A lifelogging approach to automated market research

Market research companies spend large amounts of money carrying out time-intensive processes to gather information about peo- ple’s activities, such as the place they frequent and the activities in which they partake. Due to high costs and logistical difficulties, an automated approach to this practice is needed. In this work we present an automated market research system based on computer vision and machine learning algorithms with visual lifelogging data, developed in collaboration with Sponge It, a market research com- pany. Due to some image quality constraints associated with the Sense- cam, for our prototype system we developed a visual lifelogging device using an Android smartphone. This device can capture images at higher resolutions and with additional metadata, such as location information. The aim of this project is to analyse large collections of visual lifelogs and to support both ethnographic research and audience measurement for market research. Ethnographic research is supported by high level classification of images to capture the semantics of the users activities (e.g. socialising in bar, shopping, eating). Location, time and other con- texts are also analysed, and an interactive interface supports browsing and exploration of the data based on this analysis. The system can measure audience exposure to specific advertising cam- paigns, using object recognition algorithms to automatically detect the presence of known logos in life logging images. This combination of con- cept classification for ethnographic research and object recognition for audience exposure represents a very powerful tool from a market research perspective

HIV futures NZ2: Mate araikore a muri ake nei (Tuarua)

The Living with HIV Program is a part of the Australian Research Centre in Sex, Health and Society (ARCSHS) at La Trobe University. The program conducts social research into the lived experience of HIV. The HIV Futures New Zealand 2 survey was completed by 261 HIV positive people. 75.7% were male (196), 23.9% were female (62), and one person was transgender. 60.7% were gay men, 22.7% heterosexual women, 10.1% heterosexual men, 6.1% bisexual men, and 0.4% lesbian women. The respondents’ ages ranged from 23 to 88 years with a mean of 45.6 years and a median of 44.0 years. The majority of participants were New Zealand born (69.4%) and 89.8% of the participants spoke English at home, with North African languages accounting for most of the remainder. Of the total sample, 255 indicated their ethnicity. One hundred and seventy two were European/Pakeha (65.9%), 49 were African (18.8%), 17 were Maori (6.5%), nine were Asian (3.4%) and five were Pacific Islanders (1.9%)

Multiplex ligation-dependent probe amplification (MLPA) analysis is an effective tool for the detection of novel intragenic PLA2G6 mutations: Implications for molecular diagnosis

Phospholipase associated neurodegeneration (PLAN) comprises a heterogeneous group of autosomal recessive neurological disorders caused by mutations in the PLA2G6 gene. Direct gene sequencing detects 85% mutations in infantile neuroaxonal dystrophy. We report the novel use of multiplex ligation-dependent probe amplification (MLPA) analysis to detect novel PLA2G6 duplications and deletions. The identification of such copy number variants (CNVs) expands the PLAN mutation spectrum and may account for up to 12.5% of PLA2G6 mutations. MLPA should thus be employed to detect CNVs of PLA2G6 in patients who show clinical features of PLAN but in whom both disease-causing mutations cannot be identified on routine sequencin

Dislocation-induced structural and luminescence degradation in InAs quantum dot emitters on silicon

We probe the extent to which dislocations reduce carrier lifetimes and alter luminescence and growth morphology in InAs quantum dots (QD) grown on silicon. These heterostructures are key ingredients to achieving a highly reliable monolithically integrated light source on silicon necessary for photonic integrated circuits. We find up to 20-30% shorter carrier lifetimes at spatially resolved individual dislocations from both the QD ground and excited states at room temperature using time-resolved cathodoluminescence spectroscopy. These lifetimes are consistent with differences in the intensity measured under steady-state excitation suggesting that trap-assisted recombination limits the minority carrier lifetime, even away from dislocations. Our techniques also reveal the dramatic growth of misfit dislocations in these structures under carrier injection fueled by recombination-enhanced dislocation glide and III-V/Si residual strain. Beyond these direct effects of increased nonradiative recombination, we find the long-range strain field of misfit dislocations deeper in the defect filter layers employed during III-V/Si growth alter the QD growth environment and introduce a crosshatch-like variation in the QD emission color and intensity when the filter layer is positioned close to the QD emitter layer. Sessile threading dislocations generate even more egregious hillock defects that also reduce emission intensities by altering layer thicknesses, as measured by transmission electron microscopy and atom probe tomography. Our work presents a more complete picture of the impacts of dislocations relevant for the development of light sources for scalable silicon photonic integrated circuits.Comment: 15 pages, 6 figure

Defect filtering for thermal expansion induced dislocations in III–V lasers on silicon

Epitaxially integrated III–V semiconductor lasers for silicon photonics have the potential to dramatically transform information networks, but currently, dislocations limit performance and reliability even in defect-tolerant InAs quantum dot (QD)-based lasers. Despite being below the critical thickness, QD layers in these devices contain previously unexplained misfit dislocations, which facilitate non-radiative recombination. We demonstrate here that these misfit dislocations form during post-growth cooldown due to the combined effects of (1) thermal-expansion mismatch between the III–V layers and silicon and (2) mechanical hardening in the active region. By incorporating an additional sub-critical thickness, indium-alloyed “misfit dislocation trapping layer,” we leverage these mechanical hardening effects to our advantage, displacing 95% of misfit dislocations from the QD layer in model structures. Unlike conventional dislocation mitigation strategies, the trapping layer reduces neither the number of threading dislocations nor the number of misfit dislocations. It simply shifts the position of misfit dislocations away from the QD layer, reducing the defects' impact on luminescence. In full lasers, adding a misfit dislocation trapping layer both above and below the QD active region displaces misfit dislocations and substantially improves performance: we measure a twofold reduction in lasing threshold currents and a greater than threefold increase in output power. Our results suggest that devices employing both traditional threading dislocation reduction techniques and optimized misfit dislocation trapping layers may finally lead to fully integrated, commercially viable silicon-based photonic integrated circuits

Ethanol reversal of tolerance to the respiratory depressant effects of morphine

Opioids are the most common drugs associated with unintentional drug overdose. Death results from respiratory depression. Prolonged use of opioids results in the development of tolerance but the degree of tolerance is thought to vary between different effects of the drugs. Many opioid addicts regularly consume alcohol (ethanol), and post-mortem analyses of opioid overdose deaths have revealed an inverse correlation between blood morphine and ethanol levels. In the present study, we determined whether ethanol reduced tolerance to the respiratory depressant effects of opioids. Mice were treated with opioids (morphine, methadone, or buprenorphine) for up to 6 days. Respiration was measured in freely moving animals breathing 5% CO(2) in air in plethysmograph chambers. Antinociception (analgesia) was measured as the latency to remove the tail from a thermal stimulus. Opioid tolerance was assessed by measuring the response to a challenge dose of morphine (10 mg/kg i.p.). Tolerance developed to the respiratory depressant effect of morphine but at a slower rate than tolerance to its antinociceptive effect. A low dose of ethanol (0.3 mg/kg) alone did not depress respiration but in prolonged morphine-treated animals respiratory depression was observed when ethanol was co-administered with the morphine challenge. Ethanol did not alter the brain levels of morphine. In contrast, in methadone- or buprenorphine-treated animals no respiratory depression was observed when ethanol was co-administered along with the morphine challenge. As heroin is converted to morphine in man, selective reversal of morphine tolerance by ethanol may be a contributory factor in heroin overdose deaths

Adherence to antiparkinsonian medication: An in-depth qualitative study

Background: Adherence to prescribed medication is low. It is a major problem as following practitioners’ recommendations is strongly associated with good patient outcomes. Little research has been undertaken with people in the early stages of Parkinson's disease although achieving symptom control depends on regularly timing doses. Research questions: How do people with Parkinson's disease adhere to prescribed medication, and what are the antecedents of non-adherence to antiparkinsonian medication? Design: Exploratory qualitative study using semi-structured interviews. Setting: Specialist Parkinson's disease clinic in one National Health Service hospital in England. Participants: Fifteen consecutive patients not yet in the advanced stages of Parkinson's disease living at home and responsible for managing their own medication or managing medication with the help of their carer. Methods: Semi-structured interviews with open questions. Findings: Each respondent demonstrated at least one type and in most cases several different types of non-adherent behaviour. Inadvertent minor non-adherence occurred because patients forgot to take tablets or muddled doses. Minor deliberate deviations occurred when patients took occasional extra tablets or brought forward doses to achieve better symptom control, often to cater for situations that were anticipated as especially demanding. Deliberate major non-adherence was very common and always related to over-use of medication. The experiences of parkinsonism were particular to the individual. The specific circumstances that prompted an episode of non-adherence varied between patients. Nevertheless there was evidence of negotiation between respondents and the Parkinson's disease nurse specialist; medication regimes were altered in conjunction with the patient during formal consultations and by telephone. Conclusion: Non-adherence to prescribed medication for people with chronic conditions is complex and for people with Parkinson's disease it was possible to identify different types of non-adherence. The possible existence of a typology of non-adherence for people with other chronic conditions merits investigation. Further research is needed to establish whether the findings of this small scale qualitative study can be replicated with a larger, more representative sample and establish how people with Parkinson's disease might be encouraged to adhere to medication regimes to improve symptom control

Homozygosity for a missense mutation in the 67 kDa isoform of glutamate decarboxylase in a family with autosomal recessive spastic cerebral palsy: parallels with Stiff-Person Syndrome and other movement disorders

Background Cerebral palsy (CP) is an heterogeneous group of neurological disorders of movement and/or posture, with an estimated incidence of 1 in 1000 live births. Non-progressive forms of symmetrical, spastic CP have been identified, which show a Mendelian autosomal recessive pattern of inheritance. We recently described the mapping of a recessive spastic CP locus to a 5 cM chromosomal region located at 2q24-31.1, in rare consanguineous families. Methods Here we present data that refine this locus to a 0.5 cM region, flanked by the microsatellite markers D2S2345 and D2S326. The minimal region contains the candidate gene GAD1, which encodes a glutamate decarboxylase isoform (GAD67), involved in conversion of the amino acid and excitatory neurotransmitter glutamate to the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Results A novel amino acid mis-sense mutation in GAD67 was detected, which segregated with CP in affected individuals. Conclusions This result is interesting because auto-antibodies to GAD67 and the more widely studied GAD65 homologue encoded by the GAD2 gene, are described in patients with Stiff-Person Syndrome (SPS), epilepsy, cerebellar ataxia and Batten disease. Further investigation seems merited of the possibility that variation in the GAD1 sequence, potentially affecting glutamate/GABA ratios, may underlie this form of spastic CP, given the presence of anti-GAD antibodies in SPS and the recognised excitotoxicity of glutamate in various contexts

Defective Leukocyte Adhesion and Chemotaxis Contributes to Combined Immunodeficiency in Humans with Autosomal Recessive MST1 Deficiency.

PURPOSE: To investigate the clinical and functional aspects of MST1 (STK4) deficiency in a profoundly CD4-lymphopenic kindred with a novel homozygous nonsense mutation in STK4. Although recent studies have described the cellular effects of murine Mst1 deficiency, the phenotype of MST1-deficient human lymphocytes has yet to be fully explored. Patient lymphocytes were therefore investigated in the context of current knowledge of murine Mst1 deficiency. METHODS: Genetic etiology was identified by whole exome sequencing of genomic DNA from two siblings, combined with linkage analysis in the wider family. MST1 protein expression was assessed by immunoblotting. The ability of patient lymphocytes to adhere to ICAM-1 under flow conditions was measured, and transwell assays were used to assess chemotaxis. Chemokine receptor expression was examined by flow cytometry and receptor signalling by immunoblotting. RESULTS: A homozygous nonsense mutation in STK4 (c.442C > T, p.Arg148Stop) was found in the patients, leading to a lack of MST1 protein expression. Patient leukocytes exhibited deficient chemotaxis after stimulation with CXCL11, despite preserved expression of CXCR3. Patient lymphocytes were also unable to bind effectively to immobilised ICAM-1 under flow conditions, in keeping with a failure to develop high affinity binding. CONCLUSION: The observed abnormalities of adhesion and migration imply a profound trafficking defect among human MST1-deficient lymphocytes. By analogy with murine Mst1 deficiency and other defects of leucocyte trafficking, this is likely to contribute to immunodeficiency by impairing key aspects of T-cell development and function such as positive selection in the thymus, thymic egress and immune synapse formation in the periphery.This is thepublished version. It first appeared at http://link.springer.com/article/10.1007%2Fs10875-016-0232-2