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Professor Jay Spencer Birnbrauer peacefully passed away on November 1, 2017, aged 83, in Perth, Western Australia. Known to his friends and colleagues in Australia as ‘Birny’, he was a pioneer of applied behaviour analysis on both the Australian and world stage. He contributed to the development of behaviour-analytic technology for children with intellectual and developmental disabilities in the 1960s and played a central part in the formation of the Australian Behaviour Modification Association (known today as the Australian Association for Cognitive and Behaviour Therapy) in the 1970s. He was a purist in the field of applied behaviour analysis (ABA) and was relentless in his efforts to see ABA being provided to children with a developmental disability and their families. Birny's influence in Australia, and particularly Western Australia, was mainly imparted through his role with the Master of Applied Psychology program at Murdoch University. His most widely known piece of work, the Murdoch Early Intervention Program, was an early and important replication of Lovaas's evaluation of early intensive behavioural intervention for children with autism. Birny contributed significantly to our field and to many people's lives. He is remembered often and fondly by his many friends and colleagues.
FFQ are commonly used to examine the association between diet and disease. They are the most practical method for usual dietary data collection as they are relatively inexpensive and easy to administer. In Australia, the Cancer Council of Victoria FFQ (CCVFFQ) version 2 and the online Commonwealth Scientific and Industrial Research Organisation FFQ (CSIROFFQ) are used. The aim of our study was to establish the level of agreement between nutrient intakes captured using the online CSIROFFQ and the paper-based CCVFFQ. The CCVFFQ and the online CSIROFFQ were completed by 136 healthy participants. FFQ responses were analysed to give g per d intake of a range of nutrients. Agreement between twenty-six nutrient intakes common to both FFQ was measured by a variety of methods. Nutrient intake levels that were significantly correlated between the two FFQ were carbohydrates, total fat, Na and MUFA. When assessing ranking of nutrients into quintiles, on average, 56 % of the participants (for all nutrients) were classified into the same or adjacent quintiles in both FFQ, with the highest percentage agreement for sugar. On average, 21 % of participants were grossly misclassified by three or four quintiles, with the highest percentage misclassification for fibre and Fe. Quintile agreement was similar to that reported by other studies, and we concluded that both FFQ are suitable tools for dividing participants’ nutrient intake levels into high- and low-consumption groups. Use of either FFQ was not appropriate for obtaining accurate estimates of absolute nutrient intakes.
Autobiographical memory (ABM), personal semantic memory (PSM), and autonoetic consciousness are affected in individuals with mild cognitive impairment (MCI) but their relationship with Alzheimer's disease (AD) biomarkers are unclear.
Forty-five participants (healthy controls (HC) = 31, MCI = 14) completed the Episodic ABM Interview and a battery of memory tests. Thirty-one (HC = 22, MCI = 9) underwent β-amyloid positron emission tomography (PET) and magnetic resonance (MR) imaging. Fourteen participants (HC = 9, MCI = 5) underwent one imaging modality.
Unlike PSM, ABM differentiated between diagnostic categories but did not relate to AD biomarkers. Personal semantic memory was related to neocortical β-amyloid burden after adjusting for age and apolipoprotein E (APOE) ɛ4. Autonoetic consciousness was not associated with AD biomarkers, and was not impaired in MCI.
Autobiographical memory was impaired in MCI participants but was not related to neocortical amyloid burden, suggesting that personal memory systems are impacted by differing disease mechanisms, rather than being uniformly underpinned by β-amyloid. Episodic and semantic ABM impairment represent an important AD prodrome.
Studies on the efficacy of parent training programs have mostly been conducted with preadolescents, with only a few studies investigating family treatment models in adolescents. In this article, a study is described that evaluates Standard Teen Triple P (Positive Parenting Program), a behavioural family intervention for parents of 11- to 16-year-old teenagers. Participants were 46 families with a teenager who was experiencing detectable behavioural and emotional problems. Compared to parents in the waitlist control condition, parents participating in the intervention condition reported decreased levels of teen disruptive behaviours and parent adolescent conflict, as well as a reduction in the use of ineffective parenting strategies and conflict over child-rearing issues. These positive changes were maintained at the 3-month follow-up. Results suggest that Standard Teen Triple P is a promising parenting intervention for tackling adolescent externalising problems.
The Australian Imaging, Biomarkers and Lifestyle (AIBL) Flagship Study of Ageing is a prospective study of 1,112 individuals (211 with Alzheimer's disease (AD), 133 with mild cognitive impairment (MCI), and 768 healthy controls (HCs)). Here we report diagnostic and cognitive findings at the first (18-month) follow-up of the cohort. The first aim was to compute rates of transition from HC to MCI, and MCI to AD. The second aim was to characterize the cognitive profiles of individuals who transitioned to a more severe disease stage compared with those who did not.
Eighteen months after baseline, participants underwent comprehensive cognitive testing and diagnostic review, provided an 80 ml blood sample, and completed health and lifestyle questionnaires. A subgroup also underwent amyloid PET and MRI neuroimaging.
The diagnostic status of 89.9% of the cohorts was determined (972 were reassessed, 28 had died, and 112 did not return for reassessment). The 18-month cohort comprised 692 HCs, 82 MCI cases, 197 AD patients, and one Parkinson's disease dementia case. The transition rate from HC to MCI was 2.5%, and cognitive decline in HCs who transitioned to MCI was greatest in memory and naming domains compared to HCs who remained stable. The transition rate from MCI to AD was 30.5%.
There was a high retention rate after 18 months. Rates of transition from healthy aging to MCI, and MCI to AD, were consistent with established estimates. Follow-up of this cohort over longer periods will elucidate robust predictors of future cognitive decline.
Although previous studies have shown that individuals with autism spectrum disorder (ASD) excel at visual search, underlying neural mechanisms remain unknown. This study investigated the neurofunctional correlates of visual search in children with ASD and matched typically developing (TD) children, using an event-related functional magnetic resonance imaging design. We used a visual search paradigm, manipulating search difficulty by varying set size (6, 12, or 24 items), distractor composition (heterogeneous or homogeneous) and target presence to identify brain regions associated with efficient and inefficient search. While the ASD group did not evidence accelerated response time (RT) compared with the TD group, they did demonstrate increased search efficiency, as measured by RT by set size slopes. Activation patterns also showed differences between ASD group, which recruited a network including frontal, parietal, and occipital cortices, and the TD group, which showed less extensive activation mostly limited to occipito-temporal regions. Direct comparisons (for both homogeneous and heterogeneous search conditions) revealed greater activation in occipital and frontoparietal regions in ASD than in TD participants. These results suggest that search efficiency in ASD may be related to enhanced discrimination (reflected in occipital activation) and increased top-down modulation of visual attention (associated with frontoparietal activation). (JINS, 2008, 14, 990–1003.)
A tendency to extract spurious, message-like meaning from meaningless noise was assessed as a risk factor leading to shizophrenia-spectrum disorders by assessing word length of speech illusions elicited by multispeaker babble in 43 people with prodromal symptoms. These individuals were randomised to olanzapine v. placebo groups during year 1 followed by no pharmacological treatment for those with no disorder conversion during year 2. A time-dependent Cox regression analysis of conversion to schizophrenia-spectrum disorder revealed a significant interaction between condition (olanzapine v. no drug) and length of speech illusion, with the latter strongly predicting subsequent conversion during medication-free intervals but not during olanzapine treatment.
Adenocarcinoma of the breast usually presents as a small painless mass (Figures A–a,b). The disease rarely occurs in the second and third decades but then increases in incidence through and past the menopause. Because of the seriousness and great range in age incidence of the disease, any mass in the breast must be viewed as cancer until proven otherwise (see letter in Introduction).
The stem cell population of the breast that will give rise to the milk-producing acini are located in the small ductules and persist in the fibrotic stroma of the senile breast. These stem cells are the target in carcinogenesis (Figures A–2 a,b,c). The majority of adenocarcinomas of the breast arise in these same small ductules. They may present in several ways: the vast majority develop as small solitary painless nodules, but some within the ductules may present with a bloody discharge from the nipple as the nodule develops. As the adenocarcinomas grow, they infiltrate surrounding tissues and eventually become fixed to the deep tissues and to the skin. This may cause dimpling of the skin or, if it invades the nipple, retraction of the nipple (Figure A–1a). With further growth and development it may spread first to the lymph nodes in the axilla, and shortly thereafter to the lungs, pleura, and to the bones of the spine and pelvis.
For the first time in the history of the world, every human being is now subjected to contact with dangerous chemicals, from the moment of conception until death.
Rachel Carson, Silent Spring, 1962
Our environment has been described as a “sea of carcinogens” awash with a variety of chemicals and, to a lesser extent, with oncogenic viruses and high-energy radiations, all of which may contribute significantly to cancer incidence in humans. Although much of our attention has been focused on the proliferation of synthetic chemicals and their waste byproducts, an examination of these substances has revealed that, in fact, most chemicals are not carcinogenic. Testing by the U.S. National Toxicology Program (NTP), an agency within the Department of Health and Human Services charged with the responsibility of defining human carcinogens in the United States (Huff et al. 1988), and the International Agency for Research in Cancer (IARC), a part of the World Health Organization (WHO) with a similar but broader mission (Tomatis 1988), has shown that only one-fourth to one-third of those substances even suspected of being carcinogenic on the basis of their chemistries actually are cancer-causing agents. In fact, of the more than 80,000 chemicals listed for commercial use with the NTP, thus far only 228 have been categorized as being “known” or “reasonably anticipated” as human carcinogens according to the tenth Report on Carcinogens (released December, 2002).
Some may read this book because they or a loved one has cancer, students of science may read it because they are about to make career decisions, and students of cancer may read it because of a desire to be acquainted with aspects of cancer other than those with which they work. Although most students of cancer have never seen a malignancy in a human, they are nevertheless expert in one or more of the many fascinating and important aspects of the disease. They contribute to the understanding of DNA and its replication, control of gene expression, receptors and growth factors, developmental aspects, immunology, prevention, and treatment of cancer and a myriad of other important parts of the cancer problem. We are all impressed by the recent compounding of knowledge, but even more so by our lack of knowledge and understanding of how important facts generated in one aspect of investigation bear on another. Students, unaware of the clinical aspects of the disease, lack the information to make the correlations and see the important problems that result. In addition, they may be driven in their endeavors only by the intellectualism of their part of the problem. This book is designed to provide insight and understanding into the human aspects of cancer.
It is not our purpose here to present all-encompassing details of the clinical behavior of patients with cancer that are necessary for diagnosis, medical practice, and patient management.
Our first task is to provide you with a working knowledge of the pathologic terms and concepts used throughout the text. This chapter defines terminology, compares and contrasts malignant and benign tumors, considers characteristics and behavior of malignant cells, and discusses how invading malignancies kill an individual. Tumors, with time, undergo changes that lead to autonomy. This progression of events is also examined.
An appreciation of embryology leads to a consideration of the origin of stem cells and the concepts of determination and differentiation. Both are important to understanding the origin of cancer cells, and such comprehension may lead to new modalities for treating cancers. Most textbooks of cancer biology begin with a discussion of cells. But we start with an examination of what cancer is to help you get a better grasp of the material that follows. Metastasis is difficult to understand without a prior foundation in the concepts of pathology. Similarly, carcinogenesis or chemotherapy is incomprehensible without knowledge of what a malignant cell is and how it behaves.
Much of our knowledge about tumors dates from antiquity. The streaks of hard gray tissue that extend from a tumor into the normal tissues reminded the Ancients of a crab, so they named the condition cancer (from the Greek word meaning crab). The term “tumor” denotes a mass, whether neoplastic, inflammatory, pathologic, or even physiologic. Today, tumor is used generically to describe any neoplasm, irrespective of its origin or biologic behavior.
In the previous chapter, the biology of malignancies and their caricature of normal tissue renewal suggested important principles that guide the development and use of treatment strategies. The current chapter presents how the treatment principles have been reduced to practice and how treatment principles relate to biological principles governing malignant growth. The chapter is organized around the four conventional treatment modalities available today: surgery, radiotherapy, cytotoxic chemotherapy and targeted therapy. (The term “conventional” refers to therapy accepted as the best available standard treatment.) Because of their different strategies, each modality is associated with specific risks and side effects, and this chapter builds a scientific understanding of the modalities' approved uses, successes, limitations, and toxicities. As explained in the preceding chapter, the goal of using the modalities is cytoreduction – hopefully the complete eradication of all cancer cells from the body. If not possible, then the goal becomes reducing the number of cancer cells in the body to the point that the time required for malignant stem cells to replace them is longer than the patient's life, giving rise to a cure. If sufficient cytoreduction is not achievable, then relapse ensues at some point in the future that depends on the amount of surviving malignant tissue and its rate of repopulation. The younger the patient at time of diagnosis, the more effective the treatment must be at eradicating malignant cells.