1,721,521 research outputs found
Sliding on a Nanotube: Interplay of Friction, Deformations and Structure
No full textThe frictional properties of individual carbon nanotubes (CNTs) are studied by sliding an atomic force microscopy tip across and along its principle axis. This direction-dependent frictional behavior is found to correlate strongly with the presence of structural defects, surface chemistry, and CNT chirality. This study shows that it is experimentally possible to tune the frictional/adhesion properties of a CNT by controlling the CNT structure and surface chemistry, as well as use friction force to predict its structural and chemical properties. Copyright �� 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
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Influences of Physical Activity on Risk of Parkinson’s Disease and Cognitive Decline in Elderly Hispanics
Full text linkThe number of persons aged 65 years and older is expected to double to 92 million in the US by 2060, representing a potentially large social and financial burden of age-related neurodegenerative diseases such as Alzheimer’s disease (AD) and dementias and Parkinson’s disease (PD).Thus effective preventative public health strategies are essential. Regular physical activity (PA) and an active lifestyle have many health benefits, and evidence has accumulated that PA preserves brain structures and functions via multiple physiologic mechanisms, including mediation of inflammation and a general reduction of cardiovascular risk factors. In the Parkinson’s Environment and Gene (PEG) case-control population-based study, we enrolled 357 incident PD cases and 341 controls in central California and assessed PA levels via self-report of (1) overall PA over 4 age periods; (2) competitive sports; and (3) occupational histories. Our findings suggest that higher lifetime moderate to vigorous activity, especially consistently high level of such activities throughout adulthood and sports activities in youth were negatively associated with PD risk, but we found no beneficial role for occupational physical activity. We further examine how PA at the late-life influence the risk of dementia/cognitive impairment without dementia (CIND) using a prospective cohort, Sacramento Area Latino Study on Aging (SALSA) study, in which 1789 older Mexican Americans were enrolled at baseline and a majority actively followed between 1998 and 2008. We used Cox proportional hazards regression models to estimate the individual and joint effects of PA, apolipoprotein E (APOE) ε4 and diabetes status on risk of dementia/CIND and observed a nearly 10-fold increased risk among those with all three risk factors. Results from mediation analyses indicate that some of the PA effects on mortality and dementia/CIND but not depression might be mediated through well-known inflammatory pathways represented by biomarkers, specifically interleukins 6 (IL-6) and/or tumor necrosis factor - alpha (TNF-α). However, a large proportion of the PA effects on mortality, cognition, and mood seems to operate independently of the inflammatory pathways or the biomarkers we had available and thus remain unexplained. Taken together, our results provide support for the hypothesis that PA protects against the onset of neurodegenerative diseases and all-cause mortality, and they suggest that anti-inflammatory action may partly explain the protective effects of PA on dementia/CIND and mortality
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Prenatal Exposure to Perfluoroalkyl Substances and Birth Outcomes; A Pooled Analysis in the Danish National Birth Cohort
Full text linkPerfluoroalkyl substances (PFASs) are widespread industrial pollutants that are extremely persistent in the environment. Animal studies have indicated that in-utero PFAS exposures can affect fetal growth, but findings from human studies are inconclusive. Few human studies have sufficient sample size to study the influence of PFASs on adverse birth outcomes. Here, we conducted a pooled analysis using data of 3,535 mothers and infant pairs using three sub-samples originating from the Danish National Birth Cohort (DNBC), and we evaluated the associations between prenatal PFASs exposures and birth outcomes. Maternal plasma concentrations of six types of PFASs in early pregnancy (around 8.7 gestational weeks) were studied. We found that each LN-ng/ml increase in PFOS, PFOA, PFNA and PFHpS was associated with a 65g, 51g, 52g or 56g decrease in birth weight. Moreover, we also found that prenatal PFOS, PFHpS, PFDA levels were associated with the risks for preterm birth (< 37 completed gestational week). Our findings strengthen the evidence that in-utero PFAS exposures may affect fetal growth. These findings raise concerns considering the ubiquitous contamination of PFASs in the environment. Public health strategies to prevent or lower PFASs exposures in pregnant women are needed
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Prenatal Exposure to Per- and Polyfluoroalkyl Substances (PFAS) and Risk of Autism Spectrum Disorder in the California Central Valley, 2004-2010
No full textThere is mixed evidence regarding the association between prenatal exposure to per- andpolyfluoroalkyl substances (PFAS) and autism spectrum disorder (ASD). ASD cases (n = 294)
born in the California Central Valley from 2004 – 2010 were identified from California
Department of Developmental Services (DDS) records. Controls (n = 286) born in the California
Central Valley were identified from California birth records and were matched to cases by sex,
year of birth, and exposure to selected pesticides and air pollution. Three PFAS were measured
through high-resolution metabolomic profiling in >60% of maternal serum samples collected
mid-pregnancy from mothers who participated in the California Prenatal Expanded Alpha-
fetoprotein Screening Program: perfluorooctanoic acid (PFOA), perfluorohexanesulfonic acid
(PFHxS), and perfluorooctane sulfonate (PFOS). Adjusted odds ratios (aORs) and 95%
confidence intervals (CIs) were estimated using logistic regression to examine relationships
between individual PFAS and ASD. We also tested for non-linear associations between prenatal
PFAS exposure and ASD using restricted cubic spline regression models. Additionally, we
utilized a quantile-based g-computation approach to examine associations between a total PFAS
mixture and ASD. We founded an elevated aOR for ASD comparing the highest to the lowest
PFOA exposure quartile (aOR = 1.71; 95% CI: 0.96, 3.06), but the confidence interval included
the null. Additionally, for PFOA we saw a non-linear J-shaped exposure-outcome relationship in
a restricted cubic spline regression model. No apparent associations were found for the PFAS
mixture and ASD. Associations with several PFAS were modified by maternal education. For
example, among children of mothers with low levels of education (high school or less), the
highest PFOA quartile was strongly associated with ASD compared to the lowest exposure
quartile (aOR = 2.97; 95% CI: 1.43, 6.18), and such association was not seen among mothers
with higher education levels (aOR = 0.62; 95% CI: 0.24, 1.64). Using an untargeted
metabolomic profiling approach, we found that prenatal exposure to PFOA was associated with
ASD in children, particularly among mothers with lower education levels. Larger studies are
warranted to replicate our findings, and more research is necessary to elucidate the underlying
mechanisms driving this association
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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Prenatal Risk and Protective Factors for Childhood Cancer: Investigating the Effects of Ultraviolet Radiation, Pesticide Exposure, and Maternal Diet
Full text linkChildhood cancer is a rare disease that may be triggered prenatally. The few known causes of pediatric cancers include ionizing radiation, Down syndrome, and some genetic or chromosomal anomalies. Additional risk factors have been suggested, but due to the rarity of childhood cancers, it has been difficult to establish causes and hence targets for prevention. We investigated ultraviolet radiation (UVR), pesticides, and maternal dietary patterns as possible risk and protective factors. Studies have shown that higher solar UVR may be related to lower risk of some cancers in adults and children. In a large, population-based case-control study we tested the hypothesis that childhood cancers may be influenced by UVR. Cancers in children ages 0 to 5 years were identified from California Cancer Registry records for 1988-2007 and linked to birth certificate data. Controls were sampled from birth certificates. Based on birth address, we assigned UVR exposure using a geostatistical exposure model developed with data from the National Solar Radiation Database. Our preliminary findings suggest that UVR during pregnancy may decrease the odds of some childhood cancers. In the same study population we evaluated the associations of exposure to specific pesticide types during pregnancy with glial tumors in young children in California using a validated geographic exposure model. We observed increased odds of astrocytoma for residential pesticide exposure to herbicides, insecticides and fungicides, as well as for several chemical classes of pesticides. Additionally, using data from a multi-institutional case-control study of retinoblastoma in the United States and Canada, we investigated the association of maternal prenatal diet with the risk for unilateral retinoblastoma among children less 15 years of age. Previous studies have shown that mother's diet during pregnancy may affect her offspring's risk of cancer. Our results suggest that a dietary pattern with high fruit and vegetable consumption and low consumption of fried foods and sweets during pregnancy, as well as a dietary pattern with high fruit and vegetable consumption and low consumption of red and cured meats, may reduce the odds of unilateral retinoblastoma in offspring
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Perinatal Risk Factors and Autism in Los Angeles County: The Role of Air Pollution, Maternal Race/Ethnicity and Nativity
Full text linkBackground: Autistic Disorder (AD) is a serious developmental condition with a wide range of symptoms and the prevalence has risen dramatically over the past two decades. The pathogenic mechanisms of autism have yet to be determined or are not well understood. Epidemiologic investigations support a prenatal or early postnatal origin of autism and it is likely that multiple genes interacting with one or more environmental factors cause some cases. However, high-quality population-based research addressing etiology is limited. There may be phenotypic differences in the presentation of autism in minority groups that may indicate etiologic heterogeneity, but it is unknown whether maternal race/ethnicity and nativity are risk factors for childhood autism in the U.S. Few studies to date have examined the impact of air pollution on brain development in general during pregnancy, although epidemiologic studies have associated air pollution exposure during the prenatal period to a variety of adverse birth outcomes. Few studies to date have examined the impact of air pollution on brain development in general during pregnancy, although epidemiologic studies have associated air pollution exposure during the prenatal period to a variety of adverse birth outcomes. Our first aim was to investigate the association between traffic related air pollution exposures during pregnancy and autism using: 1) ambient criteria air pollutant measurements, and 2) land-use regression (LUR) to model traffic related air pollution exposures, using a matched case-control design. The second and third aim was to determine whether the risk of autism and autistic phenotypes, i.e., comorbid mental retardation, expressive language, and emotional/behavioral deficits, differ by maternal race/ethnicity and nativity. Using U.S.-born white mothers as reference, we examined autism relative risks in Hispanics and black mothers born in or outside of the U.S of which mothers born in Mexico or Central/South America were specified. In addition, we examined the association between autism and maternal Asian race/ethnicity in women born in the U.S., China, Japan, Korea, Philippines, or Vietnam. Methods: Children of mothers who gave birth in Los Angeles who were diagnosed with a primary AD diagnosis at ages 3-5 years during 1998-2009 were identified through the California Department of Developmental Services and linked to 1995-2006 California birth certificates. For 7,603 children with autism, in the first study we selected 10 controls per case matched by sex, birth year, and minimum gestational age, birth addresses were mapped and linked to the nearest air monitoring station and a LUR model. For the second study, 6,485 children with AD were selected from a cohort of 1,461,610 births from white, Hispanic, and black mothers; and for the final study 2,532 children with AD were selected from a cohort of 401,091 births from Asian and U.S.-born white mothers. We further identified a subgroup of children with AD and a secondary diagnosis of mental retardation (AD-MR). To appropriately investigate language and behavior heterogeneity, we restricted assessments to 5-year olds. We identified from DDS evaluation records two subgroups with either "impaired" or "less impaired" expressive language; and two subgroups with "severe" or "less severe" emotional outburst behavior. Summary of findings: Per interquartile range (IQR) increase, we estimated a 12-15% relative increase in odds of autism for O3 (11.54ppb) and PM2.5 (4.68 μg/m3) when mutually adjusting for both pollutants. Furthermore, we estimated 3-9% relative increases in odds per IQR increase for LUR-based NO (9.4ppb) and NO2 (5.4ppb) exposure estimates. LUR-based associations were strongest for children of mothers with less than a high school education. We found increases in risk for AD and AD-MR for children of foreign-born (FB) black mothers and Hispanic mothers from Central/South America, as well as of mothers who immigrated from the Philippines and Vietnam compared to U.S.-born whites. We estimated a 52% and 53% relative increase in risk of having a child with AD-MR for both U.S.-born African American/black and Hispanic mothers, respectively. Compared to children with autism of U.S.-born white mothers, most other maternal subgroups, except for foreign-born Chinese or Japanese mothers, had children with a higher risk of impaired expressive language. Severity of emotional outbursts was higher in children of foreign-born black and Centra/South American mothers, as well as in U.S.-born Hispanics. However, severe emotional outbursts seem to co-occur with impaired language
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Bias Analyses in Population-Based Studies of Parkinson’s Disease
Full text linkThis dissertation work investigates two types of biases in population-based studies of Parkinson’s disease (PD), one is survivor bias in estimating the association between PD and cancer, the other is exposure misclassification due to residential mobility and time-varying exposure. Negative associations between PD and cancer have been found in epidemiological studies. Several mechanisms were proposed to explain such reported inverse associations. In the first and second part of this work we propose two similar survivor bias mechanisms that may account for the observed negative associations with cancer both prior to and after the diagnosis of PD as an alternative explanation. Using a large Danish population-based case-control study of Parkinson’s disease as an example, we utilize causal theory, Monte Carlo methods and inverse probability-of-censoring weights techniques to quantitatively investigate how the observed negative association can be explained by the hypothesized bias. These results suggest that for cancer both before and after the diagnosis of PD, survivor bias could be an alternative explanation for the observed association between cancer and PD with reasonable bias structure and assumptions. In the last part of this work we investigate possible exposure misclassification due to residential mobility and changes in pesticide application using a California population-based case-control study of Parkinson’s disease as an illustration. We simulate scenarios where detailed residential histories were lacking and only the enrollment address was used as a proxy for all addresses to estimate long-term pesticide exposures. Results show that the exposures could be either over- or under- estimated depending on pesticide, time period of interest, as well as threshold for identifying the binary exposure variables. The exposure misclassification is not necessarily non-differential and the direction of the bias is inconsistent. When estimating long-term environmental exposures using one address only it may result in exposure misclassification and not always guarantee non-differentiality
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