Dexamethasone ; therapeutic use ; Glucocorticoids ; pharmacology ; therapeutic use ; Humans ; Infant, Newborn ; Meconium Aspiration Syndrome ; drug therapy ; physiopathology ; Methylprednisolone ; therapeutic use ; Prednisolone ; therapeutic use

Objective To study the influence on STR typing for low copy number(LCN)DNA using different methods of amplifcation and detection.Methods Control DNA 9947A was diluted and then amplifled with Identifiler~(TM) or DNATyper15~(TM).The heat cycles were set to 28 or 28 add 6.Each template wag amplified three times in parallel,and then the amplified products or the product mixture of three amplifictions were deteced with 310 or 3130 Genetic Analyzer.Results The success rate of STR typing with the method 28+6 cycles was higher than that of 28 cycles.There are no correlation between the allele imbalance or allele dropout and STR locus.With the reduction in the amount of template DNA,allele imbalance and dropout gradually increased,and the allele dropout was more common than allele imbalance when the amount of template DNA Wag very small.When the product mixture of three amplifictions were deteced.the occurrence of allele imbalance and dropout reduce obviously.Conclusion The success rate of STR typing of LCN DNA can be obviously increased by detecting the product mixture of three amplifictions in parallel combined with the 28+6 heat cycle condition.

Aged ; Bone and Bones ; pathology ; Carcinoma, Small Cell ; complications ; pathology ; Female ; Humans ; Hyoid Bone ; pathology ; Plasmacytoma ; complications ; Small Cell Lung Carcinoma ; Thyroid Gland ; pathology ; Thyroid Neoplasms ; pathology

Objective Developing an internal quality control substance of Ureaplasma urealyticum(UU)‐DNA for real‐time PCR to establish an internal quality control system and preliminary evaluation its clinical value .Methods Internal quality control sub‐stance was prepared by mixing samples which Ct value were 24-25(positive sample) and 32 -33(weak positive sample) ,respec‐tively .At the same time ,selecting samples that test results were negative as negative control .The target value ,standard deviation (s) and coefficient of variation(CV) of internal quality control substance were defined by“instant method”for the first 20 runs and Levey‐Jennings quality control(QC) chart after the first 20 runs .Using the“Westdard” multi‐rule quality control methods to ana‐lyze the detection results .Exporting OPSPecs chart by quality control rules in Unity Real Time (URT ) system and setting up new quality control rules according with OPSPecs chart .Results 131 times of the detection of quality control substance were performed totally .The first 20 runs were defined by“instant method”and later 111 runs were defined by Levey‐Jennings QC chart ,the results were stable of quality control substance and reasonable quality control rules .Conclusion Preparing of internal quality control sub‐stance of UU‐DNA used in real‐time PCR might be easy and stable .So ,the internal quality control substance of UU‐DNA could be worthy for practical application in this PCR laboratory .Design internal quality control rules based OPSPecs chart in molecular de‐tection is very simple and practical .

Adult ; Altitude ; Asian Continental Ancestry Group ; genetics ; Female ; Humans ; Janus Kinase 2 ; genetics ; Male ; Middle Aged ; Mutation ; Polycythemia ; diagnosis ; ethnology ; genetics

Objective To detect the expression pattern of microRNA in A549 cells treated by lipopolysaccharide, study the expression of miRNA-1247-3P in A549 cells under LPS treatment and explore the possible mechanism of miRNA-1247-3P in A549 cells under LPS treatment. Methods A549 cells were divided into experimental and control groups. Immunocytochemical method and RT-PCR were used to detect the changes of SP-A and SP-C. The expression of miRNAs were detected using miRNAs array in different groups. The key miR-1247-3P was collected to detect the changes of miR-1247-3P in all groups using quantitative real-time polymerase chain reaction. Results Compared with control group, the expressions of SP-A and SP-C were significantly decreased in the experimental groups (P < 0.05). MiRNA array showed that 31 miRNAs were up-regulated and 3 miRNAs were down-regulated. Compared with control group, the expression of miR-1247-3P was significantly increased in the experimental groups (P < 0.05). Conclusion The increased expression of miR-1247-3P may play an important role in the pathogenesis of ARDS.

[Abstract ] Objective High-mobility group box-1 (HMGB1) is abundantly released in the epileptogenic brain tissue , but few reports are seen about the effect of HMGB 1 on the expression of P-glycoprotein ( P-gp) in the vascular endothelial cells of the epi-leptogenic tissue .This study is to explore whether HMGB 1 can regulate P-gp expression in the brain microvascular endothelial cells of the mouse in vitro . Methods Immortalized brain microvascular endothelial bEnd .3 cells of the mouse were cultured in vitro and al-located to different concentration groups ( treated with culture medium containing 10 , 100 , 500 , and 1000 ng/mL HMGB1 for 8 hours), treatment duration groups (treated with culture medium containing 100 ng/mL HMGB1 for 4, 8, 16, 24, and 32 hours), and a control group ( treated with culture medium without HMGB 1 ) .The mRNA expression of P-gp-encoding gene-multidrug resistance gene 1a (mdr1a) was detected by real-time qPCR, and its protein expression determined by Western blot and immunocytochemistry . Results The results of qPCR manifested that the expressions of mdr 1a mRNA were 1.646 ±0.176, 1.777 ±0.135, 1.617 ±0.043, and 1.398 ±0.182 in the 10, 100, 500, and 1000 ng/mL HMGB1 groups, respectively, significantly higher than 1.030 ±0.284 in the control group (P<0.05), and so were those in the 4, 8, 16, 24 h, and 32 h groups (2.655 ±0.112, 2.168 ±0.212, 1.823 ± 0.232, 1.418 ±0.376, and 1.445 ±0.123) than in the control (1.010 ±0.164) (P <0.05).Western blot showed a significant increase in the P-gp protein expression in all the concentration groups (P<0.05) as well as in the 8 h and 16 h treatment duration groups as compared with the control group (P<0.05).Immunocytochemis-try also revealed a higher P-gp expression in the HMGB1-treated than in the control cells (P<0.01). Conclusion HMGB1 can upregu-late the expressions of mdr1a mRNA and P-gp protein in the brain microvascular endothelial cells of the mouse , which may associated with drug resistance of central nervous system diseases , especially that of epilepsy .

Objective To investigate the effects of ursolic acid (UA) on cisplatin (CDDP)-induced expres_sion of transient receptor potential vanilloid 1 (TRPV1) in mouse cochlea .Methods Sixty BALB/c mice were ran_domly divided into 4 groups (15 mice in each group) and received introperitoneal injection once daily for 5 days:Control group (normol saline) ,UA group (80 mg/kg/day) ,CDDP group (4 .5 mg/kg/day) ,and CDPP (4 .5 mg/kg/day) plus UA group (80 mg/kg/day) .The expression of TRPV1 in mouse cochlea was determined by immuno_histochemistry ,microscope image analysis and western blot ,and auditory thresholds were evaluated by auditory brainstem response (ABR) measurement .ResuIts The expression of cochlea TRPV1 and ABR threshold shift was significantly increased in the mice treated with CDDP (P< 0 .05) ,as compared with control mice .These effects were prevented by UA treatment (all P<0 .05) .Furthermore ,a linear relationship analysis revealed that the ex_pression of cochlea TRPV1 was significantly correlated with ABR threshold shift(|r|>0 .7 , P<0 .05) .ConcIusion UA effectively attenuated CDDP -induced ototoxicity and improved auditory function through inhibition of TR_PV1 .

Objective To observe the roles of nuclear factor-κB (NF-κB) and hypoxia-inducible factor-1 o (HIF-1 α) in hippocampal neurodegeneration of status epilepticus (SE) rats, and explore whether HIF-1α activation is regulated by NF-κB.Methods A total of 110 male Sprague-Dawley rats were randomly divided into seven groups : (1) Control group treated with saline (control, n =15), (2) sham group implanted cannula into lateral ventricle and treated with saline (sham, n =15), (3) SE group treated with pilocarpine (SE, n =20), (4) NF-κB activity inhibitor pyrrolidine dithiocarbamate (PDTC) group treated only with PDTC (PDTC, n =15), (5) SE + PDTC group treated with pilocarpine plus PDTC (SE + PDTC, n =15), (6) SE + HIF-1o siRNA group implanted cannula into lateral ventricle and treated with pilocarpine plus HIF-1 α siRNA (SE + HIF-1α siRNA, n =15), (7) SE + control siRNA group implanted cannula into lateral ventricle and treated pilocarpine plus control siRNA (n =15).SE was induced by injecting lithium chloride and pilocarpine.The seizure of rats was observed.The protein expressions of NF-κB and HIF-1 α in hippocampus of rats were examined by Western blotting.The degenerating neurons in hippocampus were detected by Fluoro-Jade C (FJC) staining.Results Twenty-four hours after termination of SE, the nuclear protein expressions of NF-κB and HIF-1α in hippocampus of rats were increased in SE group (0.57 × 0.06, 0.47 ± 0.07) compared with those in control group (0.23 ± 0.03, 0.20 ± 0.03;P ＜0.05);and compared with SE group PDTC significantly decreased the nuclear protein expressions of NF-κB and HIF-1 α in SE + PDTC group (0.23 ± 0.03, 0.14 ± 0.03;P ＜ 0.05);in SE + PDTC group the numbers of FJC positive cells in CA1 area (28.33 ±5.03) were decreased compared with that in SE group (76.67 ± 13.32);HIF-1 o siRNA injected into lateral ventricle of rats significantly decreased the expression of HIF-1α in hippocampus (0.22 ±0.03) and the number of FJC positive cell in CA1 area (27.34 ±7.02) in SE + HIF-1α siRNA group compared with those in SE group (0.39 ±0.06, 76.67 ± 13.32;P ＜0.05).Conclusions These data suggest that SE can result in activation of NF-κB/HIF-1o pathway in brain.Inhibition of the pathway can attenuate hippocampal neurodegeneration caused by SE, which has the brain protective effect.

Animals ; Apigenin ; pharmacology ; Female ; Follicle Stimulating Hormone ; blood ; Gonadotropin-Releasing Hormone ; blood ; Luteinizing Hormone ; blood ; Phytoestrogens ; pharmacology ; Rats