the AR and synergistically stimulate androgen-mediated gene expression. This is at the expense of typical Wnt/TCF target genes, because the AR:β-catenin and TCF:β-catenin interactions are mutually exclusive. The effect of β-catenin on kallikrein expression was examined to further investigate the role of β-catenin in prostate cancer. Stable knockdown of β-catenin in LNCaP prostate cancer cells attenuated the androgen-regulated expression of KLK2, 3, 4 and 15, but not KLK14. To test whether KLK14 is instead a TCF:β-catenin target gene, the endogenous levels of β-catenin were increased by inhibiting its degradation. Although KLK14 expression was up-regulated by these treatments, siRNA knockdown of β-catenin demonstrated that this effect was independent of β-catenin. These results show that β-catenin is required for maximal expression of KLK2, 3, 4 and 15, but not KLK14. Developmental cells and tumour cells express a similar repertoire of signalling molecules, which means that these different cell types are responsive to one another. Previous reports have shown that stem cells and foetal tissues can reprogram aggressive cancer cells to less aggressive phenotypes by restoring the balance to developmental signalling pathways that are highly dysregulated in cancer. To investigate this phenomenon in prostate cancer, DU145 and PC-3 prostate cancer cells were cultured on matrices pre-conditioned with human embryonic stem cells (hESCs). Soft agar assays showed that prostate cancer cells exposed to hESC conditioned matrices had reduced clonogenicity compared with cells harvested from control matrices. A recent study demonstrated that this effect was partially due to hESC-derived Lefty, an antagonist of Nodal. A member of the transforming growth factor β (TGFβ) superfamily, Nodal regulates embryogenesis and is re-expressed in cancer. The role of Nodal in prostate cancer has not previously been reported. Therefore, the expression and function of the Nodal signalling pathway in prostate cancer was investigated. Western blots confirmed that Nodal is expressed in DU145 and PC-3 cells. Immunohistochemistry revealed greater expression of Nodal in malignant versus benign glands. Notably, the Nodal inhibitor, Lefty, was not expressed at the mRNA level in any prostate cell lines tested. The Nodal signalling pathway is functionally active in prostate cancer cells. Recombinant Nodal treatments triggered downstream phosphorylation of Smad2 in DU145 and LNCaP cells, and stably-transfected Nodal increased the clonogencity of LNCaP cells. Nodal was also found to modulate AR signalling. Nodal reduced the activity of an androgen-regulated KLK3 promoter construct in luciferase assays and attenuated the endogenous expression of AR target genes including prostatic kallikreins. These results demonstrate that Nodal is a novel example of a developmental signalling molecule that is reexpressed in prostate cancer and may have a functional role in prostate cancer progression. In summary, this project clarifies the role of androgens and changing cellular differentiation in prostate cancer by characterising the expression and function of the downstream genes encoding kallikrein-related serine proteases and Nodal. Furthermore, this study emphasises the similarities between prostate cancer and early development, and the crosstalk between developmental signalling pathways and the AR axis. The outcomes of this project also affirm the utility of the kallikrein locus as a model system to monitor tumour progression and the phenotype of prostate cancer cells.

Diagnostic and treatment pathways for men with prostate cancer in Queensland : investigating spatial and demographic inequalities

Background: Patterns of diagnosis and management for men diagnosed with prostate cancer in Queensland, Australia, have not yet been systematically documented and so assumptions of equity are untested. This longitudinal study investigates the association between prostate cancer diagnostic and treatment outcomes and key area-level characteristics and individual-level demographic, clinical and psychosocial factors.---------- Methods/Design: A total of 1064 men diagnosed with prostate cancer between February 2005 and July 2007 were recruited through hospital-based urology outpatient clinics and private practices in the centres of Brisbane, Townsville and Mackay (82% of those referred). Additional clinical and diagnostic information for all 6609 men diagnosed with prostate cancer in Queensland during the study period was obtained via the population-based Queensland Cancer Registry. Respondent data are collected using telephone and self-administered questionnaires at pre-treatment and at 2 months, 6 months, 12 months, 24 months, 36 months, 48 months and 60 months post-treatment. Assessments include demographics, medical history, patterns of care, disease and treatment characteristics together with outcomes associated with prostate cancer, as well as information about quality of life and psychological adjustment. Complementary detailed treatment information is abstracted from participants’ medical records held in hospitals and private treatment facilities and collated with health service utilisation data obtained from Medicare Australia. Information about the characteristics of geographical areas is being obtained from data custodians such as the Australian Bureau of Statistics. Geo-coding and spatial technology will be used to calculate road travel distances from patients’ residences to treatment centres. Analyses will be conducted using standard statistical methods along with multilevel regression models including individual and area-level components.---------- Conclusions: Information about the diagnostic and treatment patterns of men diagnosed with prostate cancer is crucial for rational planning and development of health delivery and supportive care services to ensure equitable access to health services, regardless of geographical location and individual characteristics. This study is a secondary outcome of the randomised controlled trial registered with the Australian New Zealand Clinical Trials Registry (ACTRN12607000233426)

Differential roles of the pRb and Arf/p53 pathways in murine naevus and melanoma genesis

We report on a systematic analysis of genotype-specific melanocyte (MC) UVR responses in transgenic mouse melanoma models along with tumour penetrance and comparative histopathology. pRb or p53 pathway mutations cooperated with NrasQ61K to transform MCs. We previously reported that MCs migrate from the follicular outer root sheath into the epidermis after neonatal UVR. Here, we found that Arf or p53 loss markedly diminished this response. Despite this, mice carrying these mutations developed melanoma with very early age of onset after neonatal UVR. Cdk4R24C did not affect the MC migration. Instead, independent of UVR exposure, interfollicular dermal MCs were more prevalent in Cdk4R24C mice. Subsequently, in adulthood, these mutants developed dermal MC proliferations reminiscent of superficial congenital naevi. Two types of melanoma were observed in this model. The location and growth pattern of the first was consistent with derivation from the naevi, while the second appeared to be of deep dermal origin. In animals carrying the Arf or p53 defects, no naevi were detected, with all tumours ostensibly skipping the benign precursor stage in progression.

Visual field size criteria for mobility rehabilitation referral

Purpose. To investigate evidence-based visual field size criteria for referral of low-vision (LV) patients for mobility rehabilitation. Methods. One hundred and nine participants with LV and 41 age-matched participants with normal sight (NS) were recruited. The LV group was heterogeneous with diverse causes of visual impairment. We measured binocular kinetic visual fields with the Humphrey Field Analyzer and mobility performance on an obstacle-rich, indoor course. Mobility was assessed as percent preferred walking speed (PPWS) and number of obstacle-contact errors. The weighted kappa coefficient of association (κr) was used to discriminate LV participants with both unsafe and inefficient mobility from those with adequate mobility on the basis of their visual field size for the full sample and for subgroups according to type of visual field loss and whether or not the participants had previously received orientation and mobility training. Results. LV participants with both PPWS <38% and errors >6 on our course were classified as having inadequate (inefficient and unsafe) mobility compared with NS participants. Mobility appeared to be first compromised when the visual field was less than about 1.2 steradians (sr; solid angle of a circular visual field of about 70° diameter). Visual fields <0.23 and 0.63 sr (31 to 52° diameter) discriminated patients with at-risk mobility for the full sample and across the two subgroups. A visual field of 0.05 sr (15° diameter) discriminated those with critical mobility. Conclusions. Our study suggests that: practitioners should be alert to potential mobility difficulties when the visual field is less than about 1.2 sr (70° diameter); assessment for mobility rehabilitation may be warranted when the visual field is constricted to about 0.23 to 0.63 sr (31 to 52° diameter) depending on the nature of their visual field loss and previous history (at risk); and mobility rehabilitation should be conducted before the visual field is constricted to 0.05 sr (15° diameter; critical).