Background : Nonspecific interstitial pneumonia (NSIP) has been reported recently to have shown much better response to medical treatment and better prognosis compared with idiopathic UIP. However, clinical characteristics of idiopathic NSIP discriminating it from UIP have not been clearly defined. Method : Among 120 patients with biopsy-proven diffuse interstitial lung diseases admitted to the Samsung Medical Center between July 1996 and March 2000, 18 patients with idiopathic NSIP were included in this study. Retrospective chart review and radiographic analysis were performed. Results : 1) At diagnosis, 17 patients were female and the average age was $55.2{\pm}8.4$ years (44~73 years). The average duration from development of respiratory symptom to surgical lung biopsy was $9.9{\pm}17.1$ months. Increase in bronchoalveolar lavage fluid lymphocytes ($23.0{\pm}13.1%$) was noted. On HRCT, ground glass and irregular linear opacity were observed, but honeycombing was absent in all patients. 2) Corticosteroids were initially given to 13 patients, but the medication was stopped in 3 patients due to severe side effects. Further medical therapy was not possible in 1 patient who experienced streroid-induced psychosis. Herpes zoster (n=3), tuberculosis (n=1), avascular necrosis of the hip (n=1), cataract (n=2) and diabetes mellitus (n=1) developed during prolonged corticosteroid administration. Of the 7 patients receiving oral cyclophosphamide therapy, hemorrhagic cystitis hindered one patient from continuing with the medication. 3) After medical treatment, 14 of 17 patients improved, and 3 patients remained stable (mean follow-up ; $24.1{\pm}11.2$ months). FVC increased by $20.2{\pm}11.2%$ of predicted value and the extent of ground glass opacity on HRCT decreased significantly ($15.7{\pm}14.7%$). 4) Of the 14 patients who had stopped medication, 5 showed recurrence of NSIP and 2 became aggravated during steroid tapering. All patients with recurrence showed deterioration within one year after completion of initial treatment. Conclusion : Since idiopathic NSIP has unique clinical profiles and shows good prognosis, diagnosis different from UIP, and aggressive medical treatment are needed.
Jung, Jae Woo;Lee, Young Woo;Choi, Jae Cheol;Yoo, Seung Min;Lee, Hwa Yeon;Lim, Seoung Young;Shin, Jong Wook;Kim, Jae Yoel;Park, In Whn;Kim, Mi Kyung;Choi, Byoung Whui
Tuberculosis and Respiratory Diseases
/
v.60
no.5
/
pp.523-531
/
2006
Background : Cervical tuberculous lymphadenopathy is a very common disease with a similar incidence to pulmonary tuberculosis. Dendritic cells play a role of initial antigen presentation of this illness. Nevertheless, the precise role of these antigen-presenting cells according to the clinical features in unclear. The aim of this study was to determine the clinical implication of dendritic cell infiltration in the cervical lymph nodes. Methods : A review of the clinical characteristics was carried out retrospectively based on the clinical records and radiography. Immunohistochemical staining was performed on the available histology specimens of 72 cases using the S-100b polyclonal antibody for dendritic cells. The number of dendritic cells with tuberculous granuloma were determined. A $X^2$ test, unpaired T test and multiple logistic regression analysis were performed. Results : Thirty percent of subjects had previous or concurrent pulmonary TB. Twenty one percent of cases showed a positive reaction on the AFB stain. Within a granuloma, the number of infiltrated dendritic cells was $113.0{\pm}7.0$. The incidence of fever and cough decreased with increasing infiltration of dendritic cells Multivariate regression analysis showed that the infiltration of dendritic cells could significantly contribute to fever. Conclusion : Overall, dendritic cells can control a Mycobacterium tuberculosis infection and modulate the immune response, as well as resolve the clinical manifestations of TB lymphadenopathy.
Kim, Chae-Gi;Yoon, Wern Chan;Song, Yong-Ho;Kim, Sang-Gyung;Choe, Jung-Yoon
IMMUNE NETWORK
/
v.1
no.3
/
pp.244-249
/
2001
The transforming growth $factor-{\beta}$ ($TGF-{\beta}$) is a multifunctional cytokine modulating the onset and course of autoimmune disease as shown in experimental models. In synovial inflammation, there is a potential role for $TGF-{\beta}$ in repairment, the inhibition of cartilage and bone destruction, and the down-regulation of immune response. The biologic effects of $TGF-{\beta}$ depend on the cell type, the isoform and the availability of active $TGF-{\beta}$. We investigated $TGF-{\beta}$ expression in patients with rheumatoid arthritis (RA) and compared to those of osteoarthritis (OA). And we determined a correlation between $TGF-{\beta}1$ and $TGF-{\beta}2$, and also the relationships between each $TGF-{\beta}$ isoform and the parameters for disease activity of RA. Methods: The study population consisted of 20 patients with RA and 20 patients with OA. The commercial ELISA kit was used to study $TGF-{\beta}1$ and $TGF-{\beta}2$ levels in peripheral blood (PB) and synovial fluids (SF). Results: 1) While PB $TGF-{\beta}1$ level was of no difference between RA and OA patient groups, SF $TGF-{\beta}1$ level was higher in RA group than OA group. Similarly, PB $TGF-{\beta}2$ levels of RA and OA groups was not different, but SF $TGF-{\beta}2$ levels was higher in RA group than OA group. 2) In patients with RA, the $TGF-{\beta}1$ levels were higher than $TGF-{\beta}2$ in both the PB and SF, while in patients with OA, there showed higher readings for $TGF-{\beta}1$ than $TGF-{\beta}2$ in SF but no difference between $TGF-{\beta}1$ and $TGF-{\beta}2$ levels in PB. 3) In patients with RA, there were no correlations between PB $TGF-{\beta}1$ and PB $TGF-{\beta}2$ levels, nor between SF $TGF-{\beta}1$ and SF $TGF-{\beta}2$ levels. At the same way, there was no correlation between PB $TGF-{\beta}1$ and SF $TGF-{\beta}1$ levels, nor between each levels of $TGF-{\beta}2$ in patients with RA. 4) There was also no correlation between each $TGF-{\beta}$ isoform and the parameters for disease activity such as ESR, CRP, tender joint count, swollen joint count, rheumatoid factor, and the duration of morning stiffness except between in PB $TGF-{\beta}1$ and disease duration of RA (r=0.637, p<0.01). Conclusion: Each $TGF-{\beta}$ isoforms were higher in synovial fluid of patients with RA than that of patients with OA. The data from the RA patients demonstrated different patterns of expressions of the isoforms depending on which compartment (PB or SF) was investigated. The quantification of different $TGF-{\beta}$ isoform is thought to be important when $TGF-{\beta}$ is measured under disease conditions of RA.
Lee, Ji Hyun;Jang, Kyoung Soo;Choi, Yong Ho;Kim, Jin-Cheol;Choi, Gyung Ja
Research in Plant Disease
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v.22
no.2
/
pp.72-80
/
2016
Gummy stem blight, caused by the fungus Didymella bryoniae, is major disease of watermelons worldwide. The objective of the present study was to establish an efficient screening system to identify watermelon resistant to D. bryoniae. An GSB3 isolate was prepared from a watermelon plant showing typical symptoms of gummy stem blight in Haman-gun and identified as D. bryoniae based on molecular analysis of internal transcribed spacer sequence. A simple mass-production technique of inoculum was developed based on spore production of D. bryoniae GSB3 under several incubation conditions and their virulence on watermelon plants. Resistance degrees of 22 commercial watermelon cultivars to the GSB3 isolate were evaluated. Among them, four watermelon cultivars showing different degree of resistance response were selected for further study. Development of disease on the cultivars according to various conditions including inoculum concentrations, incubation periods in dew chamber, and incubation temperatures was investigated. From the results, we suggest an efficient screening method for resistant watermelon cultivars to gummy stem blight. Seeds of watermelon cultivar are sown and grown in a greenhouse until plant stage of 2-fully expanded leaves. Seedlings are inoculated with D. bryoniae by spraying spore suspension of the fungus at a concentration of $5.0{\times}10^5spores/ml$. The infected plants are incubated in humidity chamber at $25^{\circ}C$ for 48 hours and then transferred to a growth chamber at $25^{\circ}C$ and 80% relative humidity with 12-hour light a day. Three to four days after inoculation, disease severity of the plant are measured using percentage of infected leaf area.
Chung, Hyunjung;Roh, Jae-Hwan;Yang, Jung-Wook;Shim, Hyeong-Kwon;Jeong, Da Gyeong;Kim, Joo Yeon;Shin, Jin Young;Kang, In Jeong;Heu, Sunggi
Research in Plant Disease
/
v.25
no.4
/
pp.164-172
/
2019
Rice blast disease caused by Magnaporthe oryzae is the most important disease of rice in both South and North Korea. Cultivation of disease-resistant cultivar is the best way to prevent this notorious disease, but M. oryzae races have been continuously changed to adapt a new cultivar. Therefore, it is important to get the information about the race and avirulence genes of the pathogen for developing blast-resistant rice cultivar. Since the entrance of North Korea was prohibited, the information about the races of M. oryzae in North Korea border areas and South Korea was collected to get the information about the diversity of rice blast pathogen in North Korea. The disease occurrence on monogenic lines carrying single resistant gene was investigated in Jeonju, Suwon, Cheorwon, Goseong, and Baengnyeongdo in Korea, and Dandong in China. The monogenic lines in Jeonju and Suwon showed diverse ranges of the response, while those in Baengnyeongdo and Dandong showed relatively high resistant responses to rice blast. All the field isolates of M. oryzae were characterized for rice blast races by the Korean differential varieties and screened for known avirulence genes to determine the spatial distribution of avirulence genes and the population of M. oryzae.
Background: High-dose chemotherapy is increasingly employed in many refractory malignant diseases. This therapy has been reported to increase response rate and survival benefits but it is also associated with higher treatment-related morbidity and mortality. We evaluated clinical characteristics and course of the pulmonary toxicity following high-dose chemotherapy with peripheral blood stem cell transplantation. Methods: Ninety-seven patients who had received high-dose chemotherapy with peripheral blood stem cell transplantation were evaluated. Five patients who developed lung lesions which were not related to infection nor primary malignant disease underwent transbronchial lung biopsy. The patients' clinical characteristics, treatments, and prognosis were reviewed retrospectively. Results: Five patients(5.1%) developed idiopathic pneumonia syndrome. The high dose chemotherapy regimens employed were cyclophosphamide, BCNU, and cisplatin in 3 cases, one case of BCNU, etoposide, Ara-C, and cyclophosphamide combination, and a regimen consisting of BCNU, etoposide, Ara-C, and melphalan. The total dose of BCNU used was 300-400 mg/$m^2$ and that of cyclophosphsmide was 6,000 mg/$m^2$. All of 5 patients received radiation therapy before this treatment. After an average duration of 14 weeks (4-26 weeks) of high-dose chemotherapy, patients developed cough, dyspnea and fever. The chest X-rays showed bilateral diffuse infiltration in 3 cases and the focal infiltration in the other 2 cases. All the patients received corticosteroid therapy as a treatment for the lung lesions. Two of them progressed to acute respiratory distress syndrome and died. Three patients recovered without residual lung lesion but one of them died of dilated cardiomyopathy. Conclusion: High-dose chemotherapy with peripheral blood stem cell transplantation especially which containing BCNU regimen may develop idiopathic pneumonia syndrome related to pulmonary toxicity and corticosteroid therapy may be bel1eficial in some cases.
Kang, Jin-Han;Kim, Jong Hyun;Park, Yong-Soo;Choi, Young-Chul;Noh, Heil;Yang, Hoon Shik;Kim, Kyu Sung;Moon, Yeon Sook;Hong, Young Jin
Clinical and Experimental Pediatrics
/
v.46
no.5
/
pp.459-466
/
2003
Purpose : AOM is the most common bacterial URI in children. The bacteriology and antibiotic Tx of AOM in children has been studied in many countries. But, there is few study of causative pathogens and antibiotic Tx of AOM in our country. In this aspect, we performed prospective clinical study to confirm the causative pathogens and assess the clinical responses of cefprozil in AOM patients. Methods : Thirty three AOM patients enrolled in this study. Tympanocentesis for isolation of causative pathogens were performed before Tx of cefprozil. The study patients received cefprozil with dose of 15 mg/kg/bid.po/day for 10-12 days, and initially assessed the clinical response at 4-5 days after receiving cefprozil and finally at the end visit. In vitro susceptibility tests of cefprozil to isolated pathogens were done by disc diffusion method, and in vitro susceptibility tests of cefaclor and cefixime to isolated pathogens were simultaneously performed. Results : Bacterial pathogens[S. pneumoniae(10), H. influenzae(5), S. aureus(2), M. catarrhalis(1) and Group A stretococcus(1)] were isolated from 19 patients. Clinically, all patients had history of abrupt high fever except one. Tympanic perforation was dominant in pathogens isolated cases, and otalgia was significantly developed in non-pathogens isolated cases. The ages of pathogens isolated cases were usually below 2 years. Eighty four point nine percent of the patients including two cases with isolation of intermediate resistant S. pneumoniae were clinically improved. Antimicrobial in vitro activity to S. pneumoniae of cefprozil were superior than that of cefacor and cefixime. Conclusion : We confirm that bacteria has the causative role in about 60% cases, and S. pneumoniae is the most common pathogen. Clinically, there were some differences in symptoms, signs and ages between pathogens isolated and non-pathogens isolated cases. The clinical responses of cefprozil in our patients revealed similar outcomes to other countries. And we reconfirm that cefprozil may be clinically effective in cases of AOM due to intermediate resistant S. pneumoniae.
Park, Hee-Kyung;Chun, Yang-Hyun;Hong, Jung-Pyo;Auh, Q-Schick
Journal of Oral Medicine and Pain
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v.33
no.3
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pp.247-256
/
2008
The belief that stress leads to illness has a long history. A number of the orofacial disease are also closely associated with stress. Despite research in the relationship of stress and the orofacial diseases leading to statistically significant correlations, the pathology remains vague. In the present study, the expression of clusterin, a stress protein responsible for antiapoptosis and cytoprotection, under restraint stress condition was observed in the submandibular gland, one of the major salivary glands. Sprague-Dawley rats were divided into 2 groups: normal group and restraint stress group. The rats of restraint stress group were placed in the stress cages and then sacrificed at day 0, 3 and 5 day of the experiment. After that, the submandibular glands of all the rats were excised immediately. The levels of clusterin proteins and mRNA in the tissues were measured by immunohistochemistry and Northern blot analyses, respectively. The results were as follows: 1. In the immunohistochemistry, clusterin protein was detected only immediately after the application of restraint stress. 2. In the restraint stress group, at day 3 and 5, histologically apoptosis was induced with karyorrhectic and pyknotic changes. 3. By the restraint stress, acinic cells were destructed earlier than ductal cells. 4. In the Northern blot, mRNA of clusterin was expressed only immediately after the application of restraint stress. The overall results suggest that as an early response to stress, clusterin is expressed in the glands to protect the glandular cells from the stress. But if stress is so strong and prolonged that it can exceed the stress adaptability of the cells, then the cells may undergo apoptosis instead of producing clusterin. An Epidemiologic Study of Symptoms of Temporomandibular Disorders in Korean College Students.
Athletic performance is an important criteria used for the selection of superior horses. However, little is known about exercise-related epigenetic processes in the horse. DNA methylation is a key mechanism for regulating gene expression in response to environmental changes. We carried out comparative genomic analysis of genome-wide DNA methylation profiles in the blood samples of two different thoroughbred horses before and after exercise by methylated-DNA immunoprecipitation sequencing (MeDIP-Seq). Differentially methylated regions (DMRs) in the pre-and post-exercise blood samples of superior and inferior horses were identified. Exercise altered the methylation patterns. After 30 min of exercise, 596 genes were hypomethy-lated and 715 genes were hypermethylated in the superior horse, whereas in the inferior horse, 868 genes were hypomethylated and 794 genes were hypermethylated. These genes were analyzed based on gene ontology (GO) annotations and the exercise-related pathway patterns in the two horses were compared. After exercise, gene regions related to cell division and adhesion were hypermethylated in the superior horse, whereas regions related to cell signaling and transport were hypermethylated in the inferior horse. Analysis of the distribution of methylated CpG islands confirmed the hypomethylation in the gene-body methylation regions after exercise. The methylation patterns of transposable elements also changed after exercise. Long interspersed nuclear elements (LINEs) showed abundance of DMRs. Collectively, our results serve as a basis to study exercise-based reprogramming of epigenetic traits.
Background : Steroid therapy has been shown to improve the clinical outcome in acute respiratory distress syndrome (ARDS) patients with histological evidence of fibroproliferation in the lung tissue and no identifiable source of infection. Because the histopathological features of acute interstitial pneumonia(AIP) are identical with that of ARDS, early steroid therapy was used in AIP patients who had histological evidence of fibroproliferation in the lung tissue and no identifiable source of infection. We analyzed seven years of our experience to evaluate the efficacy of early steroid therapy in AIP. Materials and Methods : A retrospective review was performed on AIP patients who received steroid therapy within 7 days of mechanical ventilatory support in Dankook university Hospital between May 1995 and May 2002. AIP was diagnosed clinically by ARDS without a known cause of the etiology and pathologically by a lung biopsy showing a fibroproliferative stage of diffuse alveolar damage. The clinical response and physiologic parameters were evaluated during steroid therapy. Results : Five AIP patients received intravenous methylprednisolone (1-2 mg/kg every 6 hours) after $0.6{\pm}1.7$ days of mechanical ventilatory support. Lung biopsies were performed after $1.8{\pm}1.4$ days of mechanical ventilatory support. Four patients(80%) survived and were extubated after $2.8{\pm}0.4$ days of steroid therapy with improvement in the $PaO_2/FiO_2$ ratio ($127.4{\pm}10.0$ at day 0 to $223.8{\pm}37.6$ at day 7) by steroid therapy. However, one patient(20%) died of respiratory failure after 15 days of steroid therapy. Conclusion : Early steroid therapy sppears to be beneficial in AIP patients without evidence of infection. However, as our study group was too small, further large scale studies to define the effectiveness of steroids are required.
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