• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.831-839
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• 2002

Allergy has a born predominant cause of atopy in body and react oversenstively several meterial. The cause of allergy are tick, house dust, egg, milk, bean, cosmetics, virus, bacteria, flesh and meat in Western medicine. While, Oriental medicine did not have an application on the allergy, but recognized that allergy is connected with fetal toxicosis, heat-syndrome in new born, syndrome characterized by dyspnea, sneezing, stuffy nose, nasal discharge and phlegm. Therefor, We knowed method of medical treatment following cause of disease and pathogenesis against allergy. Allergic disease(atopic dermatitis, bronchial asthma, rhinitis) were related with lung, spleen, kidney. To prevent allergic disease in born, Oriental medicine taked a serious view of fetal education. In Western medicine, The cause of allergy applied to exopathogen of Oriental medicine. In Oriental medicine, Treatment of allergy used generally strengthening the body resistance to eliminate pathogenic factors.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.15 no.2
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• pp.74-78
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• 2012

With a markedly increased prevalence of obesity, non-alcoholic fatty liver disease (NAFLD) now becomes the most common cause of chronic liver disease in both adults and children. The etiology and pathogenesis of NAFLD are multifactorial and remain incompletely understood. According to the "two-hit" theory, inflammatory cytokines and adipokines are activated by oxidative stress and they are involved in insulin resistance, necroinflammatory steatohepatitis and fibrosis. This review discusses the latest updates on the role of some of important inflammatory adipokines and cytokines in the pathogenesis of NAFLD with an emphasis on their potential therapeutic implications.

• Journal of Yeungnam Medical Science
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• v.24 no.1
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• pp.11-23
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• 2007

Hirschsprung's disease is one of the most common causes of intestinal obstruction in neonates and infants. The underlying pathology of this disease is the absence of the ganglion cells in both the myenteric (Auerbach's) plexus and the submucosal (Meissner's) plexus. Since Hirschsprung's report in 1886, there have been thousands of papers on Hirschsprung's disease but the cause of the absence of the ganglion cells has not been identified. Hirschsprung's disease can be successfully treated with the Swenson, the Duhamel, and the Soave operations even though the pathogenesis is unknown. With the recent progress of molecular biology and genetics, a more detailed approach to the pathogenesis of Hirschsprung's disease can be undertaken. In addition, there have been recent developments in the surgical approach. In this review, recent advances in surgery for Hirschsprung's disease are presented.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.1
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• pp.1-10
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• 2013

We can understand "Shanghanlun(傷寒論)" and "Wenbingtiaobian(溫病條辨)" which are major books on externally contracted diseases well by making a comparative study of their similarities and differences. After studying etiological causes and characteristics of disease, disease pattern, syndrome differentiation, transmutation rules, following conclusions are derived. While cold is an etiological cause of Cold damage and harms Yang qi, heat is an etiological cause of Warm disease and harms Yin qi. Cold damage and Warm disease have something in common in the respect of damage to fluid and humor and Yang qi. Exuberant heat symptom of Yang brightness disease and lesser yin heat transformation pattern have similar damage to fluid and humor as Warm disease does. Warm disease can reach qi collapse syndrome through damage to Yang qi following fluid and humor damage. In the respect of water qi, as Cold damage makes water-dampness retain easily due to cold congealing, dampness-draining diuretic medicinal and warm yang medicinal are used together. As warm disease damages fluid and humor, yin-tonifying medicinal is used and dampness-draining diuretic medicinal can be used in the case of Warm disease with dampness. In the respect of disease pattern, cold syndromes arise mostly by Cold damage except heat syndrome of grater yang disease, chest bind syndrome, stuffiness syndrome, reverting yin disease and yang brightness disease. Warm disease is classified as pure heat syndrome and heat syndrome with bowel excess, damage to yin, qi collapse or damage to blood.

• Advances in pediatric surgery
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• v.8 no.1
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• pp.68-70
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• 2002

Enterocolitis associated with Hirschsprung's disease has been a major cause of morbidity and even mortality, and before and after definitieve surgical treatment. It shows typical clinical characteristics, however, its pathogenesis has been poorly understood. Treatment is diverse, and consists of conservative tertment with intravenous hydration, antibiotics and rectal wash out, and surgical tertment with temporatory enterostomy, and other surgical procedures.

• Journal of Microbiology
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• v.43 no.spc1
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• pp.118-131
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• 2005

Vibrio vulnificus is an opportunistic pathogen of humans that has the capability of causing rare, yet devastating disease. The bacteria are naturally present in estuarine environments and frequently contaminate seafoods. Within days of consuming uncooked, contaminated seafood, predisposed individuals can succumb to sepsis. Additionally, in otherwise healthy people, V. vulnificus causes wound infection that can require amputation or lead to sepsis. These diseases share the characteristics that the bacteria multiply extremely rapidly in host tissues and cause extensive damage. Despite the analysis of virulence for over 20 years using a combination of animal and cell culture models, surprisingly little is known about the mechanisms by which V. vulnificus causes disease. This is in part because of differences observed using animal models that involve infection with bacteria versus injection of toxins. However, the increasing use of genetic analysis coupled with detailed animal models is revealing new insight into the pathogenesis of V. vulnificus disease.

• BMB Reports
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• v.52 no.12
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• pp.679-688
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• 2019

The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis.

• Microbiology and Biotechnology Letters
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• v.52 no.3
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• pp.221-232
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• 2024

Zoonotic diseases are rare but the transmission of disease to humans may cause serious illness. Nipah virus (NiV) is a bat-borne zoonotic pathogen, which can cause severe encephalitis and respiratory distress. The transmission of Nipah virus from bats to humans was first reported in Malaysia in 1998. Different strains of NiV show different epidemiological and clinical features. Few of the strains are highly lethal and can spread to the community resulting in a global threat. However, the availability of effective management or prophylactic measures are only limited. Thus, it is essential to contain such outbreaks by implementing proper infection control and surveillance measures. Many serological and molecular diagnostic techniques have been developed for diagnosis of this infection. This review mainly focuses on the epidemiology, transmission of Nipah virus, pathogenesis and management of NiV infection. The review also throws light on the immune response of NiV in humans and the role of One Health approach in prevention and control of NiV infection.

• Molecules and Cells
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• v.27 no.6
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• pp.621-627
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• 2009

Spinocerebellar ataxia type 1 (SCA1) is an autosomal-dominant neurodegenerative disorder characterized by ataxia and progressive motor deterioration. SCA1 is associated with an elongated polyglutamine tract in ataxin-1, the SCA1 gene product. As summarized in this review, recent studies have clarified the molecular mechanisms of SCA1 pathogenesis and provided direction for future therapeutic approaches. The nucleus is the subcellular site where misfolded mutant ataxin-1 acts to cause SCA1 disease in the cerebellum. The role of these nuclear aggregates is the subject of intensive study. Additional proteins have been identified, whose conformational alterations occurring through interactions with the polyglutamine tract itself or non-polyglutamine regions in ataxin-1 are the cause of SCA-1 cytotoxicity. Therapeutic hope comes from the observations concerning the reduction of nuclear aggregation and alleviation of the pathogenic phenotype by the application of potent inhibitors and RNA interference.

• BMB Reports
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• v.42 no.8
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• pp.467-474
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• 2009

The modification of proteins by reversible phosphorylation is a key mechanism in the regulation of various physiological functions. Abnormal protein kinase or phosphatase activity can cause disease by altering the phosphorylation of critical proteins in normal cellular and disease processes. Alzheimer' disease (AD), typically occurring in the elderly, is an irreversible, progressive brain disorder characterized by memory loss and cognitive decline. Accumulating evidence suggests that protein kinase and phosphatase activity are altered in the brain tissue of AD patients. Tau is a highly recognized phosphoprotein that undergoes hyperphosphorylation to form neurofibrillary tangles, a neuropathlogical hallmark with amyloid plaques in AD brains. This study is a brief overview of the altered protein phosphorylation pathways found in AD. Understanding the molecular mechanisms by which the activities of protein kinases and phosphatases are altered as well as the phosphorylation events in AD can potentially reveal novel insights into the role aberrant phosphorylation plays in the pathogenesis of AD, providing support for protein phosphorylation as a potential treatment strategy for AD.