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The criteria for objective memory impairment in mild cognitive impairment (MCI) are vaguely defined. Aggregating the number of abnormal memory scores (NAMS) is one way to operationalise memory impairment, which we hypothesised would predict progression to Alzheimer’s disease (AD) dementia.
As part of the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing, 896 older adults who did not have dementia were administered a psychometric battery including three neuropsychological tests of memory, yielding 10 indices of memory. We calculated the number of memory scores corresponding to z ≤ −1.5 (i.e., NAMS) for each participant. Incident diagnosis of AD dementia was established by consensus of an expert panel after 3 years.
Of the 722 (80.6%) participants who were followed up, 54 (7.5%) developed AD dementia. There was a strong correlation between NAMS and probability of developing AD dementia (r = .91, p = .0003). Each abnormal memory score conferred an additional 9.8% risk of progressing to AD dementia. The area under the receiver operating characteristic curve for NAMS was 0.87 [95% confidence interval (CI) .81–.93, p < .01]. The odds ratio for NAMS was 1.67 (95% CI 1.40–2.01, p < .01) after correcting for age, sex, education, estimated intelligence quotient, subjective memory complaint, Mini-Mental State Exam (MMSE) score and apolipoprotein E ϵ4 status.
Aggregation of abnormal memory scores may be a useful way of operationalising objective memory impairment, predicting incident AD dementia and providing prognostic stratification for individuals with MCI.
The concept of information has penetrated almost all areas of human inquiry, from physics, chemistry, and engineering through biology to the social sciences. And yet its status as a physical entity remains obscure. Traditionally, information has been treated as a derived or secondary concept. In physics especially, the fundamental bedrock of reality is normally vested in the material building blocks of the universe, be they particles, strings, or fields. Because bits of information are always instantiated in material degrees of freedom, the properties of information could, it seems, always be reduced to those of the material substrate. Nevertheless, over several decades there have been attempts to invert this interdependence and root reality in information rather than matter. This contrarian perspective is most famously associated with the name of John Archibald Wheeler, who encapsulated his proposal in the pithy dictum ‘it from bit?’ (Wheeler, 1999).
In a practical, everyday sense, information is often treated as a primary entity, as a ‘thing in its own right’ with a measure of autonomy; indeed, it is bought and sold as a commodity alongside gas and steel. In the life sciences, informational narratives are indispensable: biologists talk about the genetic code, about translation and transcription, about chemical signals and sensory data processing, all of which treat information as the currency of activity, the ‘oil’ that makes the ‘biological wheels go round’. The burgeoning fields of genomic and metagenomic sequencing and bioinformatics are based on the notion that informational bits are literally vital. But beneath this familiar practicality lies a stark paradox. If information makes a difference in the physical world, which it surely does, then should we not attribute to it causal powers? However, in physics causation is invariably understood at the level of particle and field interactions, not in the realm of abstract bits (or qubits, their quantum counterparts). Can we have both? Can two causal chains coexist compatibly? Are the twin narratives of material causation and informational causation comfortable bedfellows? If so, what are the laws and principles governing informational dynamics to place alongside the laws of material dynamics?
Recent advances suggest that the concept of information might hold the key to unravelling the mystery of life's nature and origin. Fresh insights from a broad and authoritative range of articulate and respected experts focus on the transition from matter to life, and hence reconcile the deep conceptual schism between the way we describe physical and biological systems. A unique cross-disciplinary perspective, drawing on expertise from philosophy, biology, chemistry, physics, and cognitive and social sciences, provides a new way to look at the deepest questions of our existence. This book addresses the role of information in life, and how it can make a difference to what we know about the world. Students, researchers, and all those interested in what life is and how it began will gain insights into the nature of life and its origins that touch on nearly every domain of science.
Aberrant microbiota composition and function have been linked to several pathologies, including type 2 diabetes. In animal models, prebiotics induce favourable changes in the intestinal microbiota, intestinal permeability (IP) and endotoxaemia, which are linked to concurrent improvement in glucose tolerance. This is the first study to investigate the link between IP, glucose tolerance and intestinal bacteria in human type 2 diabetes. In all, twenty-nine men with well-controlled type 2 diabetes were randomised to a prebiotic (galacto-oligosaccharide mixture) or placebo (maltodextrin) supplement (5·5 g/d for 12 weeks). Intestinal microbial community structure, IP, endotoxaemia, inflammatory markers and glucose tolerance were assessed at baseline and post intervention. IP was estimated by the urinary recovery of oral 51Cr-EDTA and glucose tolerance by insulin-modified intravenous glucose tolerance test. Intestinal microbial community analysis was performed by high-throughput next-generation sequencing of 16S rRNA amplicons and quantitative PCR. Prebiotic fibre supplementation had no significant effects on clinical outcomes or bacterial abundances compared with placebo; however, changes in the bacterial family Veillonellaceae correlated inversely with changes in glucose response and IL-6 levels (r −0·90, P=0·042 for both) following prebiotic intake. The absence of significant changes to the microbial community structure at a prebiotic dosage/length of supplementation shown to be effective in healthy individuals is an important finding. We propose that concurrent metformin treatment and the high heterogeneity of human type 2 diabetes may have played a significant role. The current study does not provide evidence for the role of prebiotics in the treatment of type 2 diabetes.
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.
Trans-generational transfer of gregarious-phase traits in the desert locust Schistocerca gregaria (Forskål, 1775) is mediated by primer gregarizing pheromonal signals produced by ovipositing females that experience crowding. We monitored time-course proteomic events in eggs from solitary-reared locusts that had been exposed for 1, 3, 5, 7, 10 and 12 days to different levels of the sand-associated gregarizing signal originating from 0, 3, 5 or 10 ovipositions by crowd-reared females. Evidence for the phase transition was sought by comparing the protein patterns of embryos thus exposed with those from crowd-reared (gregarious) controls; this comparison was continued until the stage of the first instars. Expressed proteins were analysed by two-dimensional protein gel electrophoresis, and patterns from the different treatments within stages were compared by profile matching and χ2 analyses. Eggs derived from crowd- and solitary-reared females showed essentially similar protein patterns at early stages of embryogenesis; however, mature stages (particularly, days 10 and 12) and hatchlings demonstrated significantly different patterns. Protein patterns of eggs from solitary-reared females that were incubated in sand contaminated with the pheromonal signal and of the hatchlings that emerged were similar to those derived from gregarious females and dependent on the level of the pheromone to which the embryos had been exposed. The results confirm the gregarizing effect of the signal and constitute a useful basis for unravelling the mechanism of the signalling cascades associated with gene expressions triggered by the pheromone.
We compared findings of an audit of New Zealand's version of the second opinion appointed doctor (SOAD) scheme with published information on the equivalent scheme for England and Wales, to consider what might be learnt from the different jurisdictions' experience.
Strong similarities exist between the two schemes in the demographic profile of individuals subject to the SOAD process and rates of approval of compulsory treatment. The clearer legal framework for the English scheme and its supervision by an independent national agency may offer significant advantages in terms of consistency and transparency, compared with the informal, decentralised structure of New Zealand's scheme.
Clinicians may not always favour greater formality or elaborate national structures for administering the Mental Health Act, but there are advantages in promoting clarity and consistency in a mandatory statutory process designed to protect compulsory patients' rights.
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.
Although beta-amyloid, anxiety and depression have been linked cross-sectionally to reduced memory function in healthy older adults without dementia, prospective data evaluating these associations are lacking. Using data from an observational cohort study of 178 healthy older adults without dementia followed for 3 years, we found that anxiety symptoms significantly moderated the relationship between beta-amyloid level and decline in verbal (Cohen's d = 0.65) and episodic (Cohen's d = 0.38) memory. Anxiety symptoms were additionally linked to greater decline in executive function, irrespective of beta-amyloid and other risk factors. These findings suggest that interventions to mitigate anxiety symptoms may help delay memory decline in otherwise healthy older adults with elevated beta-amyloid.