Urine specimens from 120 patients attending urologic clinics were screened by blot hybridization for the presence of a polyomavirus DNA. Detected viral DNA was then identified as BK or JC by fine restriction enzyme analysis. BK and JC viral DNA was found in 5 (4%) and 35 (29%) patients, respectively. Detection rates were compared among three age groups: 0-29, 30-59, and 60-89 years. Detection of JC viral DNA increased with age and reached the highest value (45%) in the group aged 60-89 years. For BK viral DNA a correlation between detection and age was not clear because the rate of detection was low, although the highest rate (9%) occurred in the oldest group. To confirm the active urinary excretion of polyomavirus DNA in older patients, urine specimens from 23 patients (60-90 years) treated at an internal medicine clinic were examined for viral DNA. BK and JC viral DNA were in 2 (9%) and 12 patients (52%), respectively. These results suggest that JC virus is frequently reactivated in older individuals.

ObjectiveTo clarify therapeutic effects of azithromycin, clarithromycin, minocycline and tosufloxacin against macrolide-resistant Mycoplasma pneumoniae (MRMP) pneumonia and against macrolide-sensitive Mycoplasma pneumoniae (MSMP) pneumonia in pediatric patients.MethodsA prospective, multicenter observational study was conducted from July 2013 to August 2015. The therapeutic effects of azithromycin, clarithromycin, minocycline and tosufloxacin were evaluated in 59 patients with pneumonia caused by MRMP and in 50 patients with pneumonia caused by MSMP. In vitro activities of antimicrobial agents against isolates of Mycoplasma pneumoniae were also measured.ResultsMean durations of fever following commencement of treatment in patients infected with MRMP and MSMP were 5.2 and 1.9 days, respectively (log-rank test, P < 0.0001). Among patients infected with MRMP, mean durations of fever were 4.6, 5.5, 1.0 and 7.5 days for patients treated with azithromycin, clarithromycin, minocycline and tosufloxacin, respectively (log-rank test, P < 0.0001). Among patients infected with MSMP, mean durations of fever were 2.5, 1.7, 0.9 and 4.3 days for patients treated with azithromycin, clarithromycin, minocycline and tosufloxacin, respectively (log-rank test, P = 0.0162). The MIC90s of azithromycin and clarithromycin among the 27 isolates of MRMP were 64 and 256 μg/ml, respectively, and those among the 23 isolates of MSMP were <0.000125 and 0.001 μg/ml, respectively. The MIC90s of minocycline and tosufloxacin among the 27 isolates of MRMP were 1.0 and 0.25 μg/ml, respectively, and those among the 23 isolates of MSMP were 1.0 and 0.5 μg/ml, respectively.ConclusionBoth minocycline and tosufloxacin showed good in vitro activities against MRMP. Minocycline, but not tosufloxacin, shortened the duration of fever in pediatric patients infected with MRMP compared to the duration of fever in patients treated with macrolides.

From nonimmunocompromised individuals, we have recently identified a possible archetypal JC virus DNA sequence from which various regulatory sequences of JC virus isolates derived from patients with progressive multifocal leukoencephalopathy (PML) could have evolved. In this study, we analyzed the regulatory sequences of JCV DNAs cloned from urine samples of a PML risk group (renal transplant patients on immunosuppressive therapy). A number of JC virus DNAs were molecularly cloned from virions excreted in the urine of eight patients. Furthermore, fragments containing the regulatory region were amplified by the polymerase chain reaction and subsequently molecularly cloned from cell-associated JC virus excreted in the urine of two patients. The regulatory regions in all clones were analyzed with restriction enzymes, and those in representative clones were sequenced. We found that clones with the archetypal regulatory sequence were predominant in all urine samples, but a few clones carried regulatory sequences that diverged from the archetypal sequence by deletion or duplication. The finding that sequence rearrangement in the archetypal regulatory region occurs in the course of infection in immunosuppressed hosts is consistent with the adaptation hypothesis which has been put forward to explain the divergence of the regulatory regions in PML-derived JC virus isolates.

Temperature-programmed desorption (TPD) of toluene was carried out on various zeolites, and theoretically analyzed to determine thermodynamic parameters. The TPD process was identified as the case of equilibrium control, showing that the analytical method, the same as that for ammonia TPD, can be applied to the toluene TPD to calculate the adsorption heat. It was observed that approximately one toluene molecule was adsorbed on one Na + cation for MFI and BEA. The heat of toluene adsorption on Na + was MOR > MFI > BEA > FAU, similar to the heat of ammonia adsorption on the corresponding H-form zeolite. A linear relationship was observed between both adsorption heats. It suggests that the adsorption of toluene on Na + is controlled by the electron-withdrawing nature of the ion exchange site, as well as the Brønsted acid strength of the H-form zeolite.

We molecularly cloned a number of BK virus (BKV) DNAs from urine samples collected from a patient with systemic lupus erythematosus undergoing immunosuppressive therapy. On the basis of the structure of the noncoding regulatory region, cloned viral DNAs were classified into a major group and several minor groups. The major group contained a single 68-base-pair (bp) promoter-enhancer element and a 63-bp sequence identified in the genomes of many BKV strains. Most of the minor groups retained a variety of duplications within the transcriptional control region and the origin of DNA replication. We assayed various cloned viral DNAs for the capacity to induce viral growth in transfected human embryonic kidney cells. While major viral DNAs induced slow viral replication, a minor viral DNA retaining partial duplication of the 68-bp element induced rapid viral growth. We concluded that reiteration of the promoter-enhancer element, which is required for efficient growth of BKV in cell culture, is not advantageous for replication of BKV in natural hosts.