1,334 research outputs found

    The promoter -1031(T/C) polymorphism in tumor necrosis factor-alpha associated with polycystic ovary syndrome

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    <p>Abstract</p> <p>Background</p> <p>A <it>tumor necrosis factor-alpha </it>is a multifunctional pro-inflammation cytokine, which has been considered as one of pathogenic factors for various diseases. The promoter -1031(T/C) polymorphism in the <it>tumor necrosis factor-alpha </it>gene was reported that it plays a part in reproduction-related diseases. Among these, polycystic ovary syndrome (PCOS) is known to be a common gynecological disease of women in reproductive age women. Here, we performed a comparative study of -1031(T/C) polymorphism of <it>TNF-alpha </it>gene with PCOS in a Korean population.</p> <p>Methods</p> <p>The -1031(T/C) polymorphism of <it>TNF-alpha </it>gene was analyzed by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) in a total of 217 PCOS patients and 144 matched female controls of healthy women. And statistical analysis was performed using HapAnalyzer. <it>X</it><sup>2 </sup>test and logistic regression were utilized analyze the association between two groups. A <it>p</it>-value under 0.05 was considered statistically significant.</p> <p>Results</p> <p>The genotype and allelic frequencies were in Hardy-Weinberg equilibrium (HWE). There was strong association between the -1031(T/C) polymorphism in the promoter region of <it>TNF-alpha </it>gene and PCOS (<it>p</it>-value = 0.0003, odd ratio (OR) = 2.53). In addition, the frequency of C allele was significantly higher in PCOS patients compared with controls. Sequence analyses also showed the -1031(T/C) polymorphism of <it>TNF-alpha </it>gene.</p> <p>Conclusion</p> <p>This is the first study on the -1031(T/C) polymorphism of <it>TNF-alpha </it>gene in PCOS. We concluded that the -1031(T/C) polymorphism of <it>TNF-alpha </it>gene is associated with PCOS in a Korean population. Therefore, it is possible that it may be considered as a clinical biomarker to diagnose for PCOS, and is helpful in understanding the etiology for the pathogenesis of PCOS.</p

    Antimicrobial peptide from Bacillus subtilis CSB138: characterization, killing kinetics, and synergistic potency

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    We studied the prospect of synergy between the antimicrobial peptide p138c and non-peptide antibiotics for increasing the potency and bacterial killing kinetics of these agents. The production of p138c was maximized in the late exponential growth phase of Bacillus subtilis CSB138. Purification of p138c resulted in a total of 4800 arbitrary units (AU) with 19.15-fold and 3.2% recovery. Peptide p138c was thermo-tolerant up to 50 &deg;C and stable at pH 5.8 to 11. The biochemical nature of p138c was determined by a bioassay, similar to tricine-SDS-PAGE, indicating inhibition at 3 kDa. The amino acid sequence of p138c was Gly-Leu-Glu-Glu-Thr-Val-Tyr-Ile-Tyr-Gly-Ala-Asn-Met-X-Ser. Potency and killing kinetics against vancomycin-resistant Staphylococcus aureus improved considerably when p138c was synergized with oxacillin, ampicillin, and penicillin G. The minimal inhibitory concentration (MIC) of p138c showed a 4-, 8-, and 16-fold improvement when p138c was combined with oxacillin, ampicillin, and penicillin G, respectively. The fractional inhibitory concentration index for the combination of p138c and oxacillin, ampicillin, and penicillin G was 0.3125, 0.25, and 0.09, respectively. Synergy with non-peptide antibiotics resulted in enhanced killing kinetics of p138c. Hence, the synergy between antimicrobial peptide and non-peptide antibiotics may enhance the potency and bacterial killing kinetics, providing more potent and rapidly acting agents for therapeutic use. [Int Microbiol 20(1):43-53 (2017)]Keywords: Bacillus subtilis &middot; antimicrobial peptides &middot; killing kinetic

    Mucosal and salivary microbiota associated with recurrent aphthous stomatitis

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    This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.Abstract Background Recurrent aphthous stomatitis (RAS) is a common oral mucosal disorder of unclear etiopathogenesis. Although recent studies of the oral microbiota by high-throughput sequencing of 16S rRNA genes have suggested that imbalances in the oral microbiota may contribute to the etiopathogenesis of RAS, no specific bacterial species associated with RAS have been identified. The present study aimed to characterize the microbiota in the oral mucosa and saliva of RAS patients in comparison with control subjects at the species level. Results The bacterial communities of the oral mucosa and saliva from RAS patients with active lesions (RAS, nā€‰=ā€‰18 for mucosa and nā€‰=ā€‰8 for saliva) and control subjects (nā€‰=ā€‰18 for mucosa and nā€‰=ā€‰7 for saliva) were analyzed by pyrosequencing of the 16S rRNA genes. There were no significant differences in the alpha diversity between the controls and the RAS, but the mucosal microbiota of the RAS patients showed increased inter-subject variability. A comparison of the relative abundance of each taxon revealed decreases in the members of healthy core microbiota but increases of rare species in the mucosal and salivary microbiota of RAS patients. Particularly, decreased Streptococcus salivarius and increased Acinetobacter johnsonii in the mucosa were associated with RAS risk. A dysbiosis index, which was developed using the relative abundance of A. johnsonii and S. salivarius and the regression coefficients, correctly predicted 83Ā % of the total cases for the absence or presence of RAS. Interestingly, A. johnsonii substantially inhibited the proliferation of gingival epithelial cells and showed greater cytotoxicity against the gingival epithelial cells than S. salivarius. Conclusion RAS is associated with dysbiosis of the mucosal and salivary microbiota, and two species associated with RAS have been identified. This knowledge may provide a diagnostic tool and new targets for therapeutics for RAS

    An autoregulatory loop controlling orphan nuclear receptor DAX-1 gene expression by orphan nuclear receptor ERRĪ³

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    The estrogen receptor-related receptor gamma (ERRĪ³/ERR3/NR3B3) is a member of the nuclear receptor superfamily that activates transcription in the absence of ligand. However, the detailed mechanism of gene regulation by ERRĪ³ is not fully understood. In this study we have found that the orphan nuclear receptor ERRĪ³ activates the DAX-1 promoter, which, in turn, represses transactivation by ERRĪ³. Serial deletions of mouse DAX-1 (mDAX-1) gene promoter have revealed that the region responding to ERRĪ³ is located between āˆ’129 and āˆ’121 bp and āˆ’334 and āˆ’326 bp. Gel shift assays and chromatin immunoprecipitation (ChIP) assays demonstrated that ERRĪ³ binds directly to the mDAX-1 promoter. Site-directed mutagenesis results demonstrated that ERRE1 (āˆ’129 to āˆ’121 bp) is more important than ERRE2 (āˆ’334 to āˆ’326 bp) which is not conserved in the human DAX-1 promoter. In addition, adenovirus-mediated overexpression of ERRĪ³ induced DAX-1 gene expression in MCF-7 breast cancer cells that co-expressed ERRĪ³ and DAX-1. Moreover, yeast two-hybrid and glutathione S-transferase (GST)-pull down assays demonstrated that DAX-1 physically interacted with ERRĪ³ and inhibited ERRĪ³ transactivation, and that this interaction was dependent on the AF-2 domain of ERRĪ³. In addition, in vitro competition assays showed that DAX-1 inhibited PGC-1Ī± mediated ERRĪ³ transactivation, via competition between these two factors for the AF-2 binding domain. We thus propose a novel autoregulatory loop that controls DAX-1 gene expression by ERRĪ³

    Manumycin from a new Streptomyces strain shows antagonistic effect against methicillin-resistant Staphylococcus aureus (MRSA)/vancomycin-resistant enterococci (VRE) strains from Korean Hospitals

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    An antimicrobial compound, highly effective against multidrug-resistant (MDR) bacteria, purified from a Streptomyces strain was identified as manumycin. The minimal inhibitory concentrations (MICs) of manumycin against 8 different strains of methicillin-resistant Staphylococcus aureus (MRSA) were ranged 2 to 32 Ī¼g/ml. Similarly, MICs of manumycin against 4 vancomycin-resistant enterococci (VRE) strains were ranged 8 to 32 Ī¼g/ml while it remained ineffective against 4 other VRE strains. Compared to vancomycin, manumycin provided slightly weaker activity against MRSA strains but stronger activity against 4 VRE strains. This is the first report of antagonistic effect of manumycin against MDR pathogens.Keywords: Manumycin, methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE)African Journal of Biotechnology Vol. 12(17), pp. 2249-225

    Electronic structures of hexagonal RMnO3 (R = Gd, Tb, Dy, and Ho) thin films

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    We investigated the electronic structure of multiferroic hexagonal RMnO3 (R = Gd, Tb, Dy, and Ho) thin films using both optical spectroscopy and first-principles calculations. Using artificially stabilized hexagonal RMnO3, we extended the optical spectroscopic studies on the hexagonal multiferroic manganite system. We observed two optical transitions located near 1.7 eV and 2.3 eV, in addition to the predominant absorption above 5 eV. With the help of first-principles calculations, we attribute the low-lying optical absorption peaks to inter-site transitions from the oxygen states hybridized strongly with different Mn orbital symmetries to the Mn 3d3z2-r2 state. As the ionic radius of the rare earth ion increased, the lowest peak showed a systematic increase in its peak position. We explained this systematic change in terms of a flattening of the MnO5 triangular bipyramid

    Simulation Study on a New Hybrid Autonomous Underwater Vehicle with Elevators

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    This study aims to design a new hybrid twin autonomous underwater vehicle (HTAUV) consisting of dual cylinder hulls and analyze its pitching motion. The kinematic model for the HTAUV is established, followed by the execution of hydrodynamic simulation CFD of the HTAUV using Ansys Fluent. These simulations are conducted to obtain the hydrodynamic force equation of the HTAUV, which relates to the deflection angle of the elevator. Through the motion simulation of the HTAUV, under the same net buoyancy condition, notable differences emerge when the elevator is deflected. Specifically, parameters such as gliding speed, gliding angle, and pitch angle of the HTAUV are larger when the elevator is deflected, as compared to cases where no deflection is applied

    The Effect of Clonidine Pretreatment on Epidural Resiniferatoxin in a Neuropathic Pain Rat Model

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    Resiniferatoxin (RTX) is an ultrapotent synthetic TRPV1 (transient receptor potential vanilloid subtype 1) agonist with significant initial transient hyperalgesia followed by a prolonged analgesic effect in response to thermal stimulus. Using a rat model of neuropathic pain, we evaluated the effect of pretreatment with clonidineļ¼which has been shown to relieve intradermal capsaicin-induced hyperalgesiaļ¼on the initial hyperalgesic response and the thermal analgesic property of RTX. Thirty-six male rats were divided into 6 treatment groups (nļ¼6 each):RTX 500ng, RTX 1Ī¼g, clonidine 20Ī¼g (Cl), Clļ¼‹RTX 500ng, Clļ¼‹RTX 1Ī¼g, or normal saline 20Ī¼L (control). We evaluated the short-term (180min) and long-term (20 days) analgesic effects of RTX after thermal stimulation and mechanical stimulation. RTX had significant initial transient hyperalgesia followed by a prolonged analgesic effect in response to the thermal stimulus, but the RTX 500ng and RTX 1Ī¼g groups showed no initial short-term thermal hyperalgesic responses when pretreated with clonidine. The Clļ¼‹RTX 1Ī¼g ratsŹ¼ behavior scores indicated that they were more calm and comfortable compared to the RTX 1Ī¼g rats. Even though we cannot precisely confirm that pretreatment with clonidine potentiates or adds to the analgesic effect of RTX, clonidine pretreatment with epidural RTX eliminated the initial RTX-associated hyperalgesic response and systemic toxicity in this neuropathic pain rat model
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