• 제목/요약/키워드: family pathogenesis

검색결과 120건 처리시간 0.028초

다형성선종에서 연골유래형성단백의 발현 (EXPRESSION OF CARTILAGE DERIVED MORPHOGENIC PROTEIN IN PLEOMORPHIC ADENOMA)

  • 이황재;김철환;김경욱
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제33권3호
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    • pp.247-255
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    • 2007
  • The bone morphogenic protein(BMP) can promote migration and growth of mesenchymal cells and initiate process for bone and cartilage formation. Cartilage-derived morphogenic protein(CDMP)-1 and -2 belong to the bone morphogenetic protein family in the transforming growth factor(TGF)-${\beta}$ superfamily. Although pleomorphic adenoma of the salivary glands is an epithelial tumor, it frequently shows ectopic cartilaginous formation with biomolecular studies. The mechanism of pathogenesis in cartilaginous formation is still controversy. We examined the expression and localization of CDMP-1 and -2, in comparison with the localization of cartilaginous matrix proteins, in human normal salivary glands and 20 cases of pleomorphic adenoma using immunohistochemical methods. The results were followed. 1. CMP-1 was immunolocalized in the striated ducts and the intercalated ducts, but not expressed in excretory duct, CDMP-2 was not expressed in the normal salivary glands. 2. CMP-1 was immunolocalized in the ductal cell and cuboidal neoplastic myoepithelial cells around the chondroid areas of the pleomorphic adenomas, whereas these molecules were not localized in the spindle-shaped neoplastic myoepithelial cells of the myxoid element in these tumors. CDMP-2 was expressed neither in normal salivary glands nor in any elements of the pleomorphic adenomas. 3. In transmission electron microscopic view, the tumor cells are composed of modifed myoepithelial cells between hyaline and myxoid stroma. 4. In Immuno-blot analysis, strong overexpression of CDMP-1 was frequently seen in pleomorphic adenomas, but the level of CDMP-2 was expressed minimally in pleomorphic adenoma. From the these results, it should be suggested that undifferentiated neoplastic myoepithelial cells around the chondroid areas expressed CDMP-1 and suggested that this molecule may play a role in the differentiation of neoplastic myoepithelial cells in pleomorphic adenoma, but not CDMP-2.

Vero-E6 세포에서 한탄바이러스의 증식에 관한 전자현미경적 연구 (Electron Microscopic Study on the Replcation of Hantaan Virus in Vero-E6 Cells)

  • 박경희;성인화
    • 대한바이러스학회지
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    • 제29권4호
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    • pp.201-209
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    • 1999
  • Results of the studies on the morphologic and molecular biologic characteristics of Hantaan virus (HTNV), one of the etiologic agents of Hemorrhagic fever with renal syndrome (HFRS), revealed that HTNV was a member of Family Bunyaviridae and its RNA divided into three segments. And the nucleotide sequences of these segments also were known and the differences in nucleotide sequences of HTNV from other members of genus Hantavirus were clearly evaluated. But the morphorgenesis, pathogenesis of HFRS and the replication time had not been clearly determined. In this study, to estimate the replication time of HTNV in Vero E-6 cells, Vero cells were infected with HTNV 76/118 strain, and cells were harvested from two hours post-infection up to 24 hours at two hours-intervals. Harvested cells were treated with ordinary techniques for electron microscopy and immune-electron microscopy. And then thin sections were observed under transmission electron microscope. HTNV particles were not found in the cytoplasm and in the extracellular space between $2{\sim}8$ hours after inoculation of virus, but virus particles were observed in extracellular space near the cell membrane of Vero-E6 cells 10 hours after infection. In immune electron microscopy, mature HTNV particles in extracellular spaces and immature virus labelled with gold particles in the cytoplasm of Vero E-6 cell 10 hours after infection of HTNV could be seen. This results suggest that the replication time of HTNV might be about 10 hours.

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Cloning of celC, Third Cellulase Gene, from Pectobacterium carotovorum subsp. carotovorum LY34 and its Comparison to Those of Pectobacterium sp.

  • LIM WOO JIN;RYU SUNG KEE;PARK SANG RYEOL;KIM MIN KEUN;AN CHANG LONG;HONG SU YOUNG;SHIN EUN CHULE;LEE JONG YEOUL;LIM YONG PYO;YUN HAN DAE
    • Journal of Microbiology and Biotechnology
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    • 제15권2호
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    • pp.302-309
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    • 2005
  • Phytopathogenic Pectobacterium carotovorum subsp. carotovorum (Pcc) LY34 secretes multiple isozymes of the plant cell wall degrading enzyme endoglucanases. We have cloned a third cel gene encoding CMCase from Pcc LY34. The structural organization of the celC gene (AY188753) consisted of an open reading frame (ORP) of 1,116 bp encoding 371 amino acid residues with a signal peptide of 22 amino acids within the NH$_2$-terminal region of pre-CelC. The predicted amino acid sequence of CelC was similar to that of Peetobaeterium ehrysanthemi Cel8Y (AF282321). The CelC has the conserved region of the glycoside hydrolase family 8. The apparent molecular mass of CelC was calculated to be 39 kDa by CMC-SDS-PAGE. The cellulase­minus mutant of Pee LY34 was as virulent as the wild-type in pathogenicity tests on tubers of potato. The results suggest that the CelC of Pce LY34 is a minor factor for the pathogenesis of soft-rot.

갑상선 질환에서 표피성장인자 수용체 발현 (The Expression of Epidermal Growth Factor Receptor in Thyroid Diseases)

  • 민병철;이용진;차성재;박용검;지경천;임현묵;박성일;박성준
    • 대한두경부종양학회지
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    • 제15권2호
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    • pp.156-161
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    • 1999
  • Objectives: The epidermal growth factor receptor(EGFR) family has been increasingly recognized as an important component in the control of normal cell proliferation and the pathogenesis of cancer. To confirm the usefulness of epidermal growth factor receptor as a tumor marker, we initiated this study. Materials and Methods: EGFR was measured by immunohistochemical staining using EGFR antibody. It was performed on section from paraffin blocks of 65 thyroid tissue including 33 paillary carcinoma, 11 follicular carcinoma, 11 nodular hyperplasia, 5 follicular adenoma and 5 normal thyroid tissue. We evaluated morphologic characteristic of various thyroid neoplasms, and the relationship between EGFR and other prognostic factors in papillary thyroid carcinomas. Results: The expression of EGFR was commonly found in neoplasms of thyroid, with trend for stronger staining in the more malignant tumor(p=0.000). Also the expression of EGFR in papillary thyroid cancer related to tumor characters including tumor size(p=0.042), extent(p=0.024) and prognostic features including AMES scores(p=0.019). The strong EGFR staining in papillary carcinoma was significantly associated with tumor recurrence(p=0.003). Conclusions: EGFR may have a role in the regulation of normal and neoplastic thyroid cell growth. EGFR status may help predict the clinical course of patients with malignant thyroid neoplasms. However, the study of more cases will be needed for significance of the information about the EGFR as an independent prognostic factor.

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Effects of analgesics and antidepressants on TREK-2 and TRESK currents

  • Park, Hyun;Kim, Eun-Jin;Han, Jaehee;Han, Jongwoo;Kang, Dawon
    • The Korean Journal of Physiology and Pharmacology
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    • 제20권4호
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    • pp.379-385
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    • 2016
  • TWIK-related $K^+$ channel-2 (TREK-2) and TWIK-related spinal cord $K^+$ (TRESK) channel are members of two-pore domain $K^+$ channel family. They are well expressed and help to set the resting membrane potential in sensory neurons. Modulation of TREK-2 and TRESK channels are involved in the pathogenesis of pain, and specific activators of TREK-2 and TRESK may be beneficial for the treatment of pain symptoms. However, the effect of commonly used analgesics on TREK-2 and TRESK channels are not known. Here, we investigated the effect of analgesics on TREK-2 and TRESK channels. The effects of analgesics were examined in HEK cells transfected with TREK-2 or TRESK. Amitriptyline, citalopram, escitalopram, and fluoxetine significantly inhibited TREK-2 and TRESK currents in HEK cells (p<0.05, n=10). Acetaminophen, ibuprofen, nabumetone, and bupropion inhibited TRESK, but had no effect on TREK-2. These results show that all analgesics tested in this study inhibit TRESK activity. Further study is needed to identify the mechanisms by which the analgesics modulate TREK-2 and TRESK differently.

Defense Genes Induced by Pathogens and Abiotic Stresses in Panax ginseng C.A. Meyer

  • Lee, Ok-Ran;Sathiyaraj, Gayathri;Kim, Yu-Jin;In, Jun-Gyo;Kwon, Woo-Seang;Kim, Ju-Han;Yang, Deok-Chun
    • Journal of Ginseng Research
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    • 제35권1호
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    • pp.1-11
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    • 2011
  • Korean ginseng is a medicinally important perennial herb from the family Araliaceae. It has been cultivated for its highly valued medicinal properties for over 1,000 years in east Asian countries such as China, Korea, and Japan. Due to its longtime cultivation in shady areas, ginseng is frequently exposed to pathogenic infections. Plants protect themselves from microbial pathogens using an array of defense mechanisms, some of which are constitutively active, while others are activated upon pathogen invasion. These induced defense responses, controlled by defense-related genes, require tradeoffs in terms of plant fitness. We hypothesize that ginseng, as with other plants, possesses regulatory mechanisms that coordinate the activation of attacker-specific defenses in order to minimize fitness costs while attaining optimal resistance. Several classes of defense-related genes are induced by infection, wounds, irradiation, and other abiotic stresses. Both salicylates and jasmonates have been shown to cause such responses, although their specific roles and interactions in signaling and development are not fully understood in ginseng. This review summarizes possible defense-related genes in ginseng based on their expression patterns against biotic and abiotic stresses and describes their functional roles.

Genetic Association between Eotaxin Genes and Asthma and Its Relationship to Birth Season in Korean Children

  • Ahn, In-Sung;Bae, Se-Eun;Kim, Jeong-Hee;Son, Byong-Kwan;Son, Hyeon-S.;Cho, Sung-Il
    • Genomics & Informatics
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    • 제9권1호
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    • pp.12-18
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    • 2011
  • Asthma is a chronic disease associated with airway constriction due to inflammation caused by eosinophils, mast cells, and T lymphocytes, leading to serious chronic illness in children. The eotaxin gene family has been shown to play an important role in the pathogenesis of asthma. We hypothesized that the distinctive variations among the four seasons in Korea may affect the expression of eotaxin polymorphisms, especially in children. We examined the possible effects of birth season (spring, March-May; summer, June-August; fall, September-November; and winter, December-February) on the phenotype of asthma in children. All SNP data sets of the eotaxin-2 and eotaxin-3 genes were collected from 78 asthma patients and 101 controls. Here, we investigated the effects of birth season on the expression of eotaxin-2 and eotaxin-3 in Korean children. Using the HAPLOTYPE procedure with the HTR method in SAS/Genetics, we showed that children born in spring and summer show significant haplotypes in both the eotaxin-2 and eotaxin-3 genes. Thus, the expression of polymorphisms in eotaxin-2 and eotaxin-3 may vary by season.

샤르코-마리-투스 질환의 진단 및 치료 (Diagnosis and treatment in Charcot-Marie-Tooth disease)

  • 김상범;박기덕;최병옥
    • Annals of Clinical Neurophysiology
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    • 제7권2호
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    • pp.65-74
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    • 2005
  • Charcot-Marie-Tooth (CMT) disease was described by Charcot and Marie in France and, independently, by Tooth in England in 1886. CMT is the most common form of inherited motor and sensory neuropathy, and is a genetically heterogeneous disorder of the peripheral nervous system. Therefore, many genes have been identified as CMT-causative genes. Traditionally, subclassification of CMT have been divided into autosomal dominant inherited demyelinating (CMT1) and axonal (CMT2) neuropathies, X-linked neuropathy (CMTX), and autosomal recessive inherited neuropathy (CMT4). Recently, intermediate type (CMT-Int) with NCVs between CMT1 and CMT2 is considered as a CMT type. There are several related peripheral neuropathies, such as $D{\acute{e}}j{\acute{e}}rine$-Sottas neuropathy (DSN), congenital hypomyelination (CH), hereditary neuropathy with liability to pressure palsies (HNPP) and giant axonal neuropathy (GAN). Great advances have been made in understanding the molecular basis of CMT, and 17 distinct genetic causes of CMT have been identified. The number of newly discovered mutations and identified genetic loci is rapidly increasing, and this expanding list has proved challenging for physicians trying to keep up with the field. Identifying the genetic cause of inherited neuropathies is often important to determine at risk family members as well as diagnose the patient. In addition, the encouraging studies have been published on rational potential therapies for the CMT1A. Now, we develop a model of how the various genes may interact in the pathogenesis of CMT disorder.

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위암의 BAD 단백질의 발현 (Immunohistochemical Analysis of BAD Protein Expression in Gastric Carcinomas)

  • 유남진;이종우;박원상;이정용;이석형
    • Journal of Gastric Cancer
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    • 제3권2호
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    • pp.75-79
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    • 2003
  • Purpose: Evidence exists that dysregulation of apoptosis is involved in the pathogenesis of cancer development. The Bcl-$x_{L}$/Bcl-2-associated death promoter (BAD), a member of the Bcl-2 family, is a critical regulatory component of the intrinsic cell-death pathway that exerts its pro-apoptotic effect upon heterodimerization with anti-apoptotic proteins Bcl-2 and Bcl-$X_{L}$. Expression of the BAD protein has been reported in several cancer types, but not in stomach cancer. The aim of this study was to explore the expression status of the BAD protein in gastric carcinomas. Materials and Methods: In the current study, we analyzed the expression of the BAD protein in 60 advanced gastric adenocarcinomas by using immunohistochemistry and a tissue microarray approach. Results: Immunopositivity (defined as $\geq\30\%$) was observed for the BAD protein in 57 ($95\%$) of the 60 cancers. Normal gastric mucosal cells showed weaker expressions of the BAD protein than gastric carcinomas. Conclusion: Taken together, these results suggest that stomach cancer cells in vivo may need BAD protein expression for apoptosis. Also, the higher expression of the BAD protein in stomach cancer cells than in normal gastric mucosal cells suggests that apoptosis might be easily triggered in susceptible stomach cancer cells, thereby producing selective pressure to make more apoptosis-resistant cells during tumor development.

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Comparative Analyses of Tomato yellow leaf curl virus C4 Protein-Interacting Host Proteins in Healthy and Infected Tomato Tissues

  • Kim, Namgyu;Kim, Jinnyun;Bang, Bongjun;Kim, Inyoung;Lee, Hyun-Hee;Park, Jungwook;Seo, Young-Su
    • The Plant Pathology Journal
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    • 제32권5호
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    • pp.377-387
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    • 2016
  • Tomato yellow leaf curl virus (TYLCV), a member of the genus Begomovirus, is one of the most important viruses of cultivated tomatoes worldwide, mainly causing yellowing and curling of leaves with stunting in plants. TYLCV causes severe problems in sub-tropical and tropical countries, as well as in Korea. However, the mechanism of TYLCV infection remains unclear, although the function of each viral component has been identified. TYLCV C4 codes for a small protein involved in various cellular functions, including symptom determination, gene silencing, viral movement, and induction of the plant defense response. In this study, through yeast-two hybrid screenings, we identified TYLCV C4-interacting host proteins from both healthy and symptom-exhibiting tomato tissues, to determine the role of TYLCV C4 proteins in the infection processes. Comparative analyses of 28 proteins from healthy tissues and 36 from infected tissues showing interactions with TYLCV C4 indicated that TYLCV C4 mainly interacts with host proteins involved in translation, ubiquitination, and plant defense, and most interacting proteins differed between the two tissues but belong to similar molecular functional categories. Four proteins-two ribosomal proteins, S-adenosyl-L-homocysteine hydrolase, and 14-3-3 family protein-were detected in both tissues. Furthermore, the identified proteins in symptom-exhibiting tissues showed greater involvement in plant defenses. Some are key regulators, such as receptor-like kinases and pathogenesis-related proteins, of plant defenses. Thus, TYLCV C4 may contribute to the suppression of host defense during TYLCV infection and be involved in ubiquitination for viral infection.