• Childhood Kidney Diseases
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• v.17 no.2
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• pp.110-116
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• 2013

Purpose: The $^{99m}Tc$-Dimercaptosuccinic acid (DMSA) renal scan is used primarily for the diagnosis of renal scarring and acute pyelonephritis in children with urinary tract infections (UTI). This study aimed to evaluate clinical differences based on the positive or negative results of DMSA scans and kidney ultrasonography (US) in pediatric UTI. Method: We retrospectively reviewed 142 pediatric patients with UTI who were admitted to Myongji Hospital from January 2004 to December 2012. We performed a comparative analysis of clinical parameters such as age, sex, white blood cell (WBC) count, neutrophil count, blood urea nitrogen (BUN) level, creatinine (Cr) level, C-reactive protein (CRP) level, and durations of hospitalization and fever, grouped by the results of the DMSA scans and kidney US. Results: The mean age of the patients was $33.8{\pm}48.3$ months, and 78 (55%) were male. Fifty-two patients had abnormal DMSA findings, and 71 patients had abormal kidney US findings (test positive groups). In the DMSA scan positive group, there were significant differences in age, WBC counts, neutrophil counts, CRP level, BUN level, Cr level, hospitalization duration, number of abnormal findings on kidney US, and incidence of vesicoureteral reflux (VUR) compared with the scan negative group. The kidney US positive group had significant differences in age, neutrophil count, CRP level, BUN level, Cr level, hospitalization duration, number of abnormal findings on the DMSA scans, and more frequent VUR compared with the US negative group. Conclusion: Our data suggest that there were no major differences in clinical parameters based on the results of the DMSA scans compared with kidney US in pediatric UTI. However, as kidney US and DMSA scan were performed to predict VUR, the sensitivity and negative predictive value was increased.

• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.451-463
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• 2006

Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.