Objective To observe the clinical efficacy of intratympanic dexamethasone injection for patients with sudden sensorineural hearing loss (SSNHL). Methods Forty-four SSNHL cases (44 ears) which failed to respond to regular treatments were divided into two groups. The intratympanic injection group (24 eases) were injected dexamethasone 2.5 mg to the tympanic cavity every two days,4 times in all. The control group (20 eases) were treated with B1,B12 and triphosaden. Pure tone average (PTA) was tested before and 3 days after treatment. Results The total effective rate of intratympanic injection group was higher than that of control group [37.5%(9/24) vs 10.0%(2/20)] (P < 0.05). In intratympanic injection group, PTA of post-injection was significantly lower than the pre-injection[ (52.75±20.14) dB vs (70.26±20.76) dB ] (P < 0.05). PTA of post-injection in intratympanic injection group was significantly better than that in control group[(52.75±20.14) dB vs (63.55±19.36) dB](P< 0.05). Conclusion Intratympanic dexamethasone injection can be applied to SSNHL patients who failed to respond to systemic corticosteroid treatment and it can avoid the side effects brought on by high dose systemic corticosteroid treatment.

Objective To improve the treatment level of serous otitis media(SOM)in children.Methods 56 patients were treated by positive pressure tympanic administration of ?-Chymotrypsin and Triamcinolone Acetonide through auripuncture into a single hole and 55 cases by myringotomy with grommet insertion.Results The total effective rate of serous otitis media by positive pressure tympanic administration through auripuncture into a single hole and by myringotomy with grommet insertion was 89.8%,90.8% respectively.But the former obviously had more advantages over the latter.Conclusion The technique is better in that it is safe,painless,economical,and non-traumatic.It is an effective method in treating serous otitis media in children.

Purpose:To study the RNA interference-mediated inhibition of survivin gene on the proliferation of human breast cancer SKBr-3 cells. Methods:SKBr-3 cells were transfected with a pSUPER-S1 vector plasmid that expressed survivin-targeted small interfering RNA, and the mRNA and protein levels of survivin gene were measured with RT-PCR and indirect immunofluorescence, respectively. The proliferation of transfected SKBr-3 cells was investigated through colony forming assay and MTT assay. The cell cycle phases were determined by flow cytometry(FCM). Results:The mRNA and protein levels of survivin declined markedly in pSUPER-S1-transfected SKBr-3 cells. And the colony forming rate of those cells(38?16.70)% was significantly lower than that of the control cells(90.3?4.04)%.The growth of the pSUPER-S1-transfected cells was decelerated and the cell cycle was mainly blocked at G_(1) phase(74.03?8.91)%. Conclusions:survivin gene silencing by RNA interference contributed to a distinctive inhibition of the proliferation of human breast cancer SKBr-3 cells in vitro.

Objective To investigate the predialysis education on dialysis timing of patients with end-stage renal disease (ESRD). Methods 129 patients with chronic renal failure (CRF) and serum creatinine(Scr)＞442μmol/L, endogenous creatinine clearance rate (Ccr)＜20 ml/min were randomly divided into the experimental group(70 cases) and the control group(59 cases), the experimental group received predialysis education, the control group received routine care.The basic situation, dialysis timing, depression and quality of life on the 6th,12th months after dialysis were assessed. Results There was no significant difference in age, sex, education background, health care payment manners, employment, serum creatinine, endogenous creatinine clearance rate before education.For the timing of dialysis, Ccr for the experimental group was (9.49 ± 0.77)ml/min, Ccr for the control group was (4.54 ±1.79) ml/min,the difference was significant, depression and quality of life between two groups after 6,12 months of dialysis was also statistically different. Conclusions Strengthening predialysis education is conducive to a timely start of dialysis and can effectively improve the quality of life in patients with ESRD.

Objective To develop a clinical laboratory information system to execute information sharing.Methods The system realized information sharing between the third-party clinical laboratory facility and HIS with Oracle 10g database and Powerbuilder 9.0.Results The system implemented information sharing and informatized storing of the delivery specimen clinical laboratory results in the hospital.Conclusion The system fulfills seamless interface between the third-party clinical laboratory information system and HIS so as to provide the doctor and patient access to information and enhance the accuracy and timeliness of diagnosis.

ObjectiveTo screen out the two-component system associated with drug resistance of Mycobacterium tuberculosis by detecting the differential expression of two-component system regulator genes between multidrug resistant Mycobacterium tuberculosis strains and drug sensitive strains. MethodsTotal RNA of MTB was extracted from cultured MTB during the logarithmic phase in the 7H9 brook medium, and then its purity was identified. Reverse transcription was further completed. The expressing levels of TCS response regulators were quantified using SYBR Green I qRT-PCR, which aimed at finding the differential expressions between multidrug resistant strains and sensitive strains. Finally, all of differentially expressed TCS were screened out under the stress of INH, SM and LFA. Results Compared with sensitive strains,multidrug resistant strains of Rv0491, Rv3133c, Rv3143 and Rv3246c were up-regulated 1. 03, 7.11,3.48and 1.37 folds, respectively (t/t' =5. 623, -4. 196, -3. 559 and -3. 016, respectively, P ＜0. 01 ). The expressing level of other regulators had no statistical significance between muhidrug resistant strains and drug sensitive strains. Under the antibiotic pressure, the expression of Rv1027c, Rv3246c and Rv3143 showed significant changes compared with no antibiotic group. ConclusionRv3246c and Rv3143 may be associated with MTB drug resistance and the differentially expressed genes in multi-drug resistant strains may be used as potential drug targets against drug resistant tuberculosis.

OBJECTIVETo study the changes in biological behaviors of meningitis E. coli K1 strain E44 after deletion of polyphosphate kinase 1 (ppk1) gene and explore the role of ppk1 in the pathogenesis of E. coli K1-induced meningitis.

METHODSThe wild-type strain E. coli K1 and ppk1 deletion mutant were exposed to heat at 56 degrees celsius; for 6 min, and their survival rates were determined. The adhesion and invasion of the bacteria to human brain microvascular endothelial cells (HBMECs) were observed using electron microscopy and quantitative tests. HBMECs were co-incubated with wild-type strain or ppk1 deletion mutant, and the cytoskeleton rearrangement was observed under laser scanning confocal microscope.

RESULTSThe survival rate of the ppk1 deletion mutant was significantly lower than that of the wild-type strain after heat exposure. The ppk1 deletion mutant also showed lowered cell adhesion and invasion abilities and weakened ability to induce cytoskeleton rearrangement in HBMECs.

CONCLUSIONSppk1 gene is important for E.coli K1 for heat resistance, cell adhesion and invasion, and for inducing cytoskeletal rearrangement in HBMECs.

Brain ; cytology ; Cells, Cultured ; Cytoskeleton ; Endothelial Cells ; cytology ; microbiology ; Escherichia coli ; genetics ; physiology ; Escherichia coli Proteins ; genetics ; Gene Deletion ; Humans ; Phosphotransferases (Phosphate Group Acceptor) ; genetics

Objective To explore the beneficial effects and mechanisms of neutrophil elastase (NE) and myeloperoxidase (MPO) on lead-induced hepatic inflammation in mice. Methods The specific pathogen free male C57BL/6 mice were randomly divided into four groups： control group, lead-exposed group, NE inhibitor group, and MPO inhibitor group, with three mice in each group. The mice in lead-exposed group, NE inhibitor group, and MPO inhibitor group were intraperitoneally injected with a dose of 10 mg/kg body mass of lead acetate solution, while the mice of control group received an equal volume of 0.9% saline three times per week for four weeks. In the last seven days, mice in both inhibitor groups were intraperitoneally injected with a dose of 40 mg/kg NE inhibitor sivelestat sodium or MPO inhibitor 4-aminobenzoic acid hydrazide (4-ABAH) once per day. Mouse body weight and liver histopathological changes were observed. The mRNA expression of genes associated with inflammation, such as tumor necrosis factor-α (Tnfa), interleukin-1β (Il1b), interleukin-6 (Il6), and nucleotide-binding oligomerization domain-like receptor protein 3(Nlrp3), apoptosis-associated speck-like protein (Asc) and cysteinyl aspartate specific proteinase (Caspase1) in the mouse liver tissues was detected by real-time quantitative polymerase chain reaction. The protein expression of NLRP3, ASC, and CASPASE-1 was detected using Western blotting. Results The activities of mice in all four groups were generally normal, and there was no significant difference in body weight (P>0.05). The results of hematoxylin-eosin staining showed that the cell size of hepatocytes varied in the lead-exposed mice, with indistinct cell boundaries, indicating early inflammatory responses in liver tissues. After intervention with NE or MPO inhibitors, the early inflammatory responses improved in the liver tissues of the mice in both inhibitor groups, with a better improvement observed in MPO inhibitor group compared with the NE inhibitor group. The mRNA expression of Tnfa, Il1b, Il6, Nlrp3, Asc, and Caspase1, as well as the protein expression of ASC, and CASPASE-1 in the livers of mice in the lead-exposed group was higher compared with those in the control group (all P<0.05). Compared with the lead-exposed group, the relative mRNA expression of Tnfa, Il1b, Il6, Nlrp3 and Asc was decreased in the liver tissues of mice in the NE inhibitor group (all P<0.05), while the relative expression of mRNA of Tnfa, Il1b, Il6, Caspase1 and the protein expression of ASC and CASPASE-1 were decreased in the liver tissues of mice in the MPO inhibitor group (all P<0.05). Conclusion Lead induce hepatic inflammation in mice by activating NLRP3 inflammasome. The inhibition of NE or MPO improve the lead-induced hepatic inflammatory responses in mice by alleviating NLRP3 inflammasome activation.

Objective To detect and analyze the susceptibility genes of methyl acetate poisoning in patients by whole exome sequencing. Methods Two patients with occupational acute severe methyl acetate poisoning and their first-degree relatives who work in the same occupation and position with similar working hours were selected as the research subjects by judgment sampling method. Peripheral blood was collected for whole exome sequencing. The sequencing data was compared with the public genome database to screen the mutation sites and find out the gene sites related to methyl acetate poisoning. The suspected pathogenic mutation genes were annotated and interpreted. Results The results of whole exome sequencing showed that there were 40 differential genes between the patients with methyl acetate poisoning and their first-degree relatives, including 80 single nucleotide polymorphisms and eight Indel with specific marker sequence index. Among these, the genes with strong correlation were carboxyesterase 1 (CES1) and mucin (MUC) 5B. The CES1 gene loci c.248C>T (p.Ser83Leu) heterozygous mutations, MUC5B gene loci c.6635C>T (p.Thr2212Met) and c.7685C>T (p.Thr2562Met) heterozygous mutations in patients with methyl acetate poisoning were detected. They were missense mutations. By constructing a protein-protein interaction network, a total of 11 pairs of interactions with high levels of evidence were identified, involving genes such as lysine methyltransferase 2C, HECT and RLD domains containing E3 ubiquitin protein ligase 2, neutrophil cytoplasmic factor 1, nicotinamide adenine dinucleotide phosphate oxidase 3, C-terminal binding protein 2, zinc finger protein 717, FSHD region gene 2 family member C, FSHD region gene 1, MUC4, MUC6, MUC5B, and MUC12. Conclusion The polymorphism of CES1 and MUC5B genes may be related to the occurrence and development of methyl acetate poisoning in patients.

Objective To explore the curative effect and complication of transcutaneous transcatheter uterine arterial embolization in the treatment of postpartum hemorrhage .Methods 76 cases with postpartum hemorrhage of conservative treatment invalid in the General Hospital of Huainan Oriental Hospital Group from January 2011 to January 2017 , received digital subtraction angiography ( DSA ) to make clear the site of hemorrhage , then bilateral uterine artery embolization was given .Results Seventy -six patients have stopped bleeding immediately after embolization,3 cases were significantly reduced .Bleeding stopped completely after nearly one week of treatment .Mild fever after embolization appearred unable to pain in the lower abdomen ,1 case had hip pain .Conclusion Transcuta-neous transcatheter uterine artery embolization in the treatment of postpartum hemorrhage has advantages of quick hemostasis,less trauma,less complications and preserving the uterus fertility ,which has high clinical value .