bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multi‐instrument observations of SED during 24–25 October 2011 storm: Implications for SED formation processes
Authors: Zou Shasha , Ridley Aaron J. , Moldwin Mark B. , Nicolls Michael J. , Coster Anthea J. , Thomas Evan G. , Ruohoniemi J. Michael 
Published: November 2013

AbstractWe present multiple instrument observations of a storm‐enhanced density (SED) during the 24–25 October 2011 intense geomagnetic storm. Formation and the subsequent evolution of the SED and the midlatitude trough are revealed by global GPS vertical total electron content maps. In addition, we present high time resolution Poker Flat Incoherent Scatter Radar (PFISR) observations of ionospheric profiles within the SED. We divided the SED observed by PFISR into two parts. Both parts are characterized by elevated ionospheric peak height (hmF2) and total electron content, compared to quiet time values. However, the two parts of the SED have different characteristics in the electron temperature (Te), the F region peak density (NmF2), and convection flows. The first part of the SED is associated with enhanced Te in the lower F region and reduced Te in the upper F region and is collocated with northward convection flows. The NmF2 was lower than quiet time values. The second part of the SED is associated with significantly increased NmF2, elevated Te at all altitudes and is located near the equatorward boundary of large northwestward flows. Based on these observations, we suggest that the mechanisms responsible for the formation of the two parts of the SED may be different. The first part is due to equatorward expansion of the convection pattern and the projection of northward convection flows in the vertical direction, which lifts the ionospheric plasma to higher altitudes and thus reduces the loss rate of plasma recombination. The second part is more complicated. Besides equatorward expansion of the convection pattern and large upward flows, evidences of other mechanisms, including horizontal advection due to fast flows, energetic particle precipitation, and enhanced thermospheric wind in the topside ionosphere, are also present. Estimates show that contribution from precipitating energetic protons is at most ~10% of the total F region density. The thermospheric wind also plays a minor role in this case.
Estimating aerodynamic roughness over complex surface terrain
Authors: Nield Joanna M. , King James , Wiggs Giles F. S. , Leyland Julian , Bryant Robert G. , Chiverrell Richard C. , Darby Stephen E. , Eckardt Frank D. , Thomas David S. G. , Vircavs Larisa H. , Washington Richard 
Published: November 2013

AbstractSurface roughness plays a key role in determining aerodynamic roughness length (zo) and shear velocity, both of which are fundamental for determining wind erosion threshold and potential. While zo can be quantified from wind measurements, large proportions of wind erosion prone surfaces remain too remote for this to be a viable approach. Alternative approaches therefore seek to relate zo to morphological roughness metrics. However, dust‐emitting landscapes typically consist of complex small‐scale surface roughness patterns and few metrics exist for these surfaces which can be used to predict zo for modeling wind erosion potential. In this study terrestrial laser scanning was used to characterize the roughness of typical dust‐emitting surfaces (playa and sandar) where element protrusion heights ranged from 1 to 199 mm, over which vertical wind velocity profiles were collected to enable estimation of zo. Our data suggest that, although a reasonable relationship (R2 > 0.79) is apparent between 3‐D roughness density and zo, the spacing of morphological elements is far less powerful in explaining variations in zo than metrics based on surface roughness height (R2 > 0.92). This finding is in juxtaposition to wind erosion models that assume the spacing of larger‐scale isolated roughness elements is most important in determining zo. Rather, our data show that any metric based on element protrusion height has a higher likelihood of successfully predicting zo. This finding has important implications for the development of wind erosion and dust emission models that seek to predict the efficiency of aeolian processes in remote terrestrial and planetary environments.
Flexible nonlinear estimates of the association between height and mental ability in early life
Authors: Murasko Jason E. 
Published: November 2013

ABSTRACTObjectivesTo estimate associations between early‐life mental ability and height/height‐growth in contemporary US children.MethodsStructured additive regression models are used to flexibly estimate the associations between height and mental ability at approximately 24 months of age. The sample is taken from the Early Childhood Longitudinal Study–Birth Cohort, a national study whose target population was children born in the US during 2001.ResultsA nonlinear association is indicated between height and mental ability at approximately 24 months of age. There is an increasing association between height and mental ability below the mean value of height, but a flat association thereafter. Annualized growth shows the same nonlinear association to ability when controlling for baseline length at 9 months.ConclusionsRestricted growth at lower values of the height distribution is associated with lower measured mental ability in contemporary US children during the first years of life. Am. J. Hum. Biol. 26:87–94, 2014. © 2013 Wiley Periodicals, Inc.
Sleep duration, quality, and timing and their associations with age in a community without electricity in haiti
Authors: Knutson Kristen L. 
Published: November 2013

ABSTRACTObjectivesSleep comprises one‐third of one's life, yet little is known about sleep in developing countries. Furthermore, many studies in industrialized countries have reported that sleep duration and quality decline with aging, but whether this association persists globally is unknown. This study's objectives were to characterize sleep in a community without electricity in Haiti and to examine associations between measures of sleep and age.MethodsFifty‐eight Haiti residents (50% women) in four age groups, 18–30, 31–50, 51–64, and ≥65 years participated. Three days of wrist actigraphy were used to estimate sleep patterns.ResultsMean (standard deviation) values of sleep measures were: 20:57 (0:40) for sleep onset, 4:54 (0:43) for sleep end, 9.3 (1.2) h for time in bed, 7.0 (1.0) h for sleep duration, 54 (24) min awake after sleep onset, and 88.7 (5.4)% for sleep maintenance (percentage of sleep period actually spent sleeping). There were no significant differences in the sleep measures between men and women. Regression analyses adjusting for sex, household size, and number of people sleeping in the same room indicated that only sleep fragmentation differed by age group. Specifically, mean fragmentation was higher in the youngest age group than all other age groups, which did not differ from one another.ConclusionsAverage time in bed in this Haitian sample was greater than previously reported for industrialized countries like the United States (9.3 versus. 7–8 h);, however, actual sleep duration averaged only 7 h. No age‐related decline in sleep duration or quality was observed in Haiti. Am. J. Hum. Biol. 26:80–86, 2014. © 2013 Wiley Periodicals, Inc.
Gender specific analysis of occupational diseases of the low back caused by carrying, lifting or extreme trunk flexion—use of a prevention index to identify occupations with high prevention needs
Authors: Thiede Markus , Liebers Falk , Seidler Andreas , Gravemeyer Stefan , Latza Ute 
Published: November 2013

ABSTRACTBackgroundGender specific analysis of the occupational disease of the lumbar spine caused by carrying, lifting, or extreme trunk flexion in Germany (OD No.2108) with the aim to identify areas of focus for prevention and research with a prevention index (PI).MethodsData from the German Statutory Accident Insurance stratified by gender are shown.ResultsFrom 2002 until 2009 there were 2,877 confirmed cases of an OD No. 2108 (40.1% male and 59.1% female). The PI indicated the highest prevention need for female nursing/midwifery associate professionals and male building frame and related trades workers. Patient transfer and working in extremely bent posture were the most frequent exposures.ConclusionsThe identified occupations with high need for prevention among men come from nearly all major occupational groups whereas women cluster in occupational groups from the health and care sectors. Am. J. Ind. Med. 57:233–244, 2014. © 2013 The Authors. American Journal of Industrial Medicine Published by Wiley Periodicals, Inc.
The Strain Index andTLVforHAL: Risk of lateral epicondylitis in a prospective cohort
Authors: Garg Arun , Kapellusch Jay M. , Hegmann Kurt T. , Thiese Matthew S. , Merryweather Andrew S. , Wang Ying‐Chih , Malloy Elizabeth J. 
Published: November 2013

BackgroundThis study's objective was to quantify exposure‐response relationships between job physical exposure (JPE) and incidence of lateral epicondylitis (LE).MethodsA cohort of 536 workers was enrolled from 10 manufacturing facilities and followed monthly for 6 years to ascertain changes in JPE and health status. JPE was individually measured and quantified using the Strain Index (SI) and TLV for HAL. Worker demographics, medical history, psychosocial factors, and current musculoskeletal disorders were obtained.ResultsFifty‐six workers developed LE. In multivariate models JPE, age, family problems, and swimming were associated with increased risk of LE. SI showed an exposure‐response relationship with maximum hazard ratio (HR) of 4.5(P = 0.04). TLV for HAL showed a non‐statistically significant trend for increased risk of LE (P = 0.19).ConclusionJPE is associated with increased risk of LE. The SI and TLV for HAL are useful metrics for estimating JPE. Am. J. Ind. Med. 57:286–302, 2014. © 2013 Wiley Periodicals, Inc.
Progressive multifocal leukoencephalopathy after natalizumab discontinuation
Authors: Fine Andrew J. , Sorbello Alfred , Kortepeter Cindy , Scarazzini Linda 
Published: November 2013

ObjectiveTo identify cases of laboratory‐ or biopsy‐confirmed progressive multifocal leukoencephalopathy (PML) in patients with multiple sclerosis (MS) who previously discontinued natalizumab (NTZ) for reasons unrelated to suspected or proven PML and assess PML risk factors in these cases.MethodsWe searched the US Food and Drug Administration Adverse Event Reporting System and MEDLINE for reports submitted from 2006 to 2012 of laboratory‐confirmed PML with symptom onset ≥30 days following NTZ withdrawal. We only analyzed cases where NTZ discontinuation was unrelated to suspected PML.ResultsSeventeen patients discontinued NTZ for reasons unrelated to PML but were subsequently diagnosed with the disease. The median NTZ duration was 47 monthly doses (range = 9–59 doses). All patients presented with compatible clinical symptoms within 6 months following withdrawal, and PML was confirmed by brain biopsy or by identifying JC virus in the cerebrospinal fluid by polymerase chain reaction. Immune reconstitution inflammatory syndrome (IRIS) was reported in 11 patients. Eleven patients (65%) received new MS treatments between NTZ discontinuation and PML confirmation. No deaths were reported. At NTZ withdrawal, 16 patients (94%) had ≥1 PML risk factor, including NTZ duration ≥2 years (n = 13), prior immunosuppressive agents (n = 8), and reported anti–JC virus seropositivity (n = 13).InterpretationNTZ‐treated patients presenting clinically with PML within 6 months after NTZ withdrawal frequently have pre‐existing PML risk factors. Clinicians need heightened awareness for new onset PML, IRIS, and MS relapse in evaluating neurological decline following NTZ discontinuation. Ann Neurol 2014;75:108–115
Cerebrospinal fluid neurofilament concentration reflects disease severity in frontotemporal degeneration
Authors: Scherling Carole S. , Hall Tracey , Berisha Flora , Klepac Kristen , Karydas Anna , Coppola Giovanni , Kramer Joel H. , Rabinovici Gil , Ahlijanian Michael , Miller Bruce L. , Seeley William , Grinberg Lea T. , Rosen Howard , Meredith Jere , Boxer Adam L. 
Published: November 2013

ObjectiveCerebrospinal fluid (CSF) neurofilament light chain (NfL) concentration is elevated in neurological disorders, including frontotemporal degeneration (FTD). We investigated the clinical correlates of elevated CSF NfL levels in FTD.MethodsCSF NfL, amyloid‐β1–42 (Aβ42), tau, and phosphorylated tau concentrations were compared in 47 normal controls (NC), 8 asymptomatic gene carriers (NC2) of FTD‐causing mutations, and 79 FTD (45 behavioral variant frontotemporal dementia [bvFTD], 18 progressive nonfluent aphasia [PNFA], 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson disease, and 17 corticobasal syndrome patients. Correlations between CSF analyte levels were performed with neuropsychological measures and the Clinical Dementia Rating scale sum of boxes (CDRsb). Voxel‐based morphometry of structural magnetic resonance images determined the relationship between brain volume and CSF NfL.ResultsMean CSF NfL concentrations were higher in bvFTD, SD, and PNFA than other groups. NfL in NC2 was similar to NC. CSF NfL, but not other CSF measures, correlated with CDRsb and neuropsychological measures in FTD, but not in other diagnostic groups. Analyses in 2 independent FTD cohorts and a group of autopsy‐verified or biomarker‐enriched cases confirmed the larger group analysis. In FTD, gray and white matter volume negatively correlated with CSF NfL concentration, such that individuals with the highest NfL levels exhibited the most atrophy.InterpretationCSF NfL is elevated in symptomatic FTD and correlates with disease severity. This measurement may be a useful surrogate endpoint of disease severity in FTD clinical trials. Longitudinal studies of CSF NfL in FTD are warranted. ANN NEUROL 2014;75:116–126
Diabetes, markers of brain pathology and cognitive function
Authors: Qiu Chengxuan , Sigurdsson Sigurdur , Zhang Qian , Jonsdottir Maria K. , Kjartansson Olafur , Eiriksdottir Gudny , Garcia Melissa E. , Harris Tamara B. , van Buchem Mark A. , Gudnason Vilmundur , Launer Lenore J. 
Published: November 2013

ObjectiveWe investigated whether, and the extent to which, vascular and degenerative lesions in the brain mediate the association of diabetes with poor cognitive performance.MethodsThis cross‐sectional study included 4,206 participants (age > 65 years; 57.8% women) of the Age, Gene/Environment Susceptibility–Reykjavik Study. Data were collected through interview, clinical examination, psychological testing, and laboratory tests. The composite scores on memory, information‐processing speed, and executive function were derived from a cognitive test battery. Markers of cerebral macrovascular (cortical infarcts), microvascular (subcortical infarcts, cerebral microbleeds, and higher white matter lesion volume), and neurodegenerative (lower gray matter, normal white matter, and total brain tissue volumes) processes were assessed on magnetic resonance images. Mediation models were employed to test the mediating effect of brain lesions on the association of diabetes with cognitive performance controlling for potential confounders.ResultsThere were 462 (11.0%) persons with diabetes. Diabetes was significantly associated with lower scores on processing speed and executive function, but not with memory function. Diabetes was significantly associated with all markers of brain pathology. All of these markers were significantly associated with lower scores on memory, processing speed, and executive function. Formal mediation tests suggested that markers of cerebrovascular and degenerative pathology significantly mediated the associations of diabetes with processing speed and executive function.InterpretationDiabetes is associated with poor performance on cognitive tests of information‐processing speed and executive function. The association is largely mediated by markers of both neurodegeneration and cerebrovascular disease. Older people with diabetes should be monitored for cognitive problems and brain lesions. Ann Neurol 2014;75:138–146
Chronic neuropathological and neurobehavioral changes in a repetitive mild traumatic brain injury model
Authors: Mouzon Benoit C. , Bachmeier Corbin , Ferro Austin , Ojo Joseph‐Olubunmi , Crynen Gogce , Acker Christopher M. , Davies Peter , Mullan Michael , Stewart William , Crawford Fiona 
Published: November 2013

ObjectiveTraumatic brain injury (TBI) is a recognized risk factor for later development of neurodegenerative disease. However, the mechanisms contributing to neurodegeneration following TBI remain obscure.MethodsIn this study, we have utilized a novel mild TBI (mTBI) model to examine the chronic neurobehavioral and neuropathological outcomes following single and repetitive mTBI at time points from 6 to 18 months following injury.ResultsOur results reveal that at 6, 12, and 18 months after injury, animals exposed to a single mTBI have learning impairments when compared to their sham controls without exhibiting spatial memory retention deficits. In contrast, animals exposed to repetitive injury displayed persistent cognitive deficits, slower rate of learning, and progressive behavioral impairment over time. These deficits arise in parallel with a number of neuropathological abnormalities, including progressive neuroinflammation and continuing white matter degradation up to 12 months following repetitive injury. Neither single nor repetitive mTBI was associated with elevated brain levels of amyloid beta or abnormal tau phosphorylation at 6 or 12 months after injury.InterpretationImportantly, these data provide evidence that, although a single mTBI produces a clinical syndrome and pathology that remain static in the period following injury, repetitive injuries produce behavioral and pathological changes that continue to evolve many months after the initial injuries. As such, this model recapitulates many aspects described in human studies of TBI, providing a suitable platform on which to investigate the evolving pathologies following mild TBI and potential strategies for therapeutic intervention. ANN NEUROL 2014;75:241–254
Hyperexcitable C nociceptors in fibromyalgia
Authors: Serra Jordi , Collado Antonio , Solà Romà , Antonelli Francesca , Torres Xavier , Salgueiro Monika , Quiles Cristina , Bostock Hugh 
Published: November 2013

ObjectiveTo test the hypothesis that peripheral C nociceptor function may be abnormal in fibromyalgia and that C nociceptor dysfunction may contribute to the symptoms reported by these patients.MethodsMicroneurography was used to record C nociceptors of 30 female patients meeting criteria for fibromyalgia and compared with recordings from 17 female patients with small‐fiber neuropathy and 9 female controls.ResultsWe obtained stable recordings of 186 C nociceptors in the fibromyalgia group, 114 from small‐fiber neuropathy patients, and 66 from controls. The mechanosensitive nociceptors in the fibromyalgia patients behaved normally, but the silent nociceptors in 76.6% of fibromyalgia patients exhibited abnormalities. Spontaneous activity was detected in 31% of silent nociceptors in fibromyalgia, 34% in small‐fiber neuropathy, and 2.2% in controls. Sensitization to mechanical stimulation was found in 24.2% of silent nociceptors in fibromyalgia, 22.7% in small‐fiber neuropathy, and 3.7% in controls. Abnormally high slowing of conduction velocity when first stimulated at 0.25Hz was more common in fibromyalgia.InterpretationWe show for the first time that the majority of fibromyalgia patients have abnormal C nociceptors. Many silent nociceptors exhibit hyperexcitability resembling that in small‐fiber neuropathy, but high activity‐dependent slowing of conduction velocity is more common in fibromyalgia patients, and may constitute a distinguishing feature. We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by patients with fibromyalgia. ANN NEUROL 2014;75:196–208
Lewy body extracts from Parkinson disease brains trigger α‐synuclein pathology and neurodegeneration in mice and monkeys
Authors: Recasens Ariadna , Dehay Benjamin , Bové Jordi , Carballo‐Carbajal Iria , Dovero Sandra , Pérez‐Villalba Ana , Fernagut Pierre‐Olivier , Blesa Javier , Parent Annabelle , Perier Celine , Fariñas Isabel , Obeso José A. , Bezard Erwan , Vila Miquel 
Published: November 2013

ObjectiveMounting evidence suggests that α‐synuclein, a major protein component of Lewy bodies (LB), may be responsible for initiating and spreading the pathological process in Parkinson disease (PD). Supporting this concept, intracerebral inoculation of synthetic recombinant α‐synuclein fibrils can trigger α‐synuclein pathology in mice. However, it remains uncertain whether the pathogenic effects of recombinant synthetic α‐synuclein may apply to PD‐linked pathological α‐synuclein and occur in species closer to humans.MethodsNigral LB‐enriched fractions containing pathological α‐synuclein were purified from postmortem PD brains by sucrose gradient fractionation and subsequently inoculated into the substantia nigra or striatum of wild‐type mice and macaque monkeys. Control animals received non‐LB fractions containing soluble α‐synuclein derived from the same nigral PD tissue.ResultsIn both mice and monkeys, intranigral or intrastriatal inoculations of PD‐derived LB extracts resulted in progressive nigrostriatal neurodegeneration starting at striatal dopaminergic terminals. No neurodegeneration was observed in animals receiving non‐LB fractions from the same patients. In LB‐injected animals, exogenous human α‐synuclein was quickly internalized within host neurons and triggered the pathological conversion of endogenous α‐synuclein. At the onset of LB‐induced degeneration, host pathological α‐synuclein diffusely accumulated within nigral neurons and anatomically interconnected regions, both anterogradely and retrogradely. LB‐induced pathogenic effects required both human α‐synuclein present in LB extracts and host expression of α‐synuclein.Interpretationα‐Synuclein species contained in PD‐derived LB are pathogenic and have the capacity to initiate a PD‐like pathological process, including intracellular and presynaptic accumulations of pathological α‐synuclein in different brain areas and slowly progressive axon‐initiated dopaminergic nigrostriatal neurodegeneration. ANN NEUROL 2014;75:351–362