Surface-mediated high antioxidant and anti-inflammatory effects of astaxanthin-loaded ultrathin graphene oxide film that inhibits the overproduction of intracellular reactive oxygen species

Abstract Background Astaxanthin (AST) is known as a powerful antioxidant that affects the removal of active oxygen and inhibits the production of lipid peroxide caused by ultraviolet light. However, it is easily decomposed by heat or light during production and storage because of the unsaturated compound nature with a structural double bond. The activity of AST can be reduced and lose its antioxidant capability. Graphene oxide (GO) is an ultrathin nanomaterial produced by oxidizing layered graphite. The chemical combination of AST with GO can improve the dispersion properties to maintain structural stability and antioxidant activity because of the tightly bonded functionalized GO surface. Methods Layered GO films were used as nanocarriers for the AST molecule, which was produced via flow-enabled self-assembly and subsequent controlled solution deposition of RGD peptide and AST molecules. Synthesis of the GO-AST complex was also carried out for the optimized concentration. The characterization of prepared materials was analyzed through transmission electron microscopy (TEM), scanning electron microscope (SEM), Fourier-transform infrared spectroscopy (FT-IR), atomic force microscope (AFM), and Raman spectroscopy. Antioxidant activity was tested by 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 2.2-diphenyl-1-picrylhydrazyl (DPPH) assays. The antibacterial effect and antioxidant effects were monitored for the ultrathin GO/RGD/AST Film. Further, reactive oxygen species (ROS) assay was used to evaluate the anti-inflammatory effects on L-929 fibroblasts. Results Cotreatment of GO-AST solution demonstrated a high antioxidant combined effect with a high ABTS and DPPH radicals scavenging activity. The GO/RGD/AST film was produced by the self-assembly process exhibited excellent antibacterial effects based on physicochemical damage against E. coli and S. aureus. In addition, the GO/RGD/AST film inhibited H2O2-induced intracellular ROS, suppressed the toxicity of lipopolysaccharide (LPS)-induced cells, and restored it, thereby exhibiting strong antioxidant and anti-inflammatory effects. Conclusion As GO nanocarrier-assisted AST exerted promising antioxidant and antibacterial reactions, presented a new concept to expand basic research into the field of tissue engineering

Cognitive and Emotional Aspects of Cupping Therapy

Cupping therapy has recently gained public attention and is widely used in many regions. Some patients are resistant to being treated with cupping therapy, as visually unpleasant marks on the skin may elicit negative reactions. This study aimed to identify the cognitive and emotional components of cupping therapy. Twenty-five healthy volunteers were presented with emotionally evocative visual stimuli representing fear, disgust, happiness, neutral emotion, and cupping, along with control images. Participants evaluated the valence and arousal level of each stimulus. Before the experiment, they completed the Fear of Pain Questionnaire-III. In two-dimensional affective space, emotional arousal increases as hedonic valence ratings become increasingly pleasant or unpleasant. Cupping therapy images were more unpleasant and more arousing than the control images. Cluster analysis showed that the response to cupping therapy images had emotional characteristics similar to those for fear images. Individuals with a greater fear of pain rated cupping therapy images as more unpleasant and more arousing. Psychophysical analysis showed that individuals experienced unpleasant and aroused emotional states in response to the cupping therapy images. Our findings suggest that cupping therapy might be associated with unpleasant-defensive motivation and motivational activation. Determining the emotional components of cupping therapy would help clinicians and researchers to understand the intrinsic effects of cupping therapy

Application of error classification model using indices based on dose distribution for characteristics evaluation of multileaf collimator position errors

Abstract This study aims to evaluate the specific characteristics of various multileaf collimator (MLC) position errors that are correlated with the indices using dose distribution. The dose distribution was investigated using the gamma, structural similarity, and dosiomics indices. Cases from the American Association of Physicists in Medicine Task Group 119 were planned, and systematic and random MLC position errors were simulated. The indices were obtained from distribution maps and statistically significant indices were selected. The final model was determined when all values of the area under the curve, accuracy, precision, sensitivity, and specificity were higher than 0.8 (p  0.9. Furthermore, the results of the DVH were related to dosiomics analysis in that it reflects the characteristics of the MLC position error. It was also shown that dosiomics analysis could provide important information on localized dose-distribution differences in addition to DVH information

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

The interstitial cells of Cajal (ICCs) are pacemakers in the gastrointestinal tract. The possibility of whether imatinib mesylate, a Kit receptor tyrosine kinase inhibitor, modulates pacemaker activities in the ICC was examined using the whole cell patch clamp technique. Imatinib decreased the amplitude of pacemaker potentials in a dose-dependent manner in current-clamp mode. Because the effects of imatinib on pacemaker potentials were the same as those of pinacidil, we examined the effect of glibenclamide on ICC exposed to imatinib. The effects of imatinib on pacemaker potentials were blocked by glibenclamide. To see whether the production of prostaglandins (PGs) is involved in the inhibitory effect of imatinib on pacemaker potentials, we tested the effects of naproxen (a non-selective cyclooxygenase inhibitor) and AH6809 (a prostaglandin EP1 and EP2 receptor antagonist). Naproxen and AH6809 blocked the inhibitory effects of imatinib on ICC. Butaprost (an EP2 receptor agonist) showed the actions on pacemaker potentials in the same manner as imatinib. However, SC 19220 (an EP1 receptor antagonist) has no effects. To investigate the involvement of cAMP and protein kinase A (PKA) in the effects of imatinib on ICC, SQ 22536 (an inhibitor of adenylate cyclase) and mPKAI (an inhibitor of myristoylated PKA) were used. Both SQ-22536 and mPKAI blocked the imatinib-mediated inhibition of pacemaker potentials. However, the protein kinase C (PKC) inhibitors did not block the imatinib-mediated inhibition of pacemaker potentials. These results indicate that imatinib inhibits the pacemaker potentials of ICC by activating ATP-sensitive K(+) channels and PKA-dependent, PKC-independent manner.Huizinga JD, 2002, GASTROENTEROLOGY, V123, P1627, DOI 10.1053/gast.2002.36549Torihashi S, 2002, J BIOL CHEM, V277, P19191, DOI 10.1074/jbc.M201728200Koh SD, 2002, J PHYSIOL-LONDON, V540, P803Porcher C, 2002, GASTROENTEROLOGY, V122, P1442, DOI 10.1053/gast.2002.33065Joensuu H, 2001, NEW ENGL J MED, V344, P1052DRUKER BJ, 2001, NEW ENGL J MED, V344, P1037Krystal GW, 2000, CLIN CANCER RES, V6, P3319Tonary AM, 2000, INT J CANCER, V89, P242Miettinen M, 1999, HUM PATHOL, V30, P1213Shimojima N, 2005, PHARMACOLOGY, V74, P95, DOI 10.1159/000084021Jun JY, 2005, BRIT J PHARMACOL, V144, P242, DOI 10.1038/sj.bjp.0706074Nakayama S, 2005, J CELL SCI, V118, P4163, DOI 10.1242/jcs.02540Kim BJ, 2005, GASTROENTEROLOGY, V129, P1504, DOI 10.1053/j.gastro.2005.08.016Choi S, 2006, CELL PHYSIOL BIOCHEM, V18, P187Kubota Y, 2006, NEUROUROL URODYNAM, V25, P205, DOI 10.1002/nau.20085Choi S, 2006, LIFE SCI, V78, P2322, DOI 10.1016/j.lfs.2005.09.032Popescu LM, 2006, EUR J PHARMACOL, V546, P177, DOI 10.1016/j.ejphar.2006.06.068Beckett EAH, 2007, DEV DYNAM, V236, P60, DOI 10.1002/dvdy.20929Lavoie B, 2007, J PHYSIOL-LONDON, V579, P487, DOI 10.1113/jphysiol.2006.122861Park CG, 2007, N-S ARCH PHARMACOL, V376, P175, DOI 10.1007/s00210-007-0187-1Hashitani H, 2008, BRIT J PHARMACOL, V154, P451, DOI 10.1038/bjp.2008.91Arunasree KM, 2008, LEUKEMIA RES, V32, P855, DOI 10.1016/j.leukres.2007.11.007Choi S, 2008, MOL CELLS, V26, P181Zhu MH, 2009, J PHYSIOL-LONDON, V587, P4905, DOI 10.1113/jphysiol.2009.176206Torihashi S, 1999, GASTROENTEROLOGY, V117, P140Huang SM, 1999, AM J PHYSIOL-GASTR L, V276, pG518Arber DA, 1998, HUM PATHOL, V29, P498Seibert K, 1997, ADV EXP MED BIOL, V400, P167Sanders KM, 1996, GASTROENTEROLOGY, V111, P492TORIHASHI S, 1995, CELL TISSUE RES, V280, P97HUIZINGA JD, 1995, NATURE, V373, P347HERSCHMAN HR, 1994, CANCER METAST REV, V13, P241JOHNSON FM, 2004, J EXP THER ONCOL, V4, P317Goto K, 2004, J PHYSIOL-LONDON, V559, P411, DOI 10.1113/jphysiol.2004.063875WARD SM, 1994, J PHYSIOL-LONDON, V480, P91HONDA A, 1993, J BIOL CHEM, V268, P7759MAEDA H, 1992, DEVELOPMENT, V116, P369FARRAWAY L, 1991, J PHARMACOL EXP THER, V257, P35JUMBLATT MM, 1991, INVEST OPHTH VIS SCI, V32, P360SANDERS KM, 1984, AM J PHYSIOL, V247, P117SANDERS KM, 1983, AM J PHYSIOL, V244, pG442HARDCASTLE J, 1982, J PHARM PHARMACOL, V34, P68