Part of the way the Levy Library support the educational, research and patient care activities of the faculty, students and staff of the Mount Sinai Medical Centers is by providing access to high quality electronic biomedical information resources, such as eJournals like The Lancet, The New England Journal of Medicine and Nature.
In order to access library resources, our users must use the same network ID credentials they use to access resources that contain not only protected health information (i.e., EPIC), but also sensitive personal information (i.e., webmail, Sinai Central). It might be tempting to share network ID credentials with non-affiliated colleagues or friends, but these credentials with unauthorized users puts our relationships with service providers at risk and may result in access to resources being terminated. That means that one person violating our license terms could potentially create major repercussions for the rest of the health system. If a licensing agreement is violated, the publisher may remove the Mount Sinai community’s access to their journals and books. Publishers price access to their content by the number of users and usage. Sharing passwords increases usage costs beyond what the library can pay, resulting in subscription cuts and unfilled requests. Additionally, sharing network ID credentials with unauthorized users is a direct violation of Mount Sinai IT Policy (IT Policy # 7 for Password Usage) and may result in disciplinary action.
Remember, be smart – protect your login info!
By Barnaby Nicolas, MSIS
In our monthly “Article Spotlight” series, we’re showcasing achievements of Mount Sinai faculty and researchers using Altmetrics. This month, we’re looking at an article co-written by Dr. Miriam Mered, MD, PhD, Professor, Oncological Sciences and Professor, Medicine, Hematology and Medical Oncology at Icahn School of Medicine at Mount Sinai.
Citation: Naik S, Bouladoux N, Linehan JL, Han SJ, Harrison OJ, Merad M, et al. Commensal-dendritic-cell interaction specifies a unique protective skin immune signature. Nature. 2015;520(7545):104-8.
Article Summary: This study examine the nature of the antigen presenting cells involved in the dialogue between the immune system and skin commensals. The researchers find that defined skin commensal bacteria elicit a dermal dendritic-cell-dependent, long-lasting and commensal-specific CD8+ T-cell response, while preserving tissue homeostasis. The CD8+ T cells are shown to enhance innate protection against a fungal pathogen.
BACKGROUND: The skin represents the primary interface between the host and the environment. This organ is also home to trillions of microorganisms that play an important role in tissue homeostasis and local immunity. Skin microbial communities are highly diverse and can be remodelled over time or in response to environmental challenges. How, in the context of this complexity, individual commensal microorganisms may differentially modulate skin immunity and the consequences of these responses for tissue physiology remains unclear. Here we show that defined commensals dominantly affect skin immunity and identify the cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis induces IL-17A(+) CD8(+) T cells that home to the epidermis, enhance innate barrier immunity and limit pathogen invasion. Commensal-specific T-cell responses result from the coordinated action of skin-resident dendritic cell subsets and are not associated with inflammation, revealing that tissue-resident cells are poised to sense and respond to alterations in microbial communities. This interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.
URL to this article on PlumX
Dr. Merad’s profile