• Journal of Industrial Convergence
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• v.21 no.2
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• pp.85-92
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• 2023

Abnormal spinal disease and function, in addition to simple musculoskeletal problems, can disrupt homeostasis and cause direct and indirect physiological side effects. Part or all of the immune function can be compromised, exposing you to more disease, especially if the nerves running through your spine do not deliver the proper signals to the organs that regulate your immune system. This study focuses on basic anatomic and physiological knowledge and seeks to consider potential mechanisms by which spinal function may potentially help maintain or improve immune function. To this end, we examine the roles of the spine in relation to hematopoiesis, stress, respiration, spine-nerve relationships, and the immune system, and confirm that these roles may influence immune function.

• Korean Journal of Poultry Science
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• v.6 no.1
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• pp.38-46
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• 1979

This study was directed to the Peizootics of Newcastle disease in Korea. Since 1960 New-castle disease epizootics have been observed at an interval of one or two years. The frequency of Newcastle disease outbreaks was related to the amount of the vaccine used, being the more sufficient vaccine produced the fewer outbreaks. Regional distribution of Newcastle disease outbreaks was most frequent in the capital area, being the center of poultry raising and Poultry product marketing, and infrequent in areas distant from the capital. Spreading of Newcastle disease appears to be mainly due to the movement of infected chickens. More than 60 percent of the total outbreaks of Newcastle disease diagnosed at the Veterinary Research Institute in Anyang were observed in young chickens aged less than 60 days. Improper vaccination, interference by maternally derived antibody with the immune response following vaccination, ana immaturity of immune systems of young chickens might have contributed to the results. This view was further supported by the findings that 23 percent of the total flocks experienced Newcastle disease were not vaccinated at all and, in vaccinated flocks, virtually all of the flocks were vaccinated by the drinking water method, which has been known less effective compared to individual application or spraying methods.

• The Journal of Pediatrics of Korean Medicine
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• v.16 no.2
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• pp.51-58
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• 2002

Crohn's disease is an indolent, chronic inflammatory bowel disease capable of involving the entire alimentary tract. The exact etiology and pathogenesis remain unknown despite a long and intensive research, but the finding of various abnormalities of the immune response in patients with Crohn's disease has led to the concepts that immune mechanism is involved in the pathogenesis of this disease. Recently, we have experienced a case of Crohn's disease. So the purpose of this study is to examine the efficacy of Oriental medicine for Crohn's disease.

• Journal of Chest Surgery
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• v.45 no.3
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• pp.199-201
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• 2012

Castleman's disease is a rare disorder characterized by benign tumors that may develop in the lymph node tissue throughout the body. Castleman's disease associated with myasthenia gravis is an especially rare disease. Only less than 10 cases have been reported in the world literature. The cause of Castleman's disease is associated with immune mediated reaction, and myasthenia gravis also develops due to an antibody-mediated process. The cause of myasthenia gravis is the immune activity of Castleman's disease, which may be the promoter of the antibody-mediated process. We report here a case of Castleman's disease, which was incidentally found in a patient diagnosed with myasthenia gravis.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.163-167
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• 2013

The dynamics of the virus-host interface in the response to respiratory virus infection is not well-understood; however, it is at this juncture that host immunity to infection evolves. Respiratory viruses have been shown to modulate the host response to gain a replication advantage through a variety of mechanisms. Viruses are parasites and must co-opt host genes for replication, and must interface with host cellular machinery to achieve an optimal balance between viral and cellular gene expression. Host cells have numerous strategies to resist infection, replication and virus spread, and only recently are we beginning to understand the network and pathways affected. The following is a short review article covering some of the studies associated with the Tripp laboratory that have addressed how respiratory syncytial virus (RSV) operates at the virus-host interface to affects immune outcome and disease pathogenesis.

• Clinical and Experimental Pediatrics
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• v.49 no.8
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• pp.830-832
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• 2006

Immune thrombocytopenic purpura(ITP) is an autoimmune disease characterized by increased peripheral platelet destruction due to antibody to platelet, which results in thrombocytopenia and cutaneous or mucosal bleeding. Bleeding generally occurs when platelet counts fall to less than $20,000/{\mu}L$. Children affected with ITP are usually healthy prior to the onset of the disease and typically present suddenly after a viral infection or insidiously with progressive petechiae, bruising, or purpura. In most cases the disease is self-limited; approximately 80% of children recover by 6 months after diagnosis, with or without treatment. Children with thrombocytopenia persisting for more than 6 months are defined as having chronic ITP. Clinical manifestations, diagnosis, laboratory findings, differential diagnosis and various treatment modalities are reviewed.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.8 no.2
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• pp.269-274
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• 2005

Esophageal candidiasis is an opportunistic infection, often reported in patients who have acquired immune deficiency syndrome (AIDS), a neoplastic disease, or undergoing protracted antibiotic therapy. Impaired cell mediated immunity was often considered as the major predisposing factor in patients of esophageal mucosal colonization of Candida spp. However, it is increasingly reported that the occurrence of esophageal candidiasis with no underlying disease or immune suppression. We have experienced a case of esophageal candidiasis in a 15-year-old girl who was immunologically normal and have no underlying disease and whose main symptoms were epigastric and retrosternal pain with dysphagia. This case suggests the possibilities of candidal infections in children without predisposing factors such as immune compromised conditions, so it will be needed to differentiate the esophageal candidiasis among healthy children with symptoms of odynophagia and dysphagia.

• Molecules and Cells
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• v.45 no.8
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• pp.513-521
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• 2022

Cytotoxic T lymphocyte antigen-4 (CTLA-4) is an immune checkpoint molecule that is mainly expressed on activated T cells and regulatory T (Treg) cells that inhibits T-cell activation and regulates immune homeostasis. Due to the crucial functions of CTLA-4 in T-cell biology, CTLA-4-targeted immunotherapies have been developed for autoimmune disease as well as cancers. CTLA-4 is known to compete with CD28 to interact with B7, but some studies have revealed that its downstream signaling is independent of its ligand interaction. As a signaling domain of CTLA-4, the tyrosine motif plays a role in inhibiting T-cell activation. Recently, the lysine motif has been shown to be required for the function of Treg cells, emphasizing the importance of CTLA-4 signaling. In this review, we summarize the current understanding of CTLA-4 biology and molecular signaling events and discuss strategies to target CTLA-4 signaling for immune modulation and disease therapy.

• Journal of Life Science
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• v.23 no.3
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• pp.448-461
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• 2013

Inflammatory bowel disease, known as Crohn's disease and ulcerative colitis, is an unexplained disease characterized by chronic inflammation that repeats a cycle of relapse, improvement, and complications. The cause of inflammatory bowel disease is not clearly known, but it is predicted that a complex of various factors precipitate its occurrence. In particular, inflammatory mediators, such as cytokine, induce an increase in cell-mediated inflammatory responses. Focal tissue damage then occurs in the intestinal mucosa because of the weakening of the immune-modulating functions of cotton. Immune and inflammatory responses do not decrease appropriately but continue until they lead to chronic inflammation. Current research has focused on the cytokine genes, which have important roles in these inflammatory responses. Cytokine is a glycoprotein that is produced mostly in activated immune cells. It connects the activation, multiplication, and differentiation between immune cells, which causes focal tissue damage and inflammatory response. Moreover, butyrate, which originates in dietary fiber and plays an important role in the structure and function of the intestinal area, shows control functions in the intestinal immune system by decreasing the proinflammatory cytokine and increasing the anti-inflammatory cytokine. Therefore, this research investigated the molecular mechanism of the anti-inflammatory effects of butyrate to comprehend the cytokine controlling abilities of butyrate in the immune cells. Butyrate is expected to have potential in new treatment strategies for inflammatory bowel disease.

• The Journal of Internal Korean Medicine
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• v.32 no.2
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• pp.203-216
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• 2011

Objectives : This study was conducted to evaluate the protective effects of bee venom on lipopolysaccharide (LPS)-induced chronic obstructive pulmonary disease (COPD). Methods : In this study, LPS was administrated to Balb/c mice to induce a disease that resembles COPD. 2 hr prior to LPS administration, mice were treated with bee venom via an intraperitoneal injection. Total cell number and neutrophils number in bronchoalveolar lavage fluid were counted and pro-inflammatory cytokines were also measured. For histologic analysis, periodic acid Schiff (PAS) and hematoxylin and eosin (H&E) stains were evaluated. Proliferating cell nuclear antigens (PCNA) were also assessed by immunohistochemistry. Results : On 7 days after LPS stimulation, influx of neutrophils significantly decreased in the bee venom group, compared with the COPD group. In addition, TNF-a and IL-6 levels decreased in bee venom group. Histological results also demonstrated the attenuation effect of bee venom on LPS-induced lung inflammation. Conclusions : These data suggest that bee venom has protective effects on LPS-induced lung inflammation. Therefore, bee venom may represent a novel therapeutic agent for lung inflammation and in particular for COPD.