Résumé
Precocious puberty (PP) is a common childhood sexual dysplasia. Central precocious puberty (CPP) is a disease in which the hypothalamic-pituitary-gonadal (HPG) axis is activated in early age, leading to the early release of gonadotrophin releasing hormone, the early development of gonads, and the early onset of puberty. The occurrence of puberty is regulated by gene and environment. Current clinical studies have found that gain-of-function mutations in the KISS1 gene, and loss-of-function mutations in KISS1R (also named GPR54), MKRN3 and DLK1 genes are all important single-gene causes of central precocious puberty. KISS1 is a tumor metastasis suppressor gene. KISS1R codes a G protein-coupled receptor which with its ligand, kisspeptin, forms an excitatory neuroregulator system for GnRH secretion. They play a role in the upstream of the HPG axis. MKRN3 is a maternal-imprinted gene. DLK1 is a gene that regulates the growth of cell. They play a role in the downstream of HPG axis. Recently, the incidence of central precocious puberty has become higher and higher, which is related to the excessive exposure of environmental endocrine disruptors (EEDs) due to the continuous development of social economy. A number of investigations have found that children’s exposure to EEDs is significantly related to the incidence of precocious puberty. In humans, these EEDs also affect the metabolism of gut microbes. This paper aims to review the current studies on the single-gene pathogenesis, epigenetics, gut microbiota and environmental factors of central precocious puberty, so as to provide help for the treatment and prevention of this disease.
Résumé
Background: One leading factor responsible for resistance in Acinetobacter baumannii, an important opportunist in health care institutions globally, is the production of carbapenamases like metallo-β-lactamases (MBLs), which hydrolyze a variety of β-lactams including penicillin, cephalosporins and carbapenems. However, neither any standard guidelines are available nor any method has been found to be perfect for their detection. Various methods have shown discordant results, depending upon the employed methodology, β-lactamase substrate and MBL inhibitor used. This study aims to evaluate two phenotypic methods against PCR as gold standard among carbapenem resistant A. baumannii for identifying MBL producers. Materials and Methods: A total of 130 A. baumannii were screened for imipenem and meropenem resistance by Kirby-Bauer disc diffusion method. Phenotypic expression of MBL was detected by EDTA-imipenem-microbiological (EIM) assay and extended EDTA disc synergy (eEDS) test and presence of bla-IMP and bla-VIM was detected by PCR in all the carbapenem resistant isolates. Results: Of the 43 imipenem and/or meropenem resistant A. baumannii isolates, 4 (9.3%) were found to be MBL producers by EIM and 3 (6.97%) by eEDS. Only bla-VIM gene was detected in 7 (16.28%) by PCR. In addition EIM detected 14 (32.56%) carbapenem resistant non-metallo enzyme producers. Conclusion: Of the two MBL genes targeted, bla-VIM was only detected and that too in isolates resistant to both imipenem and meropenem. Further, EIM was useful in differentiating MBL from non-metalloenzymes producers.