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,

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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

We analyzed the effects of sensitization of BALB/c mice to the OVA peptide amino acids 323-339, on the development of an IgE response, immediate cutaneous hypersensitivity and airways responsiveness (AR). Daily aerosolization of OVA 323-339 for 20 min over a period of 10 days was as effective in the stimulation of a serum anti-OVA IgE antibody response as sensitization to native OVA by the same route. After sensitization to native OVA, the majority of the IgE anti-OVA response was directed against peptide 323-339. The antibody responses were paralleled by skin test responses in sensitized mice: 73% of OVA-sensitized mice developed immediate type reactions when tested with native OVA and 82% of the mice had positive immediate skin test responses to intradermal injection of peptide 323-339. After sensitization to the peptide, 69% of the mice had positive responses to native OVA and 77% responded to peptide 323-339. Aerosolization of OVA as well as OVA 323-339 led to a comparable increase in airway responsiveness as measured by electrical field stimulation of tracheal smooth muscle preparations. To characterize T cell subpopulations that were stimulated after allergen sensitization, the distribution of specific V beta-expressing T cells was analyzed in local draining lymph nodes of the airways and the lungs. These lymph nodes were found to be enlarged after both OVA and OVA peptide sensitization. Sensitization to native OVA resulted in an increased percentage of V beta 8.1 and V beta 8.2 T cells whereas selective stimulation of V beta 8.1 T cells was found after peptide sensitization. These data indicate that OVA peptide 323-339 represents a T and B cell epitope of OVA, which is important in the generation and development of immediate hypersensitivity responses in BALB/c mice.

Comparison of the allergenicity of ovalbumin and ovalbumin peptide 323-339. Differential expansion of V beta-expressing T cell populations.

Parainfluenza pneumonia in severe combined immunodeficiency disease.

The low affinity receptor for IgE (CD23) is reported to regulate immune and inflammatory events and as a result, it may have a role in the development of allergic airway inflammation and hyperresponsiveness (AHR). To test this hypothesis CD23-deficient mice were studied following different modes of allergic sensitization. Mice were actively sensitized either intraperitoneally with ovalbumin (OA)/alum or via the airways (10 days exposure to OA aerosol with no adjuvant). Passive sensitization was performed by intravenous injections of OA-specific IgE. Airway responsiveness, serum IgE and IgG levels were assessed together with airway inflammation. Passive sensitization followed by airway challenges resulted in increased OA-specific IgG and IgE in the serum of wild-type mice only, while both the CD23+ / + and CD23− / − groups developed tracheal smooth muscle hyperresponsiveness to electrical field stimulation, indicating that IgE/CD23-mediated immune functions may not be necessary for the development of aller...

CD23 Deficient Mice Develop Allergic Airway Hyperresponsiveness Following Sensitization with Ovalbumin

Mast cells express the receptor tyrosine kinase kit/stem cell factor receptor (SCFR) which is encoded by the proto-oncogene c-kit. Ligation of SCFR induces its dimerization and activation of its intrinsic tyrosine kinase activity leading to activation of Raf-1, phospholipases, phosphatidylinositol 3-kinase, and extracellular signal-regulated kinases. However, little is known about the downstream signals initiated by SCFR ligation except for activation of extracellular signal-regulated kinases. The murine mast cell line, MC/9, synthesizes and secretes TNF-alpha following the aggregation of high affinity Fc receptors for IgE (Fc epsilonRI). Ligation of SCFR or Fc epsilonRI on MC/9 cells resulted in the activation of all three MAP kinase family members, extracellular signal-regulated kinases, c-Jun amino-terminal kinase (JNK), and p38. Stem cell factor (SCF)-induced activation of JNK and p38 was insensitive to wortmannin, cyclosporin A, and FK506 whereas activation of these kinases through Fc epsilonRI was sensitive to these drugs. Coligation of SCFR augmented Fc epsilonRI-mediated activation of MAP kinases, especially JNK activation, and SCF augmented Fc epsilonRI-mediated TNF-alpha production in MC/9 cells, although SCF alone did not induce TNF-alpha production. This augmentation by SCF was regulated at the level of transcription, at least in part, since the promoter activity of TNF-alpha was enhanced following addition of SCF. These results demonstrate that SCF can augment Fc epsilonRI-mediated JNK activation and cytokine gene transcription but via pathways that are regulated differently than the ones activated through Fc epsilonRI.

Stem cell factor augments Fc epsilon RI-mediated TNF-alpha production and stimulates MAP kinases via a different pathway in MC/9 mast cells.

In the last 30 years patients with antibody deficiency have benefited remarkably from regular replacement therapy with intramuscular immune serum globulin. In a proportion of patients this approach has not been successful in preventing sinopulmonary infections and progressive deterioration. The introduction of preparations of immune serum globulin suitable for intravenous administration provided the potential for examining the effects of achieving higher serum IgG levels. We have therefore evaluated and compared high vs low dose therapy in patients with hypogammaglobulinemia and sinopulmonary disease. To achieve minimum trough serum IgG levels of 500 mg/dl, we administered 0.6 g/kg every 4 weeks. High dose therapy proved efficacious in reducing symptoms, decreasing the frequency of major and minor infections and significantly improving pulmonary function. The improvement appeared to correlate with a marked reduction in the isolation of Mycoplasma, particularly Urea-plasma urealyticum, an important cause of infection in patients with hypogammaglobulinemia. High dose therapy with immune serum globulin suitable for intravenous administration appears to be the treatment of choice in patients with sinopulmonary disease.

Erwin W. Gelfand

Papers

Comparison of the allergenicity of ovalbumin and ovalbumin peptide 323-339. Differential expansion of V beta-expressing T cell populations.

Parainfluenza pneumonia in severe combined immunodeficiency disease.

CD23 Deficient Mice Develop Allergic Airway Hyperresponsiveness Following Sensitization with Ovalbumin

Stem cell factor augments Fc epsilon RI-mediated TNF-alpha production and stimulates MAP kinases via a different pathway in MC/9 mast cells.

Replacement therapy with high dose intravenous gamma-globulin improves chronic sinopulmonary disease in patients with hypogammaglobulinemia