ZnO nanoparticles (NPs) were synthesized using a hydrothermal method. Scanning electron microscope (SEM) and X-ray diffraction have been used for characterizing the synthesized ZnO NPs. An electrochemical sensor was fabricated using ZnO NPs–modified glassy carbon electrode for simultaneous determination of ascorbic acid (AA), dopamine (DA), and uric acid (UA). The proposed electrochemical sensor exhibited excellent detection performance toward three analytes, demonstrating that it can potentially be applied in clinical applications. The results indicated the ZnO NPs–modified electrode can detect AA in the concentrations range between 50 and 1,000 μM. The ZnO NPs–modified electrode can detect DA in the concentrations range between 2 and 150 μM. The ZnO NPs–modified electrode can detect UA in the concentrations range between 0.2 and 150 μM. The limits of detections of AA, DA, and UA using ZnO NPs–modified electrode were calculated to be 18.4, 0.75, and 0.11 μM, respectively.

Salmonella typhimurium is a pathogenic gram-negative bacterium, which is found primarily in the intestinal lumen. it often causes diarrhea in infants and young children and leads to food poisoning. Drug resistance of Salmonella typhimurium presented serious complications in clinical patients. in this study, we investigated the antibiotic susceptibility of Salmonella typhimurium standard strain L forms to the third and forth generation cephalosporins, in order to control and eliminate Salmonella typhimurium L forms in infection treatment. Salmonella typhimurium L forms were induced by β-lactam antibiotic cefazolin in the culture medium of bacterial L forms. the antibiotic susceptibility of Salmonella typhimurium L forms was analyzed by K-B drug susceptibility testing. The change trend of drug susceptibility and resistance of Salmonella typhimurium L forms was obtained in accordance with USA clinical and laboratory standards institute (CLSI) evaluation data and statistical analysis. Drug resistance of Salmonella typhimurium L forms showed little increasing trend compared with their parent bacteria. The L form inhibition zone was smaller than in the parent bacteria. However, the drug susceptibility of L forms of Salmonella typhimurium to the third and forth generation cephalosporins remained sensitive.the antibiotic susceptibility of Salmonella typhimurium L forms to the third and forth generation cephalosporins remains sensitive, and the combined use of multi-antibiotics is a convenient and effective method to reduce Salmonella typhimurium L forms occurrence. Because of the immature immunity of infants and young children, bacterial acquired antibiotic resistance and poor sanitation, Salmonella typhimurium (S. typhimurium) has become the main pathogen in nosocomial and foodborne infection 1-3. Salmonella typhimurium possesses endotoxin, enterotoxin and extracellular enzymes as well as other pathogenic factors, so that Salmonella typhimurium has strong pathogenicity 4,5. After the use of antibiotics, it was easy to make Salmonella typhimurium form into cell wall-defective bacteria named bacterial L forms 6-8. BacteriaL L forms still have the ability to cause disease, such as leading to the delay of chronic infection, and decreased susceptibility to antibacterial drugs which act on cell walls 9,10. In these experiments, we studied the resistance of Salmonella typhimurium standard strain L forms to advanced cephalosporins and judged the susceptibility degree of Salmonella typhimurium L forms to the third and fourth generation cephalosporins, in order to guide the rational use of clinical antibacterial drugs. The study will provide the basic theory for controlling Salmonella typhimurium infection. Materials and Methods Bacterial strain. Salmonella typhimurium standard strain CMCC50115 was purchased from the National Institute for the Control of Pharmaceutical and Biological Products.

Epithelial ovarian cancer (EOC) is a common ovarian cancer in gynecological cancers today. It has been found that microRNAs and long‐chain noncoding RNA (lncRNA) regulate the gene transcriptional expression in cells. However, it is not well understood that the upstream and downstream regulatory molecules of lncRNA HOX antisense intergenic RNA (HOTAIR). The effects of miR‐200c overexpression on the invasion and nude mouse tumorigenicity, as well as lncRNA HOTAIR and snail expression of EOC SKOV3 cells, should be further explored. The expression of miR‐200c and lncRNA HOTAIR was detected by reverse transcription PCR (RT‐PCR) in EOC SKOV3 cells. The whole miR‐200c gene fragment was cloned into a lentiviral plasmid vector. The miR‐200c expression in transducted SKOV3 cells with reconstructed miR‐200c lentivirus was significantly higher than the negative control (P < .01). The lentivirus‐miR‐200c‐SKOV3 cells show that the invasion ability was significantly decreased compared with the negative control (P < .01). The nude mouse tumorigenicity was significantly decreased compared with that of the control group (P < .01). The snail protein expression in lentivirus‐miR‐200c‐SKOV3 xenograft tumor was significantly decreased compared with the negative control lentivirus‐SKOV3 group (P < .05). The miR‐200c overexpression significantly decreased the expressions of lncRNA HOTAIR and snail, but increased E‐cadherin expression in the lentivirus‐miR‐200c transducted SKOV3 cells of xenograft tumor, compared with the negative control (P < .05). The miR‐200c overexpression in SKOV3 cells with transducted lentivirus‐miR‐200c can inhibit lncRNA HOTAIR expression, decrease snail, increase E‐cadherin and significantly reduce the invasion and tumorigenicity of EOC SKOV3 cells. These results suggest that the miR‐200c and lncRNA HOTAIR could be effective therapeutic targets for human epithelial ovarian cancer treatment.

Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and excessive accumulation of dysfunctional PVAT are hallmarks of pathogenesis after angioplasty. Recent genome-wide association studies reveal that single-nucleotide polymorphism (SNP) in MIA3 is associated with atherosclerosis-relevant VSMC phenotypes. However, the role of MIA3 in the vascular remodeling response to injury remains unknown. Here, we found that expression of MIA3 is increased in proliferative VSMCs and knockdown of MIA3 reduces VSMCs proliferation, migration, and inflammation, whereas MIA3 overexpression promoted VSMC migration and proliferation. Moreover, knockdown of MIA3 ameliorates femoral artery wire injury-induced neointimal hyperplasia and increases brown-like perivascular adipocytes. Collectively, the data suggest that MIA3 deficiency prevents neointimal formation by decreasing VSMC proliferation, migration, and inflammation and maintaining BAT-like perivascular adipocytes in PVAT during injury-induced vascular remodeling, which provide a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases.

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