cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7938110.v1
title: Reactions of quinones with some aryl phenols and synthesis of new quinone derivatives

description: In the present study, the reactions of p-chloranil <b>(1a)</b> and 2,3-dichloro-1,4-naphthoquinone (DCNQ) <b>(1b)</b> with some aryl phenols were investigated. The structures of all compounds were characterized using spectroscopic methods (FT-IR, <sup>1</sup>H NMR, <sup>13</sup>C NMR, and MS) and microanalysis. The electrochemical behaviors of some benzoquinone and naphthoquinone derivatives have also been investigated in unbuffered aprotic solutions.
DOI: 10.6084/m9.figshare.7938035
title: RCCPII Tweets

description: This Twitter dataset was obtained from Tweet Binder on 2 April 2019. The dataset reflects tweets containing the hashtag #RCCPII between 1 January 2016 until 2 April 2019.<br>A link to the original report is available at https://www.tweetbinder.com/report/advanced/en/426cab61.<br>
DOI: 10.6084/m9.figshare.7938026
title: gVCF_NA12046

description: 1000 Genomes gVCF mapped to hs37d5 for NA12046. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7938029
title: Cancer-specific SNPs originate from low-level heteroplasmic variants in human mitochondrial genomes of a matched cell line pair

description: Low-level mitochondrial heteroplasmy is a common phenomenon in both normal and cancer cells. Here, we investigate the link between low-level heteroplasmy and mitogenome mutations in a human breast cancer matched cell line by high-throughput sequencing. We identified 23 heteroplasmic sites, of which 15 were common between normal cells (Hs578Bst) and cancer cells (Hs578T). Most sites were clustered within the highly conserved Complex IV and ribosomal RNA genes. Two heteroplasmic variants in normal cells were found as fixed mutations in cancer cells. This indicates a positive selection of these variants in cancer cells. RNA-Seq analysis identified upregulated L-strand specific transcripts in cancer cells, which include three mitochondrial long non-coding RNA molecules. We hypothesize that this is due to two cancer cell-specific mutations in the control region.
DOI: 10.6084/m9.figshare.7938041.v1
title: Secondary structures of rfam mobile group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938023
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7938029.v1
title: Cancer-specific SNPs originate from low-level heteroplasmic variants in human mitochondrial genomes of a matched cell line pair

description: Low-level mitochondrial heteroplasmy is a common phenomenon in both normal and cancer cells. Here, we investigate the link between low-level heteroplasmy and mitogenome mutations in a human breast cancer matched cell line by high-throughput sequencing. We identified 23 heteroplasmic sites, of which 15 were common between normal cells (Hs578Bst) and cancer cells (Hs578T). Most sites were clustered within the highly conserved Complex IV and ribosomal RNA genes. Two heteroplasmic variants in normal cells were found as fixed mutations in cancer cells. This indicates a positive selection of these variants in cancer cells. RNA-Seq analysis identified upregulated L-strand specific transcripts in cancer cells, which include three mitochondrial long non-coding RNA molecules. We hypothesize that this is due to two cancer cell-specific mutations in the control region.
DOI: 10.6084/m9.figshare.7938017
title: Association of diagnostic delays to survival in lung cancer: single center experience

description: <b>Background:</b> Rapid diagnostics and treatment approaches have been applied in many countries to enhance patient satisfaction, but it is unknown whether this leads to improvements in survival. <b>Material and methods:</b> Symptoms initiation, referral, and investigations and their timing, and survival were retrospectively collected from all the patients diagnosed for lung cancer at Oulu University Hospital 2015–2016 (<i>n</i> = 221). Correlation of treatment delays to survival was evaluated in different categories and by tumor stages. <b>Results:</b> Survival analysis showed no statistical difference between patients having below or above median time for the whole clinical pathway (from symptoms to treatment). Subsection analysis of the clinical pathway and division of patients by stage showed improved survival for patients having longer than median times in referral to diagnosis (<i>p</i> = .03) and diagnosis to treatment (<i>p</i> p <b>Conclusion:</b> Longer time on diagnostic work-up of lung cancer does not worsen the survival suggesting that fast-track approaches might not improve lung cancer outcomes.
DOI: 10.6084/m9.figshare.7938026.v1
title: gVCF_NA12046

description: 1000 Genomes gVCF mapped to hs37d5 for NA12046. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7938041.v2
title: Secondary structures of rfam mobile group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938017.v1
title: Association of diagnostic delays to survival in lung cancer: single center experience

description: <b>Background:</b> Rapid diagnostics and treatment approaches have been applied in many countries to enhance patient satisfaction, but it is unknown whether this leads to improvements in survival. <b>Material and methods:</b> Symptoms initiation, referral, and investigations and their timing, and survival were retrospectively collected from all the patients diagnosed for lung cancer at Oulu University Hospital 2015–2016 (<i>n</i> = 221). Correlation of treatment delays to survival was evaluated in different categories and by tumor stages. <b>Results:</b> Survival analysis showed no statistical difference between patients having below or above median time for the whole clinical pathway (from symptoms to treatment). Subsection analysis of the clinical pathway and division of patients by stage showed improved survival for patients having longer than median times in referral to diagnosis (<i>p</i> = .03) and diagnosis to treatment (<i>p</i> p <b>Conclusion:</b> Longer time on diagnostic work-up of lung cancer does not worsen the survival suggesting that fast-track approaches might not improve lung cancer outcomes.
DOI: 10.6084/m9.figshare.7938041.v3
title: Secondary structures of rfam mobile group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938023.v1
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7938041.v4
title: Secondary structures of rfam mobile group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938023.v2
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7938041.v5
title: Secondary structures of rfam mobile group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938041.v7
title: Secondary structures of rfam group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938023.v3
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7938023.v4
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7938041.v6
title: Secondary structures of rfam mobile group II introns

description: Structures of introns group II of RFAM RF00029 family
DOI: 10.6084/m9.figshare.7938023.v6
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7938023.v5
title: Secondary structures of the training set of mobile group II introns

description: Secondary structures of the training set of mobile group II introns
DOI: 10.6084/m9.figshare.7937888
title: gVCF_HG02733

description: 1000 Genomes gVCF mapped to hs37d5 for HG02733. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937888.v1
title: gVCF_HG02733

description: 1000 Genomes gVCF mapped to hs37d5 for HG02733. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937891
title: gVCF_NA20509

description: 1000 Genomes gVCF mapped to hs37d5 for NA20509. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937870
title: gVCF_HG02731

description: 1000 Genomes gVCF mapped to hs37d5 for HG02731. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937873
title: gVCF_NA12045

description: 1000 Genomes gVCF mapped to hs37d5 for NA12045. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937891.v1
title: gVCF_NA20509

description: 1000 Genomes gVCF mapped to hs37d5 for NA20509. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937777
title: gVCF_NA20508

description: 1000 Genomes gVCF mapped to hs37d5 for NA20508. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937744
title: gVCF_HG02728

description: 1000 Genomes gVCF mapped to hs37d5 for HG02728. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937777.v1
title: gVCF_NA20508

description: 1000 Genomes gVCF mapped to hs37d5 for NA20508. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937696
title: gVCF_NA20507

description: 1000 Genomes gVCF mapped to hs37d5 for NA20507. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937744.v1
title: gVCF_HG02728

description: 1000 Genomes gVCF mapped to hs37d5 for HG02728. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937693
title: gVCF_NA12043

description: 1000 Genomes gVCF mapped to hs37d5 for NA12043. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937696.v1
title: gVCF_NA20507

description: 1000 Genomes gVCF mapped to hs37d5 for NA20507. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937687
title: GLP-1’s role in neuroprotection: a systematic review

description: Glucagon-like peptide 1 (GLP-1) is a target for treatment of diabetes; however, its function in the brain is not well studied. In this systematic review, we aimed to analyze the neuroprotective role of GLP-1 and its defined mechanisms. <b>Methods</b>: We searched ‘Web of Science’ and ‘Pubmed’ to identify relevant studies using GLP-1 as the keyword. Two hundred and eighty-nine clinical and preclinical studies have been included. Data have been presented by grouping neurodegenerative, neurovascular and specific cell culture models. <b>Results</b>: Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer’s disease, Parkinson’s disease or vascular occlusion. Possible mechanisms that provide neuroprotection are enhancing the viability of the neurons and restoring neurite outgrowth by increased neurotrophic factors, increasing subventricular zone progenitor cells, decreasing apoptosis, decreasing the level of pro-inflammatory factors, and strengthening blood-brain barrier. <b>Conclusion</b>: Based on the preclinical studies, GLP-1 modifying agents are promising targets for neuroprotection. On the other hand, the number of clinical studies that investigate GLP-1 as a treatment is low and further clinical trials are needed for a benchside to bedside translation of recent findings.
DOI: 10.6084/m9.figshare.7937690
title: Amyotrophic lateral sclerosis mortality rates among ethnic groups in a predominant admixed population in Latin America: a population-based study in Ecuador

description: Current evidence suggests heterogeneity of amyotrophic lateral sclerosis (ALS) among geographic areas and populations. Lower mortality rates have been reported in admixed populations compared to European origin populations. We aimed to describe and compare ALS mortality rates among ethnic groups using a population-based approach in a multiethnic country. Annual mortality cause registers were searched to determine ALS deaths from the National Institute of Statistics and Censuses in Ecuador (INEC) from 1990 to 2016. Mid-year population was considered for each year. The time trend was assessed using a negative binomial regression. Rate ratio statistics were performed to compare the age and sex standardized rates based on the 2010 US population among ethnic groups. Overall, 570 ALS deaths were identified. ALS mortality showed an age-related profile with a peak between 55 and 70 years. After age–sex standardization on the 2010 US population, mortality rate was 0.33 (CI 0.30–0.36) per 100,000. The time trend showed an increase of ALS mortality (<i>p</i> p = 0.231) and black (<i>p</i> = 0.125). Differences reached statistical significance between admixed and other ethnics (<i>p</i> = 0.015). Our population-based study supports the hypothesis that ALS occurrence is lower in predominant admixed populations from Latin America compared to European and Northern American populations. Further studies are needed to clarify the role of ancestral origin in ALS susceptibility.
DOI: 10.6084/m9.figshare.7937690.v1
title: Amyotrophic lateral sclerosis mortality rates among ethnic groups in a predominant admixed population in Latin America: a population-based study in Ecuador

description: Current evidence suggests heterogeneity of amyotrophic lateral sclerosis (ALS) among geographic areas and populations. Lower mortality rates have been reported in admixed populations compared to European origin populations. We aimed to describe and compare ALS mortality rates among ethnic groups using a population-based approach in a multiethnic country. Annual mortality cause registers were searched to determine ALS deaths from the National Institute of Statistics and Censuses in Ecuador (INEC) from 1990 to 2016. Mid-year population was considered for each year. The time trend was assessed using a negative binomial regression. Rate ratio statistics were performed to compare the age and sex standardized rates based on the 2010 US population among ethnic groups. Overall, 570 ALS deaths were identified. ALS mortality showed an age-related profile with a peak between 55 and 70 years. After age–sex standardization on the 2010 US population, mortality rate was 0.33 (CI 0.30–0.36) per 100,000. The time trend showed an increase of ALS mortality (<i>p</i> p = 0.231) and black (<i>p</i> = 0.125). Differences reached statistical significance between admixed and other ethnics (<i>p</i> = 0.015). Our population-based study supports the hypothesis that ALS occurrence is lower in predominant admixed populations from Latin America compared to European and Northern American populations. Further studies are needed to clarify the role of ancestral origin in ALS susceptibility.
DOI: 10.6084/m9.figshare.7937693.v1
title: gVCF_NA12043

description: 1000 Genomes gVCF mapped to hs37d5 for NA12043. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937681
title: gVCF_HG02727

description: 1000 Genomes gVCF mapped to hs37d5 for HG02727. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937684
title: Recovery in sensory-enriched break environments: integrating vision, sound and scent into simulated indoor and outdoor environments

description: To deal with stress and exhaustion at work, personal resources need to be replenished during breaks. The aim of this laboratory study (<i>n</i> = 122 students) was to test the restorative potential of sensory-enriched break environments (SEBEs) in between-subjects with repeated measures design, focusing on the type of the environment (natural outdoor vs. built indoor environment) and sensory input (no sensory input vs. audiovisual input vs. audiovisual and olfactory input). Analyses showed that SEBEs simulating either a natural or a lounge environment were perceived as more pleasant and restorative (fascination/being away) than a standard break room, which in turn facilitated the recovery of personal resources (mood, fatigue, arousal). Moreover, adding a congruent scent to an audiovisual simulation indirectly facilitated the recovery of personal resources via greater scent pleasantness and higher fascination and being away. The current study shows the opportunities for sensory enrichment to foster restoration in break environments.
DOI: 10.6084/m9.figshare.7937687.v2
title: GLP-1’s role in neuroprotection: a systematic review

description: Glucagon-like peptide 1 (GLP-1) is a target for treatment of diabetes; however, its function in the brain is not well studied. In this systematic review, we aimed to analyze the neuroprotective role of GLP-1 and its defined mechanisms. <b>Methods</b>: We searched ‘Web of Science’ and ‘Pubmed’ to identify relevant studies using GLP-1 as the keyword. Two hundred and eighty-nine clinical and preclinical studies have been included. Data have been presented by grouping neurodegenerative, neurovascular and specific cell culture models. <b>Results</b>: Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer’s disease, Parkinson’s disease or vascular occlusion. Possible mechanisms that provide neuroprotection are enhancing the viability of the neurons and restoring neurite outgrowth by increased neurotrophic factors, increasing subventricular zone progenitor cells, decreasing apoptosis, decreasing the level of pro-inflammatory factors, and strengthening blood-brain barrier. <b>Conclusion</b>: Based on the preclinical studies, GLP-1 modifying agents are promising targets for neuroprotection. On the other hand, the number of clinical studies that investigate GLP-1 as a treatment is low and further clinical trials are needed for a benchside to bedside translation of recent findings.
DOI: 10.6084/m9.figshare.7937681.v1
title: gVCF_HG02727

description: 1000 Genomes gVCF mapped to hs37d5 for HG02727. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937687.v1
title: GLP-1’s role in neuroprotection: a systematic review

description: Glucagon-like peptide 1 (GLP-1) is a target for treatment of diabetes; however, its function in the brain is not well studied. In this systematic review, we aimed to analyze the neuroprotective role of GLP-1 and its defined mechanisms. <b>Methods</b>: We searched ‘Web of Science’ and ‘Pubmed’ to identify relevant studies using GLP-1 as the keyword. Two hundred and eighty-nine clinical and preclinical studies have been included. Data have been presented by grouping neurodegenerative, neurovascular and specific cell culture models. <b>Results</b>: Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer’s disease, Parkinson’s disease or vascular occlusion. Possible mechanisms that provide neuroprotection are enhancing the viability of the neurons and restoring neurite outgrowth by increased neurotrophic factors, increasing subventricular zone progenitor cells, decreasing apoptosis, decreasing the level of pro-inflammatory factors, and strengthening blood-brain barrier. <b>Conclusion</b>: Based on the preclinical studies, GLP-1 modifying agents are promising targets for neuroprotection. On the other hand, the number of clinical studies that investigate GLP-1 as a treatment is low and further clinical trials are needed for a benchside to bedside translation of recent findings.
DOI: 10.6084/m9.figshare.7937657
title: gVCF_NA20506

description: 1000 Genomes gVCF mapped to hs37d5 for NA20506. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937657.v1
title: gVCF_NA20506

description: 1000 Genomes gVCF mapped to hs37d5 for NA20506. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937651
title: Implementing Moran eigenvector spatial filtering for massively large georeferenced datasets

description: Moran eigenvector spatial filtering (MESF) furnishes an alternative method to account for spatial autocorrelation in linear regression specifications describing georeferenced data, although spatial auto-models also are widely used. The utility of this MESF methodology is even more impressive for the non-Gaussian models because its flexible structure enables it to be easily applied to generalized linear models, which include Poisson, binomial, and negative binomial regression. However, the implementation of MESF can be computationally challenging, especially when the number of geographic units, <i>n</i>, is large, or massive, such as with a remotely sensed image. This intensive computation aspect has been a drawback to the use of MESF, particularly for analyzing a remotely sensed image, which can easily contain millions of pixels. Motivated by Curry, this paper proposes an approximation approach to constructing eigenvector spatial filters (ESFs) for a large spatial tessellation. This approximation is based on a divide-and-conquer approach. That is, it constructs ESFs separately for each sub-region, and then combines the resulting ESFs across an entire remotely sensed image. This paper, employing selected specimen remotely sensed images, demonstrates that the proposed technique provides a computationally efficient and successful approach to implement MESF for large or massive spatial tessellations.
DOI: 10.6084/m9.figshare.7937636
title: gVCF_HG02725

description: 1000 Genomes gVCF mapped to hs37d5 for HG02725. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937645
title: gVCF_NA12006

description: 1000 Genomes gVCF mapped to hs37d5 for NA12006. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937636.v1
title: gVCF_HG02725

description: 1000 Genomes gVCF mapped to hs37d5 for HG02725. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7937645.v1
title: gVCF_NA12006

description: 1000 Genomes gVCF mapped to hs37d5 for NA12006. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307