ABSTRACT
Interleukin-33 (IL-33) is a new member of the IL-1 cytokine family which plays roles in the nucleus as a nuclear factor and is released by damaged or necrotic cells to act as a cytokine. It can be released via damaged or necrotic cells and functions as a cytokine. The released IL-33 activates the downstream NF-κB and MAPKs signaling pathways through the isomers of the specific receptor ST2 and the interleukin-1 receptor accessory protein (IL-1RAcP), resulting in danger signals and the activated multiple immune responses. IL-33 is abnormally expressed in various tumors and involves in tumorigenesis, development, and metastasis. Moreover, IL-33 can play both pro-tumor and anti-tumor roles in the same type of tumor.
Subject(s)
Humans , Cytokines , Interleukin-33/genetics , MAP Kinase Signaling System , NF-kappa B/metabolism , NeoplasmsABSTRACT
Objective Todetectthe level of plasma VEGF before and after treatment of arteriovenous mal-formationpatients,and the pathophysiological role of VEGF in arteriovenous malformationpatientswas also studied. Methods The blood samples of 17 arteriovenous malformation patients were collected according to the following three groups:group before operation(AVM),group 24 hours after operation(AVM24h)and group 30 days after operation(AVM30d).As a control(Con),22 blood samples were collected from lumbar laminectomypatients.The level of plasma VEGF was determined by ELISA assay. Results Compared with the control group,the plasma VEGF was significantly decreased in AVM group and AVM24h group(P < 0.05),while the plasma VEGF in AVM30d groupwas similarto that of the control group. Conclusions Abnormal blood vessel plays an important pathophysiological role in cerebral arteriovenous malformation,and the metabolism of VEGF is involved in the pro-cess of arteriovenous malformation.
ABSTRACT
<p><b>OBJECTIVE</b>To establish an allele-specific PCR method for detect screening of CYP21A2 gene mutation.</p><p><b>METHODS</b>Allele-specific PCR primers and analogy primers were designed based on the sequence alignment of CYP21A2 and CYP21AP genes. Genomic DNA was extracted from blood specimens of 4 patients with 21-hydroxylase deficiency and 5 healthy controls and respectively amplified with allele-specific PCR primers and analogy primers and sequenced.</p><p><b>RESULTS</b>Mutations of CYP21A2 including IVS2-13A/C>G, Arg356Trp and Arg149Pro were found with the established method in all of the 4 patients but not in the healthy controls. When detected with the analogy primers set, IVS2-13A/C>G and Arg356Trp were observed in both patients and healthy controls.</p><p><b>CONCLUSION</b>The allele-specific PCR-based method is a simple, effective and reliable method for the detection of CYP21A2 gene mutation.</p>
Subject(s)
Humans , Adrenal Hyperplasia, Congenital , Genetics , Alleles , Base Sequence , DNA Mutational Analysis , Methods , DNA Primers , Genetics , Molecular Sequence Data , Mutation , Polymerase Chain Reaction , Methods , Steroid 21-Hydroxylase , GeneticsABSTRACT
The aim of this investigation was to assess the in-vitro interaction of two antifungal agents, econazole-nitrate and chelerythrine, against ten fluconazole-resistant clinical isolates and one ATCC type strain 10231 of Candida albicans. The checkerboard microdilution method was performed according to the recommendations of the National Committee for Clinical Laboratory Standards, and the results were determined by visual examination. The interaction intensity was tested in all isolates using the fractional inhibitory concentration index [FICI]. These experiments showed synergism between econazole-nitrate and chelerythrine in antifungal activity against C. albicans, and no antagonistic activity was observed in any of the strains tested. Moreover, time-kill curves were performed with selected strains to confirm the positive interactions. The similarity between the results of the FICI values and the time-kill curves revealed that chelerythrine greatly enhances the antifungal effects of econazole-nitrate against isolates of C. albicans. This synergistic effect may markedly reduce the dose of econazole-nitrate required to treat candidiasis, thereby decreasing the econazole-nitrate toxic side effects. This novel synergism might provide a potential combination treatment against fungal infections
ABSTRACT
Mycoplasmosis caused by mycoplasma has immensely reduced the performance of commercial animal husbandry, along with prevalence and increase of drug resistance in mycoplasma, thus new agents and therapies are urgently needed. Triclosan is a broad spectrum antimicrobial agent with a favorable safety profile. In the present study, we tested the antimycoplasmal activity of triclosan alone, as well as the in-vitro interaction of triclosan and the fluoroquinolones, gatifloxacin [GAT], moxifloxacin [MXF], levofloxacin [LVX], sparfloxacin [SPX], ciprofloxacin [CIP], enrofloxacin [EFX], and norfloxacin [NOR], against five mycoplasma species. This study demonstrated that triclosan had antimycoplasmal activity against both fluoroquinolones-sensitive species and a fluoroquinolones-resistant species isolated from clinic, with minimum inhibitory concentrations [MICs] of 16.0-64.0 micro g/mL and 64.0 micro g/ mL, respectively. A synergistic antimycoplasmal effect between triclosan and GAT, MFX or EFX against the five mycoplasma species was observed, with modulation factors [MFs] of 4-8, 4-16, 8-32, respectively, and fractional inhibitory concentration indexes [FICIs] of 0.375- 0.500, 0.350-0.500, 0.281-0.375, respectively. The combination of triclosan with LVX, SPX, CIP or NOR displayed either synergistic activity or indifference against the same mycoplasma species with MFs of 2-64, 4-16, 2-16, 2-64, respectively, while FICI values range from 0.516- 0.750, 0.500-0.625, 0.306-0.750, and 0.615-0.750, respectively. No antagonism was observed for any drug combination against any of the species tested. To the best of our knowledge, this is the first report that triclosan has synergistic activity with fluoroquinolones against mycoplasma species