• Clinical and Experimental Pediatrics
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• 제57권12호
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• pp.505-513
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• 2014

While the survival of extremely premature infants with respiratory distress syndrome has increased due to advanced respiratory care in recent years, necrotizing enterocolitis (NEC) remains the leading cause of neonatal mortality and morbidity. NEC is more prevalent in lower gestational age and lower birth weight groups. It is characterized by various degrees of mucosal or transmural necrosis of the intestine. Its exact pathogenesis remains unclear, but prematurity, enteral feeding, bacterial products, and intestinal ischemia have all been shown to cause activation of the inflammatory cascade, which is known as the final common pathway of intestinal injury. Awareness of the risk factors for NEC; practices to reduce the risk, including early trophic feeding with breast milk and following the established feeding guidelines; and administration of probiotics have been shown to reduce the incidence of NEC. Despite advancements in the knowledge and understanding of the pathophysiology of NEC, there is currently no universal prevention measure for this serious and often fatal disease. Therefore, new potential techniques to detect early biomarkers or factors specific to intestinal inflammation, as well as further strategies to prevent the activation of the inflammatory cascade, which is important for disease progression, should be investigated.

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2002년도 추계학술대회
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• pp.56-58
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• 2002

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.

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2004년도 International Meeting of the Microbiological Society of Korea
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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.

• 대한한의학원전학회지
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• 제12권1호
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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.

• 대한후두음성언어의학회지
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• 제25권2호
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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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• 제23권1호
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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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• 제42권2호
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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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• 제8권1호
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• pp.41-47
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• 2002

장 운동은 장근 및 점막하 신경총으로 구성된 내인성 신경계와 외인성 신경계가 합세하여 균형을 이루면서 장관이 팽창하면 상부는 수축하고 하부는 이완되어 장 내용물이 하방으로 이 동하는 운동이 연속적으로 이어지는 것이다. 신경절 세포가 없으면 내인성 신경계 억제작용 매체인 NO의 결손으로 평활근이 이완되지 않을 뿐더러 외인성 신경계 작용이 장벽에 현저히 증가되어 평소의 2-3배가 되는데 특히 adrenergic 계가 더 작용이 강하여 장벽 긴장도가 증가된 것이 무신경절 장관에서 나타나는 장 운동장애 현상의 병태생리로 설명되고 있다. 이러한 신경총의 부재는 NCC의 이동, 정착 및 성숙에 관여하는 여러 인자들의 복합적인 병적 작용 발현으로 일어나는 발생학적인 현상이며, 이러한 각종 인자들의 결함은 이와 관련된 염색체 혹은 유전자들의 변이 현상에 의한 것으로 밝혀짐에 따라 유전적인 요인들이 깊이 내재되어 있는 것이 하나씩 증명되어가고 있는 단계라고 말 할 수 있다. 지금까지는 HD와 동반되어 나타나는 이러한 현상들을 밝혀 나가고 있는 단계에 불과하며, 이러한 분자생물학적인 지식을 기초로 한다고 하여도 아직은 발병 예방이나 유전적인 치료를 고려할 수 있는 수준에는 미치지 못하는 실정이다.

• International Journal of Stem Cells
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• 제17권3호
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• pp.253-269
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• 2024

Pancreas serves endocrine and exocrine functions in the body; thus, their pathology can cause a broad range of irreparable consequences. Endocrine functions include the production of hormones such as insulin and glucagon, while exocrine functions involve the secretion of digestive enzymes. Disruption of these functions can lead to conditions like diabetes mellitus and exocrine pancreatic insufficiency. Also, the symptoms and causality of pancreatic cancer very greatly depends on their origin: pancreatic ductal adenocarcinoma is one of the most fatal cancer; however, most of tumor derived from endocrine part of pancreas are benign. Pancreatitis, an inflammation of the pancreatic tissues, is caused by excessive alcohol consumption, the bile duct obstruction by gallstones, and the premature activation of digestive enzymes in the pancreas. Hereditary pancreatic diseases, such as maturity-onset diabetes of the young and hereditary pancreatitis, can be a candidate for disease modeling using human pluripotent stem cells (hPSCs), due to their strong genetic influence. hPSC-derived pancreatic differentiation has been established for cell replacement therapy for diabetic patients and is robustly used for disease modeling. The disease modeling platform that allows interactions between immune cells and pancreatic cells is necessary to perform in-depth investigation of disease pathogenesis.

• Molecules and Cells
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• 제25권1호
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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.