Control of tuberculosis is threatened by widesread emergence of drug resistant Mycobacterium tuberculosis. Rifampin is a key component among therapeutic regimens for the tuberculosis; therefore patients in whom resistance to this drug develop have a poor outlook, particularly if rifampin resistance is associated with resistance to other tuberculosis drugs. The purpose of this study was to detect the mutation in rpoB gene of rifampin resistant M. tuberculosis in Korea and to evaluate the usefulness of the method in clinical aspects. A sample of 80 M. tuberculosis was studied, and it included 40 rifampin resistance isolates and 40 rifampin sensitive isolates by conventional methods. The detection method involved the amplification by polymerase chain reaction (PCR) of the Rif' region and the identification of mutations by single-strand DNA conformation polymorphism analysis (SSCP) of the amplification products (157 bp). Mutation were identified in 39 of 40 rifampin resistant isolates, and in 1 of 40 rifampin sensitive isolates.
Humans ; Korea ; Mycobacterium tuberculosis* ; Mycobacterium* ; Nucleic Acid Conformation ; Polymerase Chain Reaction* ; Rifampin ; Tuberculosis

Control of tuberculosis is threatened by widespread emergence of drug resistance in Mycobacterium tuberculosis. Understanding the molecular basis of resistance might lead to development of novel rapid methods for diagnosing drug resistance. Rifampin is a key component among therapeutic regimens for the tuberculosis; therefore, patients who have drug resistance do not convalesce satisfactorily. The molecular mechanism of resistance to rifampin in M. tuberulosis has been elucidated. Substitutions of a limited number of highly conserved amino acids encoded by the rpoB gene are responsible for the ""single-step"" high-level resistance of M. tuberculosis to rifampin. Currently, two genotype-based protocols allow drug test from minimally grown cultured materials: (i)mutation identification by direct sequencing of PCR-amplified material. and (ii)mutation screening by PCR-SSCP. The purpose of this study is to evaluate the usefulness of the both methods. A sample of 75 isolates of M. tuberculosis was studied, and it inculded 36 rifampin-resistant strains and 39 rifampin-sensitive strains by conventional methods. Mutaions were identified in 36 rifampin-resistant isolates but in none of 39 sensitive isolates. All mutations were clustered within a region of 23 amino acids. Both methods allow detection of rifampin resistance in 2 to 3 days and will thus help in the early management of infection by M. tuberculosis.
Amino Acids ; Drug Resistance ; Humans ; Mass Screening ; Mycobacterium tuberculosis* ; Mycobacterium* ; Rifampin ; Tuberculosis

No abstract available.
HIV-1* ; Humans* ; Tumor Necrosis Factor-alpha*

No abstract available.
Cesarean Section* ; Female ; Pregnancy

No abstract available.
Carcinoma, Basal Cell* ; Nevus*

No abstract available.
Bowen's Disease*

No abstract available.
Edema* ; Hydrops Fetalis*

No abstract available.
Adenocarcinoma* ; Fallopian Tubes* ; Female

BACKGROUND AND OBJECTIVES: The aim of this study was to determine the effect of ethanol on the regulation of vascular tone. MATERIAL AND METHODS: Using rat aorta ring, isometric contraction and 45Ca uptake were measured. Phorbol 12,13-dibutyrate (PDBu), phenylephrine, KCl were used for the regulation of smooth muscle tone. RESULTS: Ethanol induced transient contraction in rat aorta ring by dose-dependent manner. Ethanol suppressed the dose dependent contractile responses of vascular strip by phenylephrine, KCl and PDBu. Endothelium-dependent relaxation by acetylcholine was inhibited by ethanol. Ethanol depressed 45Ca uptake by high KCl but not by phenylephrine or PDBu in rat aorta. n-butanol selectively suppressed tonic contraction by high KCl, but t-butanol did not at the same concentration of butanol in rat aorta. PDBu-induced contraction was selectively suppressed by n-butanol but not by t-butanol. CONCLUSIONS: These findings suggest that the action of ethanol on phospholipase D is involved in the decreased response of rat aorta strip by vasoconstrictors.
1-Butanol ; Acetylcholine ; Animals ; Aorta* ; Ethanol* ; Isometric Contraction ; Muscle, Smooth* ; Phenylephrine ; Phorbol 12,13-Dibutyrate ; Phospholipase D ; Protein Kinase C ; Rats* ; Relaxation ; tert-Butyl Alcohol ; Vasoconstrictor Agents

No abstract available.
Abscess* ; Citrobacter koseri