No abstract available.
DNA*

No abstract available.
DNA*

BACKGROUND: Tuberculosis continues to be a major threat to health throughout the world, with an estimated 8 to 10 million new cases and 3 million deaths annually. And control of the disease is further threatened by the emergence of drug resistance. Recent major advances have been made in unravelling the molecular basis of M. tuberculosis resistance to isoniazid, streptomycin, quinolones and rifampin. And rifampin resistance is the useful indicator for the occurance of the multi-drug resistance. Hence, the rapid detection of rifampin resistant strain of M. tuberculosis is the key to have successful anti-tuberculosis therapy. Here we present our experience using PCR and line probe assay (INNO-LiPA) for easy and rapid detection of rifampin resistance of M. tuberculosis. METHODS: Thirty rifampin resistant and twenty susceptible strains of M. tuberculosis were collected from the routine culture and analyzed with INNO-LiPA. And results were compared with conventional antibiotic susceptibility testing. After amplification of the region of the RNA polymerase(rpoB), the amplified product is hybridized with a set of 10 oligonucleotides immobilized onto a membrane strip. From the pattern obtained the presence or not of rifampin resistance M. tuberculosis can be assessed. RESULTS: Ninety three percent of patients who had rifampin resistant strain revealed the multidrug resistance while only two showed resistance to rifampin only. The INNO-LiPA test results were generally agreeable with that of the conventional susceptibility testing(90%). The mutations in codon 531 (absence of 55 probe) were most commonly observed. In 55.2% of the 31 rifampin resistance M. tuberculosis confirmed on mutation by R-probes on the INNO-LiPA strips. CONCLUSIONS: The line probe assay after polymerase chain reaction is a fast and convenient method to detect both presence of M. tuberculosis complex strains and its resistance to rifampin in clinical specimens. We have suggested that detection of rifampin resistance may play a key role in monitoring multi-drug resistance. Consequently, the INNO-LiPA test may constitute an important tool for the control of tuberculosis.
Codon ; Drug Resistance ; Drug Resistance, Multiple ; Humans ; Isoniazid ; Membranes ; Mycobacterium tuberculosis* ; Mycobacterium* ; Oligonucleotides ; Polymerase Chain Reaction ; Quinolones ; Rifampin* ; RNA ; Streptomycin ; Tuberculosis

No abstract available.
Humans

No abstract available.
Creatine Kinase* ; Electrophoresis*

BACKGROUND AND OBJECTIVES: Rhinovirus enters into airway epithelial cells via the membrane bound receptor ICAM-1. Infected epithelial cells secrete the cytokines such as IL-6 and IL-8, which induce neutrophil migration into the epithelium. Clarithromycin has been found to inhibit ICAM-1 production and secretion of IL-6 and IL-8. We hypothesized that these properties of clarithromycin may be applicable in treating rhinovirus infection. MATERIALS AND METHOD: We assayed the effects of clarithromycin on rhinovirus infected A549 cells. ICAM-1 expression was assessed by flow cytometry, and cytokine secretion was assayed by ELISA. The level of viral replication was expressed as viral titer, which was determined through viral culture on MRC-5 cells. RESULTS: The mean fluorescence intensity of ICAM-1 in rhinovirus infected cells decreased from 12.4+/-0.59 to 9.2+/-0.72 after treatment with clarithromycin. The production of IL-1beta, IL-6, and IL-8 was decreased after rhinovirus infected cells were treated with clarithromycin. In the absence of rhinovirus infection, clarithromycin had no effect on ICAM-1 expression or cytokine secretion. The rhinovirus titer in infected cells was 10(3.71) TCID 50 U/ml, which was reduced following clarithromycin treatment to 10(2.14) TCID 50 U/ml. CONCLUSION: These findings suggest that clarithromycin treatment of rhinovirus infected A549 cells inhibited rhinovirus induction of increased ICAM-1 expression, cytokine elaboration, and viral replication.
Clarithromycin* ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells ; Epithelium ; Flow Cytometry ; Fluorescence ; Intercellular Adhesion Molecule-1 ; Interleukin-6 ; Interleukin-8 ; Macrolides ; Membranes ; Neutrophils ; Rhinovirus

No abstract available.
Cystitis*

BACKGROUND: Recent studies have shown that men with diabetes have lower testosterone levels than healthy men. However, studies on the correlation between testosterone and diabetes are rare in Korea. We examined the relationship between testosterone deficiency and markers related to diabetes in adult Korean men. METHODS: A total 464 men with diabetes who visited an outpatient clinic at Ajou University Hospital and had serum total testosterone and serum insulin levels measured between January 2000 and September 2013 were selected. Blood samples were collected after the subjects had fasted overnight. We divided the participants into testosterone deficient and normal groups. Testosterone deficiency was defined as having a serum total testosterone level <3.5 ng/mL. RESULTS: Of 464 subjects, 34.9% had a testosterone deficiency. The mean levels of fasting plasma glucose (P=0.007) and glycated hemoglobin (HbA1c; P=0.038) were significantly higher in the testosterone deficiency group than in the normal group. To clarify the relationship between serum total testosterone level and fasting plasma glucose or HbA1c values, Pearson's correlation test was performed. Fasting plasma glucose levels (r=-0.142, P=0.002) and HbA1c values (r=-0.097, P=0.040) showed a significant negative correlation with serum testosterone levels in men with diabetes. CONCLUSION: Major markers of diabetes that are associated with testosterone deficiency are fasting plasma glucose and HbA1c values. Poor glycemic control appears to be associated with testosterone deficiency in Korean men with diabetes.
Adult ; Ambulatory Care Facilities ; Blood Glucose ; Fasting ; Glucose ; Hemoglobin A, Glycosylated ; Humans ; Insulin ; Korea ; Male ; Testosterone*

BACKGROUND: Propofol, 2,6-diisopropyl phenol, is a short-acting, potent intravenous anesthetics agent. In both general anesthetic care and the anesthetic care of patients undergoing cardiovascular surgery, the unique characteristics of propofol might make it a logical part of the anesthetic plan for patients such as pulmonary hypertension. But there are limited experimental and clinical data on the effects of propofol on pulmonary vascular resistance, and they are somewhat contradictory. the purpose of this study was to investigated.the effect and mechanism of vasodilation induced by propofol using isolated rat pulmonary artery rings. METHODS: Cumulative dose-response curves for propofol(10(-6)~10(-3)M) were obtained from tension measurements of rings that contracted with phenylephrine(10(-6)M) and KCI(40 mM) in the presence and absence of endothelium, and in the pretreatment of L-NAME(3x10(-4)M) and substance P(3x10(-4)M). Thereafter the effect of propofol(10(-4)M) on vascular smooth muscle contration in response to Ca++ mobilization in vscular rings were investigated. RESULTS: Propofol(10(-6)~10(-3)M) produced dose-dependent relaxation and had no signficant effect from endothelium. Pretreatment of L-NAME and substance P failed to have influence on cumulative dose-respose curves. Therefore vasodilator effect of propofol was not endothelium-dependent. And 10(-4)M propofol attenuated a contraction in response to CaCl2 in vascular rings depolarized by KCI, and vasoconstraction in response to calcium entry in the presence of phenylephine was attenuated by 10(-4)M propofol. Ryanodine preteament had not influence on contractile response. CONCLUSIONS: These results suggest that vasodilation produced by propofol is not endothelium-dependent but is probably due to nonspecific intracellular Ca++ influx blockade through voltage-operated calcium channels and receptor-operated channels.
Anesthetics ; Anesthetics, Intravenous ; Animals ; Calcium ; Calcium Channels ; Endothelium ; Humans ; Hypertension, Pulmonary ; Logic ; Muscle, Smooth, Vascular ; NG-Nitroarginine Methyl Ester ; Phenol ; Propofol* ; Pulmonary Artery* ; Rats* ; Relaxation ; Ryanodine ; Substance P ; Vascular Resistance ; Vasodilation

PURPOSE: To evaluate the sonographic findings of plantar fasciitis. MATERIALS AND METHODS: Both feet of 30patients(mean age, 44years) in whom plantar fasciitis had been clinically diagnosed, and those of healthyvolunteers(mean age, 34years) were evaluated with ultrasound(US) using a 7.0MHz linear array transducer. Heel painwas unilateral in 26 patients and bilateral in four. Sagittal sonograms were obtained in the prone position, andthe thickness of the plantar fascia was measured at its proximal end near its insertion into the calcaneus. Wealso evaluated hypoechoic fascia, perifascial fluid collection, fiber rupture, calcaneal spur and calcifications. RESULTS: Plantar fascia thickness was significantly greater in the heels of patients with plantarfasciitis(3.2-8mm; mean, 5.1 +/-1.12) than in their asymptomatic heels(1.3-5mm; mean, 3.5 +/-0.78)(p<0.0001), inwhich it was similar to that of heels of patients in the control group(1.8-5mm; mean, 3.0 +/-0.71)(p<0.0001). Theproximal plantar fascia was hypoechoic in 31 symptomatic heels(91.2%), in four asymptomatic heels(15.4%), and innone of the patients in the control group. Calcaneal spurs were identified in sixteen symptomatic heels(47.1%),and in two which were asymptomatic(7.7%). Perifascial fluid collection was identified in only two symptomaticheels(5.9%). CONCLUSION: In plantar fasciitis, sonography demonstrates that the fascia is thicker as well ashypoechic. For the clinical diagnosis of planter fasciitis, US can therefore be used as an adjunct to clinicaldiagnosis.
Calcaneus ; Diagnosis ; Fascia ; Fasciitis ; Fasciitis, Plantar* ; Foot ; Heel ; Heel Spur ; Humans ; Prone Position ; Rupture ; Transducers ; Ultrasonography*