OBJECTIVE To study the patterns of the resistance to erythromycin mediated by ermB and mefE in Streptococcus pneumoniae isolates in children.METHODS Totally 1012 sputums obtained from upper and lower respiratory tract of children were collected.Clindamycin disks were used to detect macrolide resistance mediated by ermB and mefE in S.pneumoniae isolates from children.RESULTS 252 nonduplicate clinical isolates of S.pneumoniae obtained.the ermB gene(63.6%) was predominant among isolates from children,while mefE was 36.4%.CONCLUSIONS Isolates containing ermB gene are highly resistant to clindamycin.The resistance mediated by ermB is higher than that by mefE.

Serum sialic acid (SA) levels were detected by neuraminidase method in 366 patients with malignant tumor, 40 patients with benign diseases and 40 healthy subjects.For 277 malignant tumor patients, serum SA levels were monitored before and after treatment.The serum SA levels in malignant tumor group were significantly higher than those in benign diseases and control groups (P ＜0.01 ), but there were no differences between normal and benign groups (P ＞0.05 ).Serum SA levels were decreased in malignant tumor patients with remission and stable disease after treatment.In remission or stable patients the decrease of serum SA levels occurred in the first three months and no changes were found from the fourth to sixth month; meanwhile SA levels were elevated in patients with instablc condition.

BRCA1 is a well-established tumor suppressor gene, which is frequently mutated in familial breast and ovarian cancers. The gene product of BRCA1 functions in a number of cellular pathways that maintain genomic stability, including DNA damage-induced cell cycle checkpoint activation, DNA damage repair, protein ubiquitination, chromatin remodeling, as well as transcriptional regulation and apoptosis. In this review, we discuss recent advances regarding our understanding of the role of BRCA1 in tumor suppression and DNA damage response, including DNA damage-induced cell cycle checkpoint activation and DNA damage repair.
Apoptosis ; genetics ; BRCA1 Protein ; genetics ; physiology ; Breast Neoplasms ; genetics ; DNA Damage ; genetics ; DNA Repair ; genetics ; Female ; Genes, Tumor Suppressor ; Genes, cdc ; physiology ; Humans ; Mutation ; Ovarian Neoplasms ; genetics ; Signal Transduction ; genetics