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Vitiligo

Vitiligo is a chronic autoimmune disorder characterized by the loss of pigment-producing cells (melanocytes) in the skin, resulting in the appearance of white patches.
This condition can have a significant impact on an individual's physical appearance and self-esteem.
PubCompare.ai, an AI-powered platform, can enhance your Vitiligo research by helping you locate the best protocols from literature, pre-prints, and patents, while providing accurate comparisons to optimize reproducibility and accuracy.
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Most cited protocols related to «Vitiligo»

We selected 11 autoimmune traits enriched in Th1 H3K27Ac as shown in Fig 3 of Ref. 28 (link). We made predictions for 413 lead SNPs associated with 11 autoimmune diseases enriched in Th1 H3K27Ac regions (T1D: Type 1 Diabetes, CRO: Crohn’s Disease, MS: Multiple Sclerosis, CEL: Celiac Disease, PBC: Primary Biliary Cirrhosis, RA: Rheumatoid Arthritis, Allergy, ATD: Autoimmune Thyroid Disease, UC: Ulcerative Colitis, VIT: Vitiligo, SLE: Systemic Lupus Erythematosus)28 (link). We trained a gkm-SVM on the top 10,000 500 bp Th1 DHS regions, after excluding regions that were DHS in more than 30% of human ENCODE cell lines, or near promoters (< 2 kb from TSS), against an equal size GC and repeat matched training set. We scored the lead SNP and all flanking off-lead candidates in LD as defined by (R2 > .5 and PICS28 (link) probability > .0275), yielding 3113 total SNPs. Since the significance of the maximum deltaSVM score in a locus will depend on the number of SNPs in that locus, as a random control we scored random SNPs and equal size flanking sets. To determine the cutoff, we first determined 2nd percentile deltaSVM score from 10,000 random permutations for each number of flanking SNPs (1~30), and then calculated mean and standard deviation of the 100 repeated experiments as the final cutoff. We identified 17 high scoring deltaSVM SNPs which we predict to be expression perturbing SNPs with high confidence (P < .02), while at this threshold random sampling produced 8 SNPs (binomial test P < 0.004, Supplementary Figure 4). deltaSVM scores for all 3113 SNPs are provided as Supplementary Table 6.
Publication 2015
Autoimmune Diseases Celiac Disease Cell Lines Crohn Disease Diabetes Mellitus, Insulin-Dependent Homo sapiens Hypersensitivity Lupus Erythematosus, Systemic Multiple Sclerosis Primary Biliary Cholangitis Rheumatoid Arthritis Single Nucleotide Polymorphism Thyroid Diseases Thyroid Gland Ulcerative Colitis Vitiligo
The genome-wide portion of this study included unrelated cases from our three generalized vitiligo GWAS: GWAS14 (link) (n = 1514), GWAS26 (link) (n = 450), and the current GWAS3 (n = 1090). All cases were of non-Hispanic-Latino European-derived white ancestry (EUR) from North America and Europe, and met strict clinical criteria for generalized vitiligo59 . All controls were EUR individuals not specifically known to have any autoimmune disease or malignant melanoma, for whom genome-wide genotypes were obtained from the NCBI database of Genotypes and Phenotypes (dbGaP; phs000092.v1.p1, phs000125.v1.p1, phs000138.v2.p1, phs000142.v1.p1, phs000168.v1.p1, phs000169.v1.p1, phs000206.v3.p2, phs000237.v1.p1, phs000346.v1.p1, and phs000439.v1.p1 for GWAS1; phs000203.v1.p1, and phs000289.v2.p1 for GWAS2; phs000196.v2.p1, phs000303.v1.p1, phs000304.v1.p1, phs000368.v1.p1, phs000381.v1.p1, phs000387.v1.p1, phs000389.v1.p1, phs000395.v1.p1, phs000408.v1.p1, phs000421.v1.p1, phs000494.v1.p1, and phs000524.v1.p1 for GWAS3). Control datasets were matched to each of the three GWAS case datasets based on platforms used for genotyping. The independent replication study included 1827 unrelated EUR vitiligo cases and 2181 unrelated EUR controls not included in any of the GWAS. All subjects provided written informed consent. This study was carried out under the jurisdiction of each local IRB with overall oversight of the Colorado Multiple Institutional Review Board (COMIRB).
Publication 2016
Autoimmune Diseases DNA Replication Ethics Committees, Research Europeans Genome Genome-Wide Association Study Genotype Hispanics Latinos Melanoma Phenotype Vitiligo
GFP-PMEL CD8+ T cells were isolated from the spleen of GFP-PMEL TCR transgenic mice through negative selection on microbeads (Miltenyi Biotech, Auburn, CA) according to the manufacturer’s instructions. Purified CD8+ T cells (1 × 106) were injected i.v. into sublethally irradiated (500 rads one day prior to transfer) Krt14-Kitl* hosts (12–16 wk of age). Recipient mice also received i.p. injection of 1 × 106 pfu rVV-hPMEL (N. Restifo, NCI, NIH) on the same day of transfer. IFN-γ blockade was through i.p. injection of 100–500 μg of IFN-γ neutralizing antibody (XMG-6) beginning at the indicated times and twice weekly for the duration of the observation period (5–7 wks). Mice used as controls for vitiligo were sublethally irradiated but did not receive rVV-hPMEL or PMEL CD8+ T cell transfer. Mice with vitiligo used as treatment controls for IFN-γ blockade were treated with either no antibody or with an equal quantity of Rat IgG.
Publication 2011
CD8-Positive T-Lymphocytes Immunoglobulins Interferon Type II KRT14 protein, human Mice, Transgenic Microspheres Mus Passive Immunization RRAD protein, human SILV protein, human Spleen Vitiligo
GFP-PMEL CD8+ T cells were isolated from the spleen of GFP-PMEL TCR transgenic mice through negative selection on microbeads (Miltenyi Biotech, Auburn, CA) according to the manufacturer’s instructions. Purified CD8+ T cells (1 × 106) were injected i.v. into sublethally irradiated (500 rads one day prior to transfer) Krt14-Kitl* hosts (12–16 wk of age). Recipient mice also received i.p. injection of 1 × 106 pfu rVV-hPMEL (N. Restifo, NCI, NIH) on the same day of transfer. IFN-γ blockade was through i.p. injection of 100–500 μg of IFN-γ neutralizing antibody (XMG-6) beginning at the indicated times and twice weekly for the duration of the observation period (5–7 wks). Mice used as controls for vitiligo were sublethally irradiated but did not receive rVV-hPMEL or PMEL CD8+ T cell transfer. Mice with vitiligo used as treatment controls for IFN-γ blockade were treated with either no antibody or with an equal quantity of Rat IgG.
Publication 2011
CD8-Positive T-Lymphocytes Immunoglobulins Interferon Type II KRT14 protein, human Mice, Transgenic Microspheres Mus Passive Immunization RRAD protein, human SILV protein, human Spleen Vitiligo
DNA purification, genotyping, and quality-control procedures are described in the Supplementary Appendix. In the genomewide association study, we determined the genotypes of patients with vitiligo for approximately 610,000 markers by using the Illumina 610-Quad BeadChip. All mitochondrial markers and Y-chromosome markers were excluded, leaving 579,146 SNPs that were present in both patients and controls in the genomewide association data set. Genotype data were then subjected to extensive quality-control filtering. In the two replication studies, genotyping of the SNPs that showed genomewide significance (P<5×10−8) or near significance in the genomewide association study was performed with the use of the Sequenom MassArray iPLEX genotyping system. We also imputed genotypes for rs12206499, which is related to major-histocompatibility-complex (MHC) class I molecules and for technical reasons could not be genotyped, and genotyped several SNPs in the NLRP1 (NLR family, pyrin domain–containing 1 gene) region, which was previously shown to be associated with vitiligo (see the Supplementary Appendix).
Publication 2010
Chromosome Markers DNA Replication Genes Genome-Wide Association Study Histocompatibility Antigens Class I Iplex Mitochondria Patients Pyrin Domain Single Nucleotide Polymorphism Vitiligo

Most recents protocols related to «Vitiligo»

To study protein–protein interactions at crossover targets, the STRING database19 (link) (https://stringdb.org/) was used to construct a PPI network of crossover genes of AM sapiens for vitiligo and COVID-19. "Homo sapiens" was selected in the parameter Organism, "Medium confidence 0.400)" was selected in the "Minimum required interaction score", and the other parameters were kept at their default values. Then, we filtered out the top 5 ranked core crossover genes by cytohubba plugin in Cytoscape software.
Finally, we constructed the "active ingredient-crossover genes" network by Cytoscape software and screened the top 10 ranked core ingredients. The core crossover geness in the PPI network were matched with those in the "active ingredient-crossover geness" network and imported into the Venny 2.1 online website, which was presented as a Venn diagram. The overlap between the two crossover) is the most important core crossover target for AM for vitiligo and COVID-19.
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Publication 2023
COVID 19 Gene Regulatory Networks Genes Genes, vif Homo sapiens Protein Targeting, Cellular Vitiligo
This research does not involve the ethics of human and animal experiments.To identify potential targets of AM for vitiligo and COVID-19, we searched the comprehensive gene expression database GEO16 (link), (http://www.ncbi.nlm.nih.gov/geo). The species "human" was selected as the study subject and the dataset GSE75819 with samples from healthy volunteers and vitiligo lesion skin samples. Differentially expressed genes (DEGs) between lesioned and healthy volunteers were screened by GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r). Probe sets without corresponding gene symbols or multiple probe sets were removed or averaged, respectively. adj. P values < 0.05 and |LogFC|< 1 were considered statistically significant.
To identify the disease targets of AM for the treatment of COVID-19, we used the Genecards website (https://www.genecards.org) to search for COVID-19 disease related targets using "COVID-19", "coronavirus disease", and "coronary pneumonia" as search terms.
Then the disease targets of vitiligo and COVID-19 were matched with the targets of the active ingredients of AM and imported into Venny 2.1 online website (https://bioinfogp.cnb.csic.es/tools/venny/index.html), which was displayed as a Venn diagram, and the overlapping part intersection of the two was the crossover genes of AM for vitiligo and COVID-19.
To investigate the clustering of the crossover genes in the GSE75819 dataset, we finally drew the clustering heatmap of the crossover genes through the ImageGP website (http://www.ehbio.com/ImageGP/index.php/Home/Index/index.html).
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Publication 2023
Coronavirus COVID 19 Gene Expression Genes Healthy Volunteers Heart Homo sapiens Pneumonia Skin Vitiligo
For histological evaluation of HND, a histological database at the Yonsei University Severance Hospital was utilized. A query search of AD patients from 2011 who underwent facial skin biopsy was performed, and five patients were randomly selected from 9 candidates.
Histological analysis of non-HND face specimens was performed through a query search of AD patients who underwent skin biopsy on the face from 2013 for suspected concomitant vitiligo (usually the biopsy is conducted with non-lesional normal skin and lesional skin with vitiligo to compare the melanocyte population). Crude age filtering was performed to age-match AD patients. Among the 10 candidates, five patients were randomly selected for image analysis.
At 200x magnification, the longest distance from the subcorneal level to the basal layer was chosen arbitrarily for epidermal thickness after calibrating the scale bar to pixels. The number of vessels/mm2 was counted in the dermis of each slide section within a 100 µm distance from the epidermal–dermal junction.
Immunohistochemical staining was performed using paraffin-embedded sections with antibodies against factor VIII-related antigen (1:100, ab236284, Abcam), stromal cell-derived factor-1-alpha (SDF1-α) (1:100, ab25117, Abcam, Cambridge, United Kingdom), Interleukin-1-beta (IL-1-β) (1:100, ab2105, Abcam), tumor necrosis factor-alpha (TNF-α) (1:50, ab1793, Abcam), transforming growth factor-beta (TGF-β) (1:100, ab66043, Abcam), and vascular endothelial growth factor (VEGF) (1:200, ab1316, Abcam). Staining intensity was determined at 400x magnification at a randomly chosen area of the upper dermis. Images were quantified using ImageJ analysis tools (National Institutes of Health, Bethesda, MA).
To calculate the stained area of the antibody, we converted the original image to an 8-bit grayscale image (ImageJ>Image>8-bit), applied a binary threshold, and calculated the percentage positive for the stained part in the standard image. Quantification was performed relative to the entire selected region. The threshold for each staining was set as the average threshold of multiple immunostaining analyses performed by three independent experimenters.
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Publication 2023
Antibodies Biopsy Blood Vessel CXCL12 protein, human Dermis Epidermis Face Factor VIII-Related Antigen Immunoglobulins Interleukin-1 beta Melanocyte Paraffin Embedding Patients Skin Strains Stromal Cell-Derived Factor-1alpha TGF-beta1 TNF protein, human Transforming Growth Factor beta Vascular Endothelial Growth Factors Vitiligo
This was a prospective study where the cohort was recruited from the patients attending the outpatient pigmentary clinic of the dermatology department of Post Graduate Institute of Medical Education and Research, Chandigarh. Institute Ethics Committee approvals (Intramural) were obtained before initiation of the study and all research was performed in accordance with relevant guidelines/regulations. Thirty patients aged 12–60 years with a clinical diagnosis of unstable, non-segmental vitiligo with a body surface area of 10–50% and having both acral and non-acral lesions were included in the study. Unstable disease was defined as the occurrence of new lesion(s), progression of existing lesion(s), or Koebnerisation with a VIDA score of 4 + . Patients with segmental vitiligo and universal vitiligo, pregnant and lactating mothers, any contraindication to NBUVB therapy like xeroderma pigmentosa, systemic lupus erythematosus and other photo-induced or photo-aggravated dermatoses, patients who have received any systemic treatment in the past 4 weeks and patients with unrealistic expectations were excluded from the study. After obtaining informed consent from the included patients, baseline characteristics, history, and clinical examination findings of the patient were noted. Disease activity and extent were evaluated by Vitiligo disease activity score (VIDA) and Vitiligo Area Severity Index (VASI), respectively. Lesions distal to the elbows and knees were considered acral lesions. Lesional VASI was calculated separately for acral and non-acral lesions.
Publication 2023
3'-O-methyl-nordihydroguaiaretic acid Body Surface Area Diagnosis Disease Progression Education, Medical, Graduate Elbow Ethics Committees Knee Lupus Erythematosus, Systemic Mothers Patients Physical Examination Pigmentation Skin Diseases Vitiligo Xeroderma
We conducted a population-based study using both cohort design and nested case-control design in parallel, with the intention to preserve the advantages and complement the limitations of the other as we consider that cohort studies conventionally have a higher level of evidence, whereas case-control analysis was more appropriate for evaluating rare outcomes. The study period started in January 2014 and ended in December 2020. The cohort consisted of all incident patients aged above 10 years with diagnosis codes for depression (ICD-9-CM codes: 296.2, 296.3, 300.4, 311) between January 2014 and December 2016 without history of diagnosis for depression since 1993, when the database first became available. Patients were excluded if they had history of studied autoimmune diseases before onset of depression, or if they died immediately after cohort entry.
Throughout the study, patients were defined as treatment-resistant (exposed) if they had taken at least two antidepressant regimens of adequate duration (same antidepressant or combined therapy of at least 28 days with gaps of no longer than 14 days within regimens, whilst the 28-day duration was the minimum recommended duration to assess treatment responsiveness [26 ]) and had a third antidepressant regimen to confirm failure of the previous two trials. Patients who did not fulfil the criteria for TRD were considered as non-TRD (unexposed). Onset of outcome was confirmed on the date of the first autoimmune diagnosis in (1) organ-specific diseases including inflammatory bowel diseases, spondyloarthritis, psoriasis, insulin-dependent diabetes mellitus, Hashimoto’s thyroiditis, Graves’ disease, coeliac disease, vitiligo, alopecia areata, pemphigus vulgaris, dermatitis herpetiformis, pernicious anaemia, immune thrombocytopenic purpura, iridocyclitis and pemphigoid, and (2) systemic diseases including systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s disease, systemic sclerosis, polymyositis/dermatomyositis, multiple sclerosis and juvenile arthritis, captured across all settings including outpatient, inpatient and emergency services. List of ICD-9-CM codes to identify the cohort and outcomes is presented in Supplementary Table 1. Using the comorbidity rates reported from a previously similar population-based study, the sample sizes required for data collection were 5403 and 12545 for the analyses in systemic and organ-specific autoimmune diseases, respectively, to achieve an 80% statistical power in the cohort study [17 (link), 27 ].
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Publication 2023
Alopecia Anemia, Pernicious Antidepressive Agents Autoimmune Diseases Bullous Pemphigoid Celiac Disease Dermatitis Herpetiformis Dermatomyositis Diabetes Mellitus, Insulin-Dependent Diagnosis Graves Disease Hashimoto Disease Inflammatory Bowel Diseases Inpatient Iridocyclitis Juvenile Arthritis Lupus Erythematosus, Systemic Multiple Sclerosis Outpatients Patients Pemphigus Vulgaris Psoriasis Psychotherapy, Multiple Rheumatoid Arthritis Service, Emergency Medical Sjogren's Syndrome Spondylarthritis Systemic Scleroderma Thrombocytopenic Purpura, Immune Treatment Protocols Vitiligo

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Human Melanocyte Growth Supplement is a cell culture medium supplement designed to support the growth and maintenance of human melanocyte cells in vitro. The product contains a proprietary blend of essential nutrients, growth factors, and other components required for the optimal proliferation and survival of these specialized skin cells.
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More about "Vitiligo"

Vitiligo is a chronic dermatological condition characterized by the loss of melanocytes, the pigment-producing cells in the skin.
This autoimmune disorder results in the appearance of white patches, often on visible areas like the face, hands, and feet.
Impacting both physical appearance and self-esteem, vitiligo can be a challenging condition to manage.
Researchers studying vitiligo may utilize a variety of tools and techniques to understand the underlying causes and explore potential treatments.
PubCompare.ai, an AI-powered platform, can streamline the research process by helping scientists locate the best protocols from scientific literature, preprints, and patents, while providing accurate comparisons to optimize reproducibility and accuracy.
Vitiligo research may involve the use of cell culture techniques, such as those employing Medium 254 and Human Melanocyte Growth Supplement, to study the behavior and characteristics of melanocytes.
The TRIzol reagent may be used for RNA extraction, and the SYBR Green kit for gene expression analysis.
Prism software, such as GraphPad Prism 5, can be utilized for data analysis and visualization.
By leveraging the insights and tools provided by PubCompare.ai, researchers can gain deeper understanding of vitiligo and accelerate the development of effective treatments, ultimately improving the quality of life for those affected by this condition.