• 제목/요약/키워드: causative form

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피동·사동과 관련한 국어사전의 뜻풀이에 대하여 (A Study on Definition Related to Passive and Causative in Korean Dictionary.)

  • 최호철
    • 한국어학
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    • 제48권
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    • pp.333-354
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    • 2010
  • When defining the word related to passive and causative in Korean dictionary, the meaning of headword can be explained by linking them to other related words. The link could be expressed into two forms; the one is 'passive verb causative verb of A' and the other is 'passive form causative form of A.' Whichever the dictionary takes, the important thing is that the content to which it refer should be correct. However the format of 'passive verb causative verb of A' and 'passive form causative form of A' is problematic because the definition of headword does not contain semantic information but syntactic or morphological information. Generic concept 'passive form causative form' and 'passive verb causative verb' refers to respectively morphological and syntactic level but specific concept 'A' refers to semantic level. These morphological, syntactic and semantic level can not be a same dimension so the size of their denotation can not be compared. The way of transform syntactic dimension 'passive verb causative verb' and morphological dimension 'passive form causative form' into semantic dimension is removing 'verb' and 'form' from 'passive verb causative verb' and 'passive form causative form' respectively. Therefore the expression 'passive verb causative verb of A' or 'passive form causative form of A' ought be changed into 'passive causative of A.'

Progress Towards Control of a Mycobacterial Pathogen, Mycobacterium aviumsubsp. paratuberculosis, the Causative Agent of Johne's Disease in Cattle and Humans

  • Davis, William C.;Park, Kun Taek
    • 한국식품위생안전성학회지
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    • 제33권4호
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    • pp.221-228
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    • 2018
  • 19세기말 Mycobacterium avium subsp. paratuberculosis(Map)이 요네병(Johne's disease)의 원인균임이 밝혀진 이후, 불현성 감염된 동물들의 국제적 이동은 요네병을 전세계로 퍼뜨리기 시작하였다. 이러한 요네병이 축산분야에 나타남과 동시에 새로운 형태의 대장염으로서 요네병과 같은 증상을 나타내는 질병(크론병)이 사람에게서도 나타나기 시작하였다. 그러나 Map이 이러한 새로운 대장염의 원인균이며 인수공통전염병의 원인체라는 인식은 20세기 후반 이러한 질병을 앓고 있는 사람의 조직으로부터 Map을 검출할 수 있게 되고서야 나타나기 시작했다. 본 총설은 어떻게 Map이 축산분야와 사람의 공중보건 측면에서 심각한 문제를 야기시키게 되었고, Map 감염에 의한 대장염 환자의 치료가 어떻게 발전되어 왔는지 간단히 요약하고, 축산에서 Map의 통제를 위한 새로운 백신개발 전략에 대하여 소개한다.

하지불안증후군과 정신과 약물 (Restless Leg Syndrome and Psychotropic Drug)

  • 우정민;장성만
    • 수면정신생리
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    • 제17권1호
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    • pp.5-10
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    • 2010
  • Restless legs syndrome (RLS) is a common sensorimotor disorder that is characterized by an urge to move the legs and peculiar, unpleasant sensations deep in the legs and its prevalence in the general population is between 3.2% and 15%. RLS significantly impairs patients' lives, often by severely disrupting sleep. However, both clinicians and patients under-recognize the RLS. RLS phenotypes include an idiopathic form and secondary form that is usually resulted from various causative conditions. The pathophysiology of RLS may be related with the dopaminergic system, which is closely linked to a number of psychotropic medications, including antidepressant and antipsychotics. Several antidepressants and antipsychotics have been shown to induce or exacerbate RLS. We need pay attention to the fact that commonly prescribed medications can be the cause of RLS.

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Isovaleric Acidemia 3례 (3 Case of Isovaleric Acidemia)

  • 이동환;전경수;안영민
    • 대한유전성대사질환학회지
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    • 제2권1호
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    • pp.7-11
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    • 2002
  • 저자들은 잘 교정되지 않는 대사성 산혈증을 주소로 내원한 3세된 남아와 원인 모르는 기면과 구토로 5차례 입원했던 과거력을 가진 8세된 남아 형제가 유기산 분석에서 isovalerylglycine의 현저한 증가를 보여 만성 간헐형의 isovaleric acidemia로 진단된 예와 탄뎀질량분석검사에서 isovaleric acidemia로 진단되어 조기치료하고 있는 예를 경험하였기에 보고하는 바이다.

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Molecular Pharmacological Interaction of Phenylbutazone to Human Neutrophil Elastase

  • Kang, Koo-Il
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권3호
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    • pp.385-393
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    • 1998
  • Human neutrophil elastase (HNElastase, EC 3.4.21.37), a causative factor of inflammatory diseases, was purified by Ultrogel AcA54 gel filtration and CM-Sephadex ion exchange chromatography. HNElastase was inhibited by phenylbutazone in a concentration dependent manner up to 0.4 mM, but as the concentration increased, the inhibitory effect gradually diminished. Binding of phenylbutazone to the human neutrophil elastase caused strong Raman shifts at 200, 440, and 1194 $cm^{-1}$. The peak at 1194 $cm^{-1}$ might be evidence of the presence $of\;-N=N-{\Phi}$ radical. The core area of the elastase, according to the visual molecular model of human neutrophil elastase, was structurally stable. A deeply situated active center was at the core area surrounded by hydrophobic amino acids. Directly neighboring the active site was one positively charged atom and two atoms carrying a negative charge, which enabled the enzyme and the drug to form a strong interaction. Phenylbutazone may form a binding, similar to a key & lock system to the atoms carrying opposite charges near the active site of the enzyme molecule. Furthermore, the hydrophobicity of the surrounding amino acid near the active site seemed to enhance the binding strength of phenylbutazone. Binding of phenylbutazone near the active site may cause masking of the active site, preventing the substrate from approaching the active site and inhibiting elastase activity.

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Clostridium difficile Toxin A Upregulates Bak Expression through PGE2 Pathway in Human Colonocytes

  • Kim, Young Ha;Kim, Ho
    • Journal of Microbiology and Biotechnology
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    • 제29권10호
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    • pp.1675-1681
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    • 2019
  • Clostridium difficile toxin A is known to cause colonic epithelial cell apoptosis, which is considered the main causative event that triggers inflammatory responses in the colon, reflecting the concept that the essential role of epithelial cells in the colon is to form a physical barrier in the gut. We previously showed that toxin A-induced colonocyte apoptosis and subsequent inflammation were dependent on prostaglandin E2 ($PGE_2$) produced in response to toxin A stimulation. However, the molecular mechanism by which $PGE_2$ mediates cell apoptosis in toxin A-exposed colonocytes has remained unclear. Here, we sought to identify the signaling pathway involved in toxin A-induced, $PGE_2$-mediated colonocyte apoptosis. In non-transformed NCM460 human colonocytes, toxin A exposure strongly upregulated expression of Bak, which is known to form mitochondrial outer membrane pores, resulting in apoptosis. RT-PCR analyses revealed that this increase in Bak expression was attributable to toxin A-induced transcriptional upregulation. We also found that toxin A upregulation of Bak expression was dependent on $PGE_2$ production, and further showed that this effect was recapitulated by an Prostaglandin E2(PGE2) receptor-1 receptor agonist, but not by agonists of other EP receptors. Collectively, these results suggest that toxin A-induced cell apoptosis involves $PGE_2$-upregulation of Bak through the EP1 receptor.

Alzheimer's Disease and Apoptosis

  • Kim, Young-Hoon;Kim, Hye-Sun;Park, Cheol-Hyoung;Jeong, Sung-Jin;Kim, Young-Kyung;Kim, Sun-Hee;Lee, Sang-Kyeng;Suh, Yoo-Hun;Kim, Sung Su
    • 생물정신의학
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    • 제5권1호
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    • pp.66-70
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    • 1998
  • Apoptosis is a form of cell death in which the cells shrink and exhibit nuclear chromatin condensation and DNA fragmentation, and yet maintain membrane integrity. Many lines of evidence have shown that brain neurons are vulnerable to degeneration by apoptosis. Also it has been suggested that apoptosis is one of the mechanism contributing neuronal loss in Alzheimer's disease(AD), since the conditions in the disease($A{\beta}$ peptide, oxidative stress, low energy metabolism) are the inducers that activate apoptosis. Indeed some neurons in vulnerable regions of the AD brain show DNA damage, chromatin condensation, and apoptic bodies. Consistently, mutations in AD causative genes(Amyloid precursor protein, Presenilin-1 and Presenilin- 2) increase $A{\beta}$ $peptide_{1-42}(A{\beta}_{1-42})$ and sensitize neuronal cell to apoposis. However, several lines of evidence have shown that the location of neuronal loss and $A{\beta}$ peptide deposition is not correlated in AD brain and transgenic mice brain over-expressing $A{\beta}_{1-42}$. Taken together, these data may indicated that $A{\beta}$ peptide(and other causative factors of AD) can interact with other cellular insults or risk factors to exacerbate pathological mechansim of AD through apoptosis. Thus, this review discusses possible role and mechanism of apoptosis in AD.

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Isolation and identification of insect pathogenic fungus from silkworms with suspected white muscardine disease

  • Seul Ki Park;Chan Young Jeong;Hyeok Gyu Kwon;Ji Hae Lee;Sang Kuk Kang;Seong-Wan Kim;Seong-Ryul Kim;Jong Woo Park
    • International Journal of Industrial Entomology and Biomaterials
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    • 제48권1호
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    • pp.42-47
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    • 2024
  • The value of silkworms as functional health food materials has increased, as has the interest in its disease control for stable production, and in the economic value of entomopathogenic microorganisms. In this study, we isolated and identified disease-causing fungi from white muscardine silkworms, and confirmed whether this strain could produce white muscardine silkworms. For the analysis of the cause of white muscardine disease in the infected silkworms, the fungi and prokaryotes causing the disease were identified, isolated, and identified using metagenome analysis. Metagenomic analysis detected a large amount of the fungus Metarhizium rileyi in silkworms, and a large amount of the bacterium Enterococcus mundtii, which was presumed to be the causative agent of the disease. For accurate identification of the fungi, these were purified by culture medium, and sequencing and phylogenetic tree analyses were performed using an internal transcribed spacer. As a result, M. rileyi, Cladosporium cladosporioides, and C. tenuissimum were identified. In general, M. rileyi is known to form green conidia, but in this study, white-yellow conidia were formed, indicating that the exact causative agent of the fungal disease cannot be estimated by diagnosing the symptoms. Thus, a diagnostic method is necessary for the continuously collection of required pathogens, and identifying their morphological and genetic characteristics.

Epidemiological Characteristics of Nontuberculous Mycobacterial Pulmonary Disease in South Korea: A Meta-analysis of Individual Participant Data

  • Geunin Lee;Sol Kim;Shihwan Chang;Hojoon Sohn;Young Ae Kang;Youngmok Park
    • Tuberculosis and Respiratory Diseases
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    • 제87권3호
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    • pp.386-397
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    • 2024
  • Background: Despite the global increase in nontuberculous mycobacterial pulmonary disease (NTM-PD), clinical characteristics show geographical variations. We investigated the clinical characteristics of patients with NTM-PD in South Korea. Methods: We systematically reviewed articles concerning patients with NTM-PD in South Korea until February 2022. Individual participant data, regardless of treatment, were collected using a standard case report form. Results: Data of 6,489 patients from 11 hospitals between 2002 and 2019 were analyzed. The mean age was 61.5±11.7 years, of whom 57.7% were women. Mycobacterium avium (41.4%) and Mycobacterium intracellulare (38.4%) comprised most of the causative species, followed by Mycobacterium abscessus subspecies abscessus (8.6%) and M. abscessus subspecies massiliense (7.8%). Bronchiectasis (59.4%) was the most common pulmonary comorbidity. Although reported cases of NTM-PD increased over the years, the proportions of causative species and radiologic forms remained similar. Distinct clinical characteristics were observed according to age and sex. Men were older at the time of diagnosis (median 63.8 years vs. 59.9 years, p<0.001), and had more cavitary lesions than women (38.8% vs. 21.0%, p<0.001). The older group (≥65 years) had higher proportions of patients with body mass index <18.5 kg/m2 (27.4% vs. 18.6%, p<0.001) and cavitary lesions (29.9% vs. 27.6%, p=0.009) than the younger group. Conclusion: We conducted a meta-analysis of the clinical characteristics of patients with NTM-PD in South Korea, and found age- and sex-related differences in disease-specific severity. Further investigation would enhance our comprehension of the nature of the disease, and inherited and acquired host factors.

Molecular cloning, Expression and purification of Anthrax toxin from Bacillus anthracis

  • Yoon, Moon-Young
    • Journal of Photoscience
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    • 제9권2호
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    • pp.323-325
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    • 2002
  • Bacillus Anthracis is the causative agent of anthrax. The major virulence factors are a poly-D glutamic acid capsule and three-protein component exotoxin, which is collectively known as anthrax toxin, protective antigen (PA, 83 kDa), lethal factor (LF, 90 kDa), and edema factor (EF, 89 kDa). These three proteins individually have no known toxic activities, but in combination with PA form two toxins (lethal toxin and edema toxin), causing different pathogenic responses in animals and cultured cells. However, it remains to be elucidated for pathogenic mechanism of anthrax toxin. In this study, we constructed toxin component in bacterial overexpression system and purified the native toxin from Bacillus anthracis delta sterne F32 using FPLC system. Recombinant toxin showed high homogeneity and rapid purification processes. Also, this recombinant toxin was comparable to B. anthracis native toxin in terms of cytotoxic effects on cultured cell lines.

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