cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5443153
title: Coding of stopping and economic values in OFC

description: The task followed standard stop signal task paradigm (Logan, 1994; Logan and Cowan, 1984). Subjects were placed in front of a computer monitor (1920x1080px) with black background. Following a brief (300 msec) central fixation on a white circle (radius 25px, <i>Figure 1A</i>), the fixation spot disappeared on the appearance of eccentric saccade target (90px white square, positioned at 288px in left or 1632px in right of screen, 50% chance). A go trial (67% of trials, randomly selected) was indicated by a go signal which is the peripheral target, whereas a stop trial (33% of trials, randomly selected) was indicated by an additional appearance of a stop signal—a central gray square delayed relative to the go signal presentation. Stop signal delays (SSD) in the task were set to stabilize at a delay causing 50% successful inhibition out of all stop trials recorded for the task in that day; SSDs were modulated through a staircase procedure with intervals of 16 msec. On go trials, subjects were rewarded for a saccade to the go signal and fixating on it for 50 msec; and on stop trials, subjects were rewarded for inhibiting their saccade to go signal and fixating at the stop signal for 400 msec. Water rewards were provided as feedback, and they were contingent on subject’s choice. Rewards were always 125 μl. The inter trial interval was 800 msec.<br>The <i>neuroeconomic</i> <i>stopping task</i> had a similar task framework to stop signal task, interleaved with the other in an interval picked randomly from range 1-3 trials. In go trials (random 67% of the total), a peripheral target called go offer (90px white square, positioned at 288px in left or 1632px in right of the screen, 50% chance) was presented, and it was randomly associated with low (15μl), medium (125μl), or high (250μl) reward offers, as indicated by yellow, blue and magenta colored squares, respectively. In stop trials (random 33% of the total), a center stop offer delayed with respect to the appearance of go offer was presented in addition. The stop-offer was also randomly associated with yellow, blue and magenta colors to indicate low, medium and high reward sizes. The go offer in stop trials was always in blue color to represent medium reward sized offer. This setup allowed the subject to make a choice through reward comparison in case of stop trials, and through a forced choice in case of go trials. All other parameters were the same as stop signal task.
DOI: 10.6084/m9.figshare.5442652
title: Supplementary Material for: Identification of Genomic Alterations Associated with the Aggressiveness of Pancreatic Cancer Using an Ultra-High-Resolution CGH Array

description: <i>Background:</i> Genomic alterations present in pancreatic adenocarcinoma have been described only partially. In addition, the relations between these alterations and the aggressiveness of the phenotype remain unknown. <i>Methods:</i> Genomic DNA and total RNA from 5 pancreatic cell lines, of which 2 have an aggressive phenotype and are gemcitabine-resistant (Mia-Paca2 and Panc-1), and 3 less aggressive and gemcitabine-sensitive (Capan-1, Capan-2 and BxPC3), have been purified. DNA abnormalities have been analyzed using an ultra-high-resolution CGH array and mRNA expression was studied with an Affymetrix GeneChip expression array. <i>Results:</i> We identified 573 amplified and 30 deleted genes common to all 5 cell lines. Some of them have already been described, whereas other genes, implicated in signal transduction, apoptosis, cell cycle or cell migration, are described for the first time as being related to this cancer. Comparison of genomic abnormalities between the 2 most aggressive and the 3 less aggressive cell lines led to the identification of 368 genes specifically amplified in the aggressive cell lines. However, no specific gene deletion seems to be associated with the aggressive phenotype. <i>Conclusion:</i> Using a high-resolution approach, we could precisely describe the genomic alterations associated with pancreatic adenocarcinoma and determine those associated with an aggressive phenotype.
DOI: 10.6084/m9.figshare.5443153.v1
title: Coding of stopping and economic values in OFC

description: The task followed standard stop signal task paradigm (Logan, 1994; Logan and Cowan, 1984). Subjects were placed in front of a computer monitor (1920x1080px) with black background. Following a brief (300 msec) central fixation on a white circle (radius 25px, <i>Figure 1A</i>), the fixation spot disappeared on the appearance of eccentric saccade target (90px white square, positioned at 288px in left or 1632px in right of screen, 50% chance). A go trial (67% of trials, randomly selected) was indicated by a go signal which is the peripheral target, whereas a stop trial (33% of trials, randomly selected) was indicated by an additional appearance of a stop signal—a central gray square delayed relative to the go signal presentation. Stop signal delays (SSD) in the task were set to stabilize at a delay causing 50% successful inhibition out of all stop trials recorded for the task in that day; SSDs were modulated through a staircase procedure with intervals of 16 msec. On go trials, subjects were rewarded for a saccade to the go signal and fixating on it for 50 msec; and on stop trials, subjects were rewarded for inhibiting their saccade to go signal and fixating at the stop signal for 400 msec. Water rewards were provided as feedback, and they were contingent on subject’s choice. Rewards were always 125 μl. The inter trial interval was 800 msec.<br>The <i>neuroeconomic</i> <i>stopping task</i> had a similar task framework to stop signal task, interleaved with the other in an interval picked randomly from range 1-3 trials. In go trials (random 67% of the total), a peripheral target called go offer (90px white square, positioned at 288px in left or 1632px in right of the screen, 50% chance) was presented, and it was randomly associated with low (15μl), medium (125μl), or high (250μl) reward offers, as indicated by yellow, blue and magenta colored squares, respectively. In stop trials (random 33% of the total), a center stop offer delayed with respect to the appearance of go offer was presented in addition. The stop-offer was also randomly associated with yellow, blue and magenta colors to indicate low, medium and high reward sizes. The go offer in stop trials was always in blue color to represent medium reward sized offer. This setup allowed the subject to make a choice through reward comparison in case of stop trials, and through a forced choice in case of go trials. All other parameters were the same as stop signal task.
DOI: 10.6084/m9.figshare.5442460
title: Supplementary Material for: Proteomic Analysis of Pancreatic Ductal Adenocarcinoma Compared with Normal Adjacent Pancreatic Tissue and Pancreatic Benign Cystadenoma

description: <i>Background:</i> Dual expression of potential biomarkers in both benign and malignant pancreatic tumors was a major obstacle in the development of diagnostic biomarkers of early pancreatic cancer. <i>Methods:</i> To better understand the limitations of potential protein biomarkers in pancreatic cancer, we employed two-dimensional difference gel electrophoresis technology and tandem mass spectrometry to study protein expression profiles in pancreatic cancer tissues, benign pancreatic adenoma and normal adjacent pancreas. Seven differently expressed proteins were selected for validation by Western blot and/or immunohistochemistry. <i>Results:</i> 21 spots were overexpressed and 24 spots were downexpressed in pancreatic cancer compared with benign and normal adjacent tissues. Our study demonstrated that three candidate pancreatic ductal adenocarcinoma biomarkers identified in previous studies, fructose-bisphosphate aldolase A, α-smooth muscle actin and vimentin, were also overexpressed in pancreatic cystadenoma, which might lower their further utility as biomarkers for pancreatic cancer. Aflatoxin B<sub>1</sub> aldehyde reductase (AKR7A2) was confirmed to be only highly expressed in pancreatic cancer, not in normal adjacent pancreas and benign tumors. <i>Conclusions:</i> The protein profile pattern of pancreatic cystadenoma was more similar to normal adjacent pancreas than pancreatic cancer. We identified panels of the upregulated proteins in pancreatic cancer, which have not been reported in prior proteomic studies. AKR7A2 may be a novel potential biomarker for pancreatic cancer.
DOI: 10.6084/m9.figshare.5442457
title: Assembly in the translation milieu imposes evolutionary constraints on homomeric proteins

description: <b>Supplementary Video 1. Simulation</b> <b>of Tet@N with short linker. </b>For all movies the red segment is the Tet, and yellow is the YFP beta-barrel. Both cotranslational folding and misassembly take place once the Tet appear outside of the ribosome tunnels.<br> <b>Supplementary Video 2. Simulation</b> <b>of Tet@C with short linker. </b>There was no cotranslational assembly as the Tet of the leading ribosome leaves the ribosomal tunnel prior to the translation of the second ribosome, which allows it time to diffuse before the second Tet leaves the ribosome tunnel. <b> </b> <b>Supplementary Video 3. Simulation</b> <b>of Tet@N with long linker. </b>Cotranslational assembly takes place, but not misassembly. Similarly to movies S1-S2, the red segment is the Tet and the yellow is the YFP reporter-gene, the cyan segment is the long-linker. The less frequent misassembly events fit the observed <i>in vivo and in vitro</i> data. <b> </b>
DOI: 10.6084/m9.figshare.5442460.v1
title: Supplementary Material for: Proteomic Analysis of Pancreatic Ductal Adenocarcinoma Compared with Normal Adjacent Pancreatic Tissue and Pancreatic Benign Cystadenoma

description: <i>Background:</i> Dual expression of potential biomarkers in both benign and malignant pancreatic tumors was a major obstacle in the development of diagnostic biomarkers of early pancreatic cancer. <i>Methods:</i> To better understand the limitations of potential protein biomarkers in pancreatic cancer, we employed two-dimensional difference gel electrophoresis technology and tandem mass spectrometry to study protein expression profiles in pancreatic cancer tissues, benign pancreatic adenoma and normal adjacent pancreas. Seven differently expressed proteins were selected for validation by Western blot and/or immunohistochemistry. <i>Results:</i> 21 spots were overexpressed and 24 spots were downexpressed in pancreatic cancer compared with benign and normal adjacent tissues. Our study demonstrated that three candidate pancreatic ductal adenocarcinoma biomarkers identified in previous studies, fructose-bisphosphate aldolase A, α-smooth muscle actin and vimentin, were also overexpressed in pancreatic cystadenoma, which might lower their further utility as biomarkers for pancreatic cancer. Aflatoxin B<sub>1</sub> aldehyde reductase (AKR7A2) was confirmed to be only highly expressed in pancreatic cancer, not in normal adjacent pancreas and benign tumors. <i>Conclusions:</i> The protein profile pattern of pancreatic cystadenoma was more similar to normal adjacent pancreas than pancreatic cancer. We identified panels of the upregulated proteins in pancreatic cancer, which have not been reported in prior proteomic studies. AKR7A2 may be a novel potential biomarker for pancreatic cancer.
DOI: 10.6084/m9.figshare.5442379
title: Supplementary Material for: Total Number of Genome Alterations in Sporadic Gastrointestinal Cancer Inferred from Pooled Analyses in the Literature

description: <i>Background/Aims:</i> A previous study based on the age distribution of human cancers has demonstrated that about 6 or 7 mutations are required for gastrointestinal cancer to develop. This study aims to provide further insight into this issue through a systematic review of current knowledge found in the literature. <i>Methods:</i> The PubMed database was searched for entries up to December 2007 for eligible studies pertaining to chromosome aberrations and gene mutations in sporadic esophageal, gastric, colorectal and pancreatic cancers. <i>Results:</i> Of 29,308 potentially eligible titles, 302 representative reports were included in the pooled analysis. Frequently reported genome alterations were: the +3q27 and +8q24 mutations of <i>TP53 </i>for esophageal cancer; +20q13 for gastric cancer; –18q22 and +20q12–q13 mutations of <i>APC</i>, <i>TP53</i> and <i>KRAS </i>for colorectal cancer, and the –18q22 mutation of <i>KRAS</i> and <i>TP53 </i>for pancreatic cancer. Based on the frequencies of major events, which represents the expected value of the occurrence, the total number of genome alterations was estimated at 8.99 for esophageal, 4.18 for gastric, 7.36 for colorectal and 5.74 for pancreatic cancer. <i>Conclusion:</i> The genetic changes summarized here, predominantly chromosome alterations, constitute a major factor in the development of these cancers, so that it may be advisable on focus molecular strategies for diagnosis and treatment of these events.
DOI: 10.6084/m9.figshare.5442418
title: Supplementary Material for: Genome-Wide Analysis of Pancreatic Cancer Using Microarray-Based Techniques

description: <i>Background/Aims:</i> Microarray-based comparative genomic hybridisation (CGH) has allowed high-resolution analysis of DNA copy number alterations across the entire cancer genome. Recent advances in bioinformatics tools enable us to perform a robust and highly sensitive analysis of array CGH data and facilitate the discovery of novel cancer-related genes. <i>Methods:</i> We analysed a total of 29 pancreatic ductal adenocarcinoma (PDAC) samples (6 cell lines and 23 microdissected tissue specimens) using 1-Mb-spaced CGH arrays. The transcript levels of all genes within the identified regions of genetic alterations were then screened using our Pancreatic Expression Database. <i>Results:</i> In addition to 238 high-level amplifications and 35 homozygous deletions, we identified 315 minimal common regions of ‘non-random’ genetic alterations (115 gains and 200 losses) which were consistently observed across our tumour samples. The small size of these aberrations (median size of 880 kb) contributed to the reduced number of candidate genes included (on average 12 Ensembl-annotated genes). The database has further specified the genes whose expression levels are consistent with their copy number status. Such genes were <i>UQCRB</i>, <i>SQLE</i>, <i>DDEF1</i>, <i>SLA</i>, <i>ERICH1</i> and <i>DLC1</i>, indicating that these may be potential target candidates within regions of aberrations. <i>Conclusion:</i> This study has revealed multiple novel regions that may indicate the locations of oncogenes or tumour suppressor genes in PDAC. Using the database, we provide a list of novel target genes whose altered DNA copy numbers could lead to significant changes in transcript levels in PDAC.
DOI: 10.6084/m9.figshare.5442364
title: Supplementary Material for: Application of a Global Proteomic Approach to Archival Precursor Lesions: Deleted in Malignant Brain Tumors 1 and Tissue Transglutaminase 2 Are Upregulated in Pancreatic Cancer Precursors

description: <i>Background:</i> Pancreatic cancer is an almost uniformly fatal disease, and early detection is a critical determinant of improved survival. A variety of noninvasive precursor lesions of pancreatic adenocarcinoma have been identified, which provide a unique opportunity for intervention prior to onset of invasive cancer. Biomarker discovery in precursor lesions has been hampered by the ready availability of fresh specimens, and limited yields of proteins suitable for large scale screening. <i>Methods:</i> We utilized Liquid Tissue®, a novel technique for protein extraction from archival formalin-fixed material, and mass spectrometry to conduct a global proteomic analysis of an intraductal papillary mucinous neoplasm (IPMN). Tissue microarrays comprised of 38 IPMNs were used for validation of candidate proteins. <i>Results:</i> The proteomic analysis of the IPMN Liquid Tissue lysate resulted in identification of 1,534 peptides corresponding to 523 unique proteins. A subset of 25 proteins was identified that had previously been reported as upregulated in pancreatic cancer. Immunohistochemical analysis for two of these, deleted in malignant brain tumors 1 (DMBT1) and tissue transglutaminase 2 (TGM2), confirmed their overexpression in IPMNs. <i>Conclusion:</i> Global proteomics analysis using the Liquid Tissue workflow is a feasible approach for unbiased biomarker discovery in limited archival material, particularly applicable to precursor lesions of cancer.
DOI: 10.6084/m9.figshare.5442298
title: SFO-example

description: fMRI and anatomical T1-weighted image from an example subject for fMRI processing using SPM12 (http://www.fil.ion.ucl.ac.uk/spm/) through the spm12r R package (https://cran.rstudio.com/web/packages/spm12r/index.html).
DOI: 10.6084/m9.figshare.5442349
title: Exoneurella eremophila dissections, Mildura Australia

description: Dissection data from nests of Exoneurella eremophila collected in Mildura, Victoria, Australia in summer (January 2014) and autumn (April 2014). <br>All females in each nest were dissected. Females were labelled from '1' onwards in the order they were dissected (variable: 'female'). Combined with the nest number this provides a unique identifier for each individual who was dissected. <br>Wing length ('wlength') was measured in eye piece micrometer units from the tip of the submarginal cell to the axilliary sclerites. 'wlmm' provides the measurement in mm. <br>The number of wing nicks from 0 - 21 (21 = wing edges completely ragged) were counted ('nicks'). <br>The spermatheca was observed and evidence of insemination was coded '1' while unmated individuals were coded '0'. <br>The length of the 3 largest oocytes were measured in eye piece micrometer units ('ov1', 'ov2', 'ov3'). The mean oocyte size was calculated ('meanOV') and converted to mm ('meanOVmm'). The sum of the oocytes was also calculated ('sumOV') and converted to mm ('sumOVmm').<br>'SOCYN' indicates if the nest was social ('soc') or solitary ('sol'). <br><br><br><br><br><br>
DOI: 10.6084/m9.figshare.5442364.v1
title: Supplementary Material for: Application of a Global Proteomic Approach to Archival Precursor Lesions: Deleted in Malignant Brain Tumors 1 and Tissue Transglutaminase 2 Are Upregulated in Pancreatic Cancer Precursors

description: <i>Background:</i> Pancreatic cancer is an almost uniformly fatal disease, and early detection is a critical determinant of improved survival. A variety of noninvasive precursor lesions of pancreatic adenocarcinoma have been identified, which provide a unique opportunity for intervention prior to onset of invasive cancer. Biomarker discovery in precursor lesions has been hampered by the ready availability of fresh specimens, and limited yields of proteins suitable for large scale screening. <i>Methods:</i> We utilized Liquid Tissue®, a novel technique for protein extraction from archival formalin-fixed material, and mass spectrometry to conduct a global proteomic analysis of an intraductal papillary mucinous neoplasm (IPMN). Tissue microarrays comprised of 38 IPMNs were used for validation of candidate proteins. <i>Results:</i> The proteomic analysis of the IPMN Liquid Tissue lysate resulted in identification of 1,534 peptides corresponding to 523 unique proteins. A subset of 25 proteins was identified that had previously been reported as upregulated in pancreatic cancer. Immunohistochemical analysis for two of these, deleted in malignant brain tumors 1 (DMBT1) and tissue transglutaminase 2 (TGM2), confirmed their overexpression in IPMNs. <i>Conclusion:</i> Global proteomics analysis using the Liquid Tissue workflow is a feasible approach for unbiased biomarker discovery in limited archival material, particularly applicable to precursor lesions of cancer.
DOI: 10.6084/m9.figshare.5442337
title: Supplementary Material for: Novel STIL Compound Heterozygous Mutations Cause Severe Fetal Microcephaly and Centriolar Lengthening

description: STIL (SCL/TAL1 interrupting locus) is a core component of the centriole duplication process. <i>STIL</i> mutations have been associated with both autosomal recessive primary microcephaly (MCPH) and holoprosencephaly. In this report, we describe a family with multiple miscarriages and 2 terminations of pregnancy due to marked fetal microcephaly, delayed cortical gyrification, and dysgenesis of the corpus callosum. Whole exome sequencing allowed us to identify novel compound heterozygous mutations in <i>STIL.</i> The mutations lie, respectively, in the CPAP/CENPJ and the hsSAS6 interacting domains of STIL. M-phase synchronized amniocytes from both affected fetuses did not display an aberrant number of centrioles, as shown previously for either STIL-depleted or overexpressing cells. However, we observed an elongation of at least 1 centriole for each duplicated centrosome. These preliminary results may point to a novel mechanism causing MCPH and embryonic lethality in humans.
DOI: 10.6084/m9.figshare.5442349.v1
title: Exoneurella eremophila dissections, Mildura Australia

description: Dissection data from nests of Exoneurella eremophila collected in Mildura, Victoria, Australia in summer (January 2014) and autumn (April 2014). <br>All females in each nest were dissected. Females were labelled from '1' onwards in the order they were dissected (variable: 'female'). Combined with the nest number this provides a unique identifier for each individual who was dissected. <br>Wing length ('wlength') was measured in eye piece micrometer units from the tip of the submarginal cell to the axilliary sclerites. 'wlmm' provides the measurement in mm. <br>The number of wing nicks from 0 - 21 (21 = wing edges completely ragged) were counted ('nicks'). <br>The spermatheca was observed and evidence of insemination was coded '1' while unmated individuals were coded '0'. <br>The length of the 3 largest oocytes were measured in eye piece micrometer units ('ov1', 'ov2', 'ov3'). The mean oocyte size was calculated ('meanOV') and converted to mm ('meanOVmm'). The sum of the oocytes was also calculated ('sumOV') and converted to mm ('sumOVmm').<br>'SOCYN' indicates if the nest was social ('soc') or solitary ('sol'). <br><br><br><br><br><br>