• Asian-Australasian Journal of Animal Sciences
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• 제23권7호
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• pp.880-888
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• 2010

The ameliorative effect of salts and ascorbic acid polyphosphate supplementation on heat stress was studied in buffaloes. Adult buffaloes of either sex were randomly divided into 2 groups of 4 animals each. Group I served as control and Group II was supplemented with sodium bicarbonate, potassium carbonate and ascorbic acid polyphosphate. All the animals were exposed to two conditions of temperature and humidity: hot-dry and hot-humid in a psychrometric chamber for 4 h daily for 10 days. Blood was collected on day 1, 5 and 10 of treatment. The activities of catalase and superoxide dismutase (SOD), concentrations of serum glutathione (GSH), cortisol, sodium, potassium, and chloride and lipid peroxidation were estimated in serum. Lymphocyte proliferation was assessed in blood. The activities of catalase and SOD, serum concentration of GSH, sodium, potassium and chloride decreased while lipid peroxidation and serum cortisol increased in both groups when subjected to heat stress. Dietary supplementation resulted in further decreasing of the enzyme activities but increasing of the serum concentrations of GSH, sodium, potassium and chloride. Lipid peroxidation and serum cortisol increased in the supplemented group in both types of stress. Dietary supplementation caused an increase in lymphoproliferative response to con A. Thus, supplementation of ascorbate in addition to electrolytes relieves the animals of oxidative stress and boosts cell mediated immunity.

• Journal of Hospice and Palliative Care
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• 제8권1호
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• pp.52-56
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• 2005

Herpes zoster (HZ) is an acute infection of the unilateral sensory dermatome caused by varicella-zoster virus (VZV) and is characterized by vesicular eruption and unilateral pain along the involved dermatome. Although the pathogenesis of HZ is incompletely understood, it is thought that when cell-mediated immunity falls below a critical level, dormant VZV within cells of the sensory ganglia are allowed to replicate and infect the host with the resultant clinical presentation of HZ. It has been associated with immunosuppressed states, such as advanced age, leukemia, lymphoma, chemotherapy and/or radiation treatment. We present a case of a 62-year-old female patient with malignant lymphoma suffering herpes zoster ophthalmicus who did not respond to conventional treatment, and in whom the application of various nerve blocks and patient-controlled analgesia produced moderate pain relief. The patient died twenty days later due to cardiopulmonary failure.

• 정신신체의학
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• 제6권2호
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• pp.188-192
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• 1998

저자는 6년 동안 만성적으로 양손에 사마귀가 재발한 20세 남자 환자를 5회의 단기 최면치료를 통해 성공적으로 치료하였기에 문헌고찰과 함께 보고하였다. 증례의 사마귀는 7개월이 지난 추적때까지 재발하지 않았다. 화학요법이나 전기소작 등과 같은 일반적인 치료법에 만족스런 반용이 없거나, 이완을 통해 긴장을 완화하고 자아를 강화하여 증상 통제를 할 필요가 있는 경우 자기최면 연습을 포함한 최면치료가 적용될 수 있다. 또한 papova 바이러스에 의한 피부질환에 세포면역의 역할과 더불어 정신과 신체의 상호 연관을 연구하는 피부의 정신면역학 분야에 사마귀의 최면치료가 시사하는 바를 논의하였다.

• 약학회지
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• 제33권1호
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• pp.20-29
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• 1989

The humoral immune response of Eicosapentanoic acid(EPA) was investigated in mice. ICR male mice were divided into 8 groups and received intraperitoneal injection of EPA(5 mg, 10 mg, 20 mg/kg) for 4 weeks. Cyclophosphamide(5 mg/kg) was administered i.p. 2 days prior to secondary immunization. Humoral immune response was evaluated by antibody titer, hypersensitivity to SRBC (Arthus), plaque forming cell(PFC) and organ weight. The ontanined results were as followings: The increased rate of body weight, the ratio of liver weight, spleen weight to body weight were decreased by all EPA administration groups as compared to normal group. HA titer, HY titer and Arthus reaction were enhanced according to the increase of EPA doses as compared to normal group. PFC was significantly enhanced by EPA 10 mg administration group. These results suggest that EPA enhances humoral immune response to SRBC in mice, indicating that EPA may block a immunoglobulin synthesis inhibition of arachidonic acid.

• The Plant Pathology Journal
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• 제32권3호
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• pp.266-272
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• 2016

A bacterial tyrosine sulfotransferase, RaxST, is required for activation of rice XA21-mediated immunity, and it catalyzes sulfation of tyrosine residues of Omp1X and RaxX in Xanthomonas oryzae pv. oryzae, a causal agent of bacterial blight in rice. Although RaxST is biochemically well-characterized, biological functions of tyrosine sulfation have not been fully elucidated. We compared protein expression patterns between the wildtype and a raxST knockout mutant using shotgun proteomic analysis. Forty nine proteins displayed a more than 1.5-fold difference in their expression between the wildtype and the mutant strains. Clusters of orthologous groups analysis revealed that proteins involved in cell motility were most abundant, and phenotypic observation also showed that the twitching motility of the mutant was dramatically changed. These results indicate that tyrosine sulfation by RaxST is essential for Xoo movement, and they provide new insights into the biological roles of RaxST in cellular processes.

• 한국작물학회:학술대회논문집
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• 한국작물학회 2017년도 9th Asian Crop Science Association conference
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• pp.164-164
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• 2017

High throughput transcriptome investigations of immunity in plants highlight the complexity of gene networks leading to incompatible interaction. To identify genes crucial to resistance against Xanthomonas oryzae pv oryzae, functional genetic analysis of selected differentially expressed genes from our microarray data set was carried out. A total of 13 overexpression vector constructs were made using 35S CaMV promoter which drive constitutive expression in rice. Most of the genes are developmentally expressed especially during maximum tillering stage and are commonly highly expressed in the leaves. When screened against Xoo strain K2, the transgenic plants displayed shorter lesion length compared with wild type Dongjin which indicates partial resistance. The levels of ROS continuously magnified after inoculation which indicates robust cellular sensing necessary to initiate cell death. Elevated transcripts levels of several defense-related genes at the downstream of defense signal network also corroborate the phenotype reaction of the transgenic plants. Moreover, expression assays revealed regulation of these genes by cross-communicating signal-transductions pathways mediated by salicylic and jasmonic acid. These collective findings revealed the key immune signaling conduits critical to mount full defense against Xoo.

• 한국임상수의학회지
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• 제20권1호
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• pp.79-85
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• 2003

Dietary conjugated linoleic acid(CLA) has been shown to affect immune function. Thus, the objective of this study was to investigate the effects of CLA on the mice that treated prednisone. Mice were randomized into 6 groups and fed diet containing either 0(control, P), 0.5%(CLA1, CP1) or 1.5%(CLA2, CP2) CLA for Sweets. Before 1 week of finishing diet supplement CP1, CP2, and P group treated the prednisone by subcutaneous injection. The levels of serum immunoglobulin A, G, E, gut lumen s-IgA, MLN immunoglobulin A, body weight, mucosal protein was compared. The level of serum IgA in CLA1, CLA2, CP1, and CP2 group increased, while which of P group was decreased. The level of serum IgG in CLA 1 group increased, while which of the other group no differences. Serum IgE level showed no difference and the immunoglobulin production in MLN lymphocyte in CLA 1 group increased. The level of gut lumen s-IgA in P group showed decreased, while which of the other group showed no differences. These results support the view that CLA supplement partially enhance the cell-mediated immunity and overcome the immunosuppressive effect of prednisone.

• BMB Reports
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• 제50권7호
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• pp.345-354
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• 2017

Autophagy, a catabolic process necessary for the maintenance of intracellular homeostasis, has recently been the focus of numerous human diseases and conditions, such as aging, cancer, development, immunity, longevity, and neurodegeneration. However, the continued presence of autophagy is essential for cell survival and dysfunctional autophagy is thought to speed up the progression of neurodegeneration. The actual molecular mechanism behind the progression of dysfunctional autophagy is not yet fully understood. Emerging evidence suggests that basal autophagy is necessary for the removal of misfolded, aggregated proteins and damaged cellular organelles through lysosomal mediated degradation. Physiologically, neurodegenerative disorders are related to the accumulation of amyloid ${\beta}$ peptide and ${\alpha}-synuclein$ protein aggregation, as seen in patients with Alzheimer's disease and Parkinson's disease, respectively. Even though autophagy could impact several facets of human biology and disease, it generally functions as a clearance for toxic proteins in the brain, which contributes novel insight into the pathophysiological understanding of neurodegenerative disorders. In particular, several studies demonstrate that natural compounds or small molecule autophagy enhancer stimuli are essential in the clearance of amyloid ${\beta}$ and ${\alpha}-synuclein$ deposits. Therefore, this review briefly deliberates on the recent implications of autophagy in neurodegenerative disorder control, and emphasizes the opportunities and potential therapeutic application of applied autophagy.

• 대한기관식도과학회지
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• 제11권1호
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• pp.37-41
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• 2005

Deep neck infections mean infection in the potential spaces and facial planes of the neck, either abscess formation or cellulitis. Deep neck infections are caused by dental, salivary gland, pharyngeal and tonsillar infections. Sometimes, deep neck infection may be caused by tuberculosis in case of immunodefiecient patients. Acquired immunodeficiency syndrome(AIDS) is a disease associated with defective cell-mediated immunity after infected with human immunodeficiency virus(HIV). The chance of opportunistic infection in patients of AIDS increases as the level of immunodeficienty progresses. Human immunodeficiency virus infection is the most single significant risk factor for progression of pulmonary tuberculosis to extrapulmonary sites. In patients infected with HIV, the rate of extrapulomonary tuberculosis rises upto $60\%$. We report a case of a 47 year old male patient with AIDS associated with deep neck infection by tuberculosis.

• BMB Reports
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• 제55권10호
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• pp.473-480
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• 2022

Neutrophils, the most abundant innate immune cells, play essential roles in the innate immune system. As key innate immune cells, neutrophils detect intrusion of pathogens and initiate immune cascades with their functions; swarming (arresting), cytokine production, degranulation, phagocytosis, and projection of neutrophil extracellular trap. Because of their short lifespan and consumption during immune response, neutrophils need to be generated consistently, and generation of newborn neutrophils (granulopoiesis) should fulfill the environmental/systemic demands for training in cases of infection. Accumulating evidence suggests that neutrophils also play important roles in the regulation of adaptive immunity. Neutrophil-mediated immune responses end with apoptosis of the cells, and proper phagocytosis of the apoptotic body (efferocytosis) is crucial for initial and post resolution by producing tolerogenic innate/adaptive immune cells. However, inflammatory cues can impair these cascades, resulting in systemic immune activation; necrotic/pyroptotic neutrophil bodies can aggravate the excessive inflammation, increasing inflammatory macrophage and dendritic cell activation and subsequent T_H1/T_H17 responses contributing to the regulation of the pathogenesis of autoimmune disease. In this review, we briefly introduce recent studies of neutrophil function as players of immune response.