View options
Result details

Results per page
Articles per page View Sort by

6 results matched your search query
Keywords = Genes

  • Open Access Research Article
    Export citation: APA   BibTeX   EndNote   RIS  
    Trends Journal of Sciences Research 2018, 3(2), 69-74. http://doi.org/10.31586/Physiology.0302.02
    447 Views 71 Downloads 3 Shares PDF Full-text (2.323 MB)  HTML Full-text
    Abstract
    Heat stress can affect reproduction potential as an environmental factor. This Study was carried out to investigate the effects of rosemary extract on spermatogenesis and sexual hormones of laboratory mice under heat stress. 50 male mature mice were examined in five groups including a control group and four experimental groups
    [...] Read more.
    Heat stress can affect reproduction potential as an environmental factor. This Study was carried out to investigate the effects of rosemary extract on spermatogenesis and sexual hormones of laboratory mice under heat stress. 50 male mature mice were examined in five groups including a control group and four experimental groups [0, 100, 200 and 400 mg/kg of rosemary extract]. Samples were kept under heat stress four hours a day and received the extract doses for 30 days. At the end of the experiment, the amount of testosterone, LH, and FSH hormones plus the number of spermatogenic cells were measured. Obtained data were analyzed using the SPSS program. Heat stress in zero doses reduced testosterone, LH, and FSH significantly whereas rosemary extract increased testosterone and LH in 200 and 400 doses and FSH in 100,200, and 400 doses. Primary spermatocytes were decreased in zero doses significantly but increased significantly in other experimental groups [p<0.05]. In general, Heat stress reduces male sex hormones and spermatogenic cells but rosemary extract compensated this reduction dose-dependently and improved sexual potential under heat stress.  Full article
    Figures

    Figure 1 of 4

    References
    [1]
    Gayton A. 2011. Medical physiology (Translated by Farrukh Shadan), Tehran University. 2, 245.
    [2]
    Collier RJ, Dahl GE, Van Baali MJ. 2006. Major advances associated with environmental effects on dairy cattle. J Dairy Sci. 89, 1244-53.
    [3]
    Premkumar K, Abraham SK, Santhiya ST, Ramesh A. 2003. Protective effects of saffron (Crocus sativus L.) on genotoxin-induced oxidative stress in Swiss albini mice Phytother Research. 17, 614-17.
    [4]
    Modaresi M. 2012. A comparative analysis of the effects of garlic, elderberry and black seed extract on the immune system in mice. J Anim Vet Adv. 11 (4), 458-61.
    [5]
    Ojeda-sana A M, Van baren C M, Elechosa M A, Juarez M A, Morenos S. 2013. New insights into antibacterial and antioxidant activities of rosemary essential oils and their main components. Food Control. 31(1), 189?195.
    [6]
    Posadas S, Caz V, Largo C, De La Gandara B, Matallans B, Reglero G. et al. 2009. Protective effect of supercritical fluid rosemary extract, Rosmarinus officinalis, on antioxidants of major organs of aged rats. Experimental gerontology. 44(6), 383?389.
    [7]
    Modaresi M, Mohajer M. 2015. The Effect of Garlic Extract on Spermatogenesis and Sexual Hormones in Heat-Stressed Male Mice. zumsj. 23 (101), 88-97.
    [8]
    Ghiasi Ghalehkandi J. 2014. Garlic (Allium sativum) juice protects from semen oxidative stress in male rats exposed to chromium chloride. Anim Reprod. 15, 526-32.
    [9]
    Arts M J, Haenen G R, Voss H P, Bast A. 2001. Masking of antioxidant capacity by the interaction of flavonoids with protein. Food and Chemical Toxicology. 39(8), 787?791.
    [10]
    Satoh T, Kosaka K, Itoh K, Kobayashi A, Yamamoto M, Shimojo Y. et al. 2008. Carnosic acid,a catechol?type electrophilic compound, protects neurons both in vitro and in vivo through activation of the Keap1/Nrf2 pathway via S?alkylation of targeted cysteines on Keap1. Journal of neurochemistry. 104(4), 1116?1131.
    [11]
    Satoh T, Izumi M, Inukai Y, Tsutsumi Y, Nakayama N, Kosaka Kosaka. et al. 2008. Carnosic acid protects neuronal HT22 Cells through activation of the antioxidant-responsive element in free carboxylic acid-and catechol hydroxyl moieties-dependent manners. Neuroscience letters. 434(3), 260?265.
    [12]
    Jasim MA, Al-Tahan FJ. 2012. Study of the effect of decorticated and defatted castor seeds (Ricinus communis Linn.) on testosterone level and testicular architecture of male mice. J Tikrit University of Agriculture Sci. 12,176-80.
    [13]
    Kaur R, Kaur K. 2000. Effects of dietary selenium (SE) on morphology of testis and cauda epididymis in rats. Indian J Physiol Pharmacol. 44, 265-72.
  • Open Access Mini Review
    Export citation: APA   BibTeX   EndNote   RIS  
    Trends Journal of Sciences Research 2018, 3(2), 75-81. http://doi.org/10.31586/Nursing.0302.03
    177 Views 70 Downloads PDF Full-text (2.583 MB)  HTML Full-text
    Abstract
    Genotype and lifestyle factors have been implicated as the causes of non-communicable diseases including diabetes, cardiovascular diseases, cancer and chronic respiratory disease. Lifestyle factors constitute physical activity, smoking, alcohol intake and dietary habits. These factors alongside genetic factors have been studied over the past years on their relationships with non-communicable
    [...] Read more.
    Genotype and lifestyle factors have been implicated as the causes of non-communicable diseases including diabetes, cardiovascular diseases, cancer and chronic respiratory disease. Lifestyle factors constitute physical activity, smoking, alcohol intake and dietary habits. These factors alongside genetic factors have been studied over the past years on their relationships with non-communicable diseases. This review examined and compared the strengths of the two factors, lifestyle and genotype, in causing non-communicable diseases. A search was done online, predominantly with PubMed, to identify articles that contained the keywords, lifestyle, diet, exercise, genotype, gene, non-communicable diseases, cardiovascular diseases, cancer, chronic respiratory disease, diabetes. For diabetes, the results of this review showed that management of lifestyle factors can be used to prevent type 2 diabetes among genetically predisposed persons. Cancers studies have suggested that a Mediterranean diet is associated with lower cancer risk for both genetically susceptible people and non-susceptible individuals. Similar findings were gotten for cardiovascular diseases and chronic respiratory diseases. The results suggest a strong impact of lifestyle-related factors as a cause of non-communicable diseases though genetic factors cannot be underestimated. With good management of lifestyle factors, non-communicable diseases can be prevented and the risks reduced even among genetically high-risk individuals.  Full article
    References
    [1]
    World Health Organisation, Global action plan for the prevention and control of non-communicable diseases 2013-2020. Available at: who.int/iris/bitstream/10665/94384/1/9789241506236_eng.pdf. 2013. Accessed March 22, 2017.
    [2]
    Melaku YA, Temesgen AM, Deribew A, Tessema GA, Deribe K, Sahle BW, et al. The impact of dietary risk factors on the burden of non-communicable diseases in Ethiopia: findings from the Global Burden of Disease study 2013. International Journal of Behavioral Nutrition and Physical Activity 13 (2016) 122-134.
    [3]
    Hosseini-Esfahani F, Mirmiran P, Daneshpour MS, Mottaghi A, Aziz F. The effect of interactions of Single Nucleotide Polymorphisms of APOA1/APOC3 with food group intakes on the risk of metabolic syndrome. Avicenna J Med Biotech 9 (2017) 94-103.
    [4]
    Chikwere P, Annan RA. Dietary habit and other lifestyles and serum lipid profile of type 2 diabetes patients: a systematic review. Nutrition & Food Science 46 (2016) 161-170.
    [5]
    Chikwere P, Nsiah K, Tandoh MA. Relation of unsupported and unsupervised exercise with anthropometric and biochemical indices among type 2 diabetic patients. Turk J Med Sci 47 (2017) 85-90.
    [6]
    Naicker A, Venter CS, MacIntyre, UE, Ellis S. Dietary quality and patterns and non-communicable disease risk of an Indian community in KwaZulu-Natal. South Africa Journal of Health, Population and Nutrition 33 (2015) 12-20.
    [7]
    Chikwere P, Nsiah K, Tandoh MA, Agyenim-Boateng K. The relation of dietary pattern to serum lipid profile and uric acid among type 2 diabetes patients. J. Nutr. Ecol. Food Res 2 (2014) 207-213.
    [8]
    Neel JV. Diabetes mellitus: a ??thrifty?? genotype rendered detrimental by ??progress??? Am J Hum Genet 14 (1962) 353-362.
    [9]
    Langenberg C, Sharp S, Forouhi NG, Franks P, Schulze MB, Kerrison N, et al. The InterAct Project: An Examination of the Interaction of Genetic and Lifestyle Factors on the Incidence of Type 2 Diabetes in the EPIC Study. Diabetologia 54 (2011) 2272-2282.
    [10]
    Langenberg C, Sharp SJ, Franks PW, Scott RA, Deloukas P, Forouhi NG, et al. Gene-lifestyle interaction and type 2 diabetes: The EPIC InterAct case-cohort study. PLoS Med 11 (2014) e1001647.
    [11]
    Walker CG, Solis-Trapala I, Holzapfe C, Ambrosini GL, Fuller NR, Loos RJF, et al. Modelling the interplay between lifestyle factors and genetic predisposition on markers of type2 diabetes mellitus risk. PLoS ONE 10 (2015) e0131681.
    [12]
    Phillips CM. Nutrigenetics and metabolic disease: current status and implications for personalised nutrition. Nutrients 5 (2013) 32-57.
    [13]
    Hivert M, Jablonski KA, Perreault, L. Updated genetic score based on 34 con?rmed type 2 diabetes loci is associated with diabetes incidence and regression to normoglycemia in the diabetes prevention program. Diabetes 60 (2011) 1340-1348.
    [14]
    Chikwere P. Functional foods and nutraceuticals, wonders in cancer risks - a review. World Scientific News 64 (2017) 18-33.
    [15]
    Buckland G, Agudo A, Luj?n L, Jakszyn P, Bueno-de-Mesquita H, Palli D, et al. Adherence to a Mediterranean diet and risk of gastric adenocarcinoma within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study. Am J Clin Nutr 91 (2010) 381-390.
    [16]
    Ib??ez-Sanz G, D?ez-Villanueva A, Henar Alonso M, Rodr?guez-Moranta F, P?rez-G?mez B, Bustamante M, et al. Risk Model for Colorectal Cancer in Spanish Population Using Environmental and Genetic Factors: Results from the MCC-Spain study. Scientific Reports 7 (2017) 43263.
    [17]
    Stein B, Anderson JC, Rajapakse R, Alpern ZA, Messina CR, Walker G. Body mass index as a predictor of colorectal neoplasia in ethnically diverse screening population. Dig Dis Sci 55 (2010) 2945-2952.
    [18]
    Abul? A, Fern?ndez-Rozadilla C, Alonso-Espinaco V, Mu?oz J, Gonzalo V, Bessa X, et al. Case-control study for colorectal cancer genetic susceptibility in EPICOLON: previously identified variants and mucins. BMC Cancer 11 (2011) 339-346.
    [19]
    Huo D, Zheng Y, Ogundiran TO, Adebamowo C, Nathanson KL, Domchek SM, et al. Evaluation of 19 susceptibility loci of breast cancer in women of African ancestry. Carcinogenesis 33 (2012) 835?840.
    [20]
    Ko K-P, Kim S-W, Ma SH, Park B, Ahn Y, Lee JW, et al. Dietary intake and breast cancer among carriers and noncarriers of BRCA mutations in the Korean Hereditary Breast Cancer Study. Am J Clin Nutr 98 (2013) 1493-1501.
    [21]
    Toledo E, Salas-Salvad? J, Donat-Vargas C, Buil-Cosiales P, Estruch R, Ros E, et al. Mediterranean Diet and Invasive Breast Cancer Risk Among Women at High Cardiovascular Risk in the PREDIMED Trial: A Randomized Clinical Trial. JAMA Intern Med 175 (2015) 1752-1760.
    [22]
    Sanchez NF, Stierman B, Saab S, Mahajan D, Yeung H, Francois F. Physical activity reduces risk for polyps in a multiethnic colorectal cancer screening population. BMC Research Notes 5 (2012) 312-319.
    [23]
    Folkersen L, van?t Hooft F, Chernogubova E, Agardh HE, Hansson GK, Hedin U. Association of genetic risk variants with expression of proximal genes identifies novel susceptibility genes for cardiovascular disease. Circ Cardiovasc Genet 3 (2010) 365-373.
    [24]
    Sotos-Prieto M, Baylin A, Campos H, Qi L, Mattei J. Lifestyle Cardiovascular Risk Score, Genetic Risk Score, and Myocardial Infarction in Hispanic/Latino Adults Living in Costa Rica. J Am Heart Assoc 5 (2016) e004067.
    [25]
    Corella D, Asensio EM, Coltell O, Sorl?, J. V., Estruch, R., Martinez-Gonz?lez, M.A, et al. CLOCK gene variation is associated with incidence of type 2 diabetes and cardiovascular diseases in type 2 diabetic subjects: dietary modulation in the PREDIMED randomized trial. Cardiovascular Diabetology 15 (2016) 4-15.
    [26]
    Garg V, Muth AN, Ransom JF, Schluterman MK, Barnes R, King IN, et al. Mutation in NOTCH1 cause aortic valve disease. Nature 437 (2005) 270-274.
    [27]
    Khera AV, Emdin CA, Drake I. Genetic risk, adherence to a healthy lifestyle, and coronary disease. N Engl J Med 375 (2016) 2349-2358.
    [28]
    Micha R, Pe?alvo JL, Cudhea F, Imamura F, Rehm CD, Mozaffarian D. Association between dietary factors and mortality from heart disease, stroke, and type 2 diabetes in the United States. JAMA 317 (2017) 912-924.
    [29]
    Estruch R, Ros E, Salas-Salvad? J. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. N Engl J Med 368 (2013) 1279-1290.
    [30]
    McKeever TM, Lewis SA, Cassano PA, Ock? M, Burney P, Britton J, Smit HA, et al. Patterns of dietary intake and relation to respiratory disease, forced expiratory volume in 1 s, and decline in 5-y forced expiratory volume. Am J Clin Nutr 92 (2010) 408-415.
    [31]
    Powell R, Davidson D, Divers J, Manichaikul A, Jeffrey Carr J, Detrano R, et al. Genetic ancestry and the relationship of cigarette smoking to lung function and per cent emphysema in four race/ethnic groups: a cross-sectional study. Thorax 68 (2013) 634-642.
    [32]
    Sorli-Aguilar M, Martin-Lujan F, Flores-Mateo G, Arija-Val V, Basora-Gallisa J, Sola-Alberich R. Dietary patterns are associated with lung function among Spanish smokers without respiratory disease. BMC Pulmonary Medicine 16 (2016) 162-173.
    [33]
    Sabater-Lleal M, M?larstig A, Folkersen L, Artigas MS, Baldassarre D, Kavousi M, Almgren P, et al. Common Genetic Determinants of Lung Function, Subclinical Atherosclerosis and Risk of Coronary Artery Disease. PLoS ONE 9 (2014) e104082.
  • Open Access Research Article
    Export citation: APA   BibTeX   EndNote   RIS  
    Trends Journal of Sciences Research 2014, 1(1), 28-37. http://doi.org/10.31586/Agrophysical.0101.05
    305 Views 623 Downloads 1 Citations PDF Full-text (1.969 MB)  HTML Full-text
    Abstract
    We analyze the experimental data on the dynamics of water and mineral metabolism of tomato plants by using the methods of spectral analysis. Plants were cultivated under controlled conditions. We have used the various compositions of juvenile analogues of thin-layer soil. It is shown that the composition of the soil
    [...] Read more.
    We analyze the experimental data on the dynamics of water and mineral metabolism of tomato plants by using the methods of spectral analysis. Plants were cultivated under controlled conditions. We have used the various compositions of juvenile analogues of thin-layer soil. It is shown that the composition of the soil analogue significantly affects the dynamics of water-mineral metabolism of plants and plant productivity. It was found that the dynamics of the water and mineral metabolism of plants has a clear oscillatory structure. We have identified the most intense frequencies of this process. It was found that in order to maximize the productivity of plants it is necessary that the process of transpiration should contain simultaneously both high-frequency and low-frequency periodicities. This creates the most favorable environment for the development and functioning of the plant root system. It was shown that vibrations of water metabolism closely connected with the vibrations of the content of chemical elements in plants.  Full article
    Figures

    Figure 1 of 9

    References
    [1]
    Mukhomorov V.K., and Anikina L.M. 2012. Dynamics of Mineral Elements in Plants. Primary Soil Formation. LAP LAMBERT Academic Publishing. Germany. Saarbr?cken. (in Russian).
    [2]
    Mukhomorov V.K., Anikina L.M. Stepanova O.A. (2007) Dinamika produktivnosti i kachestva rastitel'noy produktsii i ikh svyaz's informatsionnym obmenom mezhdu sistemami organicheskoye veshchestvo-mikrobioticheskoye soobshchestvo pri pervichnom pochvoobrazovanii. (The dynamics of efficiency and quality of plant products and their relation with information exchange between systems of organic matter and biotic community during of the primary pedogenesis). In: Modern agrophysics for the high agrotechnologies. International Conference. St. Petersburg, Sept., 25-27, 2007, pp. 210-211. (in Russian).
    [3]
    Mukhomorov V.K., and Anikina L.M. (2008) Information Streams in Coupled Organic Matter-Microbiotic Community Systems of the Root-Inhabited Media under Primary Pedogenic Processes. Russian Agricultural Sciences, 34, 322-324.
    [4]
    Panova G.G., Ermakov E.I., Anikina L.M. Stepanova O.A. (2007) A method of chemical regeneration and sterilization of soil analogues. Inventor?s Certificate of Russian Fed. No. 23021004. Bull. No. 19.
    [5]
    ZheltovYu.I. (1986) Vliyaniye sposobov uvlazhneniya korneobitayemykh sred na produktivnost' rasteniy tomata v reguliruyemykh usloviyakh. (Influence of the ways of moistening of root-inhabited environments on the productivity of tomato plants under controlled conditions). Scientific and technical bulletin of agronomic physics. pp. 73-84. (in Russian).
    [6]
    Ermakov, E.I. (2009). The controllable technogenic agroecosystem of the noosphere level. In: Ermakov E.I. Selected Works. St. Petersburg. pp. 75-80.
    [7]
    Sokolov V.N. (1996) Microworld of argillaceous rocks. Soros Educational Journal. pp. 56-64.
    [8]
    PlatonovO.S., PoloveckaiaV.V. (2012) Features of the chemical compositionand biological activity of sapropel. Tula State Pedagogical University of L. Tolstoy. Bulletin ofnew medical technologies. 1, 105-111.
    [9]
    Udalova O.R. (2014) Thesis. Technological bases of cultivation of tomato plants under controlled agro-ecosystems. St. Petersburg.
    [10]
    Yagodyn BA (1987) Practical work on Agricultural Chemistry. M.
    [11]
    MineevaVG (Ed.). (2001) Workshop on Agricultural Chemistry. MSU.M.
    [12]
    Ermakov E.I., Medvedeva I.V., Mukhomorov V.K. (1997) Influence of natural organic matter in the nutrient solution on the water-mineral metabolism and productivity of tomato plants under controlled conditions. Agrochemistry. 5, 32-40.
    [13]
    GambarovG.M., JuravelN.M., and KorolevY.G. (1990) Statistical modelingand forecasting. Ed. by GrambergA.G.M. Finance and Statistics, (in Russian).
    [14]
    Ermakov, E.I., Medvedev I.V. (1985) Optimizatsiya usloviy zhiznedeyatel'nosti korney pri issledovanii vodno-mineral'nogo obmena i potentsial'noy produktivnosti rasteniy tomata. (Optimization of vital activity conditions of the roots in the study of water and mineral metabolism and potential productivity of tomato plants). In: Physiological objective laws of ontogeny and of plant productivity. pp. 155-185.
    [15]
    Pystyl?nik E.I. (1968) Statisticheskie metody analiza i odrabotki nablydenii (Statistical Methods of Analyzing and Processing Observations). Moscow. Nauka.
    [16]
    Fleiss J.L. (1973) Statistical Methods for Rates and Proportions. New York-Chichester-Brisbane-Toronto-Singapore. John Wiley & Sons.
    [17]
    Handbook of Applicable Mathematics. (1990) Chief Editor: Walter Ledermann. Vol. VI: Statistics. Part B. New York-Chichester-Brisbane-Toronto-Singapore. John Wiley & Sons.
    [18]
    Sir Kendall N. (1981) Time-Series. London and High Wycombe. Charls Griffin and Company Ltd.
  • Open Access Research Article
    Export citation: APA   BibTeX   EndNote   RIS  
    Trends Journal of Sciences Research 2018, 3(3), 124-132. http://doi.org/10.31586/Biochemistry.0303.04
    263 Views 163 Downloads PDF Full-text (921.556 KB)  HTML Full-text
    Abstract
    The bone health is an important part of healthy-life and longevity in current situation due to huge toxins and contaminants in the environment and food chain. Considering the importance of bone health in the modern era, the present study was undertaken to investigate the effect of the Consciousness Energy
    [...] Read more.
    The bone health is an important part of healthy-life and longevity in current situation due to huge toxins and contaminants in the environment and food chain. Considering the importance of bone health in the modern era, the present study was undertaken to investigate the effect of the Consciousness Energy Healing (The Trivedi Effect?) Treatment on Dulbecco's Modified Eagle Medium (DMEM) in which the human bone osteosarcoma cells - MG-63 (ATCC? CRL-1427?) was grown for the assessment of bone cell proliferation and differentiation in vitro. The study parameters were assessed using cell viability by MTT assay, alkaline phosphatase (ALP), and collagen synthesis on bone health using ELISA-based assay. The cell viability was significantly increased by 24% in the Biofield Energy Treated group supplemented with 10% charcoal-dextran with fetal bovine serum (CD-FBS) (G3) compared to the untreated cells group (G1). The level of ALP was significantly increased by 72% in the G3 group compared to the G1 group. Additionally, the level of collagen synthesis was significantly (p?0.001) increased by 19% in the G3 group compared to the G1 group. The overall results demonstrated that the Biofield Energy Treated DMEM has the potential for bone mineralization and bone cells growth as evident via increased levels of collagen and ALP. Therefore, the Biofield Energy Healing (The Trivedi Effect?) Treatment could be useful as a bone health promoter for various bone-related disorders like low bone density, osteogenesis imperfecta, and osteoporosis, etc.  Full article
    References
    [1]
    Yang Z, Xiong HR (2012) Culture conditions and types of growth media for mammalian cells. In L. Ceccherini-Nelli and B. Matteoli (ed.), Biomedical Tissue Culture (3-18). InTech. ISBN 978-953-51-0788-0. http://dx.doi. org/10.5772/3071
    [2]
    Beloti MM, Rosa AL (2005) Osteoblast differentiation of human bone marrow cells under continuous and discontinuous treatment with dexamethasone. Braz Dent J 16: 156-161.
    [3]
    Lajeunesse D, Kiebzak GM, Frondoza C, Sacktor B (1991) Regulation of osteocalcin secretion by human primary bone cells and by the human osteosarcoma cell line MG-63. Bone Miner 14: 237-250.
    [4]
    Robison R, Soames KH (1924) The possible significance of hexophosphoric esters in ossification Part II. The phosphoric esterase of ossifying cartilage. Biochem J 18: 740-754.
    [5]
    Gaur T, Lengner CJ, Hovhannisyan H, Bhat RA, Bodine PV, Komm BS, Javed A, van Wijnen AJ, Stein JL, Stein GS, Lian JB (2005) Canonical WNT signaling promotes osteogenesis by directly stimulating Runx2 gene expression. J Biol Chem 280: 33132-33140.
    [6]
    Gaur T, Rich L, Lengner CJ, Hussain S, Trevant B, Ayers D, Stein JL, Bodine PV, Komm BS, Stein GS, Lian JB (2006) Secreted frizzled related protein 1 regulates WNT signaling for BMP2 induced chondrocyte differentiation. J Cell Physiol 208: 87-96.
    [7]
    Canalis E, McCarthy TL, Centrella M (1989) Effects of platelet-derived growth factor on bone formation in vitro. J Cell Physiol 140: 530-537.
    [8]
    Canalis E (1987) Effects of tumor necrosis factor on bone formation in vitro. Endocrinology 121: 1596-1604.
    [9]
    Canalis E, Centrella M, McCarthy T (1988) Effects of basic fibroblast growth factor on bone formation in vitro. J Clin Invest 81: 1572-1577.
    [10]
    Wozney JM, Rosen V, Celeste AJ, Mitsock LM, Whitters MJ, Kriz R, Hewick R, Wang EA (1988) Novel regulators of bone formation: Molecular clones and activities. Science 242: 1528-1534.
    [11]
    Yount G, Patil S, Dave U, Alves-dos-Santos L, Gon K, Arauz R, Rachlin K (2013) Evaluation of biofield treatment dose and distance in a model of cancer cell death. J Altern Complement Med 19: 124-127.
    [12]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Gangwar M, Jana S (2015) Morphological and molecular analysis using RAPD in biofield treated sponge and bitter gourd. American Journal of Agriculture and Forestry 3: 264-270.
    [13]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Gangwar M, Jana S (2015) Effect of biofield energy treatment on chlorophyll content, pathological study, and molecular analysis of cashew plant (Anacardium occidentale?L.).?Journal of Plant Sciences 3: 372-382.
    [14]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Gangwar M, Jana S (2016) Molecular analysis of biofield treated eggplant and watermelon crops. Adv Crop Sci Tech 4: 208.
    [15]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Mondal SC, Jana S (2015) Effect of biofield treated energized water on the growth and health status in chicken (Gallus gallus domesticus). Poult Fish Wildl Sci 3: 140.
    [16]
    Trivedi MK, Patil S, Shettigar H, Mondal SC, Jana S (2015) The potential impact of biofield treatment on human brain tumor cells: A time-lapse video microscopy. J Integr Oncol 4: 141.
    [17]
    Trivedi MK, Patil S, Shettigar H, Gangwar M, Jana S (2015) In vitro evaluation of biofield treatment on cancer biomarkers involved in endometrial and prostate cancer cell lines. J Cancer Sci Ther 7: 253-257.
    [18]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Shettigar H, Mondal SC, Jana S (2015) Antibiogram pattern of Shigella flexneri: Effect of biofield treatment. Air Water Borne Diseases 3: 122.
    [19]
    Trivedi MK, Patil S, Shettigar H, Mondal SC, Jana S (2015) Antimicrobial susceptibility pattern and biochemical characteristics of Staphylococcus aureus: Impact of biofield treatment. J Microb Biochem Technol 7: 238-241.
    [20]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Shettigar H, Mondal SC, Jana S (2015) Effect of biofield energy treatment on Streptococcus group B: A postpartum pathogen. J Microb Biochem Technol 7: 269-273.
    [21]
    Trivedi MK, Patil S, Shettigar H, Bairwa K, Jana S (2015) Phenotypic and biotypic characterization of Klebsiella oxytoca: An impact of biofield treatment. J Microb Biochem Technol 7: 202-205.
    [22]
    Trivedi MK, Nayak G, Patil S, Tallapragada RM, Latiyal O, Jana S (2015) An evaluation of biofield treatment on thermal, physical and structural properties of cadmium powder. J Thermodyn Catal 6: 147.
    [23]
    Trivedi MK, Nayak G, Patil S, Tallapragada RM, Latiyal O, Jana S (2015) Effect of Biofield energy treatment on physical and structural properties of calcium carbide and praseodymium oxide. International Journal of Materials Science and Applications 4: 390-395.
    [24]
    Trivedi MK, Tallapragada RM, Branton A, Trivedi D, Nayak G, Latiyal O, Jana S (2015) Characterization of physical, thermal and structural properties of chromium (VI) oxide powder: Impact of biofield treatment. J Powder Metall Min 4: 128.
    [25]
    Trivedi MK, Branton A, Trivedi D, Gangwar M, Jana S (2015) Antimicrobial susceptibility, biochemical characterization and molecular typing of biofield treated Klebsiella pneumoniae. J Health Med Inform 6: 206.
    [26]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Gangwar M, Jana S (2015) Antibiogram, biochemical reactions, and genotypic pattern of biofield treated Pseudomonas aeruginosa. J Trop Dis 4: 181.
    [27]
    Trivedi MK, Tallapragada RM, Branton A, Trivedi D, Nayak G, Mishra R, Jana S (2015) Biofield treatment: A potential strategy for modification of physical and thermal properties of gluten hydrolysate and ipomoea macroelements. J Nutr Food Sci 5: 414.
    [28]
    Trivedi MK, Nayak G, Patil S, Tallapragada RM, Jana S, Mishra R (2015) Bio-field treatment: An effective strategy to improve the quality of beef extract and meat infusion powder. J Nutr Food Sci 5: 389.
    [29]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Singh R, Jana S (2015) Physicochemical and spectroscopic characterization of biofield energy treated gerbera multiplication medium. Plant 3: 57-63.
    [30]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Singh R, Jana S (2015) Physical, spectroscopic and thermal characterization of biofield treated fish peptone. Eur Biophys J 3: 51-58.
    [31]
    Trivedi MK, Branton A, Trivedi D, Nayak G, Singh R, Jana S (2015) Physicochemical characterization of biofield treated orchid maintenance/replate medium. J Plant Sci 3: 285-293.
    [32]
    Czekanska EM, Stoddart MJ, Richards RG, Hayes JS (2012) In search of an osteoblast cell model for in vitro research. Eur Cells Mater 24: 1-17.
    [33]
    Luo XH, Liao EY (2003) Effects of estriol on the proliferation and differentiation of human osteoblastic MG-63 cells. Endocr Res 29: 343-351.
    [34]
    Fu-Xiang Yu, Wei-Jian Hu, Bin He, Yi-Hu Zheng, Qi-Yu Zhang, and Lin Chen (2015) Bone marrow mesenchymal stem cells promote osteosarcoma cell proliferation and invasion. World J Surg Oncol 13: 52.
    [35]
    Muehlberg FL, Song YH, Krohn A, Pinilla SP, Droll LH, Leng X, Seidensticker M, Ricke J, Altman AM, Devarajan E, Liu W, Arlinghaus RB, Alt EU (2009) Tissue-resident stem cells promote breast cancer growth and metastasis. Carcinogenesis 30: 589-597.
    [36]
    Nagakawa Y, Aoki T, Kasuya K, Tsuchida A, Koyanagi Y (2002) Histologic features of venous invasion, expression of vascular endothelial growth factor and matrix metalloproteinase-2 and matrix metalloproteinase-9, and the relation with liver metastasis in pancreatic cancer. Pancreas 24: 169-178.
    [37]
    Wagner ER, Luther G, Zhu G, Luo Q, Shi Q, Kim SH, Gao JL, Huang E, Gao Y, Yang K, Wang L, Teven C, Luo X, Liu X, Li M, Hu N, Su Y, Bi Y, He BC, Tang N, Luo J, Chen L, Zuo G, Rames R, Haydon RC, Luu HH, He TC. (2011) Defective osteogenic differentiation in the development of osteosarcoma. Sarcoma 2011: 12. Article ID 325238
    [38]
    Coleman JE (1992) Structure and mechanism of alkaline phosphatase. Annu Rev Biophys Biomol Struct 21: 441-483.
    [39]
    Schoppet M, Shanahan CM (2008) Role for alkaline phosphatase as an inducer of vascular calcification in renal failure? Kidney Int 73: 989-991.
    [40]
    Lomashvili KA, Garg P, Narisawa S, Millan JL, O'Neill WC (2008) Upregulation of alkaline phosphatase and pyrophosphate hydrolysis: Potential mechanism for uremic vascular calcification. Kidney Int 73: 1024-1030.
    [41]
    Lomashvili K, Cobbs S, Hennigar R, Hardcastle K, O'Neill W (2004) Phosphate-induced vascular calcification: Role of pyrophosphate and osteopontin. J Am Soc Nephrol 15: 1392-1401.
    [42]
    Moochhala SH, Sayer JA, Carr G, Simmons NL (2008) Renal calcium stones: Insights from the control of bone mineralization. Exp Physiol 93: 43-49.
    [43]
    Huang MS, Sage AP, Lu J, Demer LL, Tintut Y (2008) Phosphate and pyrophosphate mediate PKA-induced vascular cell calcification. Biochem Biophys Res Commun 374: 553-558.
    [44]
    Whyte MP, Scriver CR, Beaudet AL, Sly WS, Valle D, Childs B, Kinzler KW (Eds.), (2012) The Metabolic and Molecular Bases of Inherited Diseases (8th Edn.), Vol IV, McGraw-Hill, New York.
    [45]
    Whyte MP (2010) Physiological role of alkaline phosphatase explored in hypophosphatasia. Ann NY Acad Sci 1192: 190-200.
    [46]
    Mill?n JL (2006) Mammalian Alkaline Phosphatases: From Biology to Applications in Medicine and Biotechnology WILEY-VCH Verlag GmbH & Co., KGaA, Weinheim.
    [47]
    Mornet E (2007) Hypophosphatasia. Orphanet J Rare Dis 2: 40.
    [48]
    Viguet-Carrin S, Garnero P, Delmas PD (2006) The role of collagen in bone strength. Osteoporos Int 17: 319-336.
    [49]
    Glimcher MJ, Muir H (1984) Recent studies of the mineral phase in bone and its possible linkage to the organic matrix by protein-bound phosphate bonds. Phil Trans R Soc B 304: 479-508.
    [50]
    Landis WJ, Song MJ, Leith A, Mcewen L, Mcewen BF (1993) Mineral and organic matrix interaction in normally calcifying tendon visualized in 3 dimensions by high-voltage electron-microscopic tomography and graphic image-reconstruction. J Struct Biol 110: 39-54.
    [51]
    Deshpande AS, Beniash E (2008) Bioinspired synthesis of mineralized collagen fibrils. Cryst Growth Des 8: 3084-3090.
    [52]
    Price PA, Toroian D, Lim JE (2009) Mineralization by inhibitor exclusion: The calcification of collagen with fetuin. J Biol Chem 284: 17092-17101.
    [53]
    Rubik B (1994) Manual healing methods. Alternative medicine: expanding medical horizons, Washington, DC, US Government Printing Office, NIH Publication No. 094-066.
  • Open Access Research Article
    Export citation: APA   BibTeX   EndNote   RIS  
    Trends Journal of Sciences Research 2018, 3(4), 161-169. http://doi.org/10.31586/Biomedicine.0304.03
    52 Views 66 Downloads PDF Full-text (1.915 MB)  HTML Full-text
    Abstract
    Background: Hepatocellular carcinoma is one of the most common malignant tumors, with rapid development and high malignancy. MicroRNAs have been reported to play important roles in hepatocellular carcinoma progression. Aim: To identify the key genes and miRNAs in HCC, and to explore their potential molecular mechanisms. Methods: Gene expression profiles
    [...] Read more.
    Background: Hepatocellular carcinoma is one of the most common malignant tumors, with rapid development and high malignancy. MicroRNAs have been reported to play important roles in hepatocellular carcinoma progression. Aim: To identify the key genes and miRNAs in HCC, and to explore their potential molecular mechanisms. Methods: Gene expression profiles of GSE15471 (mRNA profile) and GSE57555 (miRNA profile) were downloaded from gene expression omnibus, which were analysed using R software and bioconductor packages. The gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichments of DEGs were performed using the DAVID database, and the protein–protein interaction networks of the DEGs were constructed from the STRING database. In addition, targets of differentially expressed miRNAs were predicted by the online resource miRDB. Result: In total, 191 differentially expressed genes were identified, including 142 upregulated and 49 downregulated genes. Functional analysis revealed that these DEGs were associates with wound healing, endodermal cell-cell adhesion, activation of MAPK activity and negative regulation of cell proliferation. In addition, we identified five DEMs, which were upregulated and downregulated. hsa-miR-122-5p may target the PDK4, and hsa-miR-21-5p probably targets SPOCK1 and PAIP2B. Conclusions: We applied integrated bioinformatics to identify key pathogenic genes involved in hepatocellular carcinoma and provide new clues for further studies of hepatocellular carcinoma.  Full article
    Figures

    Figure 4 of 4

    References
    [1]
    Feng Y, Zu LL, Zhang L. MicroRNA-26b inhibits the tumor growth of human liver cancer through the PI3K/Akt and NF-kappaB/MMP-9/VEGF pathways. Oncol Rep. 2018;39(5):2288-96.
    [2]
    Liu H, Cheng L, Cao D, Zhang H. Suppression of miR-21 Expression Inhibits Cell Proliferation and Migration of Liver Cancer Cells by Targeting Phosphatase and Tensin Homolog (PTEN). Med Sci Monit. 2018;24:3571-7.
    [3]
    Grainger S, Traver D, Willert K. Wnt Signaling in Hematological Malignancies. Prog Mol Biol Transl Sci. 2018;153:321-41.
    [4]
    Setshedi M, Andersson M, Kgatle MM, Roberts L. Molecular and cellular oncogenic mechanisms in hepatocellular carcinoma. S Afr Med J. 2018;108(8b):41-6.
    [5]
    Kroemer G, Pouyssegur J. Tumor cell metabolism: cancer's Achilles' heel. Cancer cell. 2008;13(6):472-82.
    [6]
    Lu X, Kang Y. Hypoxia and hypoxia-inducible factors: master regulators of metastasis. Clin Cancer Res. 2010;16(24):5928-35.
    [7]
    Guo JR, Shen HC, Liu Y, Xu F, Zhang YW, Shao Y, et al. Effect of Acute Normovolemic Hemodilution Combined with Controlled Low Central Venous Pressure on Blood Coagulation Function and Blood Loss in Patients Undergoing Resection of Liver Cancer Operation. Hepatogastroenterology. 2015;62(140):992-6.
    [8]
    Sang L, Wang XM, Xu DY, Zhao WJ. Bioinformatics analysis of aberrantly methylated-differentially expressed genes and pathways in hepatocellular carcinoma. World J Gastroenterol. 2018;24(24):2605-16.
    [9]
    He JH, Han ZP, Wu PZ, Zou MX, Wang L, Lv YB, et al. Gene-gene interaction network analysis of hepatocellular carcinoma using bioinformatic software. Oncol Lett. 2018;15(6):8371-7.
    [10]
    Dang S, Zhou J, Wang Z, Wang K, Dai S, He S. MiR-299-3p functions as a tumor suppressor via targeting Sirtuin 5 in hepatocellular carcinoma. Biomed Pharmacother. 2018;106:966-75.
    [11]
    Wakasugi H, Takahashi H, Niinuma T, Kitajima H, Oikawa R, Matsumoto N, et al. Dysregulation of miRNA in chronic hepatitis B is associated with hepatocellular carcinoma risk after nucleos(t)ide analogue treatment. Cancer Lett. 2018;434:91-100.
    [12]
    Li Z, Xue TQ, Yang C, Wang YL, Zhu XL, Ni CF. EGFL7 promotes hepatocellular carcinoma cell proliferation and inhibits cell apoptosis through increasing CKS2 expression by activating Wnt/beta-catenin signaling. J Cell Biochem. 2018;10.1002
    [13]
    Yan L, Xu F, Dai CL. Relationship between epithelial-to-mesenchymal transition and the inflammatory microenvironment of hepatocellular carcinoma. J Exp Clin Cancer Res. 2018;37(1):203.
    [14]
    Pearson G, Robinson F, Beers Gibson T, Xu BE, Karandikar M, Berman K, et al. Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions. Endocr Rev. 2001;22(2):153-83.
    [15]
    Li D, Ren W, Jiang Z, Zhu L. Regulation of the NLRP3 inflammasome and macrophage pyroptosis by the p38 MAPK signaling pathway in a mouse model of acute lung injury. Mol Med Rep. 2018.
    [16]
    Si L, Xu L, Yin L, Qi Y, Han X, Xu Y, et al. Potent effects of dioscin against pancreatic cancer via miR-149-3P-mediated inhibition of the Akt1 signalling pathway. Br J Pharmacol. 2017;174(7):553-68.
    [17]
    Lee RC, Ambros V. An extensive class of small RNAs in Caenorhabditis elegans. Science. 2001;294(5543):862-4.
    [18]
    Woolbright BL, Choudhary D, Mikhalyuk A, Trammel C, Shanmugam S, Abbott E, et al. The Role of Pyruvate Dehydrogenase Kinase-4 (PDK4) in Bladder Cancer and Chemoresistance. Mol Cancer Ther. 2018;17(9):2004-12.
    [19]
    Sun S, Liu J, Zhao M, Han Y, Chen P, Mo Q, et al. Loss of the novel mitochondrial protein FAM210B promotes metastasis via PDK4-dependent metabolic reprogramming. Cell Death Dis. 2017;8(6):e2870.
    [20]
    Choiniere J, Wu J, Wang L. Pyruvate Dehydrogenase Kinase 4 Deficiency Results in Expedited Cellular Proliferation through E2F1-Mediated Increase of Cyclins. Mol Pharmacol. 2017;91(3):189-96.
    [21]
    Han H, Li W, Shen H, Zhang J, Zhu Y, Li Y. microRNA-129-5p, a c-Myc negative target, affects hepatocellular carcinoma progression by blocking the Warburg effect. J Mol Cell Biol. 2016.
    [22]
    Yang J, Yang Q, Yu J, Li X, Yu S, Zhang X. SPOCK1 promotes the proliferation, migration and invasion of glioma cells through PI3K/AKT and Wnt/beta-catenin signaling pathways. Oncol Rep. 2016;35(6):3566-76.
    [23]
    Chen D, Zhou H, Liu G, Zhao Y, Cao G, Liu Q. SPOCK1 promotes the invasion and metastasis of gastric cancer through Slug-induced epithelial-mesenchymal transition. J Cell Mol Med. 2018;22(2):797-807.
    [24]
    Veenstra VL, Damhofer H, Waasdorp C, Steins A, Kocher HM, Medema JP, et al. Stromal SPOCK1 supports invasive pancreatic cancer growth. Mol Oncol. 2017;11(8):1050-64.
    [25]
    Kachaev ZM, Lebedeva LA, Kozlov EN, Toropygin IY, Schedl P, Shidlovskii YV. Paip2 is localized to active promoters and loaded onto nascent mRNA in Drosophila. Cell Cycle. 2018;17(14):1708-20.
    [26]
    Rosenfeld AB. Suppression of cellular transformation by poly (A) binding protein interacting protein 2 (Paip2). PLoS One. 2011;6(9):e25116.
  • Open Access Research Article
    Export citation: APA   BibTeX   EndNote   RIS  
    Trends Journal of Sciences Research 2019, 4(2), 39-47. http://doi.org/10.31586/Dermatology.0402.01
    99 Views 86 Downloads PDF Full-text (764.334 KB)  HTML Full-text
    Abstract
    Objective: Colchicine has been used in recent years as an effective drug for controlling attacks in Behçet’s disease. In the present study, we investigated expression levels of IL1R, IL2R, IL12RB, IL23R, IL17, CXCR3, CXCR10 and IL8 genes in patients with active and inactive Behçet’s disease. We also evaluated how colchicine
    [...] Read more.
    Objective: Colchicine has been used in recent years as an effective drug for controlling attacks in Behçet’s disease. In the present study, we investigated expression levels of IL1R, IL2R, IL12RB, IL23R, IL17, CXCR3, CXCR10 and IL8 genes in patients with active and inactive Behçet’s disease. We also evaluated how colchicine use in patients with active and inactive disease affected these genes and evaluated their role in the etiopathogenesis of the disease. Methods: Thirty-five patients who were diagnosed with Behçet’s disease according to the International Working Group criteria (28 with active disease, 7 inactive) and were taking colchicine were enrolled in the study. Twenty healthy subjects were included as a control group. Expression levels of the IL1R, IL2R, IL12RB, IL23R, IL17, CXCR3 ,CXCR10 and IL8, genes were evaluated. Results: Expression levels of CXCR3 and IL23R were significantly lower in patients with active Behcet's disease when compared with the inactive disease and control groups. However, the differences in CXCR3 and IL23R expression between the inactive Behçet’s patient group and the control group were nonsignificant. Expression levels of the other genes did not differ statistically between the active Behçet’s patients, inactive Behçet’s patients, and control subjects. Conclusion: While the expression levels of the CXCR3 and IL23R genes in active Behçet’s patients were statistically lower than controls, there was no statistical difference between active and inactive Behçet’s patients or controls in terms of IL1R, IL2R, IL17, IL12RB, CXCR10 and IL8, gene expression levels. This study may form the basis for further studies to determine the molecular mechanism of colchicine in the treatment of Behçet's disease.  Full article
    References
    [1]
    Evereklioglu C. Current concepts in the etiology andtreatment of Behcet disease. Surv Ophthalmol.2005;50:297-350.
    [2]
    Onder M, Gurer MA. The multiple faces of Behcet'sdisease and its aetiological factors. J Eur Acad DermatolVenereol. 2001;15:126-36.
    [3]
    Arca E, Gür AR. Behçet Hastalığı. T Klin J Med Sci.2003;23:261-8.
    [4]
    Doğanavşargill E, Keser G. Behçet Hastalığı. T KlinJ Int Med Sci 2005;1:80-91.
    [5]
    Boyvat A. Behçet hastalığının etiyopatogenezi. T KlinJ Dermatol. 2004;1415-21.
    [6]
    Yıldırım M, et al. Behçet hastalığı patogenezindeki yenilikler Süleyman Demirel Üniversitesi Týp Fakültesi Dermatoloji AD, Isparta DERLEME. 2009, 16(3): 29-34.
    [7]
    Önder M, Gürer MA. Ülkemizde Behçet hastalığı epidemiyolojisi. T Klin J Int Med Sci 2007;3:4-7.
    [8]
    Doğanavşargil E, Keser G, Behçet hastalığı. In:Gümüþdiþ G, Doðanavþargil E, (eds). KlinikRomatoloji, 1. Baskı. İstanbul, Deniz matbaa, 1999;423-39.
    [9]
    Arayssi T.Hamdan A. New insights into the pathogenesis and therapy of Behçet'sdisease. Curr Opin Pharmacol , 2004:4: 183-8.
    [10]
    Ohno S. Ohguchi M. Hirose S., Matsuda H., Wakisaka A., Aizawa H. Closeassociation of HLA-BW51 with Behçet’s disease. Arch Ophthalmol .1982100(9), 1455-58
    [11]
    Öztaş P, et al.Behçet Hastalığı Etyopatogenezi THE ETIOPATHOGENESIS OF BEHCET'S DISEASE Turkiye Klinikleri J Dermatol .2006;16(4):181-5 DERLEME
    [12]
    Mege JL, Dilsen N, Sanguedolce V, et al. Overproduction ofmonocyte derived tumor necrosis factor alpha, interleukin (IL)13- IL-8 and increased neutrophil superoxide generation inBehcet's disease. A comparative study with familial Mediterraneanfever and healthy subjects. J Rheumatol .1993;20:1544-9
    [13]
    Sayinalp N, Ozcebe Ol, Ozdemir O, Haznedaroglu IC, Dundar S, Kirazli S: Cytokines in Behcet's disease. J Rheumatol 1996;23:321-2.
    [14]
    Öztas MO, Önder M, Gürer MA, Bukan N, Sancak B. Seruminterleukin 18 and tumour necrosis factor-alpha levels are increasedin Behcet's disease. Clin Exp Dermatol 2005;30:61-3.
    [15]
    Erkan Alpsoy Behçet Hastalığı: Etyopatogenezde Güncel Bilgiler. Turk J Dermatol 2013; 7: 41-5.
    [16]
    Pineton de Chambrun M, Wechsler B, Geri G, Cacoub P, Saadoun D. New insights into the pathogenesis of Behçet’s disease. Autoimmun Rev 2012;11(10):687-98.
    [17]
    Zhou ZY, Chen SL, Shen N, Lu Y. Cytokines and Behcet’s disease. Autoimmun Rev 2012;11(10):699-704.
    [18]
    Habibagahi Z, Habibagahi M, Heidari M. Raised concentration of soluble form of vascular endothelial cadherin and IL-23 in sera of patients with Behçet’s dise-ase. Mod Rheumatol 2010;20(2):154-9.
    [19]
    Ekinci NS, Alpsoy E, Karakas AA, Yilmaz SB, Yegin O. IL-17A has an important role in the acute attacks of Behçet’s disease. J Invest Dermatol 2010;130(8):2136- 8. 29.
    [20]
    Akman A, Alpsoy E. Behçet hastalığı: Etyopatogenezde güncel bilgiler. Turkderm 2009;43(.2):32-8.
    [21]
    Kapsimali VD, Kanakis MA, Vaiopoulos GA, Kaklamanis PG. Etiopathogenesis of Behçet’s disease with emphasis on the role of immunological aberrations. Clin Rheumatol 2010;29(11):1211-16.
    [22]
    Abbas AK,Lichtman AH. Basic immunology: functions and disorders of the immune system. 2nd ed. Phiadelphia, PA: W.B Saunders Co, Updated edition 2006-2007
    [23]
    Sang Jin Lee.et al.CXCL10/CXCR3 axis is associatedwith disease activity and thedevelopment of mucocutaneouslesions in patients with Behçet’sdiseaseSci Rep. 2017; 7: 14720.Published online 2017 Nov 7. doi: 10.1038/s41598-017-15189-9.
    [24]
    Houman H, Hamzaoui A, Ben Ghorbal I, Khanfir M, Feki M, Hamzaoui K.Abnormal expression of chemokine receptors in Behçet's disease: relationship to intracellular Th1/Th2 cytokines and to clinical manifestations. J Autoimmun. 2004 Nov;23(3):267-73.
    [25]
    M. L. Zoler, Updated Behτet's disease recommendations expand biologic treatment. EULAR 2016 Report, 2016.
    [26]
    Sakane T. Takeno M., Suzuki N., Inaba G. (1999): Behçet’s disease. N Engl J Med Oct,21, 341(17), 1284–912.
    [27]
    Akman-Demir G, Serdaroğlu P,Taşcı B. Clinical patterns of neurologicalinvolvement in Behcet’s disease: evaluation of 200 patients. Brain .1999; 122:2171-81.
    [28]
    Mendoza-Pinto C, García-Carrasco M, Jiménez-Hernández M, Jiménez Hernández C, Riebeling-Navarro C, Nava Zavala A, et al. Etiopathogenesis of Behcet’s disea-se. Autoimmun Rev .2010;9(4):241-5.
    [29]
    Suzuki Kurokawa M, Suzuki N. Behcet's disease. Clin Exp Med .2004;4 (1):10–20.
    [30]
    Yazici H, Esen F. Mortality in Behçet's syndrome. Clin Exp Rheumatol .2008;265 5:138–-40.
    [31]
    Ertenli S, et al. Synovial fluid cytokine levels in Behcet’s diseaseI. Clinical and Experimental Rheumatology .2001; 19 ( 24): 37-41.
    [32]
    Ozçimen AA ,et al. IL-1 cluster gene polymorphisms in Turkish patients with Behçet's disease. Int J Immunogenet. 2011 Aug;38(4):295-301.
    [33]
    Rubın LA, e tal.The soluble interleukin-2 receptor:biology, function,and clinicalapplication. Ann Intern Med .1990; 113 619-27
    [34]
    Evereklioglu C, et al. Serum levels of TNF-alpha, sIL-2R, IL-6, and IL-8 are increased and associated with elevated lipid peroxidation in patients with Behçet's disease. Mediators Inflamm. 2002. 11(2):87-93.
    [35]
    Takeuchi M, Daniel L Kastnera, and Elaine F Remmersa. The immunogenetics of Behçet’s disease: A comprehensive. J Autoimmun. 2015, 64: 137-148.
    [36]
    Xavier JM, Shahram F, Davatchi F, Rosa A, Crespo J, Abdollahi BS, et al. Association Study of IL10 and IL23R-IL12RB2 in Iran-ian patients with Behçet’sdisease. Arthritis Rheum (2012) 64: 2761–72. doi:10.1002/art.34437
    [37]
    Iwakura Y, Ishigame H. The IL-23/IL-17 axis in inflammation. J Clin Invest. 2006; 116:1218–1222.
    [38]
    Steinman L. Mixed results with modulation of TH-17 cells in human autoimmune diseases. Nat Immunol. 2010; 11:41–44.
    [39]
    Chang JT, Shevach EM, Segal BM. Regulation of interleukin (IL)-12 receptor beta2 subunit expression by endogenous IL-12: a critical step in the differentiation of pathogenic autoreactive T cells. J Exp Med. 1999; 189:969–978.
    [40]
    Mizuki N, Meguro A, Ota M, Ohno S, Shiota T, Kawagoe T, et al. Genome-wide association studies identify IL23R–IL12RB2 and IL10 as Behcet’s disease susceptibility loci. Nat Genet. 2010;42:703–706
    [41]
    Remmers EF, Cosan F, Kirino Y, Ombrello MJ, Abaci N, Satorius C, et al. Genome-wide association study identifies variants in the MHC class I, IL10, and IL23R–IL12RB2 regions associated with Behcet’s disease. Nat Genet. 2010;42:698–702.
    [42]
    Xavier JM, Shahram F, Davatchi F, Rosa A, Crespo J, Abdollahi BS, et al. Association study of IL10 and IL23R–IL12RB2 in Iranian patients with Behcet’s disease. Arthritis Rheum. 2012;64:2761–2772.
    [43]
    Fiorentino DF, Zlotnik A, Vieira P, Mosmann TR, Howard M, Moore KW, et al. IL-10 acts on the antigen-presenting cell to inhibit cytokine production by Th1 cells. J Immunol. 1991;146:3444–451
    [44]
    Mosmann TR, Coffman RL. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu Rev Immunol. 1989;7:145–73.
    [45]
    Talaat RM, Ashour ME, Bassyouni IH, Raouf AA. Polymorphisms of interleukin 6 and interleukin 10 in Egyptian people with Behcet’s disease. Immunobiology. 2014;219:573–582.
    [46]
    Kirino Y, Zhou Q, Ishigatsubo Y, Mizuki N, Tugal-Tutkun I, Seyahi E, et al. Targeted resequencing implicates the familial Mediterranean fever gene MEFV and the toll-like receptor 4 gene TLR4 in Behcet disease. Proc Natl Acad Sci U S A. 2013;110:8134–8139.
    [47]
    Yu H, Zheng M, Zhang L Li H, Zhu Y, Cheng L, Li L, Deng B, Kijlstra A, Yang P Allergy Clin Immunol. 2017 Feb;139(2):621-627. .Identification of susceptibility SNPs in IL10 and IL23R-IL12RB2 for Behçet's disease in Han Chinese. Allergy Clin Immunol. 2017 ;139(2):621-627
    [48]
    Hatemi G, Seyahi E, Fresko I, Talarico R, Hamuryudan V. Behçet’s syndro-me: a critical digest of the 2013-2014 literature. Clin Exp Rheumatol. 2014;32(84):S112-22.
    [49]
    Ling E, Shubinsky G, Press J. Increased proportion of CD3+CD4-CD8- double-negative T cells in peripheral blood of children with Behcet’s disease. Autoimmun Rev 2007;6(4):237-40.
    [50]
    Emiroglu N, at al. Serum IL-17A in Behçet's disease Postepy Dermatol Alergol. 2015 Oct; 32(5): 358–361.
    [51]
    Chi W, Zhu X, Yang P, Liu X, Lin X, Zhou H, Huang X, Kijlstra .Upregulated IL-23 and IL-17 in Behçet patients with active uveitis. Invest Ophthalmol Vis Sci. 2008 Jul;49(7):3058-64
    [52]
    Wei Chi, Peizeng Yang, Xuefei Zhu, Yuqin Wang, Lina Chen,Xiangkun Huang, and Xiaoli Liu1,2.Production of interleukin-17 in Behcet’s disease is inhibited by cyclosporin AMol Vis. 2010; 16: 880–886.
    [53]
    Juremalm M,.Chemokine receptor expression by mast cells Nilsson Chem Immunol Allergy. 2005;87:130-44
    [54]
    Houman H Hamzaoui A, Ben Ghorbal I, Khanfir M, Feki M, Hamzaoui K.Abnormal expression of chemokine receptors in Behçet's disease: relationship to intracellular Th1/Th2 cytokines and to clinical manifestations. J Autoimmun. 2004 Nov;23(3):267-73.
    [55]
    Fujii H, Haseagawa M, Takehara K, Mukaida N, Sato S.Abnormal expression and chemokine receptors in peripheralblood T lymphocytes from patients with systemic sclerosis. ClinExp Immunol .2002;130:548
    [56]
    Cosmi L, Annuziato F, Galli M, Maggi R, Nagata K,Romagnani S. CRTH2 is the most reliable marker for thedetection of circulating human Th2 and type 2 T cytotoxic cells inhealth and disease. Eur J Immunol 2000;30:2972.
    [57]
    Sallusto F, Lanzavecchia A, Mackay CR. Chemokines andchemokine receptors in T-cell priming and Th1/Th2-mediatedresponses. Immunol Today 1998;19:568.
    [58]
    Sallusto F, Lenig D, Macka CR, Lanzavecchia A. Flexibleprograms of chemokine receptor expression on human polarizedT helper 1 and 2 lymphocytes. J Exp Med 1998;187:875.
    [59]
    Kaplan AP. Chemokines, chemokine receptors and allergy. IntArch Allergy Immunol 2001;124:423.
    [60]
    Kim TW, Chung H, Yu HG.Chemokine expression of intraocular lymphocytes in patients with Behçet uveitis. Ophthalmic Res. 2011;45(1):5-14.
    [61]
    I Gür-Toy G1, Lenk N, Yalcin B, Aksaray S, Alli NSerum interleukin-8 as a serologic marker of activity in Behçet's disease. .Int J Dermatol. 2005 Aug;44(8):657-60
    [62]
    Durmazlar S.P., Ulkar G.B., Eskioglu F., Tatlican S., Mert A., Akgul A. Significance of serum interleukin-8 levels in patients with Behcet’s disease: High level may indicate vascular involvement. Int. J. Dermatol. 2009;48:259–264.
    [63]
    Sadeghi, A,et al. PMCID: PMC5447940Serum Profiles of Cytokines in Behcet’s Disease Alireza Sadeghi,1 Clin Med. 2017 May; 6(5): 49.
    [64]
    Nalbant S., Sahan B., Durna M., Ersanli D., Kaplan M., Karabudak O., Unal M. Cytokine profile in Behcet uveitis. Bratisl. Lek. Listy. 2008;109:551–554.
    [65]
    Bardak Y, Aridogan B.C. The demonstration of serum interleukin-6, interleukin-8, tumor necrosis factor-α, complement and immunoglobulin levels in BDwith ocular involvement. Ocul. Immunol. Inflamm. 2004;12:53–58.
    [66]
    Inanır I et al.Behcet Hastalığında IL-2R, IL-6 ve IL-8 Turkderm 214 2010; 44: 213-5Immunol Invest.
    [67]
    Karadağ R, et al.Comparison of serum levels of IL-6, IL-8, TNF-α, C reactiveprotein and heat shock protein 70 in patients with active orinactive Behcet’s Turk J Med Sci2010; 40 (1): 57-62.
    [68]
    Zouboulis CC ,etal. Adamantiades-Behçet's disease: interleukin-8 is increased in serum of patients with active oral and neurological manifestations and is secreted by small vessel endothelial cells. Arch Dermatol Res. 2000 Jun;292(6):279-84.
Filter options
Publication Date
From to
Refine Publication Date
Subject Areas
Show more Refine Subjects
Article Types
Refine Article Types
Countries / Territories
Show more Refine Countries / Territories