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Anorexia Nervosa and Osteoporosis: Pathophysiology and Treatment
Jeremy Steinman,Amal Shibli-Rahhal 대한골대사학회 2019 대한골대사학회지 Vol.26 No.3
Anorexia nervosa (AN) affects 2.9 million people, many of whom experience bone loss and increased fracture risk. In this article, we review data on the underlying pathophysiology of AN-related osteoporosis and possible approaches to disease management. Available research suggests that low body weight and decreased gonadal function are the strongest predictors of bone loss and fractures in patients with AN. Additionally, other metabolic disturbances have been linked to bone loss, including growth hormone resistance, low leptin concentrations, and hypercortisolemia, but those correlations are less consistent and lack evidence of causality. In terms of treatment of AN-related bone disease, weight gain has the most robust impact on bone mineral density (BMD). Restoration of gonadal function seems to augment this effect and may independently improve BMD. Bisphosphonates, insulin-like growth factor 1 supplementation, and teriparatide may also be reasonable considerations, however need long-term efficacy and safety data.
경동맥 혈류유동에서의 혈액의 비뉴우토니안 특성의 상대적 중요성 해석
이상욱(S.W. Lee),D.A. Steinman 한국전산유체공학회 2008 한국전산유체공학회 학술대회논문집 Vol.2008 No.-
In this study, we attempted to quantify the relative importance of assumptions regarding blood rheology. Three patient-specific carotid bifurcation geometries and time-varying flow rates were obtained using magnetic resonance imaging. For each subject, CFD simulations were carried out assuming two different non-Newtonian rheology models (Carreau and Ballyk models) and rescaled Newtonian viscosities based on characteristic shear rates to account for the shear-thinning property of blood. The sensitivity of WSS and oscillatory shear index (OSI) were contextualized with respect to the reproducibility of the reconstructed geometry and to assumptions regarding the inlet boundary conditions. We conclude that the assumption of Newtonian fluid is reasonable for studies aimed at quantifying the distribution of WSS-based extrema in an image-based CFD model of carotid bifurcation.
Do, Yoonkyung,Koh, Hyein,Park, Chae Gyu,Dudziak, Diana,Seo, Patrick,Mehandru, S.,Choi, Jae-Hoon,Cheong, Cheolho,Park, Steven,Perlin, David S.,Powell, Bradford S.,Steinman, Ralph M. WILEY-VCH Verlag 2010 European journal of immunology Vol.40 No.10
<P>To help design needed new vaccines for pneumonic plague, we targeted the Yersinia pestis LcrV protein directly to CD8α<SUP>+</SUP> DEC-205<SUP>+</SUP> or CD8α<SUP>−</SUP> DCIR2<SUP>+</SUP> DC along with a clinically feasible adjuvant, poly IC. By studying Y. pestis in mice, we could evaluate the capacity of this targeting approach to protect against a human pathogen. The DEC-targeted LcrV induced polarized Th1 immunity, whereas DCIR2-targeted LcrV induced fewer CD4<SUP>+</SUP> T cells secreting IFN-γ, but higher IL-4, IL-5, IL-10, and IL-13 production. DCIR-2 targeting elicited higher anti-LcrV Ab titers than DEC targeting, which were comparable to a protein vaccine given in alhydrogel adjuvant, but the latter did not induce detectable T-cell immunity. When DEC- and DCIR2-targeted and F1-V+ alhydrogel-vaccinated mice were challenged 6 wk after vaccination with the virulent CO92 Y. pestis, the protection level and Ab titers induced by DCIR2 targeting were similar to those induced by F1-V protein with alhydrogel vaccination. Therefore, LcrV targeting to DC elicits combined humoral and cellular immunity, and for the first time with this approach, also induces protection in a mouse model for a human pathogen.</P>
Siddharta, Anindya,Pfaender, Stephanie,Vielle, Nathalie Jane,Dijkman, Ronald,Friesland, Martina,Becker, Britta,Yang, Jaewon,Engelmann, Michael,Todt, Daniel,Windisch, Marc P.,Brill, Florian H.,Steinman Oxford University Press 2017 The Journal of Infectious Diseases Vol.215 No.6
<P><B>Abstract</B></P><P>The World Health Organization (WHO) published 2 alcohol-based formulations to be used in healthcare settings and for outbreak-associated infections, but inactivation efficacies of these products have not been determined against (re-)emerging viruses. In this study, we evaluated the virucidal activity of these WHO products in a comparative analysis. Zika virus (ZIKV), Ebola virus (EBOV), severe acute respiratory syndrome coronavirus (SARS-CoV), and Middle East respiratory syndrome coronavirus (MERS-CoV) as (re-)emerging viral pathogens and other enveloped viruses could be efficiently inactivated by both WHO formulations, implicating their use in healthcare systems and viral outbreak situations.</P>
Flt3 Signaling-Dependent Dendritic Cells Protect against Atherosclerosis
Choi, J.H.,Cheong, C.,Dandamudi, Durga B.,Park, C.,Rodriguez, A.,Mehandru, S.,Velinzon, K.,Jung, I.H.,Yoo, J.Y.,Oh, G.,Steinman, Ralph M. Cell Press 2011 Immunity Vol.35 No.5
Early events in atherosclerosis occur in the aortic intima and involve monocytes that become macrophages. We looked for these cells in the steady state adult mouse aorta, and surprisingly, we found a dominance of dendritic cells (DCs) in the intima. In contrast to aortic adventitial macrophages, CD11c<SUP>+</SUP>MHC II<SUP>hi</SUP> DCs were poorly phagocytic but were immune stimulatory. DCs were of two types primarily: classical Flt3-Flt3L signaling-dependent, CD103<SUP>+</SUP>CD11b<SUP>-</SUP> DCs and macrophage-colony stimulating factor (M-CSF)-dependent, CD14<SUP>+</SUP>CD11b<SUP>+</SUP>DC-SIGN<SUP>+</SUP> monocyte-derived DCs. Both types expanded during atherosclerosis. By crossing Flt3<SUP>-/-</SUP> to Ldlr<SUP>-/-</SUP> atherosclerosis-prone mice, we developed a selective and marked deficiency of classical CD103<SUP>+</SUP> aortic DCs, and they were associated with exacerbated atherosclerosis without alterations in blood lipids. Concomitantly, the Flt3<SUP>-/-</SUP>Ldlr<SUP>-/-</SUP> mice had fewer Foxp3<SUP>+</SUP> Treg cells and increased inflammatory cytokine mRNAs in the aorta. Therefore, functional DCs are dominant in normal aortic intima and, in contrast to macrophages, CD103<SUP>+</SUP> classical DCs are associated with atherosclerosis protection.
Lung dendritic cells induce migration of protective T cells to the gastrointestinal tract
Ruane, Darren,Brane, Lucas,Reis, Bernardo Sgarbi,Cheong, Cheolho,Poles, Jordan,Do, Yoonkyung,Zhu, Hongfa,Velinzon, Klara,Choi, Jae-Hoon,Studt, Natalie,Mayer, Lloyd,Lavelle, Ed C.,Steinman, Ralph M.,Mu The Rockefeller University Press 2013 The Journal of experimental medicine Vol.210 No.9
<P>Developing efficacious vaccines against enteric diseases is a global challenge that requires a better understanding of cellular recruitment dynamics at the mucosal surfaces. The current paradigm of T cell homing to the gastrointestinal (GI) tract involves the induction of α4β7 and CCR9 by Peyer’s patch and mesenteric lymph node (MLN) dendritic cells (DCs) in a retinoic acid–dependent manner. This paradigm, however, cannot be reconciled with reports of GI T cell responses after intranasal (i.n.) delivery of antigens that do not directly target the GI lymphoid tissue. To explore alternative pathways of cellular migration, we have investigated the ability of DCs from mucosal and nonmucosal tissues to recruit lymphocytes to the GI tract. Unexpectedly, we found that lung DCs, like CD103<SUP>+</SUP> MLN DCs, up-regulate the gut-homing integrin α4β7 in vitro and in vivo, and induce T cell migration to the GI tract in vivo. Consistent with a role for this pathway in generating mucosal immune responses, lung DC targeting by i.n. immunization induced protective immunity against enteric challenge with a highly pathogenic strain of <I>Salmonella</I>. The present report demonstrates novel functional evidence of mucosal cross talk mediated by DCs, which has the potential to inform the design of novel vaccines against mucosal pathogens.</P>