• Sleep Medicine and Psychophysiology
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• v.12 no.2
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• pp.105-110
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• 2005

The pathogenesis and mechanism of obstructive sleep apnea (OSA) has been under investigation for over 25 years, but its etiology and mechanism remains elusive. Skeletal (maxillary and/or mandibular hypoplasia or retrodisplacement, inferior displacement of hyoid) and soft tissue (increased volume of soft tissue, adenotonsillar hypertrophy, macroglossia, thickened lateral pharyngeal walls) factors, pharyngeal compliance (increased), pharyngeal muscle factors (impaired strength and endurance of pharyngeal dilators and fixators), sensory factors (impaired mechanoreceptor sensitivity, impaired pharyngeal dilator reflexes), respiratory control system factors (unstable respiratory control) and so on facilitate collapse upper airway. Therefore, OSA may be a heterogeneous disorder, rather than a single disease entity and various pathogenic factors contribute to the OSA varies person to person. As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

• Food Science of Animal Resources
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• v.30 no.4
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• pp.568-574
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• 2010

This study introduced a chick embryos’ infection model to elucidate the pathogenesis mechanism of Pseudomonas aeruginosa, which causes serious diseases in human after ingestion of P. aeruginosa-contaminated animal originated foods. The embryonic chick model is able to give a rapid and relatively inexpensive method to assess bacterial pathogenicity compared to embryos of other vertebrates. Embryos were infected with P. aeruginosa and elastase-deficient P. aeruginosa. After infection with P. aeruginosa cells, total bacterial cell numbers and gelatinase activities in the embryos were compared. Thereafter, precartilage condensation and chondrogenesis were assessed by peanut agglutinin (PNA) binding on day 3 and by Alcian blue staining for sulfated proteoglycans on day 5, respectively. P. aeruginosa significantly increased in embryos, resulting in abnormal limb development, whereas P. aeruginosa defective in elastase activity partly impaired proliferation. In addition, P. aeruginosa-infected chick embryos significantly stimulated the production of matrix metalloproteinases. Several analyses showed that elevated proteases suppressed the proliferation and survival of chondrogenic cells. The results show that this infection model was a useful assay to determine the virulence mechanism of P. aeruginosa in human after intake of microbiologically contaminated foods.

• Journal of Microbiology and Biotechnology
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• v.32 no.9
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• pp.1073-1085
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• 2022

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has continued for over 2 years, following the outbreak of coronavirus-19 (COVID-19) in 2019. It has resulted in enormous casualties and severe economic crises. The rapid development of vaccines and therapeutics against SARS-CoV-2 has helped slow the spread. In the meantime, various mutations in the SARS-CoV-2 have emerged to evade current vaccines and therapeutics. A better understanding of SARS-CoV-2 pathogenesis is a prerequisite for developing efficient, advanced vaccines and therapeutics. Since the outbreak of COVID-19, a tremendous amount of research has been conducted to unveil SARS-CoV-2 pathogenesis, from clinical observations to biochemical analysis at the molecular level upon viral infection. In this review, we discuss the molecular mechanisms of SARS-CoV-2 propagation and pathogenesis, with an update on recent advances.

• IMMUNE NETWORK
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• v.2 no.4
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• pp.189-194
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• 2002

Although the exact mechanism responsible for the pathogenesis of psoriasis is unclear, interferon-${\gamma}$ producing type 1 T cells have been reported to play a significant role. Infiltrating activated type 1 T cells in the lesions are believed to be responsible for stimulating keratinocytes, which produce many cytokines and growth factors. The hyperproliferative epidermis is understood to be the result of either the cytokines produced by the intraepidermal T cells or the reactive phenomenon after keratinocyte damage. The microenvironment in psoriatic lesions deviates toward the type 1 status, because of the increased type 1 cytokines and either the decreased or unchanged type 2 cytokines observed in psoriatic lesions. Therefore, this review focused on a T-cell-mediated immunological basis for the current hypothesis of the psoriasis pathogenesis.

• Journal of Genetic Medicine
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• v.12 no.1
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• pp.1-5
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• 2015

De novo variants (DNVs) can arise during parental germ cell formation, fertilization, and the processes of embryogenesis. It is estimated that each individual carries 60-100 such spontaneous variants in the genome, most of them benign. However, a number of recent studies suggested that DNVs contribute to the pathogenesis of a variety of human diseases. Applications of DNVs include aiding in clinical diagnosis and identifying disease-causing genetic factors in patients with atypical symptoms. Therefore, understanding the roles of DNVs in a trio, with healthy parents and an affected offspring, would be crucial in elucidating the genetic mechanism of disease pathogenesis in a personalized manner.

• Journal of Microbiology and Biotechnology
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• v.32 no.12
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• pp.1506-1514
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• 2022

Allergic contact dermatitis (ACD) is an allergen-specific T-cell-mediated inflammatory response, albeit with unclear pathogenesis. Exosomes are nanoscale extracellular vesicles secreted by several cell types and widely distributed in various biological fluids. Exosomes affect the occurrence and development of ACD through immunoregulation among other ways. Nevertheless, the role of exosomes in ACD warrants further clarification. This review examines the progress of research into exosomes and their involvement in the pathogenesis, diagnosis, and treatment of ACD and provides ideas for exploring new diagnostic and treatment methods for this disease.

• Journal of Korean Medical classics
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• v.27 no.4
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• pp.15-20
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• 2014

Objectives : We search the contents about Bi disease in Huang Di Nei Jing(黃帝內經), to analyze the significance of Bi disease, etiopathogenisis and pathogenesis of Bi disease, treatment of Bi disease. Methods : We find that the key feature of Bi disease is joint pain induced by impatency of Qi and blood. Exterior and interior etiological factors are involved in, such as exogenous evil of cold and dampness, emotional disorders, intemperance of taking food, dysfunction of yingqi and weiqi, strong or weak constitution, etc. Results : The important pathogenesis are invaded by exogenous evil because of deficiency, disharmony of yingqi and weiqi and disharmony of five viscera. The key points of treatments are the individual concerned therapy and climate concerned therapy, selecting the acupoint according to the differentiation of symptoms and signs. Conclusions : The combined therapy should be used such as acupuncture and moxibustion, hot application of medicine, massage, Daoyin, outside apply, etc. These supply the theory foundation for etiological factor, pathogenesis, syndrome and treatment, and to direct the diagnosis and treatment of Bi disease later generations.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.173-174
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• 2002

Oxidative modification of cellular structures and functions by redox imbalance is the basis of the current oxidative stress hypothesis of aging. The experimental support for this hypothsis has been generated from recent molecular probing on the interrelation between the age-related functional impairments and the pathogenesis. (omitted)

• Journal of Veterinary Clinics
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• v.28 no.1
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• pp.113-121
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• 2011

Foot-and-mouth disease (FMD) is a severe vesicular disease of cloven-hoofed animals including domesticated ruminants and pigs. Acute clinical signs may be mild in sheep and goats but are associated with lameness in pigs and mouth lesions with vesicles in cattle. The required condition for a successful pathogen appears to be the ability to counteract both the host innate and adaptive immune response. FMD virus (FMDV) inhibits the induction of antiviral molecules and interferes with the secretory pathway in the infected cell. The surface expression of Major Histocompatibility Complex (MHC) class I molecules is reduced in infected cells. Thus, the ability of the host to recognize and eliminate virus infected cells is decreased. Furthermore, FMDV infection results in a rapid, but transient lymphopenia, reducing the number of T and B cells, and affecting T cell function. The virus appears to premature apoptosis-mediated cell death because it has a very short replication cycle and is able to rapidly produce large amounts of virus. FMDV engages the host protective response at multiple steps to ensure its effective replication and pathogenesis. This review describes the recent pathological and immunological studies to overcome the powerful abilities of FMDV to counteract defense mechanism of host.

• Journal of Korean Neurosurgical Society
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• v.30 no.7
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• pp.849-854
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• 2001

Delayed cerebral infarction after resection of craniopharyngioma is a uncommon entity, but leads to high morbidity and mortality. We present 3 such cases and discuss the etiology and pathogenesis with review of pertinent literatures. In our cases, delayed deterioration of consciousness was observed in all cases. All of them expired. The cause may be multifactorial and the surgical approach may contribute to the pathogenesis of delayed cerebral infarction. We suspect vasospasm might be the major mechanism of pathogenesis. Vessels were primed to spasm during operation due to blood in the cistern or mechanical injury. Vasoactive materials may have been liberated from the pituitary stalk or injured hypothalamus, either at the time of surgery, or later, after portions of tumor have undergone necrosis. The high degree of suspicion to detect vasospasm should be done in the case of the delayed deterioration of mental status at an early stage of craniopharyngioma surgery. Possible mechanism underlying this delayed cerebral infarction are discussed.