351 research outputs found

    Collateral Estoppel

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    The doctrine of collateral estoppel involves the use of an old judgment in a new action to prevent the relitigation of issues resolved by that old judgment. At common law, use of the doctrine required that the party using collateral estoppel and the party against whom it was used be the same as the parties to the prior judgment. This common law requirement of mutuality has been relaxed and since the United States Supreme Court\u27s 1979 decision in ParklaneHoisery Co. v. Shore, the strict common law requirement of mutuality has all but completely vanished. In Parklane the Court sanctioned the use of collateral estoppel by a plaintiff who was a stranger to the original suit against a defendant who was party to that suit. The courts\u27 search for fair results and judicial economy in the application of the doctrine led to this application of the doctrine in circumstances in which the parties were not mutual. This note traces the un- steady course which the doctrine of collateral estoppel traveled before Parklane. The significance of the Court\u27s decision in Parklane is then analyzed. Finally, post-Parklane applications of collateral estoppel are discussed, including the effect of the use of collateral estoppel on the seventh amendment right to jury trial and its impact on substantive areas of law

    High Resolution Observations of Drop Size Distribution for GPM Ground Validation

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    During the Mid-latitude Continental Convective Cloud Experiment (MC3E), NASA's GPM GV Disdrometer and Radar Observations of Precipitation (DROP) Facility deployed an array of disdrometers and rain gauges in northern Oklahoma to sample, with high resolution, the drop size distribution for use in development of precipitation retrieval algorithms for the GPM core satellites. The DROP Facility instruments deployed during MC3E consisted of 16 autonomous Parsivel units, 5 two-dimensional video disdrometers (2dvds), a vertically pointing K band radar, and 32 tipping bucket rain gauges. There were several rainfall events during MC3E in which rain drops exceeding 6 mm in diameter were recorded. The disdrometer array revealed large rain drops with diameters exceeding 6 mm and 8 mm during two separate stratiform and convective rainfall events, respectively. The NPOL radar, which was scanning in high resolution RHI mode (every 40 sec) over the disdrometer array during the stratiform event, indicated a 1 km thick bright band with a differential reflectivity column of 2-3 dB extending below the melting layer to the surface where the large drops were recorded by the 2dvds. These large drops are important for GPM since they can have a great impact upon satellite precipitation retrieval, especially near the ground and below heavy convective rainfall cores where satellites have had problems depicting the rainfall

    Cerebrospinal fluid proteomics define the natural history of autosomal dominant Alzheimer's disease

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    Alzheimer’s disease (AD) pathology develops many years before the onset of cognitive symptoms. Two pathological processes—aggregation of the amyloid-β (Aβ) peptide into plaques and the microtubule protein tau into neurofibrillary tangles (NFTs)—are hallmarks of the disease. However, other pathological brain processes are thought to be key disease mediators of Aβ plaque and NFT pathology. How these additional pathologies evolve over the course of the disease is currently unknown. Here we show that proteomic measurements in autosomal dominant AD cerebrospinal fluid (CSF) linked to brain protein coexpression can be used to characterize the evolution of AD pathology over a timescale spanning six decades. SMOC1 and SPON1 proteins associated with Aβ plaques were elevated in AD CSF nearly 30 years before the onset of symptoms, followed by changes in synaptic proteins, metabolic proteins, axonal proteins, inflammatory proteins and finally decreases in neurosecretory proteins. The proteome discriminated mutation carriers from noncarriers before symptom onset as well or better than Aβ and tau measures. Our results highlight the multifaceted landscape of AD pathophysiology and its temporal evolution. Such knowledge will be critical for developing precision therapeutic interventions and biomarkers for AD beyond those associated with Aβ and tau

    Cerebrospinal fluid proteomics define the natural history of autosomal dominant Alzheimer’s disease

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    Alzheimer’s disease (AD) pathology develops many years before the onset of cognitive symptoms. Two pathological processes—aggregation of the amyloid- (A ) peptide into plaques and the microtubule protein tau into neurofibrillary tangles (NFTs)—are hallmarks of the disease. However, other pathological brain processes are thought to be key disease mediators of A plaque and NFT pathology. How these additional pathologies evolve over the course of the disease is currently unknown. Here we show that proteomic measurements in autosomal dominant AD cerebrospinal fluid (CSF) linked to brain protein coexpression can be used to characterize the evolution of AD pathology over a timescale spanning six decades. SMOC1 and SPON1 proteins associated with A plaques were elevated in AD CSF nearly 30 years before the onset of symptoms, followed by changes in synaptic proteins, metabolic proteins, axonal proteins, inflammatory proteins and finally decreases in neurosecretory proteins. The proteome discriminated mutation carriers from noncarriers before symptom onset as well or better than A and tau measures. Our results highlight the multifaceted landscape of AD pathophysiology and its temporal evolution. Such knowledge will be critical for developing precision therapeutic interventions and biomarkers for AD beyond those associated with A and tau

    Cerebrospinal fluid proteomics define the natural history of autosomal dominant Alzheimer's disease

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    Alzheimer's disease (AD) pathology develops many years before the onset of cognitive symptoms. Two pathological processes-aggregation of the amyloid-& beta;(A & beta;) peptide into plaques and the microtubule protein tau into neurofibrillary tangles (NFTs)-are hallmarks of the disease. However, other pathological brain processes are thought to be key disease mediators of A & beta;plaque and NFT pathology. How these additional pathologies evolve over the course of the disease is currently unknown. Here we show that proteomic measurements in autosomal dominant AD cerebrospinal fluid (CSF) linked to brain protein coexpression can be used to characterize the evolution of AD pathology over a timescale spanning six decades. SMOC1 and SPON1 proteins associated with A & beta;plaques were elevated in AD CSF nearly 30 years before the onset of symptoms, followed by changes in synaptic proteins, metabolic proteins, axonal proteins, inflammatory proteins and finally decreases in neurosecretory proteins. The proteome discriminated mutation carriers from noncarriers before symptom onset as well or better than A & beta;and tau measures. Our results highlight the multifaceted landscape of AD pathophysiology and its temporal evolution. Such knowledge will be critical for developing precision therapeutic interventions and biomarkers for AD beyond those associated with A & beta;and tau. Proteomic analysis of cerebrospinal fluid from individuals with autosomal dominant Alzheimer's disease reveals how this complex and chronic disease evolves over many decades

    Neurocognitive and Neuroimaging Predictors of Clinical Outcome in Bipolar Disorder

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    Historically, bipolar disorder has been conceptualized as a disease involving episodic rather than chronic dysfunction. However, increasing evidence indicates that bipolar disorder is associated with substantial inter-episode psychosocial and vocational impairment. Here we review the contributions of neurocognitive deficits and structural and functional neuroanatomic alterations to the observed functional impairments. In particular, compelling evidence now suggests that neurocognitive impairments, particularly in the areas of attention, processing speed, and memory, are associated with functional outcome. Although investigation of the neural correlates of functional disability in bipolar disorder is only in its nascent stages, preliminary evidence suggests that white matter abnormalities may be predictive of poor outcome. A better understanding of the relationship between neurocognitive and neuroimaging assays and functional outcome has the potential to improve current treatment options and provide targets for new treatment strategies in bipolar disorder

    Measuring Resilience in Adult Women Using the 10-Items Connor-Davidson Resilience Scale (CD-RISC). Role of Trauma Exposure and Anxiety Disorders

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    International audiencePURPOSE: Resilience is the ability of individuals to adapt positively in the face of trauma. Little is known, however, about lifetime factors affecting resilience. METHODS: We assessed the effects of psychiatric disorder and lifetime trauma history on the resilience self-evaluation using the Connor-Davidson Resilience Scale (CD-RISC-10) in a high-risk-women sample. Two hundred and thirty eight community-dwelling women, including 122 participants in a study of breast cancer survivors and 116 participants without previous history of cancer completed the CD-RISC-10. Lifetime psychiatric symptoms were assessed retrospectively using two standardized psychiatric examinations (Mini International Neuropsychiatric Interview and Watson's Post-Traumatic Stress Disorder Inventory). RESULTS: Multivariate logistic regression adjusted for age, education, trauma history, cancer, current psychiatric diagnoses, and psychoactive treatment indicated a negative association between current psychiatric disorder and high resilience compared to low resilience level (OR = 0.44, 95% CI [0.21-0.93]). This was related to anxiety and not mood disorder. A positive and independent association with a trauma history was also observed (OR = 3.18, 95% CI [1.44-7.01]). CONCLUSION: Self-evaluation of resilience is influenced by both current anxiety disorder and trauma history. The independent positive association between resilience and trauma exposure may indicate a "vaccination" effect. This finding need to be taken into account in future studies evaluating resilience in general or clinical populations
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