Institution
University of California, Los Angeles
Education•Los Angeles, California, United States•
About: University of California, Los Angeles is a education organization based out in Los Angeles, California, United States. It is known for research contribution in the topics: Population & Health care. The organization has 125991 authors who have published 282429 publications receiving 15785853 citations. The organization is also known as: UCLA & UC Los Angeles.
Topics: Population, Health care, Poison control, Cancer, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: The results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia, and disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways.
Abstract: Schizophrenia is a devastating neurodevelopmental disorder whose genetic influences remain elusive. We hypothesize that individually rare structural variants contribute to the illness. Microdeletions and microduplications >100 kilobases were identified by microarray comparative genomic hybridization of genomic DNA from 150 individuals with schizophrenia and 268 ancestry-matched controls. All variants were validated by high-resolution platforms. Novel deletions and duplications of genes were present in 5% of controls versus 15% of cases and 20% of young-onset cases, both highly significant differences. The association was independently replicated in patients with childhood-onset schizophrenia as compared with their parents. Mutations in cases disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways. These results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia.
1,762 citations
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TL;DR: It is demonstrated that ROS generation and oxidative stress are a valid test paradigm to compare NP toxicity, and particle interactions with cellular components are capable of generating oxidative stress.
Abstract: Nanomaterial properties differ from those bulk materials of the same composition, allowing them to execute novel activities. A possible downside of these capabilities is harmful interactions with biological systems, with the potential to generate toxicity. An approach to assess the safety of nanomaterials is urgently required. We compared the cellular effects of ambient ultrafine particles with manufactured titanium dioxide (TiO2), carbon black, fullerol, and polystyrene (PS) nanoparticles (NPs). The study was conducted in a phagocytic cell line (RAW 264.7) that is representative of a lung target for NPs. Physicochemical characterization of the NPs showed a dramatic change in their state of aggregation, dispersibility, and charge during transfer from a buffered aqueous solution to cell culture medium. Particles differed with respect to cellular uptake, subcellular localization, and ability to catalyze the production of reactive oxygen species (ROS) under biotic and abiotic conditions. Spontaneous ROS production was compared by using an ROS quencher (furfuryl alcohol) as well as an NADPH peroxidase bioelectrode platform. Among the particles tested, ambient ultrafine particles (UFPs) and cationic PS nanospheres were capable of inducing cellular ROS production, GSH depletion, and toxic oxidative stress. This toxicity involves mitochondrial injury through increased calcium uptake and structural organellar damage. Although active under abiotic conditions, TiO2 and fullerol did not induce toxic oxidative stress. While increased TNF-alpha production could be seen to accompany UFP-induced oxidant injury, cationic PS nanospheres induced mitochondrial damage and cell death without inflammation. In summary, we demonstrate that ROS generation and oxidative stress are a valid test paradigm to compare NP toxicity. Although not all materials have electronic configurations or surface properties to allow spontaneous ROS generation, particle interactions with cellular components are capable of generating oxidative stress.
1,761 citations
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TL;DR: In this article, a model involving symmetrical fluxes is introduced to take advantage of the oxygen data, and the measured δ34S and δ18O correspond to variations in these isotopes in sulfate of the world ocean surface.
1,759 citations
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TL;DR: Data support the hypothesis that high CACS can modify predicted risk obtained from FRS alone, especially among patients in the intermediate-risk category in whom clinical decision making is most uncertain.
Abstract: ContextGuidelines advise that all adults undergo coronary heart disease (CHD)
risk assessment to guide preventive treatment intensity. Although the Framingham
Risk Score (FRS) is often recommended for this, it has been suggested that
risk assessment may be improved by additional tests such as coronary artery
calcium scoring (CACS).ObjectivesTo determine whether CACS assessment combined with FRS in asymptomatic
adults provides prognostic information superior to either method alone and
whether the combined approach can more accurately guide primary preventive
strategies in patients with CHD risk factors.Design, Setting, and ParticipantsProspective observational population-based study, of 1461 asymptomatic
adults with coronary risk factors. Participants with at least 1 coronary risk
factor (>45 years) underwent computed tomography (CT) examination, were screened
between 1990-1992, were contacted yearly for up to 8.5 years after CT scan,
and were assessed for CHD. This analysis included 1312 participants with CACS
results; excluded were 269 participants with diabetes and 14 participants
with either missing data or had a coronary event before CACS was performed.Main Outcome MeasureNonfatal myocardial infarction (MI) or CHD death.ResultsDuring a median of 7.0 years of follow-up, 84 patients experienced MI
or CHD death; 70 patients died of any cause. There were 291 (28%) participants
with an FRS of more than 20% and 221 (21%) with a CACS of more than 300. Compared
with an FRS of less than 10%, an FRS of more than 20% predicted the risk of
MI or CHD death (hazard ratio [HR], 14.3; 95% confidence interval [CI]; 2.0-104; P = .009). Compared with a CACS of zero, a CACS of more
than 300 was predictive (HR, 3.9; 95% CI, 2.1-7.3; P<.001).
Across categories of FRS, CACS was predictive of risk among patients with
an FRS higher than 10% (P<.001) but not with an
FRS less than 10%.ConclusionThese data support the hypothesis that high CACS can modify predicted
risk obtained from FRS alone, especially among patients in the intermediate-risk
category in whom clinical decision making is most uncertain.
1,759 citations
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TL;DR: Modifications to this method that allow for cross-modality registration of MRI and PET brain images obtained from a single subject are described and validated quantitatively using data from patients with stereotaxic fiducial markers rigidly fixed in the skull.
Abstract: ObjectiveWe have previously reported an automated method for within-modality (e.g., PET-to-PET) image alignment. We now describe modifications to this method that allow for cross-modality registration of MRI and PET brain images obtained from a single subject.MethodsThis method does not require fidu
1,759 citations
Authors
Showing all 126949 results
Name | H-index | Papers | Citations |
---|---|---|---|
Albert Hofman | 267 | 2530 | 321405 |
Shizuo Akira | 261 | 1308 | 320561 |
George M. Whitesides | 240 | 1739 | 269833 |
Michael Karin | 236 | 704 | 226485 |
Trevor W. Robbins | 231 | 1137 | 164437 |
Fred H. Gage | 216 | 967 | 185732 |
Edward Giovannucci | 206 | 1671 | 179875 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Rob Knight | 201 | 1061 | 253207 |
Ronald M. Evans | 199 | 708 | 166722 |
Carlo M. Croce | 198 | 1135 | 189007 |
Raymond J. Dolan | 196 | 919 | 138540 |
Michael Marmot | 193 | 1147 | 170338 |
Alan C. Evans | 183 | 866 | 134642 |
Paul M. Thompson | 183 | 2271 | 146736 |