Myositis unrelated to the inoculation site after COVID-19 vaccination: a case report

We describe the case of a 49-year-old right hand-dominant woman with myositis of the biceps brachii muscle unrelated to the inoculation site following Pfizer-BioNTech COVID-19 vaccination on the deltoid muscle of the left shoulder. Coronavirus disease 2019 (COVID-19) pandemic has involved global spread, and different vaccines including inactivated, protein, vectored, and nucleic acid vaccines have been developed and administered. Common side effects of COVID-19 vaccines include general manifestations such as headache, fever, and fatigue, and various musculoskeletal symptoms. Here, we present a case of myositis occurring in the biceps brachii muscle unrelated to the inoculation site, which has not been reported previously, accompanied by a literature review.

Distal Femur Fractures Treated with Distal Femoral Locking Plate Fixation:A Retrospective Study of One Year Mortality and Risk Factors

Purpose@#This study examined the one-year mortality after locking plate fixation for distal femur fractures and the risk factors related to death. @*Materials and Methods@#From July 2011 to June 2020, 128 patients who underwent locking plate fixation for distal femur fractures were analyzed retrospectively. Epidemiologic information of the patients, characteristics related to fracture and surgery, and death were investigated. The risk factors related to death were investigated using Cox analysis, and a subgroup analysis was also performed based on the age of 65 years. @*Results@#The one-year mortality rate after locking plate fixation for distal femur fractures was 3.9%, and the mortality rates in patients younger than 65 years and older than 65 years were 0% and 6.7%, respectively. There were no significant risk factors related to death in the total population. On the other hand, in patients aged 65 years or older, however, high-energy fracture and high comorbidity index increased the risk of death after surgery by 6.9-fold and 1.9-fold, respectively. @*Conclusion@#The one-year mortality rate for the total patients was 3.9%, but the mortality rate for patients over 65 years of age increased to 6.7%. High-energy fractures and high comorbidity index were risk factors related to death after surgery for distal femur fractures in patients aged 65 years or older.

Occurrence and characterization of oseltamivir-resistant influenza virus in children between 2007-2008 and 2008-2009 seasons / 소아과

PURPOSE: There was a global increase in the prevalence of oseltamivir-resistant influenza viruses during the 2007-2008 influenza season. This study was conducted to investigate the occurrence and characteristics of oseltamivir-resistant influenza viruses during the 2007-2008 and 2008-2009 influenza seasons among patients who were treated with oseltamivir (group A) and those that did not receive oseltamivir (group B). METHODS: A prospective study was conducted on 321 pediatric patients who were hospitalized because of influenza during the 2007-2008 and 2008-2009 influenza seasons. Drug resistance tests were conducted on influenza viruses isolated from 91 patients. RESULTS: There was no significant difference between the clinical characteristics of groups A and B during both seasons. Influenza A/H1N1, isolated from both groups A and B during the 2007-2008 and 2008-2009 periods, was not resistant to zanamivir. However, phenotypic analysis of the virus revealed a high oseltamivir IC50 range and that H275Y substitution of the neuraminidase (NA) gene and partial variation of the hemagglutinin (HA) gene did not affect its antigenicity to the HA vaccine even though group A had a shorter hospitalization duration and fewer lower respiratory tract complications than group B. In addition, there was no significant difference in the clinical manifestations between oseltamivir-susceptible and oseltamivir-resistant strains of influenza A/H1N1. CONCLUSION: Establishment of guidelines to efficiently treat influenza with oseltamivir, a commonly used drug for treating influenza in Korean pediatric patients, and a treatment strategy with a new therapeutic agent is required.

Inhibition of Osteoclast Differentiation and Bone Resorption by Poria cocos Wolf Extract / 대한골다공증학회지

OBJECTIVES: Osteoclast differentiation and bone resorption are considered a potential therapeutic target to the treatment of erosive bone diseases, including osteoporosis and rheumatoid arthritis. Poria cocos Wolf (PCW), commonly used herbal medicine, has previously been reported to induce anti-inflammatory effect and anti-cancer effect, and to modulate immunologic responses. However, the effects of PCW on osteoclasts, and its detailed mechanisms are not proven. Therefore, we examined the inhibitory mechanism of PCW on osteoclast differentiation and bone resorption. MATERIALS AND METHODS: To analyze the effects of PCW on osteoclast differentiation, we examined osteoclast differentiation in bone marrow macrophages (BMMs) treated with or without of PCW by TRAP staining. The expression of c-Fos, NFATc1, TRAP and OSCAR mRNA was determined by RT-PCR and the protein levels of c-Fos, NFATc1, p38, ERK, JNK, Akt and IkappaB were assessed by western blot. Also, we evaluated the effect of PCW on bone resorption using hydroxyapatite plate. RESULTS: PCW significantly inhibited RANKL-mediated osteoclast differentiation without any evidence of cytotoxicity. We founded that PCW strongly inhibited RANKL-induced osteoclast formation when added during the early stage of cultures, suggesting that PCW acts on osteoclast precursors to inhibit RANKL/RANK signaling. Among the RANK signaling pathways, PCW inhibited the phosphorylation of p38 and JNK, also inhibited RANKL-induced expression of c-Fos, NFATc1, TRAP and OSCAR. In addition, PCW suppressed the bone resorption of mature osteoclasts. CONCLUSIONS: These findings suggest that PCW may be a potential novel drug for bone disorders by targeting the differentiation of osteoclasts as well as their functions.

Relationship between Initial EEG and the Prognosis of Acute Encephalitis / 대한소아신경학회지

PURPOSE: This study aimed to identify the usefulness of initial electroencephalograms (EEG) in the prediction of neurological outcomes of acute encephalitis. METHODS: Thirty-one patients diagnosed with acute encephalitis between January 2007 and March 2010 were included in the study, all of whom were less than 18 years old. Patients were divided into two groups. Those who had recovered completely were designated group A, and those who had neurological sequalae were designated group B. We compared the severity of EEG background abnormalities according to the Synek classification, and the incidence of interictal epileptiform discharges, electrographic seizures, normal sleep features, and EEG reactivity to pain stimuli between the two groups upon initial EEGs. RESULTS: Compared with group A, group B showed a higher grade of EEG background abnormalities (P = 0.004). The incidence of interictal epileptiform discharge (P = 0.004) and electrographic seizure (P = 0.049) were also higher in group B. Further, Group A had more EEG reactivity (P = 0.002) and the incidence of normal sleep features tended to be higher in group A (P = 0.081). CONCLUSION: Initial EEG features including the severity of EEG background abnormalities are helpful in predicting the prognosis of acute encephalitis.

A Case of Isoniazid Induced Systemic Lupus Erythematosus / 대한류마티스학회지

Many drugs have been known to induce lupus-like syndrome, composing approximately 10% of all SLE cases. Isoniazid-induced lupus erythematosus affects either sex equally and the most common presenting feature is arthralgia or arthritis with anemia. Fever and pleuritis occur in approximately half of the cases, and pericarditis in approximately 30% of cases. We discribe a 28-year-old woman receiving antituberculous medications including isoniazid for one month. She was hospitalized with fever, arthralgia and newly developed pleural effusion The analysis of pleural fluid and serum revealed an elevated level of antinuclear antibody. We suspected of drug induced lupus and stopped isoniazid medication. After discontinuation of isoniazid and short course of prednisolone treatment, her symptoms and pleural effusion disappeared. This case is to our knowledge, the fist report of isoniazid induced SLE in Korea.

Roles of Sphingosine-1 Phosaphate During Pathogenesis of Bone Destruction and Inflammation in Rheumatoid Arthritis Mice Model / 대한해부학회지

Sphingosine 1-phosphate (S1P) is a bioactive lipid molecule that mediates cell proliferation, differentiation, migration, and angiogenesis in vivo. However, the roles of S1P on pathogenesis of arthritis have been not completely understood. This study was designed to determine the effects of S1P modulation on collageninduced arthritis (CIA) model. DBA/1J mice were injected with collagen into the tail for induction of CIA model. S1P was administered into the peritoneal cavity every other days from day 1 to day 42 after collagen injection. To determine the degree of damage in CIA, we examined macroscopic findings of CIA. The inflammation and bone destruction of CIA mice were evaluated by histo-patholigy and radiography (CT and microradiography). The expressions of TNF-alpha, IL-6, and RANKL which have important roles in pathogenesis of rheumatoid arthritis and bone destruction were observed by immuno-histochemical staining. After injection with collagen in the DBA/1J mice, CIA was induced by swelling in the knee and ankle joint. Administration of S1P suppressed damages and incidence of arthritis elicited by collagen. In histologic and radiographic studies, S1P strongly suppressed the infiltration of inflammatory cells, the swelling of synovial membrane, erosion, and the destruction of bone on CIA mice. Injection of S1P resulted in down-regulation of the expression of the pro-inflammatory and bone destruction mediators such as TNF-alpha, IL-6, and RANKL on CIA mice. Furthermore, S1P suppressed the differentiation of bone marrow cells into osteoclasts by RANKL. In conclusion, this study suggest that S1P has protective effects on inflammation and bone destruction during pathogenesis of CIA, which indicates S1P can be a new possible therapeutic strategy for rheumatoid arthritis

Granulocyte Colony Stimulating Factor (G-CSF) Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis in Mice

BACKGROUND: Granulocyte colony stimulating factor (G-CSF) is known as a cytokine central to the hematopoiesis of blood cells and to modulate their cellular functions. Besides granulocytes and their precursors, monocytes/macrophages and endothelial cells are direct target cells of G-CSF action. G-CSF influences immune cells in an anti-inflammatory way. METHODS: To evaluate whether G-CSF has a potential for preventing or ameliorating diseases characterized by mucosal inflammation, we used a mouse model with trinitrobenzene sulfonic acid (TNBS)-induced inflammatory colitis. To the mice model G-CSF was administrated daily by intraperitoneal injection. Macroscopic evaluation and immunohistochemical analysis of colonic tissues were performed. RESULTS: Recombinant human G-CSF significantly inhibited LPS-induced TNF-alpha mRNA expression in THP-1 cells. As for in vivo relevance, G-CSF dramatically reduced the weight loss of mice, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, G-CSF suppressed the expression of tumor necrosis factor-alpha, interleukin-1beta, and intercellular adhesion molecule-1 in TNBS colitis. CONCLUSION: Current results demonstrate that G-CSF may be an effective agent for the treatment of diseases characterized by mucosal inflammation.

The Effects of Heme Oxygenase-1 on Collagen Induced Arthritis Model / 대한해부학회지

Heme oxygenase-1 (HO-1), an inducible heme-degrading enzyme, is expressed by macrophages and endothelial cells in response to inflammatory stresses. It has been known to show strong immunosuppressive properties although its mechanisms are not completely understood. This study was designed to determine the effects of HO-1 modulation on collagen induced arthritis (CIA) model. CIA model was induced by subcutaneous injection of collagen on tail of DBA/1J mice. For evaluation of HO-1 effects, an inducer of HO-1, cobalt protoporphyrin IX (CoPPIX), or an inhibitor of HO-1, tin protoporphyrin IX (SnPPIX), were administered every other days into peritoneal cavity from day 1 to day 42 after CIA induction. The macrocopic clinical findings of CIA were evaluated and histo-pathologic findings and radiographic analysis were carried out. The expressions of TNF-alpha, IL-6, and VEGF which have important roles in pathogenesis of rheumatoid arthritis were observed by immuno-histochemical staining. Collagen on DBA/1J mice induced arthritis at knee joint and ankle joint. Administration of CoPPIX significantly aggravated the severity of arthritis while SnPPIX protected collagen induced arthritis. SnPPIX strongly suppressed inflammatory cell infiltration, swelling of synovial membrane, and erosion and destruction of bone on CIA mice. Furthermore subcutaneous injection of collagen also increased expression of TNF-alpha, IL-6, and VEGF which are important pro-inflammatory mediators in rheumatoid arthritis. SnPPIX suppressed expression of the pro-inflammatory mediators on CIA mice. Finally, we suggest that HO-1 mediates the expression of pro-inflammatory mediators and bone destruction during pathogenesis of CIA, which indicates modulation of HO-1 can be a new therapeutic target of rheumatoid arthritis.

A Case of Acute Renal Failure Caused by Rhabdomyolysis due to Hyperosmolar Nonketotic Coma in Children / 소아과

Hyperosmolar nonketotic coma complicated in diabetes mellitus has been a rare cause of rhabdomyolysis, although increasingly reported recently. Acute renal failure can be complicated in 15 percent of rhabdomyolysis patients, but is rare in the case of rhabdomyolysis caused by diabetic hyperosomolar nonketotic coma. We report a 14 years-old boy with acute renal failure complicated by rhabdomyolysis caused by diabetic hyperosmolar coma.

Involvement of Protein Kinase C delta in Iron Chelator-Induced IL-8 Production in Human Intestinal Epithelial Cells / 대한해부학회지

Our previous study demonstrated that a bacterial siderophore, deferoxamine (DFO), could trigger inflammatory signals in human intestinal epithelial cells as a single stimulus, leading to IL-8 production via ERK1/2 and p38 phosphorylation and NF-kappa B-independent mechanism. In the present study, we proved that a novel protein kinase C (PKC)isoform, PKCdelta, is necessary for DFO-induced IL-8 production. Pretreatment of HT-29 cells with rottlerin showed remarkable inhibition of DFO-induced IL-8 production. In contrast, a conventional PKC inhibitor Go6976 did not show significant inhibition of DFO-induced IL-8 production. DFO induced strong phosphorylation of PKCdelta in the epithelial cells. Overexpression of PKCdelta resulted in enhanced PKCdelta phosphorylation, while transfection with dominant-negative PKCdelta vector failed DFO-induced phosphorylation. In addition, transfection of HT-29 cells with siRNA targeting endogenous PKCdelta, which suppressed PKCdelta expression, attenuated DFO-induced IL-8 production. These results demonstrate that PKCdelta plays an important role in regulating iron chelator-induced IL-8 production in human intestinal epithelial cells.

Rebamipide Protects TNBS Induced Colonic Damage Through Down-regulation of NF-kappaB Activation and Induction of Heme Oxygenase -1 Expression / 대한해부학회지

Crohn 's disease is characterized by a chronic relapsing inflammation of the bowel in which pro-inflammatory cytokines play an important role. Rebamipide is an anti-gastric ulcer drug with anti-inflammatory properties in vivo and in vitro. The effects of rebamipide on Crohn 's disease have not been carefully evaluated. This study investigated the potential of rebamipide to protect Crohn 's disease using a murine model of colitis induced by trinitrobenzene sulfonic acid (TNBS). Rebamipide dramatically improved histopathological symptom involving myeloperoxidase (MPO)activation and increase of microscopic damage score in TNBS induced colitis. Rebamipide suppressed IL-8 secretion, ICAM-1 induction and nuclear factor-kappaB (NF-kappaB) activation by TNF-alpha and induced heme oxygenase-1(HO-1)in HT-29 cells. HO-1 inducer cobalt protoporphyrin IX (CoPPIX)suppressed NF-kappaB activation by TNF-alpha in HT-29 cells like rebamipide, and mimicked the protective effects of rebamipide on TNBS induced colitis. This suggests that rebamipide exerts anti-inflammatory effects by down-regulating NF-kappaB activity via inducting HO-1 expression. In conclusion, this study suggests that rebamipide represents a potential therapeutic agent and HO-1 is an important therapeutic target for the treatment of Crohn's disease.

Clinical Features of Henoch-Schonlein Purpura Gastroenteropathy without Purpura before Diagnosis / 대한소아소화기영양학회지

PURPOSE: Henoch-Schonlein purpura (HSP) is a small-vessel vasculitic disease that most often affects the skin. Abdominal symptoms precede the typical purpuric rash of HSP in 14~36%. It is a challenge to diagnose HSP in the absence of a rash, because there are no biologic tests that can identify HSP with certainty, so we tried to find out the characteristic features of HSP gastroenteropathy without purpura before diagnosis. METHODS: This study included 82 children with HSP who had been admitted or visited outward of the Department of Pediatrics, Pusan National University Hospital from 1995 to 2000. The cases that the onset of purpura preceded or coincided that of abdominal pain were defined as purpura-positive group. The cases that the onset of abdominal pain preceded purpura more than 1 week and purpura was not presented till diagnosed as HSP gastroenteropathy were defined as purpura-negative group. We compared and analyzed the clinical features of the two groups by reviewing the medical records retrospectively. To ensure the diagnosis of HSP gastroenteropathy, we conducted upper GI series, abdominal ultrasonogram, abdominal CT, endoscopy and/or skin biopsy. RESULTS: The number of cases of purpura-positive group and purpura-negative group were 72 and 10, respectively. There is no difference between two groups in the incidence of clinical symptoms and laboratory findings. Children with HSP gastroenteropathy had characteristic erosive or ulcerative lesions in the stomach or duodenum on esophagogastroduodenoscopy, or mural thickening of the small bowel on abdominal ultrasonogram, CT or upper GI series. Skin biopsy revealed leukocytoclastic vasculitis in 3 of them, although biopsy specimen was taken from any areas of normal-appearing skin. In purpura-negative group, 9 patients improved by steroid therapy. CONCLUSION: In purpura-negative group, there is no diagnostic feature on the laboratory findings and clinical features. Therefore, to diagnose HSP gastroenteropathy in patients with abdominal pain in the absence of the characteristic rash, careful observation of clinical features and laboratory data, and prompt application of available diagnostic tools such as gastrointestinal endoscopy, radiologic study and skin biopsy are recommended. Early use of corticosteroid may reduce the suffering in these patients.

Iron Chelator Induces MIP-3alpha/CCL20 in Human Intestinal Epithelial Cells: Implication for Triggering Mucosal Adaptive Immunity / 체질인류학회지

A previous report by this laboratory demonstrated that bacterial iron chelator (siderophore) triggers inflammatory signals, including the production of CXC chemokie IL-8, in human intestinal epithelial cells(IECs). Microarray-based gene expression profiling revealed that iron chelator also induces CC chemokie MIP-3alpha/CCL20. As CCL20 is chemotactic for the cells involved in host adaptive immunity, this suggests that iron chelator may stimulate IECs to have the capacity to link mucosal innate and adaptive immunity. The basal medium from iron chelator deferoxamine (DFO)-treated HT-29 monolayers was as chemotactic as rhCCL20 at equivalent concentrations to attract CCR6+cells. The increase of CCL20 protein secretion appeared to correspond to that of CCL20 mRNA levels, as determined by real-time quantitative RT-PCR. The efficacy of DFO at inducing CCL20 mRNA was also observed in human Peripheral Blood Mononuclear Cells (PBMCs) and in THP-1 cells, but not in Human Umbillical Vein Endothelial Cells (HUVECs). Interestingly, unlike other proinflammatory cytokines, such as TNF-alpha and IL-1beta, a time-dependent experiment revealed that DFO slowly induces CCL20, suggesting a novel mechanism of action. A pharmacologic study also revealed that multiple signaling pathways are differentially involved in CCL20 production by DFO, while some of those pathways are not involved in TNF-alpha-induced CCL20 production. Collectively, these results demonstrate that, in addition to some bacterial products known to induce host adaptive immune responses, direct chelation of host iron by infected bacteria may also contribute to the initiation of host adaptive immunity in the intestinal mucosa.

The Inhibitory Effect of Methotrexate-Layered Double Hydroxide (LDH) Hybrid on Osteosarcoma Cell Lines / 대한정형외과학회잡지

PURPOSE: The purpose of this study was to observe and analyze the effect of Methotrexate-Layered Double Hydroxide (LDH) hybrids on growth inhibition and the apoptosis of human osteosarcoma cell lines (SaOS-2, MG-63) and normal fibroblasts. MATERIALS AND METHODS: FITC-LDH hybrids were added to the cells and incubated for 2, 4, 6, and 8 hours. The samples were examined by fluorescence microscopy. SaOS-2 and MG-63 cells, and a normal fibroblast cell line (Detroit 551) were treated with 500 g/mL MTX and 500 g/mL MTX-LDH hybrids for 24, 48, 72, and 96 hours, respectively. The proliferation was measured by using the MTT assay. Apoptosis was determined by DNA fragmentation analysis. RESULTS: The hybrids with LDH entered the cells effectively in a time- and dose-dependent manner. The proliferation of SaOS-2 cells in a culture treated with 500 g/mL of MTX-LDH hybrids for 24 hours was significantly inhibited (37% more) compared to those treated with MTX. MG-63 cell growth was inhibited 20% more than SaOS-2 cell growth. However, the difference in the degrees of inhibition of cells treated with MTXLDH hybrid or with MTX alone reduced with time. DNA ladders appeared in cells treated with 500 g/mL MTX-LDH hybrid for 24 hours but not in those treated with MTX and LDH alone. CONCLUSIONS: The results of this study suggest that MTX-LDH hybrid more effectively enters cells and inhibits their proliferation than MTX alone.

Impaired DNA Synthesis by Copper Cytotoxicity in LEC Mutant Rat / 대한해부학회지

Long-Evans Cinnamon (LEC) mutant rat, which spontaneously develops a necrotizing hepatic injury at 4 ~5 months of age, reveals an excess hepatic copper accumulation and is a good model for studying the detail mechanism of cellular copper toxicity. We have observed the effects of copper toxicity on DNA synthesis upon growth stimulation by treating primary-cultured hepatocytes of LEC rat with epidermal growth factor (EGF) and insulin. DNA synthesis measured by [ 3 H]-thymidine incorporation and DNA synthesis S-phase cells in LEC rat significantly decreased when compared to those of normal F344 rat. Since DNA synthesis was impaired in LEC rat, we examined the detail mechanism by determining the histone content, which are involved in DNA stability, and the phosphorylation of nuclear protein. However, the histone contents and phosphorylated nuclear protein upon growth stimulation was intact in LEC rat. These results suggest that a cellular event other than protein phosphorylation required for the initiation of DNA synthesis upon growth stimulation is impaired by copper cytotoxicity in LEC rat.

The Effect of Iron Depletion on the Monocytic Adhesion, Differentiation and SR-A Expression / 대한해부학회지

Maintenance of cellular iron homeostasis is a prerequisite for proliferation and differentiation of cells, and is also a central role in the regulation of immune function. Monocyte-macrophages play an important roles in host defense, particularly in the inflammatory process of acute and chronic disease. The reason that an iron is important in these cell is because an iron is indispensable in a generation of hydroxyl radical for bacterium killing. Because of the role of iron in the monocytic THP-1 cell differentiation is not become clear, we investigated whether THP-1 cell can differentiate to macrophage-like cell using of iron and iron chelator which cause iron depletion. The cell differentiation was not able to observe by iron treatment, by the way, the cell adhesion was increased in DFO treated monocyte and cellular pseodopodial extension, change of a nucleus-cytoplasmic ratio were showed in Differential interference contrast (DIC) and Giemsa staining, and it was inhibited by ferric citrate (FC). Increased polystyrene bead phagocytosis by DFO treatment of THP-1 cell were detected through FACS and rhodamine-phallodin staining. The SR-A expression, which was a cell differentiation marker, was increased by DFO treatment of THP-1 cell. These results suggest that iron depletion by DFO can promote THP-1 cell diffentiation into macrophage-like cell, and this may carrying out important role in the immune response.

Heme Oxygenase-1 is Involved in the Down-regulation of Nuclear Transcription Factor kappa B Activation in the Colonic Epithelium During Inflammation / 대한해부학회지

Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with anti-inflammatory activity, but the mechanisms underlying this activity are incompletely understood. Nuclear transcription factor kappa B (NF-kappa B) activation is an important factor in the pathogenesis of inflammatory bowel disease (IBD). We investigated the suppressive effects of HO-1 on the activation of NF-kappa B by pro-inflammatory cytokines in cultured colonic epithelial cells and by trinitrobenzene sulfonic acid (TNBS) in the colon of mice. The expression level of HO-1 in the colonic epithelium of a patient with inflammatory bowel disease and pseudo-membranous colitis was lower than that in a healthy control subject. In cultured human colonic epithelial HT-29 cells, pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha ) and IL-1 beta down-regulate HO-1 expression. The HO-1 inducer, cobalt protoporphyrin IX (CoPPIX), dramatically down-regulated NF-kappa B activation in HT-29 cells by TNF-alpha. In addition, bilirubin-a product of heme catabolism by HO-1-and the carbon monoxide donor tricarbonyldichlororuthenium (II) dimer also suppressed NF-kappa B activation by TNF-alpha. However, iron, another heme metabolite, did not suppress NF-kappa B activation by TNF-alpha. Furthermore, CoPPIX diminished the macroscopic and histopathological symptoms of TNBS-induced colitis and down-regulated NF-kappa B activation in mice. In conclusion, this study suggests that HO-1 plays an important role in the down-regulation of NF-kappa B activation, which is a key factor in the pathogenesis of IBD and is thus an excellent therapeutic target for the treatment of IBD.

Screening Test for Heart Diseases in the First Grade Elementary School Children in Busan

PURPOSE: We'd like to determine the incidence of congenital heart disease and arrhythmia in elementary school children in Busan, and to provide adequate prevention and treatment. METHODS: A total of 23,802(male 12,909, female 10,893) 1st grade elementary school children living in Busan were studied. All children were 7-8 years old. We obtained their medical history by questionnaire and checked elecrocardiography(ECG). Subsequent screening tests including a 2nd ECG, chest X-ray, phonocardiogram and CBC for the students who had abnormal findings at the first screening test. The third screening test was done for students who had cardiac murmurs or abnormal ECG findings in the second screening test by echocardiogram, treadmill test and 24-hour Holter monitoring. RESULTS: Among 23,802 children participants, 605(2.54%) had abnormal ECG findings at the first screening test. Q wave abnormality(0.58%) was observed most frequently, and complete right bundle branch block(RBBB)(0.26%), sinus tachycardia(0.24%), right axis deviation(0.22%) and ventricular premature contraction(VPC)(0.21%) followed in order. Four hundred and twenty four children participated in the second ECG screening test. Two hundred and two children(47.6%) had an abnormality such as sinus tachycardia(18.8%), VPC(17.8%), or complete RBBB(17.3%). After completing the third examination including echocardiogram, we couldn't find the students with ventricular tachycardia (VT) or SVT at the third arrhythmia screening test. CONCLUSION: A high incidence of arrhythmia was found in the 1st grade elementary school children in Busan despite their healthy appearances, although fatal heart diseases were not noted. Early diagnosis, adequate preventative measures and treatment will prevent and decrease the frequency of emergent situations like syncope and sudden death.

Effect of NMDA Receptor Antagonist (APV)on the Toxicity Induced by Oxygen Radicals in Cultured Myocardial Cells / 체질인류학회지

Toxic effect of oxygen radicals and cardioprotective effect of N -methyl -D -aspartate (NMDA) receptor antagonists against xanthine oxidase (XO) and hypoxanthine (HX)-induced cardiotoxicity were measured in order to elucidate the mechanism of cardiotoxicity on cultured mouse myocardial cells. MTT assay was performed after myocardial cells were cultured for 12 hours at various concentrations of XO/HX alone or with D -2 -amino -5 -phosphonovaleric acid (APV) or 6 - cyano -7 -nitroquinoxaline -2,3 -dione (CNQX). In this study, XO/HX was toxic in a time -and dose -dependent manners on cultured myocardial cells, and midcytotoxicity value 50 (MTT50) was at 30 mU/ml XO and 0.1 mM HX after myocardial cells were grown for 12 hours in media containing 1 ~50 mU/ml XO and 0.1 mM HX. When cultures were treated with 30 mU/ml XO and 0.1 mM HX flus 20 80 microM APV for 12 hours, cell viability was increased remarkably, while treatment with 30 mU/ml XO and 0.1 mM HX flus 10 ~50 microM CNQX did not show any protective effect against XO/HX -induced neurotoxicity. From the above results, it is suggested that oxygen radicals are toxic on cultured mouse myocardial cells by the decrease of cell viability, and NMDA receptor antagonists such as APV are very effective in the prevention of myocardial toxicity induced by oxygen radicals.