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880 results for “pathogenesis”
Identification of novel biomarkers related to pathogenesis and treatment of psoriasis
<p><span> Table S1.txt</span></p> <p><span>Differentially</span> <span>expressed genes</span><span> in the NL/LS cohort.</span></p> <p><span> </span><span> Table S2.txt</span></p> <p><span>Differentially</span> <span>expressed genes</span><span> in the pre/post treatment cohort.</span></p> <p><span> </span><span> Figure S1.pdf</span></p> <p><span>The heat map of differentially expressed genes.</span></p> <p><span>A: The heat map of the 50 most differentially expressed genes in NL/LS cohort.</span></p> <p><span>B: The heat map of the 50 most differentially expressed genes in pre/post treatment cohort.</span></p> <p><span> </span><span> </span><span>Figure S2.pdf</span></p> <p><span>Cluster outlier detection of NL/LS cohort.</span></p> <p><span>Figure S3.pdf</span></p> <p><span>Cluster outlier detection of pre/post treatment cohort.</span></p> <p><span> </span><span>Table S3.txt</span></p> <p><span>The results of GO enrichment analysis in </span><span>NL/LS cohort.</span></p> <p><span> </span><span>Figure S4</span><span>.pdf</span></p> <p><span>Chord diagram</span><span>: Go analysis of the key module in NL/LS cohort (Biological process).</span></p> <p><span> </span><span>Figure S5.pdf</span></p> <p><span>Chord diagram</span><span>: Go analysis of the key module in NL/LS cohort (Cellular component).</span></p> <p><span> </span><span>Figure S6.pdf</span></p> <p><span>Chord diagram</span><span>: Go analysis of the key module in NL/LS cohort (Molecular function).</span></p> <p><span> </span><span>Table S4.txt</span></p> <p><span>The results of KEGG enrichment analysis in </span><span>NL/LS cohort.</span></p> <p><span> </span><span>Table S5.txt</span></p> <p><span>The results of GO enrichment analysis in </span><span>pre/post treatment cohort.</span></p> <p><span> </span><span> Figure S7.pdf</span></p> <p><span>Chord diagram</span><span>: Go analysis of the key module in pre/post treatment cohort (Biological process).</span></p> <p><span> </span><span> Figure S8.pdf</span></p> <p><span>Chord diagram</span><span>: Go analysis of the key module in pre/post treatment cohort (Cellular component).</span></p> <p><span> </span><span> Figure S9.pdf</span></p> <p><span>Chord diagram</span><span>: Go analysis of the key module in pre/post treatment cohort (Molecular function).</span></p> <p><span> </span><span> Table S6.txt</span></p> <p><span>The results of KEGG enrichment analysis </span><span>in pre/post treatment cohort.</span></p> <p><span> Figure S10.pdf</span></p> <p><span>LASSO model</span></p> <p><span>A: </span><span>LASSO model of NL/LS cohort.</span></p> <p><span>B: LASSO model of </span><span>pre/post treatment cohort.</span></p>
Dataset: Analysis of changes in inter-cellular communications during Alzheimer's Disease pathogenesis reveals conserved changes in glutamatergic transmission in mice and humans
<p>Processed data (Seurat objects) from the entorhinal cortex of 5xFAD mice and donors, analyzed and described in the correponding manuscript (https://doi.org/10.1101/2024.04.30.591802).</p>
Sporadic pseudohypoparathyroidism type 1B in monozygotic twins: insights into the pathogenesis of methylation defects
<p>Context: Sporadic pseudohypoparathyroidism type 1B (sporPHP1B) is an imprinting disease without a defined genetic cause, characterized by broad methylation changes in differentially methylated regions (DMRs) of the <i>GNAS</i> gene.</p> <p>Objective: This work aims to provide insights into the causative event leading to the <i>GNAS</i> methylation defects through comprehensive molecular genetic analyses of a pair of female monozygotic twins concordant for sporPHP1B who were conceived naturally i.e., without assisted reproductive techniques.</p> <p>Methods: Using the leukocyte genome of the twins and family members, we performed targeted bisulfite sequencing, methylation-sensitive restriction enzyme (MSRE)-qPCR, whole-genome sequencing (WGS), high-density SNP array, and Sanger sequencing.</p> <p>Results: Methylation analyses by targeted bisulfite sequencing and MSRE-qPCR revealed almost complete loss of methylation at the <i>GNAS</i> AS, XL, and A/B DMRs and gain of methylation at the NESP55 DMR in the twins, but not in other family members. Except for the <i>GNAS</i> locus, we did not find apparent methylation defects at other imprinted genome loci of the twins. WGS, SNP array, and Sanger sequencing did not detect the previously described genetic defects associated with familial PHP1B. Sanger sequencing also ruled out any novel genetic alterations in the entire NESP55/AS region. However, the analysis of 28 consecutive SNPs could not exclude the possibility of paternal heterodisomy in a span of 22 kb comprising exon NESP55 and AS exon 5.</p> <p>Conclusion: Our comprehensive analysis of a pair of monozygotic twins with sporPHP1B ruled out all previously described genetic causes. Twin concordance indicates that the causative event was an imprinting error earlier than the timing of monozygotic twinning.</p>
Fig. 7 in Preliminary investigations on the pathogenesis-related protein expression profile of the medicinal herb Macleaya cordata and anti-bacterial properties of recombinant proteins
Fig. 7. Antibacterial effects of a series of purified McDef1 concentration against S. aureus (A), E. coli (B), S. pullorum (C) and A. hydrophila (D). 1: 30 μg/ml, 2: 40 μg/ ml, 3: 50 μg/ml, 4: 60 μg/ml, 5: 80 μg/ml, 6: 100 μg/ml, 7: Negative control, empty vector expression supernatant; 8: Positive control, for A̢B̢C: 0.2 mg/mL Ampicillin, for D: 0.5 mg/mL Kanamycin.
Fig. 6 in Preliminary investigations on the pathogenesis-related protein expression profile of the medicinal herb Macleaya cordata and anti-bacterial properties of recombinant proteins
Fig. 6. Antibacterial effects of recombinant yeasts with McDef1 or McDef2 fermentation supernatant on S. aureus (A), S. pullorum (B), E. coli (C) and A. hydrophila (D). 1: Fermentation supernatant of the recombinant McDef1; 2: Fermentation supernatant of the recombinant McDef2; 3: Negative control, empty vector expression supernatant; 4: Positive control, A̢B̢C: 0.2 mg/mL Ampicillin; D: 0.5 mg/mL Kanamycin.
Fig. 4 in Preliminary investigations on the pathogenesis-related protein expression profile of the medicinal herb Macleaya cordata and anti-bacterial properties of recombinant proteins
Fig. 4. Multiple sequence alignments of the mature peptides of McLTP1 homologs from different plants with ClustalW2. The target proteins McLTP1 of this study are highlighted with yellow fluorescent background. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2 in Preliminary investigations on the pathogenesis-related protein expression profile of the medicinal herb Macleaya cordata and anti-bacterial properties of recombinant proteins
Fig. 2. Multiple sequence alignments of the McDef1 (A) and McDef2-5 (B) homologs from different plants with ClustalW2. The conserved domains α-core and γ-core are marked under the homologous sequences respectively. The target proteins McDef1 in (A) and McDef2-5 in (B) of this study are highlighted with yellow fluorescent background. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in Preliminary investigations on the pathogenesis-related protein expression profile of the medicinal herb Macleaya cordata and anti-bacterial properties of recombinant proteins
Fig. 1. The alignment analysis of McDef1-5. The underlined amino acids represent the signal sequence predicted with SignalP. The cysteines are marked in yellow background and the putative disulfide bonds are also shown. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 8 in Preliminary investigations on the pathogenesis-related protein expression profile of the medicinal herb Macleaya cordata and anti-bacterial properties of recombinant proteins
Fig. 8. Antibacterial effects of a series of purified McDef2 concentration against S. aureus (A), E. coli (B), S. pullorum (C) and A. hydrophila (D). 1: 30 μg/ml, 2: 40 μg/ ml, 3: 50 μg/ml, 4: 60 μg/ml, 5: 80 μg/ml, 6: 100 μg/ml, 7: Negative control, empty vector expression supernatant; 8: Positive control, for A̢B̢C: 0.2 mg/mL Ampicillin, for D: 0.5 mg/mL Kanamycin.
Pathogenesis and Management of M. Ulcerans Disease, Buruli Ulcer
ClinicalTrials.gov study NCT02153034. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Potential Role of CD9 and Implication of Motility Process in Pathogenesis of TEL/ALM1-positive ALL Relapses (LAL TEL/ALM1 and CD9).
ClinicalTrials.gov study NCT01282593. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Study On the Role of Mitochondrial Dysfunction in the Pathogenesis of Metformin-associated Lactic Acidosis
ClinicalTrials.gov study NCT00942123. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The Role of Angiotensinogen Gene Polymorphism in the Pathogenesis of Non-familial Sick Sinus Syndrome
ClinicalTrials.gov study NCT01310920. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The Pathogenesis and Natural History of Sjogren's Disease
ClinicalTrials.gov study NCT01425892. IPD Sharing: NO. Countries: 1. Publications: 1.
Nitric Oxide, LPS and the Pathogenesis of Asthma Phase 1
ClinicalTrials.gov study NCT00671229. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Etiology, Pathogenesis, and Natural History of Idiopathic CD4+ Lymphocytopenia
ClinicalTrials.gov study NCT00867269. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Pathogenesis and Cerebrovascular Manifestations of Septic Encephalopathy
ClinicalTrials.gov study NCT00410111. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Predictive Immune Biomarkers for COVID-19 Pathogenesis
ClinicalTrials.gov study NCT04385108. IPD Sharing: NO. Countries: 1. Publications: 3.
Pathogenesis of Functional Hypothalamic Amenorrhea
ClinicalTrials.gov study NCT01674426. IPD Sharing: Not stated. Countries: 1. Publications: 3.
COVID-19 Associated Lymphopenia Pathogenesis Study in Blood
ClinicalTrials.gov study NCT04401436. IPD Sharing: NO. Countries: 1. Publications: 4.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.