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Mission Statement
The Rosacea Research & Development Institute [RRDi] is the first non-profit organization made by rosaceans for rosacea sufferers that will collect donations for rosacea research to be performed by physicians and biomedical research scientists and includes these specific goals:
Goal # 1: To be the first non profit organization for rosacea patient advocacy and to find the cure for rosacea.
Goal # 2: To have a majority of rosaceans the right to vote who sits on the board of directors. This is in stark contrast to other rosacea non profit organizations comprised of non rosacea sufferers who are usually businessmen or dermatologists with a vested interest in treating rosacea.
Goal # 3: To make this the first rosacea specific non profit organization to utilize most of the donations for research and treatment development. This is in stark contrast to non profit organizations that spend 50% to 60% of their donations on paying their staff, board of directors, conventions for professional members or to pay private contractors for services.
Goal # 4: To allow rosacea sufferers to guide where and how the money is spent on rosacea research and be the first non profit organization to allow rosaceans to be members of the corporation. Until June 7, 2004, the date of incorporation, there had been no other non profit organization that allowed input from rosacea sufferers.
Goal # 5: To attain a level such that the RRDi can directly impact medical articles published on the subject, information disseminated to physicians and rosacea sufferers and apply positive pressure on the medical community.
Goal #6: Continue to publish the Journal of the RRDi and fund all authors who contribute an article.
Goal #7: To allow volunteer members to have a platform to voice their concerns about rosacea and to contribute information about rosacea. Our goal is 10K members.
For more information on how and why this non profit organization for rosacea was formed click here.
Our Charter can be read by clicking here.
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Member Statistics
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Posts
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Arch Dermatol Res. 2024 Oct 14;316(10):677. doi: 10.1007/s00403-024-03433-y. ABSTRACT Dysbiosis in the skin microbiome is closely associated with various inflammatory skin diseases. However, current research on the causal relationship between the skin microbiome and inflammatory skin diseases lacks comprehensive and detailed investigation. We used a two-sample Mendelian randomization (MR) approach to explore associations between the skin microbiome and seven inflammatory skin diseases, including acne, atopic dermatitis, erysipelas, vitiligo, psoriasis, rosacea, and urticaria. The GWAS summary data for the skin microbiome was derived from 647 participants in two German population-based cohorts, and for the inflammatory skin diseases, they were sourced from the FinnGen consortium. Our primary MR analysis method was the inverse variance weighted (IVW) method, complemented by alternatives like MR-Egger regression, weighted median estimation, and constrained maximum likelihood. Sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and MR-PRESSO outlier detection, were conducted to validate and stabilize our findings. We identified significant causal relationships between the skin microbiome and seven inflammatory skin diseases: acne, atopic dermatitis, erysipelas, vitiligo, psoriasis, rosacea, and urticaria, with 7, 6, 9, 1, 7, 4, and 7 respective causal relationships for each disease. These relationships comprise 20 protective and 14 risk causal relationships. We applied the false discovery rate correction to these results. Sensitivity analysis revealed no significant pleiotropy or heterogeneity. Our study revealed both beneficial and detrimental causal relationships between diverse skin microbiota and inflammatory skin diseases. Additionally, the ecological niche of the skin microbiome was crucial to its functional impact. This research provided new insights into how skin microbiota impacted skin diseases and the development of therapeutic strategies. PMID:39400597 | DOI:10.1007/s00403-024-03433-y {url} = URL to article
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