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American Journal of Medical and Biological Research

ISSN (Print): 2328-4080

ISSN (Online): 2328-4099

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Website: http://www.sciepub.com/journal/AJMBR

   

Article

Frequency of Estrogen Receptor-1 (ESR-1) Gene Polymorphism (PvuII and XbaI) in Patients with Coronary Artery Disease

1Department of Clinical Biochemistry and Molecular Medicine, Taibah Faculty of Medicine, Taibah University, Al-Madinah Al-Munawwarah, Saudi Arabia

2Department of Medical Biochemistry, Tanta Faculty of medicine, Tanta University, Egypt

3Department of Cardiology, Tanta Faculty of medicine, Tanta University, Egypt

4Department of Clinical and Chemical Pathology, National Cancer Institute, Cairo University, Egypt

5Department of Clinical Pathology, Faculty of Medicine, 6th October University, Cairo, Egypt

6Department of Medical Education, Suez Canal Faculty of Medicine, Suez Canal University, Egypt

7Department of Medical Education, Taibah Faculty of Medicine, Taibah University, Al-Madinah Al-Munawwarah, Saudi Arabia

8Division of Pediatric cardiology, Department of Pediatrics, Maternity and Children Hospital, King Abdullah Medical City, Al-Madinah Al-Munawwarah, Kingdom of Saudi Arabia

9Department of Medical Biochemistry, Sohag Faculty of Medicine, Sohag University, Egypt


American Journal of Medical and Biological Research. 2016, 4(1), 5-9
doi: 10.12691/ajmbr-4-1-2
Copyright © 2016 Science and Education Publishing

Cite this paper:
Reham A. Mariah, Kamal El-din Ahmed, Naglaa Mostafa, Mongi Mohamed Ahmed Ayat, Tayseer Nansour, Manal Mohamed Helmy Nabo, Salah Mohamed El Sayed. Frequency of Estrogen Receptor-1 (ESR-1) Gene Polymorphism (PvuII and XbaI) in Patients with Coronary Artery Disease. American Journal of Medical and Biological Research. 2016; 4(1):5-9. doi: 10.12691/ajmbr-4-1-2.

Correspondence to: Salah  Mohamed El Sayed, Department of Clinical Biochemistry and Molecular Medicine, Taibah Faculty of Medicine, Taibah University, Al-Madinah Al-Munawwarah, Saudi Arabia. Email: drsalahpediatr@yahoo.com

Abstract

Sex hormones might be viewed as biomarkers for cardiovascular health status, as well as protective agents against heart diseases. Coronary artery disease (CAD) is the most common disease in humans and has a complex etiology. In this study, we aimed to investigate the association of CAD with ESR1 PvuII and XbaI gene mutation frequencies and to see if it's important as a genetic risk factor and the susceptibility for CAD in Tanta region, Egypt. By polymerase chain reaction with restriction fragment length polymorphism (PCR- RFLP), we determined the frequency of the ESR1 gene polymorphisms in 110 healthy and 100 CAD sample. Results revealed that there were no significant differences between CAD patients and the control group as regard the frequency AA, AG and GG of XbaI genotype. PvuII genotype frequencies were TT, TC and CC with no significant value. Regarding allele frequencies of PvuII and XbaI polymorphism, they were not statistically important. There was no significant difference among all studied subjects regarding sex, age, menopausal status, cardiac complications and lipid profile, but there was highly significant differences regarding the body mass index. In conclusion, estrogen receptor alpha gene polymorphism Pvu II and XbaI site are not associated with the coronary artery disease.

Keywords

References

[1]  M. Ezzati, M., Lopez, A.D., Rodgers, A., Vander, S. H., Murray, C.J. Comparative Risk Assessment Collaborating Group. Selected major risk factors and global and regional burden of disease. Lancet; 360: 1347-60, 2002.
 
[2]  Gupta, R., Joshi, P., Mohan, V., Reddy, S.K., and Yusuf. S. Global burden of cardiovascular disease. Epidemiology and causation of coronary heart disease and stroke in India. Heart; 94: 16-26, 2008.
 
[3]  Deschamps, A.M. & Murphy, E. (2009). Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female rats. American Journal of Physiology. Heart and Circulatory Physiology. Vol. 297, No. 5 pp. 1806-1813. Deschamps, A.M., Murphy, E. & Sun, J. (2010). Estrogen receptor activation and cardioprotection in ischemia reperfusion injury. Trends in Cardiovascular Medicine, Vol. 20, No. 3, pp. 73-78.
 
[4]  Malkin CJ, Channer KS & Jones TH. (2010). Testosterone and heart failure. Current Opinion in Endocrinology, diabetes, and obesity, Vol. 17, No. 3, pp. 262-268.
 
[5]  Karadağ B, Guven M, Hacıoğlu Y, Oz E, Batar B, Domanic N et al. Relationship bet w een two estrogen receptor-α gene polymorphisms and angiographic coronary artery disease. Anadolu Kardiyol Derg 2009; 9: 267-72.
 
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[6]  Tschugguel W, Schneeberger C, et al. Production and actions of estrogens. N Engl J Med. 2002;346:340-352. 5. Mendelsohn ME. Genomic and nongenomic effects of estrogen in the vasculature. Am J Cardiol. 2002; 90:3F-6F.
 
[7]  Hodgin JB, Krege JH, Reddick RL, et al. Estrogen receptor alpha is a major mediator of 17beta-estradiol’s atheroprotective effects on lesion size in Apoe-/- mice. J Clin Invest. 2001;107:333-340.
 
[8]  Sasaki M, Tanaka Y, Sakuragi N, Dahiya R. Six polymorphisms on estrogen receptor 1 gene in Japanese, American and Germanpopulations. Eur J Clin Pharmacol 2003; 59: 389-93.
 
[9]  Mansur ADP, Nogueira CCM, Strunz CMC, Aldrighi JM, Ramires JAF. Genetic polymorphisms of estrogen receptors in patients with premature coronary artery disease. Arch Med Res 2005; 36: 511-7.
 
[10]  Jian WX, Yang YJ, Long JR, Li YN, Deng FY, Jiang DK et al. Estrogen receptor α gene relationship with peak bone mass and body mass index in Chinese nuclear families. J Hum Genet 2005; 50: 477-82.
 
[11]  Senti M et al. Qualitative assessment of previous evidence and an updated meta-analysis confi rms lack of association betweenthe ESR1 rs2234693 (PvuII) variant and coronary heart diseasein men and women. Atherosclerosis 2009; 207: 480-6.
 
[12]  Almeida S, Hutz MH. Estrogen receptor 1 gene polymorphisms and coronary artery disease in the Brazilian population. Braz J Med Biol Res 2009; 39: 447-54.
 
[13]  Rokach A, Pollak A , Rosen L, Friedlander Y, Blumenfeld A, Reznik L et al. Estrogen receptor α gene polymorphisms are associated with the angiographic extent of coronary artery disease. J Clin Endocrinol Metab 2005; 90: 6556-60.
 
[14]  Alevizaki M, Saltiki K, Cimponeriu A, Kanakakis I, Xita N, Alevizaki CC et al. Severity of cardiovascular disease in postmenopausal women: associations with common estrogen receptor α polymorphic variants. Eur J Endocrinol 2007; 156: 489-96.
 
[15]  Lu H, Higashikata T, Inazu A, Nohara A, Yu WX, Shimizu M et al. Association of estrogen receptor-α gene polymorphismswith coronary artery disease in patients with familialhyper cholesterolemia. Arterioscler Th romb Vasc Biol 2002; 22:817-23.
 
[16]  Gensini GG. A more meaningful scoring system for determining the severity of the coronary heart disease. Am J Cardiol 1983; 51: 606.
 
[17]  Molvarec A, Széplaki G, Kovács M, et al. Estrogen receptor alpha (ESR1) PvuII and XbaI gene polymorphisms in ischemic stroke in a Hungarian population. Clin Chim Acta. 2007;382:100-105.
 
[18]  Liping Ding, Lihua Hu , Zhitao Jin , Taohong Hu, Huili Ma, et al. A meta-analysis of correlation of ER gene polymorphisms and risk in Chinese population with coronary heart disease. Life Science Journal 2013;10 (4).
 
[19]  Jin LZ, Chen YC, Ma YD.Association of estrogen receptor α gene Pvu II and XbaI polymorphisms with coronary artery disease. CHINESE JOURNAL OF BIOMEDICALENGINEERING 2010; 16: 136-9.
 
[20]  Abdussemet HAZAR, Fuat DİLMEÇ, Aydemir KOÇARSLAN, Mustafa GÖZ, et al. Th e ESR1 gene polymorphisms in patients with coronary artery disease in the southeastern Turkish population. Turk J Med Sci 2012; 42 (6): 1050-1057.
 
[21]  Xu HY, Hou XW, Wang NF, Hui B, Jin JF, Yun S et al. Gender-specific effect of estrogen receptor-1 gene polymorphisms in coronary artery disease and its angiographic severity in Chinese population. Clin Chim Acta 2008; 395: 130-3.
 
[22]  Boroumand M, Ghaedi M, Mohammadtaghvaei N, Pourgholi L, Anvari MS, Davoodi G et al. Lipid profi le and infl amatory markers associated with estrogen receptor α PvuII and XbaI gene polymorphisms. Transl Res 2009; 153: 288-95.
 
[23]  Lluis-Ganella C, Lucas G, Subirana I, Escurriol V, Tomas M, Senti M et al. Qualitative assessment of previous evidence and an updated meta-analysis confi rms lack of association between the ESR1 rs2234693 (PvuII) variant and coronary heart disease in men and women. Atherosclerosis 2009; 207: 480-6.
 
[24]  Alevizaki M, Saltiki K, Cimponeriu A, Kanakakis I, Xita N, Alevizaki CC et al. Severity of cardiovascular disease in postmenopausal women: associations with common estrogen receptor α polymorphic variants. Eur J Endocrinol 2007; 156: 489-96.
 
[25]  Karadağ B, Güven M, Hacıoğlu Y, Öz E, Batar B, Domaniç N et al. Relationship between two estrogen receptor-α gene polymorphisms and angiographic coronary artery disease. Anadolu Kardiyol Derg 2009; 9: 267-72.
 
Show Less References

Article

Risk Factor of Frequent Relapse in Pediatric Nephrotic Syndrome

1Department of Child Health, Faculty of Medicine, Universitas Padjadjaran, Dr. Hasan Sadikin General Hospital, Bandung, Indonesia


American Journal of Medical and Biological Research. 2016, 4(1), 10-12
doi: 10.12691/ajmbr-4-1-3
Copyright © 2016 Science and Education Publishing

Cite this paper:
Desman Situmorang, Nanan Sekarwana, Eddy Fadlyana. Risk Factor of Frequent Relapse in Pediatric Nephrotic Syndrome. American Journal of Medical and Biological Research. 2016; 4(1):10-12. doi: 10.12691/ajmbr-4-1-3.

Correspondence to: Desman  Situmorang, Department of Child Health, Faculty of Medicine, Universitas Padjadjaran, Dr. Hasan Sadikin General Hospital, Bandung, Indonesia. Email: dman2912@gmail.com

Abstract

Background. Nephrotic syndrome (NS) is a kidney disease with high incidence. Although steroids therapy produces a good outcome with remission (80−95%), but the relapse rates are also high (60-90%). Relapsed NS patients experienced a long period treatment and become dependent on steroids, which might cause side effects such as short stature, overweight, osteoporosis, and cardiovascular disease. Some risk factors of relapse are age, late remission, first relapsed ≤6 months after remission, and short initial therapy. Study design. A cross-sectional study with retrospective data collection from medical record of patients with frequent and infrequent relapse nephrotic syndrome from January 2010 to December 2014. There were 90 patients which were divided in two groups, 45 frequent relapse and 45 infrequent relapse. Statistical analysis used bivariate and multivariate risk factor. Result. Boys:girls ratio was 4.6:1, with median age is 5 years and 5 month (65 months). From bivariate analysis, the first diagnosis ≤5 years (p<0.001) and time on remission ≤6 month (p<0.001) were the risk factor of frequent relapse. Multivariate analysis showed time on remission ≤6 month (OR 37.113, CI 95% (7.115−193.595)) more significant than the age at diagnosis ≤5 years (OR 8.0 CI 95% (2.402−26.645)) upon frequent relapse nephrotic syndrome. Conclusion. Time on remission ≤6 month and the age at diagnosis of NS ≤5 years were risk factor of frequent relapse in nephrotic syndrome patients.

Keywords

References

[1]  Bagga A, Mantan M. Nephrotic syndrome in children. Indian J Med Res. 2005; 122(1):13-28.
 
[2]  Roth KS, Amaker BH, Chan JCM. Nephrotic syndrome: Pathogenesis and management. Pediatr Rev. 2002;23(7):237-48.
 
[3]  Konsensus tata laksana sindrom nefrotik idiopatik pada anak. 2nd Edition. Jakarta: UKK Nefrologi IDAI; 2008.
 
[4]  Pais P, Avner ED. Nephrotic syndrome. In: Kliegman RM, Stanton BF, III JWSG, Shor NF, Editor. Nelson textbook of pediatrics. 19th Edition. Philadelphia: Elsevier; 2011. p. 6483-8.
 
[5]  Teeninga N, Holthe JEK-v, Rijswijk Nv, Mos NId, Hop WCJ, Wetzels JFM, et al. Extending prednisolone treatment does not reduce relapses in childhood nephrotic syndrome. J Am Soc Nephrol. 2013;24:149-59.
 
Show More References
[6]  Sarker MN, Islam MMSU, Saad T, Shoma FN, Sharmin LS, Khan HA, et al. Risk factor for relapse in childhood nephrotic syndrome - a hospital based retrospective study. Faridpur Med Coll J. 2012;7(1):18-22.
 
[7]  ISKDC. Early identification of frequent relapsers among children with minimal change nephrotic syndrome. A report of the international study of kidney disease in children. J Pediatr. 1982;101(4):514-8.
 
[8]  Salloum AAA, Muthanna A, Bassrawi R, Shehab AAA, Ibrahim AA, Islam MZ, et al. Long-term outcome of the difficult nephrotic syndrome in children. Saudi J Kidney Dis Transpl. 2012;23(5):965-72.
 
[9]  Niaudet P. Long-term outcome of children with steroid-sensitive idiopathic nephrotic syndrome. Clin J Am Soc Nephrol. 2009;4:1547-8.
 
[10]  Liu D, Ahmet A, Ward L, Krishnamoorthy P, Mandelcorn ED, Leigh R, et al. A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy, asthma & clinical immunology. 2013;9(30):1-25.
 
[11]  Garniasih D, Djais JTB, Garna H. Hubungan antara kadar albumin dan kalsium serum pada sindrom nefrotik anak. Sari Pediatri. 2008;10(2):100-5.
 
[12]  Niaudet P, Boyer O. Idiopathic nephrotic syndrome in children: Clinical aspects. In: Avner E, Harmon W, Niaudet P, Yoshikawa N, editor. Pediatric nephrology. Edisi ke-6. Berlin: Springer; 2009. hlm. 667-702.
 
[13]  Uwaezuoke SN. Steroid-sensitive nephrotic syndrome in children: Triggers of relapse and evolving hypotheses on pathogenesis. Italian Journ of Ped. 2015;41(19):1-6.
 
[14]  Constantinescu AR, Shah HB, Foote EF, Weiss LS. Predicting first-year relapses in children with nephrotic syndrome. Pediatrics. 2000;105:492-5.
 
[15]  Shin HK, Kim JH, Yoo KH, Hong YS, Lee JW, Kim SK. Risk factor for the first-year relapse in children with nephrotic syndorome. J Korean Pediatr Soc. 2003;46:889-92.
 
[16]  Meyers KEC, Kajubu DA, Kaplan BS. Minimal-change nephrotic syndrome. In: Neilson EG, Couser WG, editor. Immunologic renal disease. Edisi. Philadelphia: Lippincot-Raven; 1997. hlm. 975-92.
 
[17]  Sureshkumar P, Hodson EM, Willis NS, Barzi F, Craig JC. Predictors of remission and relapse in idiopathic nephrotic syndrome: A prospective cohort study. Pediatr Nephrol. 2014;29:1039-46.
 
[18]  Takeda A, Matsutani H, Niimura F, Ohgushi H. Risk factors for relapse in childhood nephrotic syndrome. Pediatr Nephrol. 1996;10:740-1.
 
Show Less References

Article

Characterization of Pollen Specific Proteins SF3 and SF21 from Sunflower (Helianthus annuus L.) for the Allergenicity Potential

1Department of Science and Laboratory Technology, Dar es Salaam Institute of Technology, P. O. Box 2958, Dar es Salaam, Tanzania


American Journal of Medical and Biological Research. 2016, 4(2), 13-19
doi: 10.12691/ajmbr-4-2-1
Copyright © 2016 Science and Education Publishing

Cite this paper:
Ezekiel Amri. Characterization of Pollen Specific Proteins SF3 and SF21 from Sunflower (Helianthus annuus L.) for the Allergenicity Potential. American Journal of Medical and Biological Research. 2016; 4(2):13-19. doi: 10.12691/ajmbr-4-2-1.

Correspondence to: Ezekiel  Amri, Department of Science and Laboratory Technology, Dar es Salaam Institute of Technology, P. O. Box 2958, Dar es Salaam, Tanzania. Email: ezekielamri@yahoo.com

Abstract

Pollen from different type of plants carry different proteins that are more likely to become allergenic than others. In this study pollen specific proteins SF3 and SF21 from Sunflower (Helianthus annuus) were in-silico characterized for allergenicity potential. Bioinformatics allergen prediction tools were employed for prediction of SF3 and SF21 as candidate allergens. The phylogenetic relationship between the pollen specific proteins and protein allergens of Asteraceae family was also analyzed to unveil their similarity. The results by Bepipred Linear Epitope prediction demonstrated a good number of epitopes in pollen specific protein SF3 and SF21 signifying that both are potential allergens. However, further analysis through ConSurf revealed the presence of allergen-specific patches with remarkably higher proportion of surface-exposed hydrophobic residue in SF3 than SF21. Further prediction by AlgPred and ProAp methods with Support Vector Machines (SVMs) revealed that only SF3 contained IgE epitope thus confirming it as a potential allergen. The phylogenetic analysis revealed a close identity of SF3 with the major allergen of Ambrosia artemisiifolia pollen, Amb a 3. The study has demonstrated high allergenic activity of SF3 protein with shared similarity with the pollen protein allergens of Asteraceae family. This study forms a basis in predicting cross-reactivity of pollen specific proteins, designing of therapeutic procedures and evaluating the allergenic potential of novel proteins.

Keywords

References

[1]  Furmonaviciene, R., Sutton, B. J., Glaser, F., Laughton, C. A., Jones, N., Sewell, H. F., and Shakib, F. (2005). An attempt to define allergen-specific molecular surface features: a bioinformatic approach. Bioinformatics, 21(23): 4201-4204.
 
[2]  Songnuan, W. (2013). Wind-pollination and the roles of pollen allergenic proteins. Asian Pac J Allergy Immunol, 31:261-270.
 
[3]  Radauer, C. and Breiteneder, H. (2006). Pollen allergens are restricted to few protein families and show distinct patterns of species distribution. Journal of Allergy and Clinical Immunology, 117(1): 141-147.
 
[4]  Skjoth, C.A., Sommer, J., Stach, A., Smith, M., Brandt, J. (2007). The long-range transport of birch (Betula) pollen from Poland and Germany causes significant pre-season concentrations in Denmark. Clin Exp Allergy, 37:1204-1212.
 
[5]  Taketomi, E.A., Sopelete, M.C., Moreira, P.F.D.S. and Vieira, F.D.A.M. (2006). Pollen allergic disease: pollens and its major allergens. Revista Brasileira de Otorrinolaringologia, 72(4): 562-567.
 
Show More References
[6]  Bousquet, P.J., Bachert, C., Canonica, G.W., Casale, T.B., Mullol, J., Klossek, J.M., Zuberbier, T., and Bousquet, J. (2010) Uncontrolled allergic rhinitis during treatment and its impact on quality of life: acluster randomized trial. J Allergy Clin Immunol 126(3): 666-668.
 
[7]  Asam, C., Hofer, H., Wolf, M., Aglas, L., and Wallner, M. (2015). Tree pollen allergens—an update from a molecular perspective. Allergy, 70(10): 1201-1211.
 
[8]  Baltz, R., Schmit, A.-C., Kohnen, M., Hentges, F. and Steinmetz, A. (1999). Differential localization of the LIM domain protein PLIM-1 in microspores and mature pollen grains from sunflower, Sex. Plant Reprod., 12: 60-65.
 
[9]  Kräuter-Canham, R., Bronner, R., and Steinmetz, A. (2001). SF21 is a protein which exhibits a dual nuclear and cytoplasmic localization in developing pistils of sunflower and tobacco. Annals of Botany, 87(2): 241-249.
 
[10]  Lundberg, J. (2009). Asteraceae and relationships within Asterales. Systematics, evolution, and biogeography of Compositae, 157-169.
 
[11]  Gasteiger E., Hoogland C., Gattiker A., Duvaud S., Wilkins M.R., Appel R.D., Bairoch A. (2005). Protein Identification and Analysis Tools on the ExPASy Server; (In) John M. Walker (ed): The Proteomics Protocols Handbook, Humana Press. pp. 571-607
 
[12]  Larsen, J.E.P., Lund, O. and Nielsen, M. (2006). Improved method for predicting linear B-cell epitopes. Immunome research, 2(1): 1.
 
[13]  Berezin, C., Glaser, F., Rosenberg, J., Paz, I., Pupko, T., Fariselli, P and Ben-Tal, N. (2004). ConSeq: the identification of functionally and structurally important residues in protein sequences. Bioinformatics, 20(8): 1322-1324.
 
[14]  Saha, S., Raghava ,G.V (2006). AlgPred: prediction of allergenic proteins and mapping of IgE epitopes. Nucleic Acids Research 34(2):W202-W209
 
[15]  Wang, J., Yu, Y., Zhao, Y., Zhang, D., and Li, J. (2013). Evaluation and integration of existing methods for computational prediction of allergens. BMC bioinformatics, 14(Suppl 4), S1.
 
[16]  Singh, S., Taneja, B., Salvi, S. S., and Agrawal, A. (2009). Physical properties of intact proteins may predict allergenicity or lack thereof. PloS one, 4(7): e6273.
 
[17]  Shakushiro, K., Yamasaki, Y., Nishikawa, M. and Takakura, Y. (2004). Efficient scavenger receptor-mediated uptake and cross-presentation of negatively charged soluble antigens by dendritic cells. Immunology 112: 211-218.
 
[18]  Bowyer, P., Fraczek, M., and Denning, D.W. (2006). Comparative genomics of fungal allergens and epitopes shows widespread distribution of closely related allergen and epitope orthologues. BMC genomics, 7(1): 251.
 
[19]  Pomés, A. (2009). Relevant B cell epitopes in allergic disease. International archives of allergy and immunology, 152(1): 1-11
 
[20]  Meno, K. H. (2011). Allergen structures and epitopes. Allergy, 66(95):19-21.
 
[21]  Seong, S.Y. and Matzinger, P. (2004) Hydrophobicity: an ancient damage-associated molecular pattern that initiates innate immune responses. Nat. Rev. Immunol., 4:469-478.
 
[22]  Glaser, A. G., Menz, G., Kirsch, A. I., Zeller, S., Crameri, R., and Rhyner, C. (2008). Auto‐and cross‐reactivity to thioredoxin allergens in allergic bronchopulmonary aspergillosis. Allergy, 63(12): 1617-1623.
 
[23]  Oezguen, N., Zhou, B., Negi, S.S., Ivanciuc, O., Schein, C.H., Labesse, G., and Braun, W. (2008). Comprehensive 3D-modeling of allergenic proteins and amino acid composition of potential conformational IgE epitopes. Molecular immunology, 45(14): 3740-3747.
 
[24]  Kumar, H.G.A. and Venkatesh, Y.P. (2014). In silico analyses of structural and allergenicity features of sapodilla (Manilkara zapota) acidic thaumatin-like protein in comparison with allergenic plant TLPs. Molecular immunology, 57(2): 119-128.
 
[25]  Sharma, R., Singh, A.K., and Umashankar, V. (2009). Characterization of allergenic epitopes of Ory s1 protein from Oryza sativa and its homologs. Bioinformation, 4(1): 12-18.
 
[26]  Huby, R.D., Dearman, R.J., and Kimber, I. (2000). Why are some proteins allergens?. Toxicol. Sci., 55:235-246.
 
[27]  Umetsu, D. T., Akbari, O., DeKruyff, R.H., Shearer, W.T., Rosenwasser, L. J., and Bochner, B.S. (2003). Regulatory T cells control the development of allergic disease and asthma. Journal of Allergy and Clinical Immunology, 112(3): 480-487.
 
[28]  Dimitrov, I., Naneva, L., Doytchinova, I., and Bangov, I. (2014). AllergenFP: allergenicity prediction by descriptor fingerprints. Bioinformatics, 30(6): 846-851.
 
[29]  FAO/WHO, (2003): Evaluation of allergenicity of Genetically Modified Foods. Report of a Joint FAO/WHO Expert Consultation on Allergenicity of Foods Derived from Biotechnology, Rome.
 
[30]  Pichler, U., Hauser, M., Wolf, M., Bernardi, M. L., Gadermaier, G., Weiss, R. and Rafaiani, C. (2015). Pectate lyase pollen allergens: sensitization profiles and cross-reactivity pattern. PloS one, 10(5): e0120038.
 
[31]  Vieths, S., Scheurer, S., and BALLMER‐WEBER, B.A. (2002). Current understanding of cross‐reactivity of food allergens and pollen. Annals of the New York Academy of Sciences, 964(1): 47-68.
 
[32]  Ribeiro, H., Oliveira, M., Ribeiro, N., Cruz, A., Ferreira, A., Machado, H. and Abreu, I. (2009). Pollen allergenic potential nature of some trees species: A multidisciplinary approach using aerobiological, immunochemical and hospital admissions data. Environmental research, 109(3): 328-333.
 
Show Less References