datacite-mapping 0.2.1 → 0.2.2

data/spec/data/dash1/ucsf-ark+=b7272=q6kw5cxv-mrt-datacite.xml

@@ -1,43 +1,44 @@
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-<identifier identifierType="DOI">10.7272/Q6KW5CXV</identifier>
-<creators>
-<creator>
-<creatorName>Weiner, Michael W.</creatorName>
-</creator>
-</creators>
-<titles>
-<title>Predicting Cognitive Decline</title>
-</titles>
-<publisher>University of California, San Francisco</publisher>
-<publicationYear>2012</publicationYear>
-<subjects>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Adult</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Human</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Magnetic Resonance Imaging</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Cognition</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Neuropsychological Test</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Aged</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Middle Aged</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Dementia</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Cognition Disorders</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Risk Factors</subject>
-</subjects>
-<contributors>
-<contributor contributorType="ResearchGroup">
-<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
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-</contributors>
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-<description descriptionType="Abstract">These data were acquired with the overall goal of determining the regional and longitudinal pattern of changes in the brain which best predict future cognitive decline and dementia due to Alzheimer's disease (AD). The data set includes longitudinal clinical evaluation, cognitive testing, and neuroimaging assessments from a non-demented study population aged 65 and up who complain of memory problems and show some indication of memory and/or executive functioning below age/gender/education adjusted norm.</description>
-<description descriptionType="Methods">Data Acquisition Location: San Francisco VA Medical Center; Scanner Type: Siemens Vision 1.5T; Coronal T1 MPRAGE: TR=9ms, TE=4ms, TI=300ms, 1x1mm2, 3mm slice thickness; Axial double spin echo PD &amp; T2: TR=5000ms, TE=20/85ms, 1x1.25mm2, 3mm slice thickness</description>
-</descriptions>
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+<identifier identifierType="DOI">10.7272/Q6KW5CXV</identifier>
+<creators>
+<creator>
+<creatorName>Weiner, Michael W.</creatorName>
+</creator>
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+<title>Predicting Cognitive Decline</title>
+</titles>
+<publisher>University of California, San Francisco</publisher>
+<publicationYear>2012</publicationYear>
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+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Adult</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Human</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Magnetic Resonance Imaging</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Cognition</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Neuropsychological Test</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Aged</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Middle Aged</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Dementia</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Cognition Disorders</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Risk Factors</subject>
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+<contributors>
+<contributor contributorType="ResearchGroup">
+<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
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+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">18550226</relatedIdentifier>
+</relatedIdentifiers>
+<descriptions>
+<description descriptionType="Abstract">These data were acquired with the overall goal of determining the regional and longitudinal pattern of changes in the brain which best predict future cognitive decline and dementia due to Alzheimer's disease (AD). The data set includes longitudinal clinical evaluation, cognitive testing, and neuroimaging assessments from a non-demented study population aged 65 and up who complain of memory problems and show some indication of memory and/or executive functioning below age/gender/education adjusted norm.</description>
+<description descriptionType="Methods">Data Acquisition Location: San Francisco VA Medical Center; Scanner Type: Siemens Vision 1.5T; Coronal T1 MPRAGE: TR=9ms, TE=4ms, TI=300ms, 1x1mm2, 3mm slice thickness; Axial double spin echo PD &amp; T2: TR=5000ms, TE=20/85ms, 1x1.25mm2, 3mm slice thickness</description>
+</descriptions>
 </resource>

data/spec/data/dash1/ucsf-ark+=b7272=q6ms3qnx-mrt-datacite.xml

@@ -1,4 +1,5 @@
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@@ -39,4 +40,4 @@
     <description descriptionType="Methods">Data captured included participant vital sign values at the measurement interval with the highest shock index (pulse/SBP) within the first hour after study entry: pulse, systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP= (2 x DBP + SBP)/3), SI (pulse/SBP), and pulse pressure (SBP-DBP). Severe shock at study entry was defined as MAP less than 60 mmHg, below which perfusion of vital organs has been proposed to be inadequate. BP was measured via an automated blood pressure device or auscultatory technique with mercury sphygmomanometer. Outcomes comprised any severe adverse maternal event related to obstetric hemorrhage, and included organ system dysfunction-based criteria and intervention-based criteria. Although the outcomes for the original trials were determined prior to the development of the WHO “Near-Miss” criteria, they are very similar. The original outcomes for the studies were maternal mortality; end-organ system failure morbidity defined as clinically-diagnosed major organ failure (respiratory, renal, neurological, cardiac) lasting for 24 hours post-resuscitation; and the intervention variables ICU admission, blood transfusion, and emergency hysterectomy for intractable uterine atony. These outcomes were selected because in the majority of our study sites, laboratory-based criteria (e.g., determining DIC by platelets), were not consistently available. For the purposes of the present analysis we used the WHO maternal near-miss indicators for our outcomes. We evaluated maternal status as 1) death or 2) severe maternal outcome (SMO), a composite indicator of death or severe end-organ failure maternal morbidity. Finally we combined SMO with the WHO intervention-based near-miss criteria ICU admission, blood transfusion ≥5 units and emergency hysterectomy (uterine atony diagnoses only). WHO labels these as “critical interventions”; therefore, to be consistent with WHO criteria, we called our composite indicator of SMO and the critical interventions SMO-CI.</description>
     <description descriptionType="Other">Current dataset preparation: Bill and Melinda Gates Foundation (OPP1086183). Original data collection: MacArthur Foundation (05-84956-000-GSS), National Institutes of Health (R01HD053129) and Bill and Melinda Gates Foundation (48541).</description>
   </descriptions>
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data/spec/data/dash1/ucsf-ark+=b7272=q6mw2f2n-mrt-datacite.xml

@@ -1,61 +1,62 @@
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-<identifier identifierType="DOI">10.7272/Q6MW2F2N</identifier>
-<creators>
-<creator>
-<creatorName>Cardenas, Valerie</creatorName>
-</creator>
-<creator>
-<creatorName>Tosun, Duygu</creatorName>
-</creator>
-<creator>
-<creatorName>Chao, Linda</creatorName>
-</creator>
-<creator>
-<creatorName>Fletcher, P. Thomas</creatorName>
-</creator>
-<creator>
-<creatorName>Joshi, Sarang</creatorName>
-</creator>
-<creator>
-<creatorName>Joshi, Sarang</creatorName>
-</creator>
-<creator>
-<creatorName>Weiner, Michael W.</creatorName>
-</creator>
-<creator>
-<creatorName>Schuff, Norbert</creatorName>
-</creator>
-</creators>
-<titles>
-<title>Voxel-wise co-analysis of macro- and microstructural brain alteration in Mild Cognitive Impairment and Alzheimer's disease using anatomical and diffusion MRI</title>
-</titles>
-<publisher>University of California, San Francisco</publisher>
-<publicationYear>2012</publicationYear>
-<subjects>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Adult</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Male</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Female</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Magnetic Resonance Imaging</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Brain</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Human</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Multivariate Analysis</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Deformation Morphometry</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Anisotropy</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH"/>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH"/>
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-<contributor contributorType="ResearchGroup">
-<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
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-<dates>
-<date dateType="Collected">2005-2009</date>
-</dates>
-<resourceType resourceTypeGeneral="Dataset">application/octet-stream</resourceType>
-<descriptions>
-<description descriptionType="Abstract">Structural and diffusion data from cognitively normal elderly and those with mild cognitive impairment.  Background and Purpose: To determine if a voxel-wise &quot;co-analysis&quot; of structural and diffusion tensor magnetic resonance imaging (MRI) together reveals additional brain regions affected in mild cognitive impairment (MCI) and Alzheimer's Disease (AD) than voxel-wise analysis of the individual MRI modalities alone.  Conclusion: These results suggest that in corpus callosum and temporal regions macro- and microstructural variations in MCI can be congruent, providing potentially new insight into the mechanisms of brain tissue degeneration. </description>
-<description descriptionType="Methods">Methods: Twenty-one patients with MCI, 21 patients with AD, and 21 cognitively normal healthy elderly were studied with MRI. Maps of deformation and fractional anisotropy (FA) were computed and used as dependent variables in univariate and multivariate statistical models. Results: Univariate voxel-wise analysis of macrostructural changes in MCI showed atrophy in the right anterior temporal lobe, left posterior parietal/precuneus region, WM adjacent to the cingulate gyrus, and dorsolateral prefrontal regions, consistent with prior research. Univariate voxel-wise analysis of microstructural changes in MCI showed reduced FA in the left posterior parietal region extending into the corpus callosum, consistent with previous work. The multivariate analysis, which provides more information than univariate tests when structural and FA measures are correlated, revealed additional MCI-related changes in corpus callosum and temporal lobe.  Participants: Participants were recruited by advertisements in the community or referred by one of several memory clinics in the San Francisco Bay Area, including the Memory Disorders Clinic at the San Francisco Veterans Affairs Medical Center, the Memory and Aging Center at the University of California, San Francisco, and the Memory Disorders Clinic at the California Pacific Medical Center, for inclusion in one of several studies. Study procedures include a neurological exam, structural MRI, diffusion MRI, and comprehensive neuropsychological testing. In compliance with the Code of Ethics of the World Medical Association and the Declaration of Helsinki, study procedures were approved by review boards of the University of California San Francisco and the San Francisco VA Medical Center, explained to all participants, written informed consent was obtained. From the larger population studied, only participants with artifact-free structural and diffusion MRI were included. Twenty-one patients met Petersen's criteria for MCI, age: 71 ± 8 yrs, 11 women, MMSE (Mini-Mental State Examination): 29 ± 2. These patients were gender matched with 21 cognitively normal healthy elderly controls (CN), age: 70 ± 7 yrs, 11 women, MMSE 29 ± 1. The MCI patients were also gender matched with 21 patients who met AD criteria of the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS/ADRDA), age: 69 ± 9, 11 women, MMSE 21 ± 7. As evidenced by the high MMSE scores, the MCI patients were in an early stage of cognitive deficits and far less impaired than the AD patients.  Magnetic resonance imaging (MRI) acquisition: All scans were performed on a 4 Tesla (Bruker/Siemens) MRI system with a birdcage transmit and 8 channel receive coil arranged in the same housing. The scans included T1-weighted and T2-weighted structural MRI data for measurements of brain macro-structure and diffusion tensor MRI for measurement of micro-structure. T1-weighted images were obtained with a 3D volumetric magnetization prepared rapid gradient echo (MPRAGE) sequence, TR/TE/TI=2300/3/950 ms, timing; 7º flip angle; 1.0 x 1.0 x 1.0 mm3 resolution; 157 continuous sagittal slices; acquisition time of 5 min. T2-weighted images were acquired with a variable flip (VFL) angle turbo spin-echo sequence with TR/TE = 4000/30 ms and with the same resolution matrix and field of view of MPRAGE. DTI was based on a dual spin-echo refocused echo-planar imaging (EPI) sequence supplemented with parallel imaging acceleration (GRAPPA) (Griswold et al., 2002) with a factor 2 to reduce susceptibility distortions. Other imaging parameters were: TR/TE=6000/77 ms; 2 x 2 mm2 in-plane resolution; 40 continuous 3 mm slices. A reference image (no diffusion gradient b=0) and six diffusion-weighted images (b=800s/mm2 along six non-collinear direction) were acquired. Four DTI scans were acquired and averaged after motion correction to boost signal-to-noise. The total acquisition time of DTI was 4 min.  MRI pre-processing: An expectation maximization segmentation (EMS) algorithm including correction for intensity inhomogeneity 30,31 was applied to T1 weighted MRI, separating skull, scalp, extra-cranial tissue from the rest of brain image volume. Each individual skull-stripped and bias field corrected brain image volume was affine registered to a reference brain image to adjust for global differences in brain positioning and scale across individuals. For this study, an unbiased average brain image was used as the reference. The unbiased average brain was generated from 10 healthy elderly individual brains (i.e., age of 50 to 70) that were not part of the CN group using an unbiased atlas formation technique based on large deformations mapping 32. A large deformation diffeomorphic mapping algorithm using fluid-flow registration 33 was used to register individual scans to standard image space of the unbiased atlas brain. The Jacobian determinant of this transformation was computed at each voxel (resolution 1x1x1 mm3), giving the pattern of volume change required to force the individual anatomy to conform to the reference. The Jacobian images were log transformed to achieve a more normal distribution and then smoothed using a Gaussian filter (FWHM=10 mm) to create tissue volume maps (JAC), where the value at each voxel represents the tissue volume relative to the reference (e.g., a voxel value of 0.06 denotes a volume volrefx100.06, or about 15 percent greater than the reference voxel)  DTI pre-processing: The pre-processing pipeline aims to align a set of DTI images with the corresponding structural data through the following steps. Diffusion tensor images were corrected for eddy currents and head motion 34. Based on a mutual information metric, the T2-weighted image was rigidly aligned to the B0 image, which is a DTI maps without diffusion sensing gradients (b=0 s/mm2). A variational image-based approach was used to calculate a deformation field from the B0 image to the rigidly aligned T2-weighted image to correct for susceptibility artifacts (i.e., nonlinear geometric distortion in DTI) 35. We selected a variational approach for EPI distortion correction over the conventional field map approach, because studies have shown that the local deformations in EPI are best handled with a dense displacement field (i.e. high order deformations) 35. In contrast, field maps can fail to completely correct geometric distortions, presumably due to limits in the physical model 36. Concatenated eddy current transformation and the deformation field for nonlinear distortion correction were applied to all DTIs. Diffusion tensors were estimated for each subject from the diffusion tensor images using weighted least squares tensor estimation 37. The T2-weighted image was rigidly aligned to the T1-weighted image and the transformation was concatenated with the inverse rigid transformation from B0 image to T2-weighted image. The resulting rigid transformation was applied to the FA image to map onto the T1-weighted structural image space of the subject. The FA image was then mapped onto the standard image space by applying the diffeomorphic mapping estimated in MRI pre-processing. FA images were then smoothed using a Gaussian filter (FWHM=10 mm) in the standard image space. </description>
-</descriptions>
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+<identifier identifierType="DOI">10.7272/Q6MW2F2N</identifier>
+<creators>
+<creator>
+<creatorName>Cardenas, Valerie</creatorName>
+</creator>
+<creator>
+<creatorName>Tosun, Duygu</creatorName>
+</creator>
+<creator>
+<creatorName>Chao, Linda</creatorName>
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+<creatorName>Fletcher, P. Thomas</creatorName>
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+<creatorName>Joshi, Sarang</creatorName>
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+<creatorName>Joshi, Sarang</creatorName>
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+<creatorName>Weiner, Michael W.</creatorName>
+</creator>
+<creator>
+<creatorName>Schuff, Norbert</creatorName>
+</creator>
+</creators>
+<titles>
+<title>Voxel-wise co-analysis of macro- and microstructural brain alteration in Mild Cognitive Impairment and Alzheimer's disease using anatomical and diffusion MRI</title>
+</titles>
+<publisher>University of California, San Francisco</publisher>
+<publicationYear>2012</publicationYear>
+<subjects>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Adult</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Male</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Female</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Magnetic Resonance Imaging</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Brain</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Human</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Multivariate Analysis</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Deformation Morphometry</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Anisotropy</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/"/>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/"/>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/"/>
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+<contributor contributorType="ResearchGroup">
+<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
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+<dates>
+<date dateType="Collected">2005-2009</date>
+</dates>
+<resourceType resourceTypeGeneral="Dataset">application/octet-stream</resourceType>
+<descriptions>
+<description descriptionType="Abstract">Structural and diffusion data from cognitively normal elderly and those with mild cognitive impairment.  Background and Purpose: To determine if a voxel-wise "co-analysis" of structural and diffusion tensor magnetic resonance imaging (MRI) together reveals additional brain regions affected in mild cognitive impairment (MCI) and Alzheimer's Disease (AD) than voxel-wise analysis of the individual MRI modalities alone.  Conclusion: These results suggest that in corpus callosum and temporal regions macro- and microstructural variations in MCI can be congruent, providing potentially new insight into the mechanisms of brain tissue degeneration. </description>
+<description descriptionType="Methods">Methods: Twenty-one patients with MCI, 21 patients with AD, and 21 cognitively normal healthy elderly were studied with MRI. Maps of deformation and fractional anisotropy (FA) were computed and used as dependent variables in univariate and multivariate statistical models. Results: Univariate voxel-wise analysis of macrostructural changes in MCI showed atrophy in the right anterior temporal lobe, left posterior parietal/precuneus region, WM adjacent to the cingulate gyrus, and dorsolateral prefrontal regions, consistent with prior research. Univariate voxel-wise analysis of microstructural changes in MCI showed reduced FA in the left posterior parietal region extending into the corpus callosum, consistent with previous work. The multivariate analysis, which provides more information than univariate tests when structural and FA measures are correlated, revealed additional MCI-related changes in corpus callosum and temporal lobe.  Participants: Participants were recruited by advertisements in the community or referred by one of several memory clinics in the San Francisco Bay Area, including the Memory Disorders Clinic at the San Francisco Veterans Affairs Medical Center, the Memory and Aging Center at the University of California, San Francisco, and the Memory Disorders Clinic at the California Pacific Medical Center, for inclusion in one of several studies. Study procedures include a neurological exam, structural MRI, diffusion MRI, and comprehensive neuropsychological testing. In compliance with the Code of Ethics of the World Medical Association and the Declaration of Helsinki, study procedures were approved by review boards of the University of California San Francisco and the San Francisco VA Medical Center, explained to all participants, written informed consent was obtained. From the larger population studied, only participants with artifact-free structural and diffusion MRI were included. Twenty-one patients met Petersen's criteria for MCI, age: 71 ± 8 yrs, 11 women, MMSE (Mini-Mental State Examination): 29 ± 2. These patients were gender matched with 21 cognitively normal healthy elderly controls (CN), age: 70 ± 7 yrs, 11 women, MMSE 29 ± 1. The MCI patients were also gender matched with 21 patients who met AD criteria of the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS/ADRDA), age: 69 ± 9, 11 women, MMSE 21 ± 7. As evidenced by the high MMSE scores, the MCI patients were in an early stage of cognitive deficits and far less impaired than the AD patients.  Magnetic resonance imaging (MRI) acquisition: All scans were performed on a 4 Tesla (Bruker/Siemens) MRI system with a birdcage transmit and 8 channel receive coil arranged in the same housing. The scans included T1-weighted and T2-weighted structural MRI data for measurements of brain macro-structure and diffusion tensor MRI for measurement of micro-structure. T1-weighted images were obtained with a 3D volumetric magnetization prepared rapid gradient echo (MPRAGE) sequence, TR/TE/TI=2300/3/950 ms, timing; 7º flip angle; 1.0 x 1.0 x 1.0 mm3 resolution; 157 continuous sagittal slices; acquisition time of 5 min. T2-weighted images were acquired with a variable flip (VFL) angle turbo spin-echo sequence with TR/TE = 4000/30 ms and with the same resolution matrix and field of view of MPRAGE. DTI was based on a dual spin-echo refocused echo-planar imaging (EPI) sequence supplemented with parallel imaging acceleration (GRAPPA) (Griswold et al., 2002) with a factor 2 to reduce susceptibility distortions. Other imaging parameters were: TR/TE=6000/77 ms; 2 x 2 mm2 in-plane resolution; 40 continuous 3 mm slices. A reference image (no diffusion gradient b=0) and six diffusion-weighted images (b=800s/mm2 along six non-collinear direction) were acquired. Four DTI scans were acquired and averaged after motion correction to boost signal-to-noise. The total acquisition time of DTI was 4 min.  MRI pre-processing: An expectation maximization segmentation (EMS) algorithm including correction for intensity inhomogeneity 30,31 was applied to T1 weighted MRI, separating skull, scalp, extra-cranial tissue from the rest of brain image volume. Each individual skull-stripped and bias field corrected brain image volume was affine registered to a reference brain image to adjust for global differences in brain positioning and scale across individuals. For this study, an unbiased average brain image was used as the reference. The unbiased average brain was generated from 10 healthy elderly individual brains (i.e., age of 50 to 70) that were not part of the CN group using an unbiased atlas formation technique based on large deformations mapping 32. A large deformation diffeomorphic mapping algorithm using fluid-flow registration 33 was used to register individual scans to standard image space of the unbiased atlas brain. The Jacobian determinant of this transformation was computed at each voxel (resolution 1x1x1 mm3), giving the pattern of volume change required to force the individual anatomy to conform to the reference. The Jacobian images were log transformed to achieve a more normal distribution and then smoothed using a Gaussian filter (FWHM=10 mm) to create tissue volume maps (JAC), where the value at each voxel represents the tissue volume relative to the reference (e.g., a voxel value of 0.06 denotes a volume volrefx100.06, or about 15 percent greater than the reference voxel)  DTI pre-processing: The pre-processing pipeline aims to align a set of DTI images with the corresponding structural data through the following steps. Diffusion tensor images were corrected for eddy currents and head motion 34. Based on a mutual information metric, the T2-weighted image was rigidly aligned to the B0 image, which is a DTI maps without diffusion sensing gradients (b=0 s/mm2). A variational image-based approach was used to calculate a deformation field from the B0 image to the rigidly aligned T2-weighted image to correct for susceptibility artifacts (i.e., nonlinear geometric distortion in DTI) 35. We selected a variational approach for EPI distortion correction over the conventional field map approach, because studies have shown that the local deformations in EPI are best handled with a dense displacement field (i.e. high order deformations) 35. In contrast, field maps can fail to completely correct geometric distortions, presumably due to limits in the physical model 36. Concatenated eddy current transformation and the deformation field for nonlinear distortion correction were applied to all DTIs. Diffusion tensors were estimated for each subject from the diffusion tensor images using weighted least squares tensor estimation 37. The T2-weighted image was rigidly aligned to the T1-weighted image and the transformation was concatenated with the inverse rigid transformation from B0 image to T2-weighted image. The resulting rigid transformation was applied to the FA image to map onto the T1-weighted structural image space of the subject. The FA image was then mapped onto the standard image space by applying the diffeomorphic mapping estimated in MRI pre-processing. FA images were then smoothed using a Gaussian filter (FWHM=10 mm) in the standard image space. </description>
+</descriptions>
 </resource>

data/spec/data/dash1/ucsf-ark+=b7272=q6pn93h6-mrt-datacite.xml

@@ -1,4 +1,4 @@
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+<resource xmlns="http://datacite.org/schema/kernel-3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd">
 <identifier identifierType="DOI">10.7272/q6pn93h6</identifier>
 <creators>
 <creator><creatorName>Creasman, Jennifer</creatorName></creator>
@@ -33,20 +33,20 @@
 </relatedIdentifiers>
 <descriptions>
 <description descriptionType="Abstract">Background
-Obesity is an established and modifiable risk factor for urinary incontinence, but conclusive evidence for a beneficial effect of weight loss on urinary incontinence is lacking.<br/>
-Methods<br/>
-We randomly assigned 338 overweight and obese women with at least 10 urinary incontinence episodes per week to an intensive 6-month weight-loss program that included diet, exercise, and behavior modification (226 patients) or to a structured education program (112 patients).<br/>
-Results<br/>
-The mean (±SD) age of the participants was 53±11 years. The body-mass index (the weight in kilograms divided by the square of the height in meters) (36±6) and the weekly number of incontinence episodes as recorded in a 7-day diary of voiding (24±18) were similar for both groups at baseline. The women in the intervention group had a mean weight loss of 8.0% (7.8 kg), as compared with 1.6% (1.5 kg) in the control group (P&lt;0.001). After 6 months, the mean weekly number of incontinence episodes decreased by 47% in the intervention group, as compared with 28% in the control group (P = 0.01). As compared with the control group, the intervention group had a greater decrease in the frequency of stress-incontinence episodes (P = 0.02), but not of urge-incontinence episodes (P = 0.14). A higher proportion of the intervention group than of the control group had a clinically relevant reduction of 70% or more in the frequency of all incontinence episodes (P&lt;0.001), stress-incontinence episodes (P = 0.009), and urge-incontinence episodes (P = 0.04).<br/>
-Conclusions<br/>
+Obesity is an established and modifiable risk factor for urinary incontinence, but conclusive evidence for a beneficial effect of weight loss on urinary incontinence is lacking.<br />
+Methods<br />
+We randomly assigned 338 overweight and obese women with at least 10 urinary incontinence episodes per week to an intensive 6-month weight-loss program that included diet, exercise, and behavior modification (226 patients) or to a structured education program (112 patients).<br />
+Results<br />
+The mean (±SD) age of the participants was 53±11 years. The body-mass index (the weight in kilograms divided by the square of the height in meters) (36±6) and the weekly number of incontinence episodes as recorded in a 7-day diary of voiding (24±18) were similar for both groups at baseline. The women in the intervention group had a mean weight loss of 8.0% (7.8 kg), as compared with 1.6% (1.5 kg) in the control group (P&lt;0.001). After 6 months, the mean weekly number of incontinence episodes decreased by 47% in the intervention group, as compared with 28% in the control group (P = 0.01). As compared with the control group, the intervention group had a greater decrease in the frequency of stress-incontinence episodes (P = 0.02), but not of urge-incontinence episodes (P = 0.14). A higher proportion of the intervention group than of the control group had a clinically relevant reduction of 70% or more in the frequency of all incontinence episodes (P&lt;0.001), stress-incontinence episodes (P = 0.009), and urge-incontinence episodes (P = 0.04).<br />
+Conclusions<br />
 A 6-month behavioral intervention targeting weight loss reduced the frequency of self-reported urinary-incontinence episodes among overweight and obese women as compared with a control group. A decrease in urinary incontinence may be another benefit among the extensive health improvements associated with moderate weight reduction. (ClinicalTrials.gov number, NCT00091988.)</description>
 <description descriptionType="Methods">Eligible participants were randomly assigned at a 2:1 ratio to an intensive 6-month behavioral weight-loss program or to a structured four-session education program (the control group). Randomization
-was performed with the use of randomly permuted blocks of three or six, stratified according to clinical center, with random assignment concealed in tamper-proof envelopes. The participants were aware of their treatment assignment, but the staff members who collected the outcome data were not.<br/>
-The participants completed questionnaires concerning their demographic characteristics, medical and behavioral history, and history of incontinence that were routinely used by the investigators.<br/>
-The participants were weighed to the nearest 0.5 kg on a calibrated digital scale (Tanita BWB 800) while wearing street clothes and without shoes. Height was measured at baseline to the nearest centimeter with the use of a calibrated, wall-mounted stadiometer and a horizontal measuring block.<br/>
+was performed with the use of randomly permuted blocks of three or six, stratified according to clinical center, with random assignment concealed in tamper-proof envelopes. The participants were aware of their treatment assignment, but the staff members who collected the outcome data were not.<br />
+The participants completed questionnaires concerning their demographic characteristics, medical and behavioral history, and history of incontinence that were routinely used by the investigators.<br />
+The participants were weighed to the nearest 0.5 kg on a calibrated digital scale (Tanita BWB 800) while wearing street clothes and without shoes. Height was measured at baseline to the nearest centimeter with the use of a calibrated, wall-mounted stadiometer and a horizontal measuring block.<br />
 The participants were trained to complete a 7-day diary of voiding (see the Supplementary Appendix, available with the full text of this article at NEJM.org), and interviewers reviewed the diaries with the participants to answer questions and reconcile inconsistencies.15,16 The participants recorded the time of each void and each incontinence episode. According to the instructions provided, the participants identified each episode as stress incontinence (involuntary loss of urine with coughing, sneezing, straining, or Weight Loss to Treat Urinary Incontinence n engl j med 360;5 nejm.org january 29, 2009 37 exercise), urge incontinence (loss of urine associated with a strong need or urge to void), or other. For the purposes of analysis, each woman was then classified as having stress-only incontinence, stress-predominant incontinence (i.e., at least two thirds of the total number of episodes were stress episodes), urge-only incontinence, urge-predominant continence (i.e., at least two thirds of the total number of episodes were urge episodes), or mixed incontinence (i.e., at least two types were reported, but no type constituted two
 thirds of the total number of episodes).</description>
 <description descriptionType="SeriesInformation">Weight loss to treat urinary incontinence in overweight and obese women.
 Subak LL, Wing R, West DS, Franklin F, Vittinghoff E, Creasman JM, Richter HE, Myers D, Burgio KL, Gorin AA, Macer J, Kusek JW, Grady D; PRIDE Investigators. N Engl J Med. 2009 Jan 29;360(5):481-90. doi: 10.1056/NEJMoa0806375. PMID: 19179316 [PubMed - indexed for MEDLINE] Free PMC Article</description>
 </descriptions>
-</resource>
+</resource>

data/spec/data/dash1/ucsf-ark+=b7272=q6qj7f78-mrt-datacite.xml

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+  <identifier identifierType="DOI"/>
+  <creators>
+    <creator>
+      <creatorName>Haack, Lauren</creatorName>
+    </creator>
+  </creators>
+  <titles>
+    <title>Monroe Monroe Group Videos</title>
+  </titles>
+  <publisher>UC San Francisco</publisher>
+  <publicationYear>2016</publicationYear>
+  <subjects>
+    <subject>Monroe</subject>
+    <subject>Monroe</subject>
+    <subject>Video</subject>
+  </subjects>
+  <contributors>
+    <contributor contributorType="DataManager">
+      <contributorName>Plageman, Melissa</contributorName>
+    </contributor>
+  </contributors>
+  <relatedIdentifiers/>
+  <resourceType resourceTypeGeneral="Audiovisual">Audiovisual</resourceType>
+  <sizes>
+    <size>6707770982</size>
+  </sizes>
+  <rightsList>
+    <rights rightsURI="https://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution 4.0 International (CC-BY 4.0)</rights>
+  </rightsList>
+  <descriptions/>
+</resource>

data/spec/data/dash1/ucsf-ark+=b7272=q6qn64nk-mrt-datacite.xml

@@ -1,46 +1,47 @@
-<?xml version="1.0" encoding="utf-8"?><resource xmlns="http://datacite.org/schema/kernel-3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd">
-<identifier identifierType="DOI">10.7272/Q6QN64NK</identifier>
-<creators>
-<creator>
-<creatorName>Weiner, Michael W.</creatorName>
-</creator>
-<creator>
-<creatorName>Schuff, Norbert</creatorName>
-</creator>
-</creators>
-<titles>
-<title>Posttraumatic Stress Disorder (PTSD)</title>
-</titles>
-<publisher>University of California, San Francisco</publisher>
-<publicationYear>2012</publicationYear>
-<subjects>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Adult</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Human</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Magnetic Resonance Imaging</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Cognition</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Neuropsychological Test</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Brain</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Middle Aged</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Post-Traumatic</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Stress Disorders</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Veterans</subject>
-</subjects>
-<contributors>
-<contributor contributorType="ResearchGroup">
-<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
-</contributor>
-</contributors>
-<resourceType resourceTypeGeneral="Dataset">application/octet-stream</resourceType>
-<relatedIdentifiers>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">11750891</relatedIdentifier>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">18201876</relatedIdentifier>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">19703319</relatedIdentifier>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">20104401</relatedIdentifier>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">20194830</relatedIdentifier>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">20483375</relatedIdentifier>
-</relatedIdentifiers>
-<descriptions>
-<description descriptionType="Abstract">This data set was acquired to study various aspects associated with PTSD and includes structural neuroimaging data as well as clinical assessments including history of physical and sexual abuse or neglect, family history of violence, veteran status, presence of alcoholism, and scores on the clinician-administered PTSD scale (CAPS).</description>
-<description descriptionType="Methods">Data Acquisition Location: San Francisco VA Medical Center; Scanner Type: Siemens Vision 1.5T; Coronal T1 MPRAGE: TR=10ms, TE=4ms, TI=300ms, 1x1mm2, 1.4mm slice thickness; Axial double spin echo PD &amp; T2: TR=2500ms, TE=20/80ms, 1x1.4mm2, 3mm slice thickness</description>
-</descriptions>
+<?xml version="1.0" encoding="UTF-8"?>
+<resource xmlns="http://datacite.org/schema/kernel-3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd">
+<identifier identifierType="DOI">10.7272/Q6QN64NK</identifier>
+<creators>
+<creator>
+<creatorName>Weiner, Michael W.</creatorName>
+</creator>
+<creator>
+<creatorName>Schuff, Norbert</creatorName>
+</creator>
+</creators>
+<titles>
+<title>Posttraumatic Stress Disorder (PTSD)</title>
+</titles>
+<publisher>University of California, San Francisco</publisher>
+<publicationYear>2012</publicationYear>
+<subjects>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Adult</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Human</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Magnetic Resonance Imaging</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Cognition</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Neuropsychological Test</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Brain</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Middle Aged</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Post-Traumatic</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Stress Disorders</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Veterans</subject>
+</subjects>
+<contributors>
+<contributor contributorType="ResearchGroup">
+<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
+</contributor>
+</contributors>
+<resourceType resourceTypeGeneral="Dataset">application/octet-stream</resourceType>
+<relatedIdentifiers>
+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">11750891</relatedIdentifier>
+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">18201876</relatedIdentifier>
+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">19703319</relatedIdentifier>
+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">20104401</relatedIdentifier>
+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">20194830</relatedIdentifier>
+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">20483375</relatedIdentifier>
+</relatedIdentifiers>
+<descriptions>
+<description descriptionType="Abstract">This data set was acquired to study various aspects associated with PTSD and includes structural neuroimaging data as well as clinical assessments including history of physical and sexual abuse or neglect, family history of violence, veteran status, presence of alcoholism, and scores on the clinician-administered PTSD scale (CAPS).</description>
+<description descriptionType="Methods">Data Acquisition Location: San Francisco VA Medical Center; Scanner Type: Siemens Vision 1.5T; Coronal T1 MPRAGE: TR=10ms, TE=4ms, TI=300ms, 1x1mm2, 1.4mm slice thickness; Axial double spin echo PD &amp; T2: TR=2500ms, TE=20/80ms, 1x1.4mm2, 3mm slice thickness</description>
+</descriptions>
 </resource>

data/spec/data/dash1/ucsf-ark+=b7272=q6rf5rzx-mrt-datacite.xml

@@ -1,4 +1,5 @@
-<?xml version="1.0" encoding="utf-8"?><resource xmlns="http://datacite.org/schema/kernel-3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd">
+<?xml version="1.0" encoding="UTF-8"?>
+<resource xmlns="http://datacite.org/schema/kernel-3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd">
   <identifier identifierType="DOI"/>
   <creators>
     <creator>
@@ -34,7 +35,7 @@
     <rights rightsURI="https://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution 4.0 International (CC-BY 4.0)</rights>
   </rightsList>
   <descriptions>
-    <description descriptionType="Abstract">To understand visual functions mediated by intrinsically photosensitive melanopsin-expressing retinal ganglion cells (mRGCs), it is important to elucidate axonal projections from these cells into the brain.  Initial studies reported that melanopsin is expressed only in retinal ganglion cells within the eye. However, recent studies in Opn4-Cre mice revealed Cre-mediated marker expression in multiple brain areas. These discoveries complicate the use of melanopsin-driven genetic labeling techniques to identify retinofugal projections specifically from mRGCs. To restrict labeling to mRGCs, we developed a recombinant adeno-associated virus (AAV) carrying a Cre-dependent reporter (human placental alkaline phosphatase) that was injected into the vitreous of Opn4-Cre mouse eyes. The labeling observed in the brain of these mice was necessarily restricted specifically to retinofugal projections from mRGCs in the injected eye. We found that mRGCs innervate multiple nuclei in the basal forebrain, hypothalamus, amygdala, thalamus and midbrain. Midline structures tended to be bilaterally innervated whereas the lateral structures received mostly contralateral innervation. As validation of our approach, we found projection patterns largely corresponded with previously published results; however, we have also identified a few novel targets. Our discovery of projections to the central amygdala suggests a possible direct neural pathway for aversive responses to light in neonates. In addition, projections to the accessory optic system suggest that mRGCs play a direct role in visual tracking, responses that were previously attributed to other classes of retinal ganglion cells. Moreover, projections to the zona incerta raise the possibility that mRGCs could regulate visceral and sensory functions.  However, additional studies are needed to investigate the actual photosensitivity of mRGCs that project to the different brain areas. Also, there is a concern of &quot;overlabeling&quot; with very sensitive reporters that uncover low levels of expression.  Light evoked signaling from these cells must be shown to be of sufficient sensitivity to elicit physiologically relevant responses.</description>
+    <description descriptionType="Abstract">To understand visual functions mediated by intrinsically photosensitive melanopsin-expressing retinal ganglion cells (mRGCs), it is important to elucidate axonal projections from these cells into the brain.  Initial studies reported that melanopsin is expressed only in retinal ganglion cells within the eye. However, recent studies in Opn4-Cre mice revealed Cre-mediated marker expression in multiple brain areas. These discoveries complicate the use of melanopsin-driven genetic labeling techniques to identify retinofugal projections specifically from mRGCs. To restrict labeling to mRGCs, we developed a recombinant adeno-associated virus (AAV) carrying a Cre-dependent reporter (human placental alkaline phosphatase) that was injected into the vitreous of Opn4-Cre mouse eyes. The labeling observed in the brain of these mice was necessarily restricted specifically to retinofugal projections from mRGCs in the injected eye. We found that mRGCs innervate multiple nuclei in the basal forebrain, hypothalamus, amygdala, thalamus and midbrain. Midline structures tended to be bilaterally innervated whereas the lateral structures received mostly contralateral innervation. As validation of our approach, we found projection patterns largely corresponded with previously published results; however, we have also identified a few novel targets. Our discovery of projections to the central amygdala suggests a possible direct neural pathway for aversive responses to light in neonates. In addition, projections to the accessory optic system suggest that mRGCs play a direct role in visual tracking, responses that were previously attributed to other classes of retinal ganglion cells. Moreover, projections to the zona incerta raise the possibility that mRGCs could regulate visceral and sensory functions.  However, additional studies are needed to investigate the actual photosensitivity of mRGCs that project to the different brain areas. Also, there is a concern of "overlabeling" with very sensitive reporters that uncover low levels of expression.  Light evoked signaling from these cells must be shown to be of sufficient sensitivity to elicit physiologically relevant responses.</description>
     <description descriptionType="Methods">Methods
 
 Generating AAV-flex-plap
@@ -57,4 +58,4 @@ To visualize brain nuclei, all brain sections were counterstained with ToPro3 (L
 </description>
     <description descriptionType="Other">EY 01869</description>
   </descriptions>
-</resource>
+</resource>

data/spec/data/dash1/ucsf-ark+=b7272=q6rn35sz-mrt-datacite.xml

@@ -1,63 +1,65 @@
-<?xml version="1.0" encoding="utf-8"?><resource xmlns="http://datacite.org/schema/kernel-3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd">
-<identifier identifierType="DOI">10.7272/Q6RN35SZ</identifier>
-<creators>
-<creator>
-<creatorName>Cardenas, Valerie</creatorName>
-</creator>
-<creator>
-<creatorName>Samuelson, Kristin</creatorName>
-</creator>
-<creator>
-<creatorName>Lenoci, Maryanne A.</creatorName>
-</creator>
-<creator>
-<creatorName>Studholme, Colin</creatorName>
-</creator>
-<creator>
-<creatorName>Neylan, Thomas C.</creatorName>
-</creator>
-<creator>
-<creatorName>Marmar, Charles R.</creatorName>
-</creator>
-<creator>
-<creatorName>Schuff, Norbert</creatorName>
-</creator>
-<creator>
-<creatorName>Weiner, Michael W.</creatorName>
-</creator>
-</creators>
-<titles>
-<title>Changes in brain anatomy during the course of PTSD</title>
-</titles>
-<publisher>University of California, San Francisco</publisher>
-<publicationYear>2012</publicationYear>
-<subjects>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Adult</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Male</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Human</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Magnetic Resonance Imaging</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Brain</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Deformation Morphometry</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Longitudinal</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Neuropsychological Testing</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Stress Disorders, Post-Traumatic</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Veterans</subject>
-<subject schemeURI="http://www.nlm.nih.gov/mesh/" subjectScheme="MeSH">Vietnamese Conflict, 1961-1975</subject>
-</subjects>
-<contributors>
-<contributor contributorType="ResearchGroup">
-<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
-</contributor>
-</contributors>
-<dates>
-<date dateType="Collected">1998-2005</date>
-</dates>
-<resourceType resourceTypeGeneral="Dataset">application/octet-stream</resourceType>
-<relatedIdentifiers>
-<relatedIdentifier relatedIdentifierType="PMID" relationType="References">21683556</relatedIdentifier>
-</relatedIdentifiers>
-<descriptions>
-<description descriptionType="Abstract">Longitudinal structural T1-weighted images from middle-aged controls and veterans with PTSD (post-traumatic stress disorder). Most patients were Vietnam veterans.  The goal of this study was to determine whether PTSD was associated with an increase in time-related decline in macrostructural brain volume and whether these changes were associated with accelerated cognitive decline. To quantify brain structure, 3 dimensional T1-weighted MRI scans were performed at baseline and again after a minimum of 24 months in 25 patients with PTSD and 22 controls. Longitudinal changes in brain volume were measured using deformation morphometry. For the group as a whole PTSD+ patients did not show significant ongoing brain atrophy compared to PTSD-. PTSD+ patients were then subgrouped into those with decreasing or increasing symptoms. We found little evidence for brain markers of accelerated atrophy in PTSD+ veterans whose symptoms improved over time, with only a small left parietal region showing greater ongoing tissue loss than PTSD-. PTSD patients whose symptoms increased over time showed accelerated atrophy throughout the brain, particularly brainstem and frontal and temporal lobes. Lastly, for the sample as a whole greater rates of brain atrophy were associated with greater rates of decline in verbal memory and delayed facial recognition.</description>
-<description descriptionType="Methods">Participants: After complete description of the study to the subjects, written informed consent was obtained to a protocol approved by the review boards of both the University of California, San Francisco (UCSF) and the San Francisco Veterans Affairs (SFVA) Medical Center. Participants had previously participated in one of two earlier studies examining neuroimaging and neuropsychological correlates of PTSD (Neylan et al., 2004; Samuelson et al., 2006; Schuff et al., 2008; Schuff et al., 2001). When initially studied, participants had given consent to be re-contacted about future studies. Veterans were contacted a minimum of two years after completion of the first assessment. Study procedures included completing a neuropsychological test battery and MRI scanning. Participants met the following basic inclusion criteria at baseline: veterans 25-65 years of age; PTSD+ participants had current PTSD attributable to a traumatic life event (e.g., Vietnam or Gulf War combat, experiencing or witnessing serious accidents, illnesses, sudden death, physical and sexual assault), PTSD- participants had no current, subthreshold, or lifetime history of PTSD. Exclusion criteria at baseline were: diagnosis of drug dependence or abuse within the past 6 months, current or lifetime history of any psychiatric disorder with psychotic features, current or lifetime history of bipolar disorder, history of neurologic or systemic illness affecting CNS function, history of head injury with loss of consciousness exceeding 10 minutes, and history of head injury with any persistent post-injury symptoms. Alcohol abuse and dependence were allowable diagnoses for one of the original studies. Patients and controls were studied twice, once after enrollment (baseline) and again after a minimum of 24 months. Because we were interested in the natural course of PTSD, we did not apply exclusionary criteria at follow-up. At follow-up, three PTSD+ participants met one of the exclusionary baseline diagnoses—two exhibiting psychotic symptoms and one exhibiting symptoms of bipolar disorder not otherwise specified. These participants did not represent outliers in terms of neuropsychological functioning and were included in our previous study of longitudinal neuropsychological functioning (Samuelson et al., 2009), and were also included in this longitudinal imaging study. This analysis included 25 PTSD+ male veterans and 22 PTSD- male veterans that had complete longitudinal MRI and neuropsychological datasets.  Clinical and cognitive testing: Diagnoses of PTSD at baseline and follow-up were made by a clinical psychologist using the Clinician Administered PTSD Scale, which determines if DSM-IV diagnostic criteria were met (CAPS; (Blake et al., 1995)). Individuals with no trauma exposure received a CAPS score of 0. The Structured Clinical Interview for DSM-IV Diagnosis (SCID; (First et al., 1996)) was used to diagnose comorbid and exclusionary conditions. Lifetime alcohol use was obtained using the Lifetime Drinking History questionnaire (LDH; (Skinner and Sheu, 1982)).  All participants were administered a test battery of neuropsychological measures at both timepoints, including the California Verbal Learning Test (CVLT; (Delis et al., 1987)), Faces I, Faces II, Family Pictures I, Family Pictures II, Digit Span and Spatial Span subtests of the Wechsler Memory Scale-Third Edition (WMS-III; (Wechsler, 1987)). Samuelson and colleagues previously reported on the longitudinal neuropsychological changes observed in this dataset (Samuelson et al., 2009), and found a subtle decline in delayed facial recognition as indexed by performance on the Faces II subtest. In light of this finding and the previous reports of longitudinal changes on the CVLT due to PTSD (Yehuda et al., 2006), this study focused only on the relationships of longitudinal changes in Faces II, CVLT total (short term verbal memory) and CVLT long delay (long term verbal memory) with longitudinal measures of brain atrophy. Longitudinal change on these neuropsychological tests was defined as (scoretp1-scoretp2)/(test interval in yrs).  MRI acquisition and processing: T1-weighted images were acquired on a clinical 1.5 Tesla MR scanner (Vision, Siemens Medical Systems, Iselin NJ) using Magnetization Prepared Rapid Acquisition Gradient Echo (TR/TI/TE = 9/300/4 ms, 1x1 mm2 in-plane resolution, 1.5 mm slabs); images were acquired orthogonal to the long axis of the hippocampus.  Deformation based morphometry (DBM) analyses: Robust fluid registration was used to nonlinearly register baseline and follow-up scans of each participant to create maps of longitudinal atrophy. Each participant's baseline image was then registered to an atlas; transformations were combined to create maps of longitudinal atrophy in common space as described in (Cardenas et al., 2007). The longitudinal atrophy maps were normalized by interscan interval and these maps of annualized atrophy rate in common space were used in statistical analysis using linear models. ANCOVA at each voxel was used to test our first hypothesis that PTSD was associated with greater tissue atrophy rates; the maps of longitudinal change were the dependent variable, group status (i.e., PTSD+ or PTSD-) was the categorical predictor, and age was a covariate. Linear regressions with baseline clinical or imaging measures as the independent variable were fit at each voxel in order to identify baseline predictors of ongoing atrophy. Subsequent analyses compared PTSD+ participants with improving symptoms vs. PTSD-, and PTSD+ with worsening symptoms vs. PTSD-, in order to determine the relationship between improving mental health and ongoing brain atrophy. Using all participants, linear regression with change in neuropsychological test score as the independent variable was also fit at each voxel, covarying for age, in order to determine the relationship between rate of tissue atrophy and cognitive decline. Statistical maps were corrected for multiple comparisons by thresholding at uncorrected p=0.005, identifying suprathreshold clusters, and using nonstationary random field theory (Worsley et al., 2002) to identify clusters with corrected p&lt;0.05. Within each cluster with corrected p&lt;0.05, the estimated effects (i.e., the voxel-wise beta coefficients from the linear model) were averaged to determine the magnitude of the group effects (for ANCOVA models) or the slope (for regression models).</description>
-</descriptions>
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+<identifier identifierType="DOI">10.7272/Q6RN35SZ</identifier>
+<creators>
+<creator>
+<creatorName>Cardenas, Valerie</creatorName>
+</creator>
+<creator>
+<creatorName>Samuelson, Kristin</creatorName>
+</creator>
+<creator>
+<creatorName>Lenoci, Maryanne A.</creatorName>
+</creator>
+<creator>
+<creatorName>Studholme, Colin</creatorName>
+</creator>
+<creator>
+<creatorName>Neylan, Thomas C.</creatorName>
+</creator>
+<creator>
+<creatorName>Marmar, Charles R.</creatorName>
+</creator>
+<creator>
+<creatorName>Schuff, Norbert</creatorName>
+</creator>
+<creator>
+<creatorName>Weiner, Michael W.</creatorName>
+</creator>
+</creators>
+<titles>
+<title>Changes in brain anatomy during the course of PTSD</title>
+</titles>
+<publisher>University of California, San Francisco</publisher>
+<publicationYear>2012</publicationYear>
+<subjects>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Adult</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Male</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Human</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Magnetic Resonance Imaging</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Brain</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Deformation Morphometry</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Longitudinal</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Neuropsychological Testing</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Stress Disorders, Post-Traumatic</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Veterans</subject>
+<subject subjectScheme="MeSH" schemeURI="http://www.nlm.nih.gov/mesh/">Vietnamese Conflict, 1961-1975</subject>
+</subjects>
+<contributors>
+<contributor contributorType="ResearchGroup">
+<contributorName>UCSF Center for Imaging of Neurodegenerative Diseases</contributorName>
+</contributor>
+</contributors>
+<dates>
+<date dateType="Collected">1998-2005</date>
+</dates>
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+<relatedIdentifier relatedIdentifierType="PMID" relationType="References">21683556</relatedIdentifier>
+</relatedIdentifiers>
+<descriptions>
+<description descriptionType="Abstract">Longitudinal structural T1-weighted images from middle-aged controls and veterans with PTSD (post-traumatic stress disorder). Most patients were Vietnam veterans.  The goal of this study was to determine whether PTSD was associated with an increase in time-related decline in macrostructural brain volume and whether these changes were associated with accelerated cognitive decline. To quantify brain structure, 3 dimensional T1-weighted MRI scans were performed at baseline and again after a minimum of 24 months in 25 patients with PTSD and 22 controls. Longitudinal changes in brain volume were measured using deformation morphometry. For the group as a whole PTSD+ patients did not show significant ongoing brain atrophy compared to PTSD-. PTSD+ patients were then subgrouped into those with decreasing or increasing symptoms. We found little evidence for brain markers of accelerated atrophy in PTSD+ veterans whose symptoms improved over time, with only a small left parietal region showing greater ongoing tissue loss than PTSD-. PTSD patients whose symptoms increased over time showed accelerated atrophy throughout the brain, particularly brainstem and frontal and temporal lobes. Lastly, for the sample as a whole greater rates of brain atrophy were associated with greater rates of decline in verbal memory and delayed facial recognition.</description>
+<description descriptionType="Methods">Participants: After complete description of the study to the subjects, written informed consent was obtained to a protocol approved by the review boards of both the University of California, San Francisco (UCSF) and the San Francisco Veterans Affairs (SFVA) Medical Center. Participants had previously participated in one of two earlier studies examining neuroimaging and neuropsychological correlates of PTSD (Neylan et al., 2004; Samuelson et al., 2006; Schuff et al., 2008; Schuff et al., 2001). When initially studied, participants had given consent to be re-contacted about future studies. Veterans were contacted a minimum of two years after completion of the first assessment. Study procedures included completing a neuropsychological test battery and MRI scanning. Participants met the following basic inclusion criteria at baseline: veterans 25-65 years of age; PTSD+ participants had current PTSD attributable to a traumatic life event (e.g., Vietnam or Gulf War combat, experiencing or witnessing serious accidents, illnesses, sudden death, physical and sexual assault), PTSD- participants had no current, subthreshold, or lifetime history of PTSD. Exclusion criteria at baseline were: diagnosis of drug dependence or abuse within the past 6 months, current or lifetime history of any psychiatric disorder with psychotic features, current or lifetime history of bipolar disorder, history of neurologic or systemic illness affecting CNS function, history of head injury with loss of consciousness exceeding 10 minutes, and history of head injury with any persistent post-injury symptoms. Alcohol abuse and dependence were allowable diagnoses for one of the original studies. Patients and controls were studied twice, once after enrollment (baseline) and again after a minimum of 24 months. Because we were interested in the natural course of PTSD, we did not apply exclusionary criteria at follow-up. At follow-up, three PTSD+ participants met one of the exclusionary baseline diagnoses—two exhibiting psychotic symptoms and one exhibiting symptoms of bipolar disorder not otherwise specified. These participants did not represent outliers in terms of neuropsychological functioning and were included in our previous study of longitudinal neuropsychological functioning (Samuelson et al., 2009), and were also included in this longitudinal imaging study. This analysis included 25 PTSD+ male veterans and 22 PTSD- male veterans that had complete longitudinal MRI and neuropsychological datasets.  Clinical and cognitive testing: Diagnoses of PTSD at baseline and follow-up were made by a clinical psychologist using the Clinician Administered PTSD Scale, which determines if DSM-IV diagnostic criteria were met (CAPS; (Blake et al., 1995)). Individuals with no trauma exposure received a CAPS score of 0. The Structured Clinical Interview for DSM-IV Diagnosis (SCID; (First et al., 1996)) was used to diagnose comorbid and exclusionary conditions. Lifetime alcohol use was obtained using the Lifetime Drinking History questionnaire (LDH; (Skinner and Sheu, 1982)).  All participants were administered a test battery of neuropsychological measures at both timepoints, including the California Verbal Learning Test (CVLT; (Delis et al., 1987)), Faces I, Faces II, Family Pictures I, Family Pictures II, Digit Span and Spatial Span subtests of the Wechsler Memory Scale-Third Edition (WMS-III; (Wechsler, 1987)). Samuelson and colleagues previously reported on the longitudinal neuropsychological changes observed in this dataset (Samuelson et al., 2009), and found a subtle decline in delayed facial recognition as indexed by performance on the Faces II subtest. In light of this finding and the previous reports of longitudinal changes on the CVLT due to PTSD (Yehuda et al., 2006), this study focused only on the relationships of longitudinal changes in Faces II, CVLT total (short term verbal memory) and CVLT long delay (long term verbal memory) with longitudinal measures of brain atrophy. Longitudinal change on these neuropsychological tests was defined as (scoretp1-scoretp2)/(test interval in yrs).  MRI acquisition and processing: T1-weighted images were acquired on a clinical 1.5 Tesla MR scanner (Vision, Siemens Medical Systems, Iselin NJ) using Magnetization Prepared Rapid Acquisition Gradient Echo (TR/TI/TE = 9/300/4 ms, 1x1 mm2 in-plane resolution, 1.5 mm slabs); images were acquired orthogonal to the long axis of the hippocampus.  Deformation based morphometry (DBM) analyses: Robust fluid registration was used to nonlinearly register baseline and follow-up scans of each participant to create maps of longitudinal atrophy. Each participant's baseline image was then registered to an atlas; transformations were combined to create maps of longitudinal atrophy in common space as described in (Cardenas et al., 2007). The longitudinal atrophy maps were normalized by interscan interval and these maps of annualized atrophy rate in common space were used in statistical analysis using linear models. ANCOVA at each voxel was used to test our first hypothesis that PTSD was associated with greater tissue atrophy rates; the maps of longitudinal change were the dependent variable, group status (i.e., PTSD+ or PTSD-) was the categorical predictor, and age was a covariate. Linear regressions with baseline clinical or imaging measures as the independent variable were fit at each voxel in order to identify baseline predictors of ongoing atrophy. Subsequent analyses compared PTSD+ participants with improving symptoms vs. PTSD-, and PTSD+ with worsening symptoms vs. PTSD-, in order to determine the relationship between improving mental health and ongoing brain atrophy. Using all participants, linear regression with change in neuropsychological test score as the independent variable was also fit at each voxel, covarying for age, in order to determine the relationship between rate of tissue atrophy and cognitive decline. Statistical maps were corrected for multiple comparisons by thresholding at uncorrected p=0.005, identifying suprathreshold clusters, and using nonstationary random field theory (Worsley et al., 2002) to identify clusters with corrected p&lt;0.05. Within each cluster with corrected p&lt;0.05, the estimated effects (i.e., the voxel-wise beta coefficients from the linear model) were averaged to determine the magnitude of the group effects (for ANCOVA models) or the slope (for regression models).</description>
+</descriptions>
+</resource>
+