Institution
Ford Motor Company
Company•Dearborn, Michigan, United States•
About: Ford Motor Company is a company organization based out in Dearborn, Michigan, United States. It is known for research contribution in the topics: Internal combustion engine & Signal. The organization has 36123 authors who have published 51450 publications receiving 855200 citations. The organization is also known as: Ford Motor & Ford Motor Corporation.
Topics: Internal combustion engine, Signal, Clutch, Control theory, Torque
Papers published on a yearly basis
Papers
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TL;DR: An approach to adaptive optics in microscopy wherein the rear pupil of an objective lens is segmented into subregions, and light is directed individually to each subregion to measure, by image shift, the deflection faced by each group of rays as they emerge from the objective and travel through the specimen toward the focus.
Abstract: Biological specimens are rife with optical inhomogeneities that seriously degrade imaging performance under all but the most ideal conditions. Measuring and then correcting for these inhomogeneities is the province of adaptive optics. Here we introduce an approach to adaptive optics in microscopy wherein the rear pupil of an objective lens is segmented into subregions, and light is directed individually to each subregion to measure, by image shift, the deflection faced by each group of rays as they emerge from the objective and travel through the specimen toward the focus. Applying our method to two-photon microscopy, we could recover near-diffraction-limited performance from a variety of biological and nonbiological samples exhibiting aberrations large or small and smoothly varying or abruptly changing. In particular, results from fixed mouse cortical slices illustrate our ability to improve signal and resolution to depths of 400 microm.
559 citations
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TL;DR: An automated surveillance tool for reporting the incidence, prevalence and processes of care for patients with heart failure confirmed a chronic disease epidemic of heart failure manifested primarily by an increase in prevalence over the past decade.
551 citations
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TL;DR: Posttraumatic stress disorder influences the risk for first-onset major depression and alcohol use disorder and preexisting major depression increased women's vulnerability to the PTSD-inducing effects of traumatic events and risk for exposure to traumatic events.
Abstract: Background: The risk for first-onset major depression, anxiety, and substance use disorders associated with prior posttraumatic stress disorder (PTSD) was estimated in a sample of women. Methods: The National Institute of Mental Health Diagnostic Interview Schedule, revised according to DSMIII-R , was used to measure lifetime psychiatric disorders in a stratified random sample of 801 mothers of children, who participated in a study of cognitive and psychiatric outcomes by level of birth weight. Cox proportional hazards models with time-dependent covariates were used to calculate the hazards ratios of first onset of other disorders following PTSD. Results: The lifetime prevalence of traumatic events was 40% and of PTSD, 13.8%. Posttraumatic stress disorder signaled increased risks for first-onset major depression (hazards ratio, 2.1) and alcohol use disorder (hazards ratio, 3.0). The risk for major depression following PTSD was of the same magnitude as the risk for major depression following other anxiety disorders. Women with preexisting anxiety and PTSD had significantly increased risk for first-onset major depression. Additional analysis showed that preexisting major depression increased women's vulnerability to the PTSD-inducing effects of traumatic events and risk for exposure to traumatic events. Conclusions: Posttraumatic stress disorder influences the risk for first-onset major depression and alcohol use disorder. The causal explanation of these temporally secondary disorders is unclear and might involve the effect of PTSD or underlying vulnerabilities exposed by the traumatic experience.
545 citations
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TL;DR: Significant increases in vascular endothelial growth factor, cyclic guanosine monophosphate, angiogenesis, endogenous cell proliferation and neurogenesis and an increase in the synaptic protein, synaptophysin indicate that atorvastatin induced brain plasticity and has neurorestorative activity after experimental stroke.
Abstract: We demonstrate that the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors atorvastatin and simvastatin enhance functional outcome and induce brain plasticity when administered after stroke to rats. With atorvastatin treatment initiated 1 day after stroke, animals exhibited significant increases in vascular endothelial growth factor, cyclic guanosine monophosphate, angiogenesis, endogenous cell proliferation and neurogenesis, and an increase in the synaptic protein, synaptophysin. Atorvastatin-induced angiogenesis in a tube formation assay was reduced by an antibody against the vascular endothelial growth factor receptor 2 (FIK-1) and by the nitric oxide synthase inhibitor, N-mono-methyl-L-arginine (L-NAME). Atorvastatin also induced phosphorylation of Akt and Erk in cultured primary cortical neurons. These data indicate that atorvastatin induced brain plasticity and has neurorestorative activity after experimental stroke.
545 citations
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TL;DR: The data demonstrate that MSCs survive, migrate and differentiate into phenotypic neural cells and suggest that intracerebral transplantation of M SCs may provide a powerful autoplastic therapy for stroke.
543 citations
Authors
Showing all 36140 results
Name | H-index | Papers | Citations |
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Anil K. Jain | 183 | 1016 | 192151 |
Markus Antonietti | 176 | 1068 | 127235 |
Christopher M. Dobson | 150 | 1008 | 105475 |
Jack Hirsh | 146 | 734 | 86332 |
Galen D. Stucky | 144 | 958 | 101796 |
Federico Capasso | 134 | 1189 | 76957 |
Peter Stone | 130 | 1229 | 79713 |
Gerald R. Crabtree | 128 | 371 | 60973 |
Douglas A. Lauffenburger | 122 | 705 | 55326 |
Abass Alavi | 113 | 1298 | 56672 |
Mark E. Davis | 113 | 568 | 55334 |
Keith Beven | 110 | 514 | 61705 |
Naomi Breslau | 107 | 254 | 42029 |
Fei Wang | 107 | 1824 | 53587 |
Jun Yang | 107 | 2090 | 55257 |