BACKGROUND: Asymptomatic vancomycin-resistant enterococci (VRE) colonization precedes infection. VRE-colonized patients serve as silent reservoirs of enterococci that go on to colonize other patients. Rapidly identifying colonized patients is crucial to prevent the spread of VRE. The culture-based method of VRE screening is time-consuming. We evaluated the diagnostic performance of a recently developed multiplex real-time PCR for the detection of VRE. METHODS: We obtained 105 rectal swabs from patients who were being monitored for carriage of VRE. After 24 hour incubation of swabs in enterococcosel broth (EB) supplemented with 6 microg/mL vancomycin, multiplex real-time PCR was performed using the Anyplex(TM) VanR Real-time Detection (VanR) kit (Seegene, Inc., Seoul, Korea). The results of multiplex real-time PCR were compared to those of culture. We evaluated the specificity and detection limits of multiplex real-time PCR using VanR for VRE. RESULTS: A total of 96/105 (91.4%) samples were VRE positive according to multiplex real-time PCR with EB while 85/105 (80.9%) samples were positive in culture. Eleven discordant results (10.4%) (multiplex real-time PCR positive, culture negative) were noted. All non-enterococcal bacteria and vancomycin-susceptible enterococci were negative. The DNA detection limits of VanR were 0.035 pg per reaction (3 microL) for Enterococcus faecium and 0.35 pg for Enterococcus faecalis. CONCLUSION: The application of multiplex real-time PCR after EB incubation allows rapid and sensitive detection in 26-28 hours for VRE screening from rectal swabs. This method could facilitate the timely implementation of contact isolation to prevent the spread of VRE.
Bacteria ; Colon ; DNA ; Enterococcus ; Enterococcus faecium ; Humans ; Limit of Detection ; Mass Screening ; Real-Time Polymerase Chain Reaction ; Sensitivity and Specificity ; Vancomycin

Background: Although both obesity, measured by body mass index, and visceral obesity are known to be major risk factors of metabolic syndrome and its components, there have been debates on the relative contribution of general obesity and visceral obesity to the development of metabolic syndrome. Methods: We performed a large longitudinal cohort study of 3,093 subjects (age range, 18–65 years) who were metabolically healthy and had a normal weight who received health screenings over a 3-year follow-up period. Cox proportional hazards models were used to estimate the adjusted hazard ratios (HRs) and 95% confidence intervals (CI) for incident metabolic syndrome and its components per sex-specific 1-standard deviation (SD) increase in visceral adipose tissue (VAT) and body mass index. Results: Both obesity and visceral obesity increased the risk of incident metabolic syndrome, but when HR was compared per sex-specific 1-SD, visceral obesity appeared to confer more risk than simple obesity. The HR for 1-SD of body mass index was 1.19 (95% CI, 1.07–1.32; P=0.001) in men and 1.29 (95% CI, 1.10–1.52; P=0.002) in women, while the HR for 1-SD of VAT was 1.29 (95% CI, 1.15–1.44; P<0.001) in men and 1.50 (95% CI, 1.28–1.75; P<0.001) in women. Conclusion Visceral obesity and obesity were longitudinally associated with an increased risk of incident metabolic syndrome among metabolically healthy adults, and visceral fat accumulation appears to be better predictor of metabolic syndrome.

PURPOSE: Breast cancer survivors have slightly increased the risk of second primary cancers. Breast, colon, uterine, and ovarian cancers are common secondary cancers in breast cancer survivors. In this study, we assessed the development of second primary cancers of breast cancer survivors in Korea. METHODS: Medical records of patients with breast cancer in 3 tertiary medical institutions were reviewed retrospectively. We evaluated secondary malignancy diagnosed at least 2 months after the breast cancer diagnosis. Based on the International Classification of Disease-9 codes of malignancies, secondary primary breast cancer records were evaluated with person-year adjustment. The standardized incidence ratio (SIR) was assessed using national cancer incidence. RESULTS: A total of 3,444 treatment records were included from 3 medical centers. The cumulative incidence of overall second primary cancers was 2.8% (n = 93). The SIR was significantly higher in all sites (1.56; 95% confidence interval [CI], 1.26–1.91), endometrial cancer (5.65; 95% CI, 2.06–12.31), biliary tract cancer (3.96; 95% CI, 1.19–8.60), and thyroid cancer (2.29; 95% CI, 1.67–3.08). CONCLUSION: The incidence of cancer was higher in breast cancer survivors compared to general population. Surveillance of secondary cancer in this group should be recommended individually considering the benefit related to the prognosis of primary breast cancer.
Biliary Tract Neoplasms ; Breast Neoplasms* ; Breast* ; Classification ; Colon ; Diagnosis ; Early Detection of Cancer ; Endometrial Neoplasms ; Female ; Humans ; Incidence ; Korea ; Medical Records ; Neoplasms, Second Primary* ; Ovarian Neoplasms ; Prognosis ; Retrospective Studies ; Survivors* ; Thyroid Neoplasms

PURPOSE: Breast cancer survivors have slightly increased the risk of second primary cancers. Breast, colon, uterine, and ovarian cancers are common secondary cancers in breast cancer survivors. In this study, we assessed the development of second primary cancers of breast cancer survivors in Korea. METHODS: Medical records of patients with breast cancer in 3 tertiary medical institutions were reviewed retrospectively. We evaluated secondary malignancy diagnosed at least 2 months after the breast cancer diagnosis. Based on the International Classification of Disease-9 codes of malignancies, secondary primary breast cancer records were evaluated with person-year adjustment. The standardized incidence ratio (SIR) was assessed using national cancer incidence. RESULTS: A total of 3,444 treatment records were included from 3 medical centers. The cumulative incidence of overall second primary cancers was 2.8% (n = 93). The SIR was significantly higher in all sites (1.56; 95% confidence interval [CI], 1.26–1.91), endometrial cancer (5.65; 95% CI, 2.06–12.31), biliary tract cancer (3.96; 95% CI, 1.19–8.60), and thyroid cancer (2.29; 95% CI, 1.67–3.08). CONCLUSION: The incidence of cancer was higher in breast cancer survivors compared to general population. Surveillance of secondary cancer in this group should be recommended individually considering the benefit related to the prognosis of primary breast cancer.
Biliary Tract Neoplasms ; Breast Neoplasms* ; Breast* ; Classification ; Colon ; Diagnosis ; Early Detection of Cancer ; Endometrial Neoplasms ; Female ; Humans ; Incidence ; Korea ; Medical Records ; Neoplasms, Second Primary* ; Ovarian Neoplasms ; Prognosis ; Retrospective Studies ; Survivors* ; Thyroid Neoplasms

BACKGROUND: Idiopathic pulmonary fibrosis involves irreversible alveolar destruction. Although alveolar epithelial type II cells are key functional participants within the lung parenchyma, how epithelial cells are affected upon bleomycin (BLM) exposure remains unknown. In this study, we determined whether BLM could induce cell cycle arrest via regulation of Schlafen (SLFN) family genes, a group of cell cycle regulators known to mediate growth-inhibitory responses and apoptosis in alveolar epithelial type II cells. METHODS: Mouse AE II cell line MLE-12 were exposed to 1–10 µg/mL BLM and 0.01–100 µM baicalein (Bai), a G1/G2 cell cycle inhibitor, for 24 hours. Cell viability and levels of pro-inflammatory cytokines were analyzed by MTT and enzyme-linked immunosorbent assay, respectively. Apoptosis-related gene expression was evaluated by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Cellular morphology was determined after DAPI and Hoechst 33258 staining. To verify cell cycle arrest, propidium iodide (PI) staining was performed for MLE-12 after exposure to BLM. RESULTS: BLM decreased the proliferation of MLE-12 cells. However, it significantly increased expression levels of interleukin 6, tumor necrosis factor α, and transforming growth factor β1. Based on Hoechst 33258 staining, BLM induced condensation of nuclear and fragmentation. Based on DAPI and PI staining, BLM significantly increased the size of nuclei and induced G2/M phase cell cycle arrest. Results of qRT-PCR analysis revealed that BLM increased mRNA levels of BAX but decreased those of Bcl2. In addition, BLM/Bai increased mRNA levels of p53, p21, SLFN1, 2, 4 of Schlafen family. CONCLUSION: BLM exposure affects pulmonary epithelial type II cells, resulting in decreased proliferation possibly through apoptotic and cell cycle arrest associated signaling.
Animals ; Apoptosis ; Bisbenzimidazole ; Bleomycin ; Cell Cycle Checkpoints ; Cell Cycle ; Cell Line ; Cell Survival ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells ; Gene Expression ; Genes, vif ; Humans ; Idiopathic Pulmonary Fibrosis ; Interleukin-6 ; Lung ; Mice ; Propidium ; RNA, Messenger ; Transforming Growth Factors ; Tumor Necrosis Factor-alpha

BACKGROUND: Idiopathic pulmonary fibrosis involves irreversible alveolar destruction. Although alveolar epithelial type II cells are key functional participants within the lung parenchyma, how epithelial cells are affected upon bleomycin (BLM) exposure remains unknown. In this study, we determined whether BLM could induce cell cycle arrest via regulation of Schlafen (SLFN) family genes, a group of cell cycle regulators known to mediate growth-inhibitory responses and apoptosis in alveolar epithelial type II cells. METHODS: Mouse AE II cell line MLE-12 were exposed to 1–10 µg/mL BLM and 0.01–100 µM baicalein (Bai), a G1/G2 cell cycle inhibitor, for 24 hours. Cell viability and levels of pro-inflammatory cytokines were analyzed by MTT and enzyme-linked immunosorbent assay, respectively. Apoptosis-related gene expression was evaluated by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Cellular morphology was determined after DAPI and Hoechst 33258 staining. To verify cell cycle arrest, propidium iodide (PI) staining was performed for MLE-12 after exposure to BLM. RESULTS: BLM decreased the proliferation of MLE-12 cells. However, it significantly increased expression levels of interleukin 6, tumor necrosis factor α, and transforming growth factor β1. Based on Hoechst 33258 staining, BLM induced condensation of nuclear and fragmentation. Based on DAPI and PI staining, BLM significantly increased the size of nuclei and induced G2/M phase cell cycle arrest. Results of qRT-PCR analysis revealed that BLM increased mRNA levels of BAX but decreased those of Bcl2. In addition, BLM/Bai increased mRNA levels of p53, p21, SLFN1, 2, 4 of Schlafen family. CONCLUSION BLM exposure affects pulmonary epithelial type II cells, resulting in decreased proliferation possibly through apoptotic and cell cycle arrest associated signaling.

Mycobacteruim kansasii occasionally causes disseminated infection with poor outcome in immunocompromised patients. We report the first case of disseminated M. kansasii infection associated with multiple skin lesions in a 48-yr-old male with myelodysplastic syndrome. The patient continuously had taken glucocorticoid during 21 months and had multiple skin lesions developed before 9 months without complete resolution until admission. Skin and mediastinoscopic paratracheal lymph node (LN) biopsies showed necrotizing granuloma with many acid-fast bacilli. M. kansasii was cultured from skin, sputum, and paratracheal LNs. The patient had been treated successfully with isoniazid, rifampin, ethmabutol, and clarithromycin, but died due to small bowel obstruction. Our case emphasizes that chronic skin lesions can lead to severe, disseminated M. kansasii infection in an immunocompromised patient. All available cases of disseminated M. kansasii infection in non HIV-infected patients reported since 1953 are comprehensively reviewed.
Antitubercular Agents/therapeutic use ; Clarithromycin/therapeutic use ; Glucocorticoids/therapeutic use ; Humans ; Immunocompromised Host ; Isoniazid/therapeutic use ; Male ; Middle Aged ; Mycobacterium Infections, Nontuberculous/*diagnosis/drug therapy/immunology ; *Mycobacterium kansasii/isolation & purification ; Myelodysplastic Syndromes/drug therapy ; Rifampin/therapeutic use ; Skin Diseases, Bacterial/*diagnosis/immunology/pathology ; Sputum/microbiology ; Sweet Syndrome/diagnosis

Clinical presentations associated with acute human immunodeficiency virus (HIV) infection are various and nonspecific. Neurologic manifestations may accompany acute HIV infection. Aseptic meningitis has been described in several reports; however, acute encephalitis during acute HIV infection is rare. Some studies have suggested that antiretroviral therapy for treatment of symptomatic acute HIV infection could be beneficial, especially in severe cases. Encephalitis is life-threatening; therefore, early diagnosis and antiretroviral therapy may be needed. We report on a case of encephalitis associated with acute HIV infection. The patient received early antiretroviral therapy and recovered from encephalitis without neurological sequelae.
Early Diagnosis ; Encephalitis ; HIV ; HIV Infections ; Humans ; Meningitis, Aseptic ; Neurologic Manifestations