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

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

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.
Abscess* ; Citrobacter koseri

No abstract available.
Female ; Pregnancy ; Pregnancy, Ectopic*

This experimental study was conducted to evaluate the effect of indomethacin and methylprednisolone on PAN-induced nephrosis in rats. Sprague-Dawley rats weighing 150~200gm were used and divided into controls, group I (PAN intraperitoneally), group II(PAN intraperitoneally, followed by indomethacin peritoneally for 12 days), group III (PAN intraperitoneally, followed by methylprednisolone peritoneally for 12 days) and group IV (PAN intraperitoneally, followed by cyclosporin subcutaneously for 12 days). Twenty four-hour urinary protein excretion was measured on day 0, 5, 10 and 17. On the 17th day, rats were sacrificed for the determination of total serum protein, albumin and cholesterol levels. Foot process widths of glomerular epithelial cells were measured, and anionic sites of lamina rara externa were determined by using PEI as cationic probes. The following results were obtained. Twenty four-hour urinary protein excretion (mg/day) of group I was significantly increased to 455.7+/-188.8 on the 5th day compared to 15.2+/-3.7 on day 0 (p<0.01), and increased gradulally to 525.6+/-203.5 on the 10th day, then decreased to 280.6+/-25.2 on the 17th day. In group III, 24 hr urinary protein excretion on 17 th day (180.7+/-64.5) was significantly lower than that of group I (280.6+/-25.2). Total serum protein of group III was significantly lower than that of group I, and serum albumin and cholesterol did not show any significant difference among Group I, II, III and IV. Foot process widths (nm) of glomerular epithelial cells in group I, II, III and IV were 409.5+/-15.2, 387.8+/-49.2, 279.9+/-36.9 and 398.3+/-38.3, respectively. And the value of group of group III was significantly lower than that of group I (p<0.01). The number of anionic sites per 1micrometer length of glomerular basement membrane in Group I, II, III and IV were 10.3+/-1.3, 10.1+/-1.6, 12.5+/-1.5and 10.2+/-1.5, respectively. And the value of group III was significantly lower than that of group I (P<0.01). In conclusion, cyclosporin and indomethacin did not show any significant effect on PAN nephrosis in rat. However, methylprednisolone reduced the urinary protein excretion and showed significant recovery of foot process widths and number of anionic sites of glomerular basement membrane.
Animals ; Cholesterol ; Cyclosporine* ; Epithelial Cells ; Foot ; Glomerular Basement Membrane ; Indomethacin* ; Methylprednisolone* ; Nephrosis* ; Nephrotic Syndrome ; Rats* ; Rats, Sprague-Dawley ; Serum Albumin

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