BACKGROUND: Blood transfusion poses high risks and has a high probability of error because of the complexity and involvement of several people in the process. The purpose of this study was to share our experience in classifying reports related to blood transfusions. We included patient safety reports that were prepared over a 10-year period that began from the opening of the hospital. We then analyzed the causes and the corrective actions. METHODS: We analyzed 125 reports related to blood transfusions, and these reports were included in the patient safety reports received from November 2008 to December 2018. The events were categorized as sampling error, inspection error, testing error, issue error, disposal error, transfusing blood components error, or others error, depending on the stage of the blood transfusion process. Regardless of the cause, the event that led to an inappropriate transfusion was classified as a transfusion incident. RESULTS: The number of blood transfusions per year increased, and the rate of blood transfusion accidents ranged from 0.00% to 0.05% per year. A total of 125 reports were prepared over a 10-year period, and these included 8 blood sampling errors, 11 testing errors, 2 issuing errors, 94 disposal errors, 3 others errors, and 7 errors associated with the transfusing of blood components. After the transfusion incident, PDA was applied as a solution. Transfusing the wrong blood components did not occur, and the incidence of taking blood from the wrong patients was decreased. CONCLUSION We applied corrective actions according to the cause of the event and we confirmed that the blood transfusion incidents decreased.

The genetic variant rs16754 of Wilms tumor gene 1 (WT1) has recently been described as an independent prognostic factor in AML patients. It is of great interest to test whether WT1 single nucleotide polymorphism can be used as a molecular marker in other types of cancer, to improve risk and treatment stratification. We performed sequencing analysis of exons 7 and 9 of WT1, which are known mutational hotspots, in a total of 73 patients with BCR-ABL1-negative myeloproliferative neoplasm (MPN) and 93 healthy controls. No previously reported WT1 mutations were identified in the present study. In Korean patients with BCR-ABL1-negative MPN, WT1 genetic variant rs16754 had no significant impact on clinical outcomes. We observed a significant difference in the allelic frequencies of WT1 rs16754 in Koreans between BCR-ABL1-negative MPN cases and healthy controls. Individuals carrying variant G alleles of WT1 rs16754 showed a relatively low prevalence of BCR-ABL1-negative MPN, compared with those carrying wild A alleles of WT1 rs16754 (Hazard ratio 0.10-0.65, P<0.05). Therefore, possession of the variant G allele of WT1 rs16754 may reduce the risk of developing BCR-ABL1-negative MPN.
Adult ; Aged ; Aged, 80 and over ; Alleles ; Asian Continental Ancestry Group/*genetics ; Case-Control Studies ; Exons ; Female ; Fusion Proteins, bcr-abl/genetics ; Gene Frequency ; Genotype ; Humans ; Leukemia, Myeloid, Acute/pathology ; Male ; Middle Aged ; Myeloproliferative Disorders/*genetics/pathology ; Polymorphism, Single Nucleotide ; Prognosis ; Proportional Hazards Models ; Republic of Korea ; Risk ; Sequence Analysis, DNA ; WT1 Proteins/*genetics ; Young Adult

alpha-Asarone exhibits a number of pharmacological actions including neuroprotective, anti-oxidative, anticonvulsive, and cognitive enhancing action. The present study investigated the effects of alpha-asarone on pro-inflammatory cytokines mRNA, microglial activation, and neuronal damage in the hippocampus and on learning and memory deficits in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Varying doses of alpha-asarone was orally administered (7.5, 15, or 30 mg/kg) once a day for 3 days before the LPS (3 mg/kg) injection. alpha-Asarone significantly reduced TNF-alpha and IL-1beta mRNA at 4 and 24 hours after the LPS injection at dose of 30 mg/kg. At 24 hours after the LPS injection, the loss of CA1 neurons, the increase of TUNEL-labeled cells, and the up-regulation of BACE1 expression in the hippocampus were attenuated by 30 mg/kg of alpha-asarone treatment. alpha-Asarone significantly reduced Iba1 protein expression in the hippocampal tissue at a dose of 30 mg/kg. alpha-Asarone did not reduce the number of Iba1-expressing microglia on immunohistochemistry but the average cell size and percentage areas of Iba1-expressing microglia in the hippocampus were significantly decreased by 30 mg/kg of alpha-asarone treatment. In the Morris water maze test, alpha-asarone significantly prolonged the swimming time spent in the target and peri-target zones. alpha-Asarone also significantly increased the number of target heading and memory score in the Morris water maze. The results suggest that inhibition of pro-inflammatory cytokines and microglial activation in the hippocampus by alpha-asarone may be one of the mechanisms for the alpha-asarone-mediated ameliorating effect on memory deficits.
Animals ; Cell Size ; Cytokines* ; Head ; Hippocampus ; Immunohistochemistry ; Learning ; Maze Learning ; Memory ; Memory Disorders* ; Mice* ; Microglia ; Neurons ; RNA, Messenger ; Swimming ; Tumor Necrosis Factor-alpha ; Up-Regulation

alpha-Asarone exhibits a number of pharmacological actions including neuroprotective, anti-oxidative, anticonvulsive, and cognitive enhancing action. The present study investigated the effects of alpha-asarone on pro-inflammatory cytokines mRNA, microglial activation, and neuronal damage in the hippocampus and on learning and memory deficits in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Varying doses of alpha-asarone was orally administered (7.5, 15, or 30 mg/kg) once a day for 3 days before the LPS (3 mg/kg) injection. alpha-Asarone significantly reduced TNF-alpha and IL-1beta mRNA at 4 and 24 hours after the LPS injection at dose of 30 mg/kg. At 24 hours after the LPS injection, the loss of CA1 neurons, the increase of TUNEL-labeled cells, and the up-regulation of BACE1 expression in the hippocampus were attenuated by 30 mg/kg of alpha-asarone treatment. alpha-Asarone significantly reduced Iba1 protein expression in the hippocampal tissue at a dose of 30 mg/kg. alpha-Asarone did not reduce the number of Iba1-expressing microglia on immunohistochemistry but the average cell size and percentage areas of Iba1-expressing microglia in the hippocampus were significantly decreased by 30 mg/kg of alpha-asarone treatment. In the Morris water maze test, alpha-asarone significantly prolonged the swimming time spent in the target and peri-target zones. alpha-Asarone also significantly increased the number of target heading and memory score in the Morris water maze. The results suggest that inhibition of pro-inflammatory cytokines and microglial activation in the hippocampus by alpha-asarone may be one of the mechanisms for the alpha-asarone-mediated ameliorating effect on memory deficits.
Animals ; Cell Size ; Cytokines* ; Head ; Hippocampus ; Immunohistochemistry ; Learning ; Maze Learning ; Memory ; Memory Disorders* ; Mice* ; Microglia ; Neurons ; RNA, Messenger ; Swimming ; Tumor Necrosis Factor-alpha ; Up-Regulation

OBJECTIVESChunghyuldan (CHD), a combinatorial drug that has anti-hyperlipidemic and antiinflammatory activities, has been shown to reduce infarct volume in a focal ischemia-reperfusion rat model. To explore the molecular basis of CHD's neuroprotective effect, we examined whether CHD shows a cell-protective activity and has a regulatory effect on Bax and/or B-cell leukemia/lymphoma 2 (Bcl-2) expression in mouse neuroblastoma 2a (N2a) cells subjected to hypoxia-reoxygenation (H/R).

METHODSIn order to evaluate the effects of CHD on the cytotoxicity induced from hypoxia or H/R condition, lactate dehydrogenase (LDH) assay was performed. To explore whether the suppression of neural damage when pre-treated with CHD is associated with its anti-apoptotic effect, the CHD effect on the expression of Bcl-2 and Bax was analyzed by Western blotting analysis.

RESULTSCytotoxicity of N2a cell line was slightly increased in 42 h hypoxia condition and dramatically increased under the H/R condition. CHD treatment markedly decreased the cytotoxicity in both conditions (P<0.01, P<0.05). H/R markedly increased the expression of the pro-apoptotic protein, Bax, but slightly increased the expression of the anti-apoptotic protein, Bcl-2, compared with the normoxia or hypoxia group. CHD significantly decreased Bax expression (P<0.01) and slightly decreased Bcl-2 expression (P>0.05), resulted in a reduction of Bax/Bcl-2 ratio in N2a cells subjected to H/R.

CONCLUSIONCHD has neuroprotective effect in N2a cells subjected to H/R, which might be derived at least in part from its ability to decrease the expression of the pro-apoptotic protein, Bax.

Animals ; Cell Line, Tumor ; Drugs, Chinese Herbal ; pharmacology ; Hypoxia ; prevention & control ; Mice ; Neuroblastoma ; metabolism ; pathology ; Neuroprotective Agents ; pharmacology ; Reperfusion Injury ; prevention & control

BACKGROUND: Group A Streptococcus (GAS) is responsible for a wide spectrum of human diseases. We investigated the distribution of emm types and antibiotic resistance rates of GAS from clinical specimens in several Korean medical centers. METHODS: A total of 192 strains of GAS from throat, blood, and other specimens collected in Seoul, Busan, Ulsan, Iksan, and Jeju were studied in 2008-2009. The emm genotypes were identified using PCR and sequencing. Antimicrobial susceptibility testing was performed by disk diffusion method. Phenotypes of macrolide resistance were evaluated, and macrolide resistance genes were determined by PCR. RESULTS: The emm89 (33.9%) was most frequently detected, followed by emm1 (12.5%), emm12 (8.3%), emm4 (7.8%), and emm75 (7.3%). The distribution of emm types did not show a close relation to the type of specimen and was different for each area. The resistance rates to erythromycin (ERY) and clindamycin (CLI) were 4.6% and 3.7%, respectively. Among the nine ERY-resistant strains, the rate of constitutive resistance was 88.9%, compared with 11.1% for the M phenotype. Five of the ERY-resistant strains were emm28. CONCLUSION: This multicenter study reveals heterogenous emm genotypes by geographic area. Rates of resistance to ERY and CLI were low, and most of the ERY-resistant strains showed a constitutive macrolide-lincosamide-streptogramin B (cMLSB) phenotype.
Clindamycin ; Diffusion ; Drug Resistance, Microbial ; Erythromycin ; Genotype ; Humans ; Korea ; Molecular Epidemiology ; Pharynx ; Phenotype ; Polymerase Chain Reaction ; Streptococcus ; Streptococcus pyogenes

BACKGROUND: In addition to Klinefelter's syndrome, microdeletion of Yq is the most common genetic cause of male infertility; 15% of azoospermic or 5-10% of oligozoospermic males have Yq deletions. We evaluated a Yq microdeletion kit (LG Life Sciences, Korea) for identifying microdeletions in the azoospermic factor (AZF) regions of the Yq. METHODS: The kit was designed to amplify 3 regions of the AZF gene (AZFa, AZFb, and AZFc) using 15 sequence-tagged sites. We evaluated the preclinical performance of the kit. For clinical validation, 58 patients including 25 idiopathic azoospermic or oligozoospermic patients were examined. RESULTS: We observed clear bands on electrophoresis of DNA, up to a DNA concentration of 3.12 ng/microliter; the known microdeletion regions of all 6 reference cell-lines (Coriell, USA) were accurately detected and no false positive/negative results showed with normal female (n=11) and fertile male (n=15) specimens. This kit could identify the same microdeletions in the common regions, similar to another commercial kit. Among the 58 male infertile patients, 7 (12.1%) had microdeletions of the Yq. Among the idiopathic azoospermic (n=22) and oligozoospermic (n=3) patients, 3 (12.0%) had microdeletions. Further, 2 of 21 varicocele patients (9.5%), 1 of 4 patients with testicular failure, and 1 patient with a 45,X/46,XY mosaic had microdeletions. CONCLUSIONS: The kit was effective for detecting microdeletions of the Yq. We identified microdeletions in 12% of the infertile patients. This Y chromosome microdeletion detection kit is useful for screening Yq microdeletions in infertile patients.
Azoospermia/genetics ; *Chromosome Deletion ; *Chromosomes, Human, Y ; Electrophoresis, Agar Gel/methods ; Female ; Humans ; Infertility, Male/genetics ; Male ; Oligospermia/genetics ; Polymerase Chain Reaction/*methods ; Reagent Kits, Diagnostic ; Reproducibility of Results ; Seminal Plasma Proteins/*genetics ; Sensitivity and Specificity ; Varicocele/genetics

BACKGROUND: Antimicrobial susceptibility of Legionella spp. has rarely been studied in Korea. Therefore, we aimed to determine the susceptibility of Legionella spp. to various antibiotics. METHODS: We assessed the antimicrobial susceptibility of 66 environmental and clinical Legionella isolates collected between January 2001 and December 2008 from Korea and Japan. The minimum inhibitory concentrations (MICs) of 6 antibiotics, namely, azithromycin, ciprofloxacin, clarithromycin, clindamycin, gatifloxacin, and gemifloxacin were determined by the broth microdilution method using buffered starch yeast extract broth. RESULTS: The MIC ranges of the 6 antibiotics used against the Legionella isolates were as follows: 0.004-0.062 microgram/mL (azithromycin), 0.002-0.5 microgram/mL (ciprofloxacin), 0.004-0.5 microgram/mL (clarithromycin), 0.12-4 microgram/mL (clindamycin), 0.002-0.12 microgram/mL (gatifloxacin), and 0.008-1 microgram/mL (gemifloxacin). CONCLUSIONS: Legionella spp. isolates from Korea and Japan were most susceptible to gatifloxacin. Azithromycin, clarithromycin, ciprofloxacin, and gemifloxacin were also effective for treating legionellosis.
Anti-Bacterial Agents/*pharmacology ; Azithromycin/pharmacology ; Ciprofloxacin/pharmacology ; Clarithromycin/pharmacology ; Clindamycin/pharmacology ; Drug Resistance, Bacterial ; Fluoroquinolones/pharmacology ; Humans ; Legionella/*drug effects/isolation & purification ; Legionellosis/diagnosis/microbiology ; Microbial Sensitivity Tests ; Naphthyridines/pharmacology

No abstract available.

PURPOSE: The purpose of this study is to evaluate the effectiveness of a medical ethics course taught in medical school by examining the students' abilities to identify medical ethics issues, the applicability of a medical ethics course, and self-efficacy. METHODS: 366 subjects were recruited from three different groups (medical students, interns, and residents) who had completed a medical ethics course. Data were collected using a 20-item questionnaire. Analysis was done with a SPSS statistics program. RESULTS: Of the three groups, the students scored the highest in identifying medical ethics issues. When asked how often they see medical ethics issues in real medical situations (students were asked how often they would expect to see these ethical issues in medical settings), the students responded with the highest number, followed by the interns. The residents responded with the lowest number. Regarding the applicability of the medical ethics course, while students believed the course was highly useful and applicable to real medical settings, interns and residents did not agree. The participants' self-efficacy and satisfaction were generally low. The majority of all three groups thought that medical ethics education should be more practical and that it should be taught during internship as well as during residency. CONCLUSION: Our findings suggest two important directions for medical ethics education. First, the current medical ethics curriculum should be offered during both internship and residency. Second, the content should focus more on actual clinical scenarios ('clinical ethics') than theoretical principles.
Curriculum ; Ethics, Medical ; Humans ; Internship and Residency ; Schools, Medical ; Surveys and Questionnaires