• Proceedings of the Microbiological Society of Korea Conference
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• 2004.05a
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• pp.132-136
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• 2004

Understanding the molecular pathogenesis of the multifaceted host-pathogen interaction is critical in the development of improved treatment and prevention, as well as elucidating how certain bacteria can circumvent host defenses, multiply in the host, and cause such extensive damage. Disease caused by infection with V. vulnificus is remarkable for the invasive nature of the infection, ensuing severe tissue damage, and rapidly fulminating course. The characterization of somatic as well as secreted products of V. vulnificus has yielded a large list of putative virulence attributes, whose known functions are easily imagined to explain the pathology of disease. These putative virulence factors include a carbohydrate capsule, lipopolysaccharide, a cytolysin/hemolysin, elastolytic metalloprotease, iron sequestering systems, lipase, and pili. However, only few among the putative virulence factors has been confirmed to be essential for virulence by the use of molecular Koch's postulates. This presentation describes molecular biological characterization of the virulence factors contributing to survival as well as to toxigenesis of V. vulnificus.

• Journal of Korean Medical classics
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• v.12 no.1
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• pp.168-195
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• 1999

The hakgil is the important disease in the oriental medicine historically. In the preseant time also this disease continually appear all over the world. So purpose of this study is that consider the symptoms and pathogenesis of hakgil(瘧疾) with the point of view of oriental medicine. And in this study, the results are summarized as the followings. 1. The symptos of hakgil(瘧疾). 1) Rigor and heat spasm : The main symptoms of hakgil is the severe and periodical rigor and heat spasm. Generally the rigor first appear and later the heat spasm appear. According to the first and last, severe and weak, the hakgil is classified to hanhak(寒瘧), onhak(溫瘧), danhak(癉瘧), binhak(牝瘧). 2) The regulation of the time of spasm : The spasm occour in the same time daily or one time in two days, three days or several days. And the spasm time is regulary in day or night. 3) The term between the spasm and next one become later or faster. It can be decided that the becoming worse and better in the disease with the signs. 4) The seasonal property Generally the hakgil appear in summer and early autumn. 5) The other kind of hakgil there are five-organ hakgil(五臟瘧), six-kyung hakgil(六經瘧), janghak(瘴瘧), kuihak(鬼瘧), six-gi hakgil(六氣瘧), damhak(痰瘧), sikhak(食瘧), and so on. 6) The pulse condition of the hakgil is chiefly hyun(弦). 2. The pathogenesis of the hakgil 1) The cause of the hakgil The causes of the hakgil first are the seo(暑) or heat(熱) that make the problem in the cycle of five phases(五行). In the consequence, il open the hole of skin so that the pathogenic factors easily invade the humanbody and at the same time the pathogenic factor in the inside easily come out, that make the spasm. In the second time the pathogenic factor of yin(陰) - wind(風), cold(寒), water(水) invade through the opened skin to combine with the factor in the inside. Such condition make the hakgil and the accessory spasm. 2)The pathogenesis of hakgil(瘧疾) (1) The rigor and heat spasm of hakgil(瘧疾) appear because in summer the human body don't accomplish a task of summer because of hot weather or heat, so in autumn the ki(氣) of human body separate into yin(陰) and yang(陽), and the skin of human body is weaken so the saki(邪氣: pathogenic factors) is easily come into the human body. At this time the circulation of ki(氣) is obstructed, so the jungki(精氣: vital substance) apply to straighten the circulation of ki(氣), if the jungki(精氣: vital substance) help the yin(陰) the rigor spasm appear in the opposit direction the jungki(精氣: vital substance) help the yang(陽) the heat spasm appear. (2) The period of circulation of ki(氣) and jungki(精氣: vital substance) is one day, so the general period of spasm of hakgil(瘧疾) is one day, But if the saki(邪氣: pathogenic factors) come into the human body deeply, the jungki(精氣: vital substance) cannot apply 10 straighten the circulation of ki(氣) every day so the period of spasm become longer.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.25 no.2
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• pp.86-89
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• 2014

Functional dysphonia (FD) is a voice disorder in the absence of structural or neurologic laryngeal pathology. FD is not a single disease but a disease entity. Therefore several voice disorders, which have completely different pathogenesis, are included in this category. The first step of treatment of FD is differentiating patient's voice symptoms from other organic voice disorders and other functional voice problems. Several different treatment modalities are included in the managements of FD. Voice therapy is in charge of the main role in treatment of FD. Medical treatment is also necessary when patient has general problems which would affect voice production. Vocal folds mucosal lesions can cause FD even the lesion is minor. In this case proper surgical intervention helps to improve the symptom of FD. Psychiatric consultation should be considered when the patient has psychological problems.

• Journal of Yeungnam Medical Science
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• v.23 no.1
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• pp.138-142
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• 2006

Abdominal distension is not an uncommon symptom in the neonate; it is indistinguishable from Hirschsprung disease by symptoms and X-ray findings. In three patients, severe abdominal distension was found at early infancy and improved with conservative treatment without relapse. The findings were different from those of Hirschsprung disease. Immaturity or poor coordination of peristaltic movement is postulated as the cause. With maturation such problems can normalize. However the pathogenesis remains unclear and further investigation is needed to improve our understanding.

• Journal of Microbiology
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• v.42 no.2
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• pp.117-125
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• 2004

Propionibacterium acnes (P. acnes) plays an important role in the disease pathogenesis of acne vulgaris, a disorder of pilosebaceous follicles, seen primarily in the adolescent age group. In the present study, the presence of antibodies against P. acnes (MTCC1951) were detected in acne patient (n=50) and disease free controls (n=25) using dot-ELISA and Western blot assay. The ability of P. acnes to induce pro-inflammatory cytokines by human peripheral blood mononuclear cells (PBMCs), obtained from acne patients and healthy subjects, were also analysed. The patients (n=26) who were culture positive for skin swab culture, were found to have a more advanced disease and higher antibody titres (1:4000 to >1:16000) compared to the P. acnes negative patients (n=24) and normal controls (n=25). An analysis of patients' sera by western blot assay recognized a number of antigenic components of P. acnes, rang-ing from 29 to 205 kDa. The major reactive component was an approximately 96 kDa polypeptide, which was recognised in 92％ (24 of 26) of the patients sera. Further, the P. acnes culture supernatant, crude cell lysate and heat killed P. acnes whole cells, obtained from 72-h incubation culture, were observed to be able to induce significant amounts of IL-8 and tumor necrosis factor alpha (TNF-${\alpha}$) by the PBMCs in both the healthy subjects and patients, as analysed by cytokine-ELISA. The levels of cytokines were significantly higher in the patients than the healthy subjects. A major 96 kDa polypep-tide reactant was eluted from the gel and was found to cause dose dependent stimulation of the pro-ductions of IL-8 and TNF-${\alpha}$. Thus, the above results suggest that both humoral and pro-inflammatory responses play major roles in the pathogenesis of acne.

• Advances in pediatric surgery
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• v.8 no.1
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• pp.41-47
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• 2002

Abnormal distribution of the enteric nerves such as adrenergic, cholinergic and peptidergic nerves may cause the functional obstruction in Hirschsprung's disease (HD). Although the sustained contraction of the aganglionic segment is the main pathophysiology of HD, the etiology and pathogenesis is not thoroughly understood, With the recent progress of molecular biology and genetics,a more detailed approach to the pathogenesis of the HD can be undertaken. In this review, the roles of the nitric oxide, nitric oxide synthase and interstitial cells of Cajal on smooth muscle relaxation, the effects of extracellular matrix, cell adhesion molecules, neurotrophic factors on the migration and maturation of the neural crest cells are described. In the section of genetic factors, familial occurrences, association of chromosomal abnormalities, RET gene, glial cell line-derived neurotrophic factor gene, endothelin-3 gene and endothelin-B receptor gene and their r elationships to HD is briefly reviewed.

• Molecules and Cells
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• v.25 no.1
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• pp.7-19
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• 2008

Complexins play a critical role in the control of fast synchronous neurotransmitter release. They operate by binding to trimeric SNARE complexes consisting of the vesicle protein Synaptobrevin and the plasma membrane proteins Syntaxin and SNAP-25, which are key executors of membrane fusion reactions. SNARE complex binding by Complexins is thought to stabilize and clamp the SNARE complex in a highly fusogenic state, thereby providing a pool of readily releasable synaptic vesicles that can be released quickly and synchronously in response to an action potential and the concomitant increase in intra-synaptic $Ca^{2+}$ levels. Genetic elimination of Complexins from mammalian neurons causes a strong reduction in evoked neurotransmitter release, and altered Complexin expression levels with consequent deficits in synaptic transmission were suggested to contribute to the etiology or pathogenesis of schizophrenia, Huntington's disease, depression, bipolar disorder, Parkinson's disease, Alzheimer's disease, traumatic brain injury, Wernicke's encephalopathy, and fetal alcohol syndrome. In the present review I provide a summary of available data on the role of altered Complexin expression in brain diseases. On aggregate, the available information indicates that altered Complexin expression levels are unlikely to have a causal role in the etiology of the disorders that they have been implicated in, but that they may contribute to the corresponding symptoms.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3025-3033
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• 2016

Chronic myeloid leukaemia (CML) is a clonal myeloproliferative hematopoietic stem cell disorder. Deregulated BCR-ABL fusion tyrosine kinase activity is the main cause of CML disease pathogenesis, making BCR-ABL an ideal target for inhibition. Current tyrosine kinase inhibitors (TKIs) designed to inhibit BCR-ABL oncoprotein activity, have completely transformed the prognosis of CML. Interruption of TKI treatment leads to minimal residual disease reside (MRD), thought to reside in TKI-insensitive leukaemia stem cells which remain a potential reservoir for disease relapse. This highlights the need to develop new therapeutic strategies for CML either as small molecule master TKIs or phytopharmaceuticals derived from nature to achieve chronic molecular remission. This review outlines the past, present and future therapeutic approaches for CML including coverage of relevant mechanisms, whether ABL dependent or independent, and epigenetic factors responsible for developing resistance against TKIs. Appearance of mutant clones along the course of therapy either pre-existing or induced due to therapy is still a challenge for the clinician. A proposed in-vitro model of generating colony forming units from CML stem cells derived from diagnostic samples seems to be achievable in the era of high throughput technology which can take care of single cell genomic profiling.

• Mycobiology
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• v.37 no.3
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• pp.161-170
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• 2009

Cryptococcus neoformans is a basidiomycete human fungal pathogen that causes meningoencephalitis in both immunocompromised and immunocompetent individuals. The ability to sense and respond to diverse extracellular signals is essential for the pathogen to infect and cause disease in the host. Four major stress-activated signaling (SAS) pathways have been characterized in C. neoformans, including the HOG (high osmolarity glycerol response), PKC/Mpk1 MAPK (mitogen-activated protein kinase), calcium-dependent calcineurin, and RAS signaling pathways. The HOG pathway in C. neoformans not only controls responses to diverse environmental stresses, including osmotic shock, UV irradiation, oxidative stress, heavy metal stress, antifungal drugs, toxic metabolites, and high temperature, but also regulates ergosterol biosynthesis. The PKC(protein kinase C)/Mpk1 pathway in C. neoformans is involved in a variety of stress responses, including osmotic, oxidative, and nitrosative stresses and breaches of cell wall integrity. The $Ca^{2+}$/calmodulin- and Ras-signaling pathways also play critical roles in adaptation to certain environmental stresses, such as high temperature and sexual differentiation. Perturbation of the SAS pathways not only impairs the ability of C. neoformans to resist a variety of environmental stresses during host infection, but also affects production of virulence factors, such as capsule and melanin. A drug(s) capable of targeting signaling components of the SAS pathway will be effective for treatment of cryptococcosis.

• Molecular & Cellular Toxicology
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• v.2 no.1
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• pp.60-66
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• 2006

Methylmercury (MeHg), one of the heavy metal compounds, can cause severe damage to the central nervous system in humans. Many reports have shown that MeHg is poisonous to human body through contaminated foods and has released into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established so far. This study, using of suppression subtractive hybridization (SSH) method, was peformed to identify differentially expressed genes by MeHg in SH-SY5Y human neuroblastoma cell line. We prepared to total RNA from SH-SY5Y cells treated with solvent (DMSO) and $6.25\;{\mu}M\;(IC_{50})$ MeHg and performed forward and reverse SSH. Differentially expressed cDNA clones were screened by dot blot, sequenced and confirmed that individual clones indeed represent differentially expressed genes with real time RT-PCR. These sequences were identified by BLAST homology search to known genes or expressed sequence tags (ESTs). Analysis of these sequences may provide an insight into the biological effects of MeHg in the pathogenesis of neurodegenerative disease and a possibility to develop more efficient and exact monitoring system of heavy metals as ubiquitous environmental pollutants.