Journal of Pathology and Translational Medicine

Jiyoung Park

3 Articles

Brucella Prostatitis: A First Case Report Diagnosed in Korea.: Seong Yeol Ryu, Hyun Ah Kim, Jiyoung Park, Misun Choe, Kunyoung Kwon; Korean J Pathol. 2011;45:S66-S69.; DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.S1.S66

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Brucellosis is a zoonosis caused by several species of Brucella. Brucellosis is usually an acute or sub-acute febrile illness that histologically develops granulomatous inflammation. Brucella prostatitis is a very rare complication and is usually accompanied by epididymo-orchitis. We now report a case of histologically proven granulomatous prostatitis due to Brucella without clinical evidence of epididymo-orchitis. A 61-year-old farmer presented with myalgia, low back pain, and fever. A needle biopsy of the prostate was performed due to symptoms of urinary frequency and high prostate specific antigen levels (17.3 ng/mL). Histologically, the prostate showed granulomatous inflammation without caseous necrosis. Polymerase chain reaction (PCR) studies of blood and prostatic tissue for Brucella were positive, while a PCR study for Mycobacterium tuberculosis was negative. The patient was treated with doxycycline and rifampin. A possibility of Brucella prostatitis should be considered in the differential diagnosis of granulomatous prostatitis or prostatitis of unknown origin associated with or without epididymo-orchitis.

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An Imported Case of Brucella melitensis Infection in South Korea
Jee Young Lee, Yongduk Jeon, Mi Young Ahn, Hea Won Ann, In Young Jung, Wooyong Jung, Moo Hyun Kim, Jin Young Ahn, Je Eun Song, Yong Chan Kim, Dong Hyun Oh, Eun Jin Kim, Su Jin Jeong, Nam Su Ku, Hyunsoo Kim, Kyungwon Lee, June Myung Kim, Jun Yong Choi
Infection & Chemotherapy.2018; 50(2): 149. CrossRef
Brucellosis Prostatitis: A Neglected Diagnosis for a Tropical Disease
Jing Liu, Bhavika Kaul, Andrea Shioleno, Niraj Mehta, Rojelio Mejia
Current Tropical Medicine Reports.2016; 3(4): 181. CrossRef

Expression of Inducible Nitric Oxide Synthase and Nitric Oxide Mediated Apoptosis in Neuronal PC12 Cells after Lipopolysaccharide/Tumor Necrosis Factor-/Interferon- Treatment.: Jiyeon Kim, Jiyoung Kim, Kuseong Kang, Eunkyoung Kwak, Jiyoung Park, Taein Park, Yoonkyung Sohn; Korean J Pathol. 2002;36(4):249-256.

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Abstract PDF: BACKGROUND
Inducible nitric oxide synthase (iNOS) has been detected in a number of pathologic conditions in the central nervous system. This study was investigated the patterns of iNOS expression in the neuronal PC12 cell and the effects of nitric oxide on the apoptosis of PC12 cells.
METHODS
The stimulating agents for induction of iNOS expression in PC12 cells were bacterial lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-), and interferon-gamma (IFN-).
RESULTS
The expression iNOS mRNA and protein in PC12 cells stimulated with LPS/TNF-/IFN- were profoundly increased. The expression of iNOS mRNA arose at 6 hours, peaked at 12 hours, and declined to 48 hours after LPS/TNF-/ IFN- treatment. iNOS protein was increased up to 24 hours in LPS/TNF-/IFN- treated PC12 cells while the expression of nNOS was unaffected. Accumulation of NO derivatives in the culture media was markedly increased at least at up to 48 hours after LPS/TNF-/IFN- treatment. The induction of iNOS expression and NO production in differentiated PC12 cells was correlated with apoptotic cell death judged by transmission electron microscopy and DNA fragmentation from the results of the Terminal deoxynucleotidyl-transferase-mediated dUDP biotin nick end-labeling (TUNEL) method. After treatment with NOS inhibitor, N-monomethylarginine (NMMA), a profound decrease in NO production by LPS/TNF-/IFN- treated PC12 cells was noted. And the LPS/TNF-/IFN- induced apoptosis was prevented by the NMMA treatment.
CONCLUSIONS
From the above results it is concluded that the expression of iNOS in differentiated PC12 cells is induced by the combined application of LPS, TNF-, and IFN-. And the apoptosis of cultured PC12 cells is mediated by iNOS-derived NO.

Distribution of Free Radicals in Reperfusion Injury after Transient Brain Ischemia.: Eunkyoung Kwak, Hyungho Suh, Jiyoung Park, Yunsup Kum, Taein Park, Jungwan Kim, Yoonkyung Sohn; Korean J Pathol. 2000;34(11):893-900.

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Abstract PDF: Free radicals are known as an important factor which may act on reperfusion injury after transient or permanent brain ischemia. Numerous studies about cytotoxic function of free radical have been done. Most of these studies demonstrate the function of free radical in reperfusion injury by using radical scavenger or antioxidant as inhibitor of radicals. We used a modification of Karnovsky's Mn2 /diaminobenzidine (DAB) technique to demonstrate intravascular free radicals following transient occlusion and reperfusion of one middle cerebral artery in Sprague-Dawley rats. The MCA was occluded for 2 hours using an intraluminal suture method. The reperfusion time after transient ischemia was 1 hour, 6 hours, and 24 hours, respectively. Animals were perfused transcardially with solution containing Mn2 and DAB. After DAB perfusion, the brains were removed promptly, sectioned in frozen, and stained with methylene blue for light microscopic examination. Upon light microscopic examination, free radicals were confined within intravascular lumen and the amount of deposits increased according to the duration of reperfusion. Upon electron microscopic examination, free radicals were located in nuclear membrane and membrane of mitochondria and RER, and demonstrated as electron dense deposits. In addition, cell processes of the neuron revealed an electron dense deposits beneath the inner side of the membrane. In conclusion, free radicals demonstrated in the reperfusion injury area indicate that free radical acts as an important cytotoxic factor. Intracellular localization of free radicals may explain the relationship between free radical and delayed neuronal injury.

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