• 제목/요약/키워드: brain diseases

검색결과 880건 처리시간 0.032초

Expression of Epstein-Barr Virus Gene and Clonality of Infiltrated T Lymphocytes in Epstein-Barr Virus-associated Gastric Carcinoma

  • Lee, Jae-Myun;Kim, Ho-Guen;Noh, Sung-Hoon;Lee, Won-Young;Kim, Se-Jong;Park, Jeon-Han
    • IMMUNE NETWORK
    • /
    • 제11권1호
    • /
    • pp.50-58
    • /
    • 2011
  • Background: Epstein-Barr virus associated gastric lymphoepithelioma-like carcinoma (LELC) is characterized by the intensive infiltration of lymphoid cells, the presence of EBV, and the better prognosis over typical adenocarcinoma. Thus, it was assumable that viral latent proteins may be responsible for the recruitment of a certain T cell repertoire to EBV-associated gastric carcinoma. Methods: To examine above possibility, EBV gene expression in gastric carcinoma tissues and usage of TCR among the tumor infiltrating lymphocytes were analyzed. Results: EBV specific DNA and EBERs RNA were detected in 4 out of 30 patients. RT-PCR analysis revealed that all 4 of EBV-positive tumor tissues expressed EBNA1 mRNA and BARTs and LMP2a was detected only one sample out of 4. However, the EBNA2 and LMP-1 transcripts were not detected in these tissues. $CD8^+$ T cells were the predominant population of infiltrating lymphocytes in the EBV-positive gastric carcinoma. According to spectra type analysis of infiltrating T cells, 10 predominant bands were detected by TCR $V{\beta}$ CDR3 specific RT-PCR from 4 EBV-positive tumor tissues. Sequence analysis of these bands revealed oligoclonal expansion of T cells. Conclusion: These findings suggest that clonally expanded T cells in vivo might be a population of cytotoxic T cells reactive to EBV-associated gastric carcinoma.

CKD-712, (S)-1-(${\alpha}$-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Inhibits the NF-${\kappa}B$ Activation and Augments Akt Activation during TLR4 Signaling

  • Lee, Jeong-Gi;Yang, Eun-Jeong;Shin, Jeon-Soo;Kim, Dal-Hyun;Lee, Sung-Sook;Choi, In-Hong
    • IMMUNE NETWORK
    • /
    • 제11권6호
    • /
    • pp.420-423
    • /
    • 2011
  • Since CKD-712 has been developed as an anti-inflammatory agent, we examined the effect of CKD-712 during TLR4 signaling. Using HEK293 cells expressing TLR4, CKD-712 was pre-treated 1 hr before LPS stimulation. Activation of NF-${\kappa}B$ was assessed by promoter assay. The activation of ERK, JNK, p38, IRF3 and Akt was measured by western blotting. CKD-712 inhibited the NF-${\kappa}B$ signaling triggered by LPS. The activation of ERK, JNK, p38 or IRF3 was not inhibited by CKD-712. On the contrary the activation of these molecules was augmented slightly. The activation of Akt with stimulation of LPS was also enhanced with CKD-712 pre-treatment at lower concentration, but was inhibited at higher concentration. We suggest that during TLR4 signaling CKD-712 inhibits NF-${\kappa}B$ activation. However, CKD-712 augmented the activation of Akt as well as Map kinases. Therefore, we suggest that CKD-712 might have a role as an immunomodulator.

Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model

  • Lee, Seung Hak;Jung, Bong-Kwang;Song, Hyemi;Seo, Han Gil;Chai, Jong-Yil;Oh, Byung-Mo
    • Parasites, Hosts and Diseases
    • /
    • 제58권4호
    • /
    • pp.461-466
    • /
    • 2020
  • Toxoplasma gondii is an obligate intracellular protozoan parasite that can invade various organs in the host body, including the central nervous system. Chronic intracranial T. gondii is known to be associated with neuroprotection against neurodegenerative diseases through interaction with host brain cells in various ways. The present study investigated the neuroprotective effects of chronic T. gondii infection in mice with cerebral ischemia experimentally produced by middle cerebral artery occlusion (MCAO) surgery. The neurobehavioral effects of cerebral ischemia were assessed by measurement of Garcia score and Rotarod behavior tests. The volume of brain ischemia was measured by triphenyltetrazolium chloride staining. The expression levels of related genes and proteins were determined. After cerebral ischemia, corrected infarction volume was significantly reduced in T. gondii infected mice, and their neurobehavioral function was significantly better than that of the uninfection control group. Chronic T. gondii infection induced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) in the brain before MCAO. T. gondii infection also increased the expression of vascular endothelial growth factor after the cerebral ischemia. It is suggested that chronic intracerebral infection of T. gondii may be a potential preconditioning strategy to reduce neural deficits associated with cerebral ischemia and induce brain ischemic tolerance through the regulation of HIF-1α expression.

뇌 수막종 및 낭종에서 자기공명영상 펄스 시퀀스 변화에 따른 신호대잡음비의 통계적 접근 (Statistical Approach of Measurement of Signal to Noise Ratio in According to Change Pulse Sequence on Brain MRI Meningioma and Cyst Images)

  • 이을규;최관우;정회원;장서구;김기원;손순룡;민정환;손진현
    • 대한방사선기술학회지:방사선기술과학
    • /
    • 제39권3호
    • /
    • pp.345-352
    • /
    • 2016
  • 본 연구는 뇌 자기공명영상에서 질환관심영역(ROI)을 설정하여 신호대잡음비(SNR)를 펄스 시퀀스 별로 분석하여 MRI CAD 개발에 필요한 기초자료를 활용하고자 하는 것이 본 연구의 목적이다. 연구대상은 2005년 1월부터 2015년 12월까지 서울소재 대학병원에서 뇌 조영자기공명영상(Brain MRI Contrast Enhancement)을 검사한 환자 117명이다. 측정이 용이한 질환 2종류 수막종(Meningioma), 낭종(Cyst)을 측정대상으로 하였고, 측정방법은 Image J 프로그램을 사용하였다. 뇌질환의 SNR값을 측정하여 SPSS Statistics21 통계프로그램으로 ANOVA 분석을 하였으며 p < 0.05에서 유의한 것으로 판단하였다. 표본의 인구사회학적 특성, 시퀀스별 SNR의 평균값, 95% 신뢰 구간 값, SNR 평균차이 값 등을 분석하였다. 각 질환의 시퀀스별 분석결과는 Meningioma: T1CE > T2 > T1, FLAIR (p<0.05); Cyst: T2 > T1, T1CE > FLAIR (p < 0.05)였다. SNR 수치로 시퀀스들의 특징을 조합하여 질환의 특성을 파악할 수 있어 향후 자기공명영상검사의 정확성과 편의성을 제공하고, 판독보조진단 프로그램 개발의 기초자료로 활용될 수 있을 것으로 기대된다.

CADASIL 동물모델의 생리학적 접근 및 연구적 가치의 예측 (Physiological approach of CADASIL animal model and its predictable implication)

  • 정성철;고은아
    • Journal of Medicine and Life Science
    • /
    • 제16권3호
    • /
    • pp.55-59
    • /
    • 2019
  • Cerebral vessels are functionally and structurally specialized to provide adequate blood flow to brain which shows high metabolic rates. Cerebral hemorrhage or ischemic infarction due to cerebrovascular injury or occlusion can cause the immediate brain damage, and if not treated rapidly, can lead to serious or permanent brain damages, and sometimes life-threatening. Unlike these popular cerebrovascular diseases, there are diseases caused by genetic problems. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is one of them. CADASIL does not show the high incidence, but it is considered to be significantly affected by regional obstructiveness such as islands and therefore, to be an important genetic disease in Jeju. This paper aims to summarize the possibility of animal model research that can provide preclinical data for CADASIL disease research and to evaluate its applicability in future research plans.

Temporal Transcriptome Analysis of SARS-CoV-2-Infected Lung and Spleen in Human ACE2-Transgenic Mice

  • Jung Ah, Kim;Sung-Hee, Kim;Jung Seon, Seo;Hyuna, Noh;Haengdueng, Jeong;Jiseon, Kim;Donghun, Jeon;Jeong Jin, Kim;Dain, On;Suhyeon, Yoon;Sang Gyu, Lee;Youn Woo, Lee;Hui Jeong, Jang;In Ho, Park;Jooyeon, Oh;Sang-Hyuk, Seok;Yu Jin, Lee;Seung-Min, Hong;Se-Hee, An;Joon-Yong, Bae;Jung-ah, Choi;Seo Yeon, Kim;Young Been, Kim;Ji-Yeon, Hwang;Hyo-Jung, Lee;Hong Bin, Kim;Dae Gwin, Jeong;Daesub, Song;Manki, Song;Man-Seong, Park;Kang-Seuk, Choi;Jun Won, Park;Jun-Won, Yun;Jeon-Soo, Shin;Ho-Young, Lee;Jun-Young, Seo;Ki Taek, Nam;Heon Yung, Gee;Je Kyung, Seong
    • Molecules and Cells
    • /
    • 제45권12호
    • /
    • pp.896-910
    • /
    • 2022
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible and potentially fatal virus. So far, most comprehensive analyses encompassing clinical and transcriptional manifestation have concentrated on the lungs. Here, we confirmed evident signs of viral infection in the lungs and spleen of SARS-CoV-2-infected K18-hACE2 mice, which replicate the phenotype and infection symptoms in hospitalized humans. Seven days post viral detection in organs, infected mice showed decreased vital signs, leading to death. Bronchopneumonia due to infiltration of leukocytes in the lungs and reduction in the spleen lymphocyte region were observed. Transcriptome profiling implicated the meticulous regulation of distress and recovery from cytokine-mediated immunity by distinct immune cell types in a time-dependent manner. In lungs, the chemokine-driven response to viral invasion was highly elevated at 2 days post infection (dpi). In late infection, diseased lungs, post the innate immune process, showed recovery signs. The spleen established an even more immediate line of defense than the lungs, and the cytokine expression profile dropped at 7 dpi. At 5 dpi, spleen samples diverged into two distinct groups with different transcriptome profile and pathophysiology. Inhibition of consecutive host cell viral entry and massive immunoglobulin production and proteolysis inhibition seemed that one group endeavored to survive, while the other group struggled with developmental regeneration against consistent viral intrusion through the replication cycle. Our results may contribute to improved understanding of the longitudinal response to viral infection and development of potential therapeutics for hospitalized patients affected by SARS-CoV-2.

Statistical network analysis for epilepsy MEG data

  • Haeji Lee;Chun Kee Chung;Jaehee Kim
    • Communications for Statistical Applications and Methods
    • /
    • 제30권6호
    • /
    • pp.561-575
    • /
    • 2023
  • Brain network analysis has attracted the interest of neuroscience researchers in studying brain diseases. Magnetoencephalography (MEG) is especially proper for analyzing functional connectivity due to high temporal and spatial resolution. The application of graph theory for functional connectivity analysis has been studied widely, but research on network modeling for MEG still needs more. Temporal exponential random graph model (TERGM) considers temporal dependencies of networks. We performed the brain network analysis, including static/temporal network statistics, on two groups of epilepsy patients who removed the left (LT) or right (RT) part of the brain and healthy controls. We investigate network differences using Multiset canonical correlation analysis (MCCA) and TERGM between epilepsy patients and healthy controls (HC). The brain network of healthy controls had fewer temporal changes than patient groups. As a result of TERGM, on the simulation networks, LT and RT had less stable state than HC in the network connectivity structure. HC had a stable state of the brain network.

중풍 발병 부위별 위험요인 및 전조증상 조사연구 (Investigation on Risk Factor and Warning Signs According to Stroke Lesion)

  • 정재한;선종주;민인규;김미영;최원우;홍진우;나병조;정우상;문상관;조기호;김영석
    • 대한한방내과학회지
    • /
    • 제28권4호
    • /
    • pp.808-815
    • /
    • 2007
  • Objectives : This study investigated stroke lesions and their relationship with warning signs and risk factors in stroke patients. Methods : Three hundred fifty-three stroke patients were recruited at the Department of Cardiovascular and Neurologic Diseases (stroke center) of Kyung Hee University Oriental hospital from October 2005 to July 2007. We evaluated their stroke lesions with brain MRI, their warning signs, and risk factors. Results : 353 subjects were included in the final analysis. The frequency of diabetes was found more in presence of brain stem lesion than without. The cortex lesion showed a close relationship with smoking, drinking and the frequency of one side paralysis or weakness. These were more common in males than in females. Conclusions : We observed stroke lesions and their characteristics in stroke patients. The subjects' brain lesions seemed affectedby the risk factors. A concrete conclusion can hardly be drawn from this study; additional research is necessary.

  • PDF

Ribosomal Protein L19 and L22 Modulate TLR3 Signaling

  • Yang, Eun-Jeong;Seo, Jin-Won;Choi, In-Hong
    • IMMUNE NETWORK
    • /
    • 제11권3호
    • /
    • pp.155-162
    • /
    • 2011
  • Background: Toll-like receptor 3 (TLR3) recognizes double-stranded RNA (dsRNA) and induces inflammation. In this study we attempted to ascertain if there are endogenous host molecules controlling the production of cytokines and chemokines. Two candidates, ribosomal protein L19 and L22, were analyzed to determine if they influence cytokine production followed by TLR3 activation. In this study we report that L19 acts upon production of IP-10 or IL-8 differently in glioblastoma cells. Methods: L19 or L22 was transfected into HEK293-TLR3, A549 or A172 cells. After treatment with several inhibitors of NF-${\kappa}B$, PI3K, p38 or ERK, production of IL-8 or IP-10 was measured by ELISA. siRNA was introduced to suppress expression of L19. After Vesicular stomatitis virus infection, viral multiplication was measured by western blot. Results: L19 increased ERK activation to produce IL-8. In A172 cells, in which TLR3 is expressed at endosomes, L19 inhibited interferon regulatory factor 3 (IRF3) activation and IP-10 production to facilitate viral multiplication, whereas L19 inhibited viral multiplication in A549 cells bearing TLR3 on their cell membrane. Conclusion: Our results suggest that L19 regulates TLR3 signaling, which is cell type specific and may be involved in pathogenesis of autoimmune diseases and chronic inflammatory diseases.

Dexamethasone Downregulates Expressions of 14-3-3β and γ-Isoforms in Mice with Eosinophilic Meningitis Caused by Angiostrongylus cantonensis Infection

  • Tsai, Hung-Chin;Chen, Yu-Hsin;Yen, Chuan-Min;Chung, Li-Yu;Wann, Shue-Ren;Lee, Susan Shin-Jung;Chen, Yao-Shen
    • Parasites, Hosts and Diseases
    • /
    • 제57권3호
    • /
    • pp.249-256
    • /
    • 2019
  • Steroids are commonly used in patients with eosinophilic meningitis caused by A. cantonensis infections. The mechanism steroids act on eosinophilic meningitis remains unclear. In this mouse experiments, expressions of 14-3-3 isoform ${\beta}$ and ${\gamma}$ proteins significantly increased in the CSF 2-3 weeks after the infection, but not increasedin the dexamethasone-treated group. Expression of 14-3-3 ${\beta}$, ${\gamma}$, ${\varepsilon}$, and ${\theta}$ isoforms increased in brain meninges over the 3-week period after infection and decreased due to dexamethasone treatment. In conclusion, administration of dexamethasone in mice with eosinophilic meningitis decreased expressions of 14-3-3 isoform proteins in the CSF and in brain meninges.