Animals ; Borrelia burgdorferi ; genetics ; isolation & purification ; China ; Genotype ; Ixodidae ; microbiology

Objective To study the mutation rate of hereditary deafness genes found in the newborn babies and to explore the feasibility of routine screening of congenital deafness for the newborns.Method The cord blood were taken to tcst four common deafness genes using gene chip technology in newborn infants born in our Hospital from May 2015 to May 2017 and screening of hearing was performed 48 hours after birth.x2 test was used to analyze the results of gene screening and the hearing screening data obtained after 42 days.Result A total of 2 615 newborns were enrolled in the study and 2 455 cases passed the hearing screening test 48 hours after birth (the passing rate was 93.9％).143 cases passed the hearing screening after 42 days with the passing rate of 99.3％.The mutation of deafness gene from the newborn's cord blood was detected in 107 cases with the rate of 4.1％.96 of 107 infants with deafness gene mutations passed the hearing screening (89.7％).While in infants without this mutation,2 502 cases passed the hearing screening (99.8％,2 502/2 508).The rate of hearing defects in children with deafness gene mutation was significantly higher than those without this gene mutation,and the difference was statistically significant (x2 =160.199,P ＜0.001).Of the 107 cases,the most common mutation was GJB2 (49 cases,45.8％),followed by SLC26A4 (37 cases,34.6％) and mtDNA 12SrRNA (13 cases,12.1％),while the GJB3 was the least (8 cases,7.5％).6 cases were diagnosed the neonate hearing loss at 3 months in 17 newborns who failed to pass repeat screening test 42 days after birth.Among them,hearing loss was caused by the mutation in 5 cases.Conclusion The main mutated genes in children with deafness were GJB2 and SLC26A4 in this study.The combination of hearing screening of newborns and gene test is clinically feasible.The deafness genes in the normal hearing carriers can be detected in time.It is of great advantage for early intervention and treament of the infants early.

Objective To prepare monoclonal antibodies (mAb) against the type Ⅳ secretion system protein VirB5 of Brucella melitensis and to provide a basis for pathgenic diagnosis and research of brucellosis.Methods Four SPF female BALB/c mice were subcutaneously immunized with purified VirB5 protein at a dose of 60 μg/mice,and immunization was strengthened every 2 weeks at a dose of 30 μg/mice,three times in total.Two weeks later,the orbital venous blood of mice was taken to determine the antibody titer,and then intraperitoneally injected for the fourth time to strengthen immunization.Three days later,mouse spleen cells were fused with mouse myeloma SP2/O cells in a ratio of 5:1.After 3 times of cell screening and monoclonal cloning,the hybridoma cell lines with stable secretion of VirB5 antibody were established;one BALB/c mouse was intraperitoneally injected with hybridoma cells,and ascites were collected and antibody was purified when the mouse abdomen was significantly enlarged.The immunological characteristics of mAbs were identified by indirect enzyme-linked immunosorbent assay (ELISA) and Western blotting.Results A total of 6 monoclonal cell lines (2-2,2-12,2-19,2-25,2-31 and 2-40) capable of secreting VirB5 antibody were established.Among them,the cell line 2-19 can stably secrete an antibody that specifically recognized the VirB5 protein,and the VirB5 antibody secreted by the cell line was identified as an IgG1 subtype,a kappa light chain,a mAb affinity constant of 1.6 × 108.The titer of ascites antibody of mouse intraperitoneally injected with hybridoma cell 2-19 was 1:51 200.Conclusion The high-affinity mAb of type Ⅳ secretion system protein VirB5 is successfully prepared,and the antibody can rapidly bind specifically to pathogens,providing an alternative material for establishment of brucellosis pathogen diagnostic method.

Heart failure (HF) is a global public health problem with high morbidity and mortality. A large number of studies have shown that HF is caused by severe energy metabolism disorders, which result in an insufficient heart energy supply. This deficiency causes cardiac pump dysfunction and systemic energy metabolism failure, which determine the development of HF and recovery of heart. Current HF therapy acts by reducing heart rate and cardiac preload and afterload, treating the HF symptomatically or delaying development of the disease. Drugs aimed at cardiac energy metabolism have not yet been developed. In this review, we outline the main characteristics of cardiac energy metabolism in healthy hearts, changes in metabolism during HF, and related pathways and targets of energy metabolism. Finally, we discuss drugs that improve cardiac function