1.A Case of Fetal Hydantoin Syndrome Associated with Cardiac Anomaly.
Hae Kyung LEE ; Joo Soo PARK ; Keong Bae PARK ; Young Chang KIM
Journal of the Korean Pediatric Society 1995;38(6):853-856
No abstract available.
2.Clinical Manifestation of Necrotizing Pneumonia in Healthy Children.
Seong Phil BAE ; Do Hyun KIM ; Sang Hoon CHAE ; Ihl Sung PARK ; Keong Bae PARK ; Mi Yong SHIN ; Joon Soo PARK ; Young Tong KIM
Soonchunhyang Medical Science 2013;19(2):87-92
OBJECTIVE: Necrotizing pneumonia (NP) is a severe complication of lobar pneumonia caused by various pathogens. The immunopathogenesis and clinical characteristics of NP in children are not clearly understood. We wanted to evaluate the clinical characteristics and suggest in part the immunopathogenesis of NP. METHODS: We reviewed retrospectively the medical charts and radiographic materials of eight patients with NP, who were diagnosed by chest radiography and chest computed tomography at the Department of Pediatrics, Soonchunhyang University Hospitals at Cheonan and Bucheon from January 2002 to December 2011. RESULTS: They were previously healthy, 2.1 to 4.6 years of ages (mean, 2.8+/-1.0 years) and three boys and five girls. All of them had pleural effusion. Five patients had pneumonic consolidations in right upper lung field. Three patients had pneumatocele. They developed leukocytosis (mean, 19,400+/-6,400/mm3), higher C-reactive protein level (mean, 25.1+/-8.0 mg/dL). The etiologic agents were revealed in two patients; Streptococcus pneumonia (S. pneumonia) was revealed in one patient and S. pneumonia and Mycoplasma pneumonia in the other patient. Three patients were treated with additional intravenous immunoglobulin. Clinical improvement was prolonged: fever lasted 10 to 23 days, and length of hospitalization was 15 to 36 days. NP or pneumatocele were completely resolved on the follow-up radiographic studies in all of the patients. CONCLUSION: Although the previously healthy young children with NP had protracted clinical course, they recovered without any problematic sequelae. Our results suggest that the immunopathogenesis of NP in children may be associated with the exaggerated immune reaction of the host to insults from initial bacterial infections, rather than the pathogen-induced cytopathies.
Bacterial Infections
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C-Reactive Protein
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Child*
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Chungcheongnam-do
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Female
;
Fever
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Follow-Up Studies
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Gyeonggi-do
;
Hospitalization
;
Hospitals, University
;
Humans
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Immunoglobulins
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Leukocytosis
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Lung
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Pediatrics
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Pleural Effusion
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Pneumonia*
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Pneumonia, Mycoplasma
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Radiography
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Retrospective Studies
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Streptococcus
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Thorax
3.The Effect of Vasoactive Intestinal Peptide on Cord Blood CD34 (+) Cells.
Mi Kyong YEO ; Hwa Young BAE ; Min Kyu HUR ; Jae Sun RA ; In Seob HAN ; Min Keong KIM ; Soon Ki KIM ; Sang Kyu PARK
Korean Journal of Pediatric Hematology-Oncology 2003;10(2):262-268
PURPOSE: We investigated the expression of vasoactive intestinal peptide (VIP), VIP receptor 1 (VPAC1), VIP receptor 2 (VPAC2) genes in the human umbilical cord blood CD34 cells, and the ability of VIP to stimulate human primitive as well as monopotent hematopoietic progenitors. METHODS: We isolated RNA from umbilical cord blood CD34 cells, and then performed RT-PCR, and sequencing. The umbilical cord blood CD34 cells were cultured with the various concentrations of VIP for burst-forming unit of erythrocyte (BFU-E), colony-forming unit of granulocyte/monocyte (CFU-GM), colony-forming unit of graulocyte/erythrocyte/monocyte/megakaryocyte (CFU-GEMM), and colony-forming unit of megakaryocyte (CFU-Mk). RESULTS: The RNA coding for VPAC1 was detected in human umbilical cord blood CD34 cells. VIP significantly stimulated the growth of CFU-GEMM and CFU-Mk. CONCLUSION: The present results suggest that VIP is an important neuropeptide in the early proliferation of human primitive as well as megakaryocyte progenitors.
Clinical Coding
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Erythrocytes
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Fetal Blood*
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Humans
;
Megakaryocyte Progenitor Cells
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Megakaryocytes
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Myeloid Progenitor Cells
;
Neuropeptides
;
Receptors, Vasoactive Intestinal Peptide
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RNA
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Stem Cells
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Vasoactive Intestinal Peptide*