다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

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It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced in the detection, management,

/pdf/acc-aha-2006-guidelines-for-the-management-of-patients-with-27qfh9fc7i.pdf

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

Interleukin-10 (IL-10), first recognized for its ability to inhibit activation and effector function of T cells, monocytes, and macrophages, is a multifunctional cytokine with diverse effects on most hemopoietic cell types. The principal routine function of IL-10 appears to be to limit and ultimately terminate inflammatory responses. In addition to these activities, IL-10 regulates growth and/or differentiation of B cells, NK cells, cytotoxic and helper T cells, mast cells, granulocytes, dendritic cells, keratinocytes, and endothelial cells. IL-10 plays a key role in differentiation and function of a newly appreciated type of T cell, the T regulatory cell, which may figure prominently in control of immune responses and tolerance in vivo. Uniquely among hemopoietic cytokines, IL-10 has closely related homologs in several virus genomes, which testify to its crucial role in regulating immune and inflammatory responses. This review highlights findings that have advanced our understanding of IL-10 and its receptor, as well as its in vivo function in health and disease.

Interleukin-10 and the interleukin-10 receptor.

Prospective Cohort Study

Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma

https://www.atsjournals.org/doi/pdf/10.1164/rccm.2204001

Mice Are a Good Model of Human Airway Disease

Background Eosinophils play a major role in allergic airway inflammation because of their ability to release toxic mediators. In addition, they are able to migrate toward draining thoracic lymph nodes (TLNs) after intratracheal administration, where they can function as antigen-presenting cells. Objective In this study, we evaluated in vivo eosinophil migration toward the TLN after allergen sensitization and analyzed expression of molecules involved in antigen presentation. Methods Mice were sensitized by intraperitoneal injection of ovalbumin on days 1 and 10 and challenged once intranasally with ovalbumin on day 20. The kinetics of eosinophilia was evaluated in blood, lung tissue homogenate, bronchoalveolar lavage fluid, and TLN. Cell surface staining was analyzed by flow cytometry. Results The kinetics of eosinophil recruitment was similar in TLN, lung tissue, and blood, beginning at 12 hours and peaking at 48 hours after allergen challenge. Approximately 70% of TLN eosinophils expressed MHC class II molecules, compared with less than 25% in blood and lungs. Moreover, TLN eosinophils expressed higher levels of MHC class II and CD86 compared with blood and lung eosinophils. Most eosinophils expressed CD80 and CD54, whereas only a few eosinophils expressed CD40. Eosinophils in lungs and TLN appeared to be activated with lower CD62-ligand expression compared with blood eosinophils. Conclusion The presence of eosinophils with a different phenotype in the TLN at early time points after allergen challenge of sensitized mice supports their capacity to serve as antigen-presenting cells, sustaining allergic/inflammatory responses in the airways.

https://www.jacionline.org/article/S0091-6749(04)02214-6/pdf

Migration and accumulation of eosinophils toward regional lymph nodes after airway allergen challenge.

We investigated the effects of rapamycin (RAP) on cell cycle progression and protein synthesis in mitogen-activated primary T lymphocytes. Stimulation of resting human T lymphocytes with phorbol ester and calcium ionophore rendered cells capable of initiating DNA synthesis within 30 h; roughly 60% of the cells entered the first G2/M phase of the cell cycle within 96 h. Addition of RAP delayed the entry into S phase by 9 h, although a similar percentage (approximately 50%) of cells entered the first G2/M phase and proliferated. On this basis, we concluded that RAP primarily induced a G1 prolongation without blocking cell cycle progression. Addition of the co-mitogens to resting T lymphocytes up-regulated the translation of ribosomal protein mRNA concurrent with activation of p70s6k. RAP inhibited this translational up-regulation of ribosomal protein mRNA as well as the activation of p70s6k without affecting translation of nonribosomal protein mRNA. RAP also prevented the synthesis and accumulation of ribosomal proteins. Further, this failure to increase ribosomal proteins, which probably reflects the failure to increase numbers of ribosomes, resulted in suppression of the synthesis of total cellular protein and a delay in the escalation of cell size. RAP-treated cells eventually initiated DNA synthesis when cell size became equivalent to that of the control cells entering S phase of the cell cycle. Thus, inhibition of protein synthesis caused by the primary inhibition of ribosomal protein mRNA translation probably explains the effect of RAP on cell cycle progression of mitogen-activated resting T lymphocytes.

Rapamycin inhibits ribosomal protein synthesis and induces G1 prolongation in mitogen-activated T lymphocytes.

Rationale: There is conflicting information about the development and resolution of airway inflammation and airway hyperresponsiveness (AHR) after repeated airway exposure to allergen in sensitized mice.Methods: Sensitized BALB/c and C57BL/6 mice were exposed to repeated allergen challenge on 3, 7, or 11 occasions. Airway function in response to inhaled methacholine was monitored; bronchoalveolar lavage fluid inflammatory cells were counted; and goblet cell metaplasia, peribronchial fibrosis, and smooth muscle hypertrophy were quantitated on tissue sections. Bone marrow–derived dendritic cells were generated after differentiation of bone marrow cells in the presence of growth factors.Results: Sensitization to ovalbumin (OVA) in alum, followed by three airway exposures to OVA, induced lung eosinophilia, goblet cell metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased levels of interleukin (IL)-4, IL-5, IL-13, granulocyte-macrophage colony–stimulating factor, trans...

/pdf/importance-of-myeloid-dendritic-cells-in-persistent-airway-2rfi0wggax.pdf

Importance of myeloid dendritic cells in persistent airway disease after repeated allergen exposure.

The role of T cells expressing specific V beta elements was examined in the regulation of allergen-specific immunoglobulin (Ig)E production and airways responsiveness (AR). In BALB/c mice, inhalation of the allergen ovalbumin (OVA) induced an IgE anti-OVA response, immediate cutaneous reactivity, and increased AR. These results were associated with an expansion of V beta 8.1/8.2 T cells in local draining lymph nodes of the airways and the lung. Transfer of V beta 8.1/8.2 T cells from sensitized mice stimulated an IgE anti-OVA response, immediate cutaneous hypersensitivity, and increased AR in naive syngeneic recipients. In contrast, OVA-reactive V beta 2 T cells inhibited these effects. These data demonstrate for the first time that T cells with different V beta specificities play a critical role in the in vivo regulation of allergen-specific IgE production and AR.

https://rupress.org/jem/article-pdf/177/4/1175/1103727/1175.pdf

Erwin W. Gelfand

Papers

Mice Are a Good Model of Human Airway Disease

Migration and accumulation of eosinophils toward regional lymph nodes after airway allergen challenge.

Rapamycin inhibits ribosomal protein synthesis and induces G1 prolongation in mitogen-activated T lymphocytes.

Importance of myeloid dendritic cells in persistent airway disease after repeated allergen exposure.

T cells expressing specific V beta elements regulate immunoglobulin E production and airways responsiveness in vivo.