Evaluation of the Impact of a Public Bicycle Share Program on Population Bicycling in Vancouver, BC

Public bicycle share programs have been implemented in cities around the world to encourage bicycling. However, there are limited evaluations of the impact of these programs on bicycling at the population level. This study examined the impact of a public bicycle share program on bicycling amongst residents of Vancouver, BC. Using an online panel, we surveyed a population-based sample of Vancouver residents three times: prior to the implementation of the public bicycle share program (T0, October 2015, n=1111); in the early phase of implementation (T1, October 2016, n=995); and one-year post implementation (T2, October 2017, n=966). We used difference in differences estimation to assess whether there was an increase in bicycling amongst those living and/or working in close proximity (≤500 m) to Vancouver\u27s Mobi by Shaw Go public bicycle share program, compared to those living and working outside this area. Results suggest that only living or only working inside the bicycle share service area was not associated with increases in bicycling at T1 or T2 relative to those outside the service area. Both living and working inside the bicycle share service area was associated with increases in bicycling at T1 (OR: 2.26, 95% CI: 1.07, 4.80), however not at T2 (OR: 1.37, 95% CI: 0.67, 2.83). These findings indicate that the implementation of a public bicycle share program may have a greater effect on bicycling for residents who both live and work within the service area, although this effect may not be sustained over time.&nbsp

Contact lens physical properties and lipid deposition in a novel characterized artificial tear solution

Lorentz, H., Heynen, M., Kay, L. M. M., Dominici, C. Y., Khan, W., Ng, W. W. S., & Jones, L. (2011). Contact lens physical properties and lipid deposition in a novel characterized artificial tear solution. Molecular Vision, 17, 3392–3405.Purpose: To characterize various properties of a physiologically-relevant artificial tear solution (ATS) containing a range of tear film components within a complex salt solution, and to measure contact lens parameters and lipid deposition of a variety of contact lens materials after incubation in this ATS.Methods: A complex ATS was developed that contains a range of salts, proteins, lipids, mucin, and other tear film constituents in tear-film relevant concentrations. This ATS was tested to confirm that its pH, osmolality, surface tension, and homogeneity are similar to human tears and remain so throughout the material incubation process, for up to 4 weeks. To confirm that silicone hydrogel and conventional hydrogel contact lens materials do not alter in physical characteristics beyond what is allowed by the International Organization for Standardization (ISO) 18369–2. The diameter, center thickness, and calculated base curve were measured for five different lens materials directly out of the blister pack, after a rinse in saline and then following a two week incubation in the modified ATS. To test the ATS and the effect of its composition on lipid deposition, two lens materials were incubated in the ATS and a modified version for several time points. Both ATS solutions contained trace amounts of carbon-14 cholesterol and phosphatidylcholine, such that deposition of these specific lipids could be quantified using standard methods.Results: This ATS is a complex mixture that remains stable at physiologically relevant pH (7.3–7.6), osmolality (304–306 mmol/kg), surface tension (40–46 dynes/cm) and homogeneity over an incubation period of three weeks or more. The physical parameters of the lenses tested showed no changes beyond that allowed by the ISO guidelines. Incubations with the ATS found that balafilcon A lenses deposit significantly more cholesterol and phosphatidylcholine than omafilcon A lenses (p<0.05) and that removing lactoferrin and immunoglobulin G from the ATS can significantly decrease the mass of lipid deposited.Conclusions: This paper describes a novel complex artificial tear solution specially designed for in-vial incubation of contact lens materials. This solution was stable and did not adversely affect the physical parameters of the soft contact lenses incubated within it and showed that lipid deposition was responsive to changes in ATS composition.This study was sponsored by ALCON Research Ltd. Special thanks to Michelle Senchyna, Peggy Stauffer and Rekha Rangarajan for fruitful discussions. One of the authors (L.J.) has received funding over the past 3 years from the following companies who either are directly involved in products used in this manuscript or are involved in the manufacture of competing products - Alcon, AMO, B&L, CIBA Vision, CooperVision, and Johnson & Johnson

Behavioral Priming: It's All in the Mind, but Whose Mind?

The perspective that behavior is often driven by unconscious determinants has become widespread in social psychology. Bargh, Chen, and Burrows' (1996) famous study, in which participants unwittingly exposed to the stereotype of age walked slower when exiting the laboratory, was instrumental in defining this perspective. Here, we present two experiments aimed at replicating the original study. Despite the use of automated timing methods and a larger sample, our first experiment failed to show priming. Our second experiment was aimed at manipulating the beliefs of the experimenters: Half were led to think that participants would walk slower when primed congruently, and the other half was led to expect the opposite. Strikingly, we obtained a walking speed effect, but only when experimenters believed participants would indeed walk slower. This suggests that both priming and experimenters' expectations are instrumental in explaining the walking speed effect. Further, debriefing was suggestive of awareness of the primes. We conclude that unconscious behavioral priming is real, while real, involves mechanisms different from those typically assumed to cause the effect

Different aspects of emotional processes in apathy: Application of the French translated dimensional apathy scale

Apathy is a behavioural symptom that occurs in neuropsychiatric, neurological and neurodegenerative disease. It is defined as a lack of motivation and/or a quantitative reduction of goal-directed behaviour. Levy and Dubois Cerebral Cortex, 16(7), 916–928 (2006) proposed a triadic substructure of apathy and similar subtypes can be assessed using the Dimensional Apathy Scale (DAS), via the Executive, Emotional and Initiation subscales. The aim of this study was to translate the DAS in to French (f-DAS), examine its psychometric properties and the substructure of apathy using Confirmatory Factor Analysis (CFA). The results showed an acceptable internal consistency reliability of the f-DAS and a similar relationship to depression as in the original DAS development study. The CFA supported a triadic dimensional substructure of the f-DAS, similar to the original DAS but suggested a more complex substructure, specifically, two further processes of the Emotional apathy dimension relating to “Social Emotional” and “Individual Emotional” aspects of demotivation. To conclude, the f-DAS is a robust and reliable tool for assessing multidimensional apathy. Further research should explore the utility of the f-DAS in patients with neuropsychiatric diseases in view of social emotional aspects in apathy

The relationship between anti-HPV-16 IgG seropositivity and cancer of the cervix, anogenital organs, oral cavity and pharynx, oesophagus and prostate in a black South African population

BACKGROUND: Human papillomavirus type 16 (HPV-16) infection is an important cause of cervical cancer, other anogenital cancers and, possibly, some oral and pharyngeal cancers. The association of HPV-16 with oesophageal and with prostate cancers has not been firmly established. METHODS: We analysed sera from 3,757 HIV seronegative black South Africans using an anti-HPV IgG enzyme-linked immunosorbent assay (ELISA). The subjects were recruited from 1995 to 2000 as part of an ongoing cancer case control study. Cases were patients with newly diagnosed cancers of the cervix (n = 946), other anogenital organs (n = 80), the oral cavity and pharynx (n = 102), the oesophagus (n = 369) or the prostate (n = 205). The comparison group consisted of 2,055 age and sex-matched patients randomly selected from the same data base, diagnosed at the same hospitals, but with a vascular disease or with a cancer unrelated to HPV infection. Subjects' sera were randomly and blindly allocated onto ELISA plates. Optical density (OD) levels of anti-HPV-16 IgG of > 0.45 and ≥ 0.767 were taken to be cut-offs for negative, medium and high antibody levels. RESULTS: After adjustment for potential confounders, cancer types that showed a statistically significant association with increased anti-HPV-16 IgG antibody (Ab) levels were cancer of the cervix (OR for medium Ab levels = 1.6, and for high = 2.4, p < 0.0001), cancers of other anogenital organs (OR for medium or high Ab levels = 2.5, p = 0.002), and cancer of the oesophagus (OR for medium Ab = 1.3, and high Ab levels = 1.6 p = 0.002). Cancers of the oral cavity and pharynx showed a borderline significant association in the unadjusted model (p = 0.05) but after adjustment for confounding the trend in relation to Ab levels was positive but not statistically significant (OR for medium Ab = 1.1, and high Ab = 1.5 p = 0.13). Prostate cancer was not associated with HPV-16 seropositivity (OR for medium Ab level = 1.4, and for high Ab level = 1.3, p = 0.3). CONCLUSION: If there is indeed an association between HPV-16 and oesophageal and possibly also some oral cavity and pharyngeal cancers, then emerging HPV vaccines may also reduce, at least in part, the incidence of these leading cancer types

Novel Associations between Common Breast Cancer Susceptibility Variants and Risk-Predicting Mammographic Density Measures.

Mammographic density measures adjusted for age and body mass index (BMI) are heritable predictors of breast cancer risk, but few mammographic density-associated genetic variants have been identified. Using data for 10,727 women from two international consortia, we estimated associations between 77 common breast cancer susceptibility variants and absolute dense area, percent dense area and absolute nondense area adjusted for study, age, and BMI using mixed linear modeling. We found strong support for established associations between rs10995190 (in the region of ZNF365), rs2046210 (ESR1), and rs3817198 (LSP1) and adjusted absolute and percent dense areas (all P < 10(-5)). Of 41 recently discovered breast cancer susceptibility variants, associations were found between rs1432679 (EBF1), rs17817449 (MIR1972-2: FTO), rs12710696 (2p24.1), and rs3757318 (ESR1) and adjusted absolute and percent dense areas, respectively. There were associations between rs6001930 (MKL1) and both adjusted absolute dense and nondense areas, and between rs17356907 (NTN4) and adjusted absolute nondense area. Trends in all but two associations were consistent with those for breast cancer risk. Results suggested that 18% of breast cancer susceptibility variants were associated with at least one mammographic density measure. Genetic variants at multiple loci were associated with both breast cancer risk and the mammographic density measures. Further understanding of the underlying mechanisms at these loci could help identify etiologic pathways implicated in how mammographic density predicts breast cancer risk.ABCFS: The Australian Breast Cancer Family Registry (ABCFR; 1992-1995) was supported by the Australian NHMRC, the New South Wales Cancer Council, and the Victorian Health Promotion Foundation (Australia), and by grant UM1CA164920 from the USA National Cancer Institute. The Genetic Epidemiology Laboratory at the University of Melbourne has also received generous support from Mr B. Hovey and Dr and Mrs R.W. Brown to whom we are most grateful. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Breast Cancer Susceptibility Variants and Mammographic Density 5 Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. BBCC: This study was funded in part by the ELAN-Program of the University Hospital Erlangen; Katharina Heusinger was funded by the ELAN program of the University Hospital Erlangen. BBCC was supported in part by the ELAN program of the Medical Faculty, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg. EPIC-Norfolk: This study was funded by research programme grant funding from Cancer Research UK and the Medical Research Council with additional support from the Stroke Association, British Heart Foundation, Department of Health, Research into Ageing and Academy of Medical Sciences. MCBCS: This study was supported by Public Health Service Grants P50 CA 116201, R01 CA 128931, R01 CA 128931-S01, R01 CA 122340, CCSG P30 CA15083, from the National Cancer Institute, National Institutes of Health, and Department of Health and Human Services. MCCS: Melissa C. Southey is a National Health and Medical Research Council Senior Research Fellow and a Victorian Breast Cancer Research Consortium Group Leader. The study was supported by the Cancer Council of Victoria and by the Victorian Breast Cancer Research Consortium. MEC: National Cancer Institute: R37CA054281, R01CA063464, R01CA085265, R25CA090956, R01CA132839. MMHS: This work was supported by grants from the National Cancer Institute, National Institutes of Health, and Department of Health and Human Services. (R01 CA128931, R01 CA 128931-S01, R01 CA97396, P50 CA116201, and Cancer Center Support Grant P30 CA15083). Breast Cancer Susceptibility Variants and Mammographic Density 6 NBCS: This study has been supported with grants from Norwegian Research Council (#183621/S10 and #175240/S10), The Norwegian Cancer Society (PK80108002, PK60287003), and The Radium Hospital Foundation as well as S-02036 from South Eastern Norway Regional Health Authority. NHS: This study was supported by Public Health Service Grants CA131332, CA087969, CA089393, CA049449, CA98233, CA128931, CA 116201, CA 122340 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services. OOA study was supported by CA122822 and X01 HG005954 from the NIH; Breast Cancer Research Fund; Elizabeth C. Crosby Research Award, Gladys E. Davis Endowed Fund, and the Office of the Vice President for Research at the University of Michigan. Genotyping services for the OOA study were provided by the Center for Inherited Disease Research (CIDR), which is fully funded through a federal contract from the National Institutes of Health to The Johns Hopkins University, contract number HHSN268200782096. OFBCR: This work was supported by grant UM1 CA164920 from the USA National Cancer Institute. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. SASBAC: The SASBAC study was supported by Märit and Hans Rausing’s Initiative against Breast Cancer, National Institutes of Health, Susan Komen Foundation and Agency for Science, Technology and Research of Singapore (A*STAR). Breast Cancer Susceptibility Variants and Mammographic Density 7 SIBS: SIBS was supported by program grant C1287/A10118 and project grants from Cancer Research UK (grant numbers C1287/8459). COGS grant: Collaborative Oncological Gene-environment Study (COGS) that enabled the genotyping for this study. Funding for the BCAC component is provided by grants from the EU FP7 programme (COGS) and from Cancer Research UK. Funding for the iCOGS infrastructure came from: the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692), the National Institutes of Health (CA128978) and Post- Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112 - the GAMEON initiative), the Department of Defence (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund.This is the author accepted manuscript. The final version is available via American Association for Cancer Research at http://cancerres.aacrjournals.org/content/early/2015/04/10/0008-5472.CAN-14-2012.abstract

Identification of a novel locus on chromosome 2q13, which predisposes to clinical vertebral fractures independently of bone density.

OBJECTIVES: To identify genetic determinants of susceptibility to clinical vertebral fractures, which is an important complication of osteoporosis. METHODS: Here we conduct a genome-wide association study in 1553 postmenopausal women with clinical vertebral fractures and 4340 controls, with a two-stage replication involving 1028 cases and 3762 controls. Potentially causal variants were identified using expression quantitative trait loci (eQTL) data from transiliac bone biopsies and bioinformatic studies. RESULTS: A locus tagged by rs10190845 was identified on chromosome 2q13, which was significantly associated with clinical vertebral fracture (P=1.04×10-9) with a large effect size (OR 1.74, 95% CI 1.06 to 2.6). Bioinformatic analysis of this locus identified several potentially functional SNPs that are associated with expression of the positional candidate genes TTL (tubulin tyrosine ligase) and SLC20A1 (solute carrier family 20 member 1). Three other suggestive loci were identified on chromosomes 1p31, 11q12 and 15q11. All these loci were novel and had not previously been associated with bone mineral density or clinical fractures. CONCLUSION: We have identified a novel genetic variant that is associated with clinical vertebral fractures by mechanisms that are independent of BMD. Further studies are now in progress to validate this association and evaluate the underlying mechanism

Using positional information to provide context for biological image analysis with MorphoGraphX 2.0

Positional information is a central concept in developmental biology. In developing organs, positional information can be idealized as a local coordinate system that arises from morphogen gradients controlled by organizers at key locations. This offers a plausible mechanism for the integration of the molecular networks operating in individual cells into the spatially-coordinated multicellular responses necessary for the organization of emergent forms. Understanding how positional cues guide morphogenesis requires the quantification of gene expression and growth dynamics in the context of their underlying coordinate systems. Here we present recent advances in the MorphoGraphX software (Barbier de Reuille et al., 2015)⁠ that implement a generalized framework to annotate developing organs with local coordinate systems. These coordinate systems introduce an organ-centric spatial context to microscopy data, allowing gene expression and growth to be quantified and compared in the context of the positional information thought to control them

Pattern of Relapse and Treatment Response in WNT- Activated Medulloblastoma

Over the past decade, wingless-activated (WNT) medulloblastoma has been identified as a candidate for therapy de-escalation based on excellent survival; however, a paucity of relapses has precluded additional analyses of markers of relapse. To address this gap in knowledge, an international cohort of 93 molecularly confirmed WNT MB was assembled, where 5-year progression-free survival is 0.84 (95%, 0.763-0.925) with 15 relapsed individuals identified. Maintenance chemotherapy is identified as a strong predictor of relapse, with individuals receiving high doses of cyclophosphamide or ifosphamide having only one very late molecularly confirmed relapse (p = 0.032). The anatomical location of recurrence is metastatic in 12 of 15 relapses, with 8 of 12 metastatic relapses in the lateral ventricles. Maintenance chemotherapy, specifically cumulative cyclophosphamide doses, is a significant predictor of relapse across WNT MB. Future efforts to de-escalate therapy need to carefully consider not only the radiation dose but also the chemotherapy regimen and the propensity for metastatic relapses