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  • Corporate Membership is open to the public and rosaceans are welcome

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    1. RRDi members (including guests) must be polite and respectful to fellow members taking into consideration the individual fellow member's religious, ethical, and cultural values, as well as age, race and sex. The institute determines what is polite and respectful and may or may not give warnings for violating this rule. Removal from the membership is possible for violating this rule. It is a privilege to be a member of the RRDi and not a right.

    2. To be a legal corporate voting member a name, mailing address, two email addresses, and a statement of whether the member is a rosacean or not a rosacean is required. Non voting members are only required to provide an email address.

    3. Members (including guests) may not profit from the institute; however, any Medical Advisory Consultants (or Committee) member or any other member may be compensated for services rendered to the institute.

    4. Members (including guests) who sell items or services for rosacea may comment on a treatment, product, book or service sold by the member when another member asks for information. However, the institute may at any time stop the discussion, delete the posts or ban the member at the sole discretion of the institute. Warnings may or may not be given to the member by the institute. Profiting from contacts of fellow members through the institute is not the purpose of this non profit institute. However, information is acceptable to post when asked and appropriate comments are allowed subject to the approval by the institute. The RRDi determines if the post is appropriate or not and you agree to this decision.

    5. Members should state if they have a diagnosis of rosacea from a physician and failure to discuss this may be grounds for dismissal as a member. The institute needs to know which voting members are rosaceans to determine the percentage of voting members who have a diagnosis of rosacea from a physician and which voting members are not rosacea sufferers. Non voting members are also required to state if they have a diagnosis of rosacea if another member inquires.  

    6. Privacy is of concern to the institute. Names, mailing and email addresses are not given out to the public or to fellow members by the institute. Your public profile is available to anyone to view but only shows your location, country, and whether you are a rosacean if you put data into these public profile boxes. Your personal profile like first and last name, etc., is never shown to the public and only RRDi staff members can view your personal profile. You agree to allow your public profile to be shown. Members should not release names, mailing or email addresses of fellow members if you are aware of the personal contact information of a fellow member without the consent of the fellow member. A Privacy Policy is available for the public. Members who donate to the institute will be listed with their name and the amount unless the donor requests anonymity. If you want to remain anonymous please let the institute know when you donate otherwise your name will be posted without any address, phone, or email address.

    7. Members (including guests) will adhere, agree to and obey the Guidelines, Charter, Articles of Incorporation, the Bylaws, the Conflict of Interest Policy and these Rules of the Institute. Violation of any of these rules may be grounds for being removed as a corporate voting member or non voting member. You may view these documents by request or check the site index.

    8. A 'rosacean' is a rosacea sufferer. 'Institute' refers to the RRDi. RRDi refers to the Rosacea Research & Development Institute. You accept these terms.

    9. Guests are NOT allowed to post for free since the end of June 2022 in the Guest Forum and are required to donate for a subscription and certain areas of the website open to guests for free and guests are never allowed to post. All these rules apply to registered members and guests who are not registering an email (or account) and post in our Guest Forum or member areas of our website. To remain as an active member requires a donation with a subscription of at least a minimum of $2/month donation (or $1/month for three or more months subscription). After thirty days a subscribed registered member becomes an inactive member who has stopped donating for a subscription or has not posted in the last thirty days (whichever comes first) and has the same access to our website as a guest who is not allowed in the member areas of our website. An inactive member may be an active member by simply logging into their registered account and subscribing for a minimum of $2/month donation (or $1/month for three or more months subscription). Subscribers may opt for a discounted ($1/month) three, six, twelve, hundred twenty month or a lifetime donation subscription plan. Volunteers may request a waived subscription.

       10.  The Rules of the Institute may be changed at any time at the sole discretion of the institute. 

     

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    • Redox Biol. 2022 Aug 5;55:102427. doi: 10.1016/j.redox.2022.102427. Online ahead of print. ABSTRACT Reactive oxygen species (ROS)-activated proinflammatory signals in keratinocytes play a crucial role in the immunoregulation of inflammatory skin diseases, including rosacea and psoriasis. Nav1.8 is a voltage-gated sodium ion channel, and its abnormal expression in the epidermal layer contributes to pain hypersensitivity in the skin. However, whether and how epidermal Nav1.8 is involved in skin immunoregulation remains unclear. This study was performed to identify the therapeutic role of Nav1.8 in inflammatory skin disorders. We found that Nav1.8 expression was significantly upregulated in the epidermis of rosacea and psoriasis skin lesions. Nav1.8 knockdown ameliorated skin inflammation in LL37-and imiquimod-induced inflammation mouse models. Transcriptome sequencing results indicated that Nav1.8 regulated the expression of pro-inflammatory mediators (IL1β and IL6) in keratinocytes, thereby contributing to immune infiltration in inflammatory skin disorders. In vitro, tumor necrosis factor alpha (TNFα), a cytokine that drives the development of various inflammatory skin disorders, increased Nav1.8 expression in keratinocytes. Knockdown of Nav1.8 eliminated excess ROS production, thereby attenuating the TNFα-induced production of inflammatory mediators; however, a Nav1.8 blocker did not have the same effect. Mechanistically, Nav1.8 reduced superoxide dismutase 2 (SOD2) activity by directly binding to SOD2 to prevent its deacetylation and mitochondrial localization, subsequently inducing ROS accumulation. Collectively, our study describes a central role for Nav1.8 in regulating pro-inflammatory responses in the skin and indicates a novel therapeutic strategy for rosacea and psoriasis. PMID:35952475 | DOI:10.1016/j.redox.2022.102427 {url} = URL to article
    • Ann Dermatol. 2022 Aug;34(4):261-269. doi: 10.5021/ad.21.223. ABSTRACT BACKGROUND: Rosacea is a chronic inflammatory skin disease with a pathophysiological mechanism that remains unclear. Recently, dysregulation of the sensory nerve system has been implicated in the development of this condition. OBJECTIVE: This study aimed to investigate the effect of capsaicin on neuroinflammatory mediators in rosacea. In addition, this study aimed to evaluate the attenuating effects of capsazepine, a transient receptor potential vanilloid type 1 (TRPV1) antagonist. METHODS: We obtained skin tissue from both rosacea patients and normal individuals for an in vivo study. In addition, normal human epidermal keratinocytes (NHEKs) were cultured, and treated with capsaicin and capsazepine for an in vitro study. Quantitative changes in neuroinflammatory mediators were evaluated by semi-quantitative reverse transcription-polymerase chain reaction (PCR), real-time PCR, enzyme-linked immunosorbent assay, and immunofluorescence staining. RESULTS: The data showed the increase of TRPV1, TRPV4, cathelicidin (LL37) and tumor necrosis factor-α (TNF-α) in skin tissue by real-time PCR. In addition, the data showed that cathelicidin (LL37), kallikrein-5 (KLK-5), TNF-α, vascular endothelial growth factor (VEGF), interleukin (IL)-1α, IL-1β, IL-8, and protease-activated receptor 2 (PAR2) increased in capsaicin-treated NHEKs. Capsazepine attenuated the expression of TRPV1 and other mediators, except for IL-8, in capsaicin-treated NHEKs. CONCLUSION: We confirmed that TRPV1, TRPV4, cathelicidin (LL37) and TNF-α are increased in rosacea skin, and that capsaicin is associated with increase of neuroinflammatory mediators such as LL37, KLK-5, TNF-α, VEGF, IL-1α, IL-1β, IL-8, and PAR2. Modulators or inhibitors of neuroinflammatory mediators including TRPV1 could be potential therapeutic option in the treatment of patients with rosacea. PMID:35948328 | DOI:10.5021/ad.21.223 {url} = URL to article If you want to deep dive into this subject it is related to the Immune System Disorder Theory which one of many theories on the cause of rosacea. Find more information here (requires subscription😞 https://irosacea.org/forums/forum/67-immune-system-disorder-theory/
    • J Clin Aesthet Dermatol. 2022 Jul;15(7):E60-E62. ABSTRACT Rosacea is a chronic disease requiring long-term management. However, it is often treated according to package label instructions, which reflect the conditions of a Phase III study rather than a chronic disease. Furthermore, due to a lack of clinical data or guidelines on long-term treatment, many clinicians choose to discontinue treatment once success has been reached, rather than continuing with maintenance therapy. As experienced practicing dermatologists and investigators in the field, in this article we address the current evidence gaps in rosacea management and provide practical advice to clinicians on how optimal outcomes can be achieved and maintained in patients with rosacea in real-world practice, based on our own experience and the available clinical data. PMID:35942011 | PMC:PMC9345196 {url} = URL to article
    • Clin Cosmet Investig Dermatol. 2022 Aug 1;15:1465-1473. doi: 10.2147/CCID.S373534. eCollection 2022. ABSTRACT INTRODUCTION: Rosacea is a common chronic inflammatory disease occurring on the face, whose diagnosis is mainly based on symptoms and physical signs. Due to some overlap in symptoms and signs with other inflammatory skin diseases, young and inexperienced doctors often make misdiagnoses and missed diagnoses in clinical practices. We analyze the results of skin physiology and dermatoscopy using machine learning method and identify the characteristics of acne rosacea, which differentiate it from other common facial inflammatory skin diseases so as to improve the accuracy of clinical and differential diagnosis of rosacea. METHODS: A total of 495 patients who were jointly diagnosed by two experienced doctors were included. Basic data, clinical symptoms, physiological skin detection, and dermatoscopy results were collected, and the clinical characteristics of rosacea and other common facial inflammatory diseases were summarized according to the descriptive analysis results. The model was established using a machine learning method and compared with the judgment results of young and inexperienced doctors to verify whether the model can improve the accuracy of clinical diagnosis and differential diagnosis of rosacea. RESULTS: The proportion of yellow and red halos, vascular polygons, as well as follicular pustules, showed by dermatoscopy, and the melanin index in physiological skin detection revealed statistical significance in differentiating rosacea and other common facial inflammatory diseases (all P < 0.01). After adopting the machine learning, we found that GBM (Gradient Boosting Machine) algorithm was the best, and the error rate of this model in the validation set was 5.48%. In the final man-machine comparison, the accuracy of the GBM algorithm model for the classification of skin disease was significantly higher than that of young and inexperienced doctors. CONCLUSION: Dermatoscopy combined with machine learning can effectively improve the diagnosis and differential diagnosis accuracy of rosacea and other facial inflammatory skin diseases. PMID:35935599 | PMC:PMC9354760 | DOI:10.2147/CCID.S373534 {url} = URL to article
    • Pharmacol Ther. 2022 Aug 4:108259. doi: 10.1016/j.pharmthera.2022.108259. Online ahead of print. ABSTRACT Mas-related G protein-coupled receptors (GPCRs) of subfamily X, designated MRGPRX, are primate-specific orphan receptors that belong to the δ-branch of rhodopsin-like, class A GPCRs. Four distinct subtypes exist, MRGPRX1, -2, -3, and -4, MRGPRX2 having the lowest degree of similarity with the others. Due to their expression on sensory neurons and immune cells, and their roles in pain perception and transmission, itch, inflammation, immune defense, pseudo-allergic reactions, wound healing, and possibly cancer, they have recently attracted much attention as novel drug targets. In particular MRGPRX2 was identified as an important mast cell receptor responsible for anaphylactoid drug reactions, and involved in skin and mucosal diseases, e.g. urticaria, atopic dermatitis, rosacea, and allergic rhinitis. A major hurdle has been the lack of animal models for studying these primate-specific receptors. However, recently humanized mice have been created. Moreover, a mouse ortholog of MRGPRX2, MRGPRB2, was identified, both receptors having a certain degree of similarity. MRGPRX1 and -2 can be activated by various peptides and small (partly peptidomimetic) molecules. MRGPRX2 is additionally activated by a very broad range of basic molecules, positively charged at physiologic pH value of 7.4, including many drugs. MRGPRX4 is activated by small acidic molecules including bile acids. For MRGPRX3, no ligands have been reported yet. Antagonists with reasonable potency and selectivity have been described for MRGPRX1, and few antagonists also for MRGPRX2, but not for the other subtypes. The recent elucidation of cryogenic electron microscopy structures of MRGPRX2 and -4 is expected to facilitate and advance drug development for these receptors. Currently, research on MRGPRX is still in its infancy, and exciting discoveries can be awaited. These receptors have great potential as future drug targets. PMID:35934214 | DOI:10.1016/j.pharmthera.2022.108259 {url} = URL to article
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