BackgroundPubertal timing in mammals is triggered by reactivation of the hypothalamic-pituitary-gonadal (HPG) axis and modulated by both genetic and environmental factors. Strain-dependent differences in vaginal opening among inbred mouse strains suggest that genetic background contribute significantly to the puberty timing, although the exact mechanism remains unknown.Methodology/Principal FindingsWe performed a genome-wide scanning for linkage in reciprocal crosses between two strains, C3H/HeJ (C3H) and C57BL6/J (B6), which differed significantly in the pubertal timing. Vaginal opening (VO) was used to characterize pubertal timing in female mice, and the age at VO of all female mice (two parental strains, F1 and F2 progeny) was recorded. A genome-wide search was performed in 260 phenotypically extreme F2 mice out of 464 female progeny of the F1 intercrosses to identify quantitative trait loci (QTLs) controlling this trait. A QTL significantly associated was mapped to the DXMit166 marker (15.5 cM, LOD = 3.86, p<0.01) in the reciprocal cross population (C3HB6F2). This QTL contributed 2.1 days to the timing of VO, which accounted for 32.31% of the difference between the original strains. Further study showed that the QTL was B6-dominant and explained 10.5% of variation to this trait with a power of 99.4% at an alpha level of 0.05.The location of the significant ChrX QTL found by genome scanning was then fine-mapped to a region of ∼2.5 cM between marker DXMit68 and rs29053133 by generating and phenotyping a panel of 10 modified interval-specific congenic strains (mISCSs).Conclusions/SignificanceSuch findings in our study lay a foundation for positional cloning of genes regulating the timing of puberty, and also reveal the fact that chromosome X (the sex chromosome) does carry gene(s) which take part in the regulative pathway of the pubertal timing in mice.

Background Health-care-associated infections characterised by antibiotic drug resistance are a global medical challenge that claims billions of dollars of health-care expenditure. Bacterial adhesion and subsequent formation of biofi lms on catheters and tubes are the primary mechanisms through which these infections are initiated and propagated. We tested the effi cacy and safety for clinical treatment of a coating based on natural protein, in which immunogenicity was eliminated through physical plasticising, applied to the surfaces of medical devices to inhibit bacterial adhesion. Methods We did a randomised clinical trial in two hospitals in China (Shanghai Changzheng Hospital and 254th Hospital of Chinese People's Liberation Army in Tianjin), in men and women without urinary tract infection, aged 18-75 years, who required urethral catheterisation. Patients who were pregnant, perinatal, or allergic to silicon rubber or protein, or who had any other diseases (eg, cystitis, stress incontinence, mental or neurological disorders, or severe heart, liver, lung, or kidney failures) not suitable for the study were excluded. All patients who provided written informed consent were enrolled and assigned to groups using a random envelope. Patients received Foley catheters with (test group) and without (controls) the coating. Primary outcomes were diff erences between groups in bacterial colony count and amount of mineral deposition, analysed by Fisher exact test, and leucocytes and occult blood in urine, analysed by χ²/Fisher exact test. To reduce uncertainty owing to participants' use of antibiotics, we designed two-section sampling projects to assess catheter sections in the bladder and out of the urinary meatus. Chinese Food and Drug Administration (Jiangsu province) regulatory code 2014-ZC-440; hospital ethics committee coding EC-Device-2014-18 and EC-Device-2015-08. Findings Between July, 2014, and November, 2015, we randomly assigned 67 patients to the test group and 65 to the control group. Urinary mineral deposition occurred in fi ve (8%) patients in test group and 22 (34%) in control group (χ²=14•11, OR 0•16, 95% CI 0•06-0•45, p=0•0002). Bacterial colonisation was present in catheter sections out of the urinary meatus for 18 test patients (27%) and 44 (68%) controls (OR 0•16, 95% CI 0•08-0•37, p<0•0001), and in bladder for 27 (40%) test patients and 44 (68%) controls (0•32, 0•16-0•66, p<0•0001). There were no signifi cant diff erences between the groups in leucocytes and occult blood in urine before, during, or after catheterisation (p>0•05). No adverse events occurred in either group. Interpretation The coating can eff ectively and safely inhibit biofi lm formation on catheter surface and reduce urinary mineral deposition.

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This study was performed to discover SNPs for genetic polymorphism analysis of mitochondrial DNA from wild house mice. Universal primer florescent PCR, fluorescence-based conformation sensitive gel electrophoresis (F-CSGE) and DNA sequencing were conducted to analyze the coding region of mitochondrial DNA. Different types of unknown mutations were recorded by variable F-CSGE patterns without false positive. Twenty-four SNPs, sixteen of which were first discovered in the coding region of mitochondrial DNA, were found in 64 wild house mice from 4 districts in Shanghai. Therefore, F-CSGE was proved to be powerful technique for SNP discovery in the coding region mitochondrial DNA. The novel SNPs can be used as molecular markers to analyze population structure and genetic polymorphisms of the wild house mice in Shanghai.