RESUMO
We report the first occurrence of New Delhi metallo-ß-lactamase 5 (NDM-5) in carbapenem-resistant Escherichia coli isolated from blood cultures of three leukemia patients in northern China. These patients had at some time been hospitalized in the hematology department of the same hospital. All isolates were ST167 with identical pulsed-field gel electrophoresis patterns, suggesting a likely hospital transmission.
Assuntos
Bacteriemia/microbiologia , Escherichia coli/enzimologia , Leucemia/microbiologia , beta-Lactamases/biossíntese , Adulto , Carbapenêmicos/farmacologia , China , Eletroforese em Gel de Campo Pulsado , Escherichia coli/efeitos dos fármacos , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
OBJECTIVES: To investigate mechanism for the increasing level of serum vascular endothelial growth factor(VEGF) in tumour patients during radiotherapy and the inhibitory action of the antisense oligodeoxynucleotide (AS-ODN) to the expression of VEGF protein by radiotherapy in the prostate cancer cell line (PC3M). METHODS: To observe the changes of serum VEGF in the prostate cancer patients during radiotherapy dynamically and the inhibitory action of the antisense oligodeoxynucleotide to the expression of VEGF by radiotherapy in PC3M. RESULTS: The changes of serum VEGF in three patients receiving radiotherapy had been observed continuously. The levels of serum VEGF began to increase when the patients received radiotherapy and rised up to peak value after fifteen days, then declined to the range of pre-radiotherapy. Irradiating the PC3M cells with X-rays significantly increased the VEGF expression and secretion. The expression of VEGF protein in the group treated by VEGF AS-ODNs and X-ray irradiation decreased significantly than the group treated only by X-ray irradiation. CONCLUSIONS: The induction of VEGF protein expression by X-ray irradiation in tumor cells may result in the increasing of the VEGF in the prostate cancer patients during radiotherapy and the induction can be blocked by VEGF AS-ODNs.
Assuntos
DNA Antissenso/farmacologia , Fatores de Crescimento Endotelial/antagonistas & inibidores , Expressão Gênica/efeitos dos fármacos , Linfocinas/antagonistas & inibidores , Neoplasias da Próstata/sangue , Fatores de Crescimento Endotelial/sangue , Fatores de Crescimento Endotelial/genética , Expressão Gênica/efeitos da radiação , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/sangue , Peptídeos e Proteínas de Sinalização Intercelular/genética , Linfocinas/sangue , Linfocinas/genética , Masculino , Neoplasias da Próstata/patologia , Radioterapia/efeitos adversos , Células Tumorais Cultivadas , Fator A de Crescimento do Endotélio Vascular , Fatores de Crescimento do Endotélio VascularRESUMO
To evaluate the molecular mechanism of fluoroquinolones resistance in Mycoplasma hominis (MH) clinical strains isolated from urogenital specimens. 15 MH clinical isolates with different phenotypes of resistance to fluoroquinolones antibiotics were screened for mutations in the quinolone resistance-determining regions (QRDRs) of DNA gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE) in comparison with the reference strain PG21, which is susceptible to fluoroquinolones antibiotics. 15 MH isolates with three kinds of quinolone resistance phenotypes were obtained. Thirteen out of these quinolone-resistant isolates were found to carry nucleotide substitutions in either gyrA or parC. There were no alterations in gyrB and no mutations were found in the isolates with a phenotype of resistance to Ofloxacin (OFX), intermediate resistant to Levofloxacin (LVX) and Sparfloxacin (SFX), and those susceptible to all three tested antibiotics. The molecular mechanism of fluoroquinolone resistance in clinical isolates of MH was reported in this study. The single amino acid mutation in ParC of MH may relate to the resistance to OFX and LVX and the high-level resistance to fluoroquinolones for MH is likely associated with mutations in both DNA gyrase and the ParC subunit of topoisomerase IV.