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4. MAOB rs3027452 Modifies Mood Improvement After Tryptophan Supplementation

Author

Gonzalez I, Polvillo R, Ruiz-Galdon M, Reyes-Engel A, and Royo JL

Subjects
tryptophan, serotonin, 5-ht, mood, pharmacogenetics, monoamine oxidase, Medicine (General), R5-920
Abstract

Irene Gonzalez,1 Rocio Polvillo,1,2 Maximiliano Ruiz-Galdon,1 Armando Reyes-Engel,1 Jose Luis Royo1 1Department of Surgery, Biochemistry and Immunology School of Medicine, University of Malaga, Malaga, Spain; 2Centro Andaluz de Biología del Desarrollo, Seville, 41013, SpainCorrespondence: Armando Reyes-Engel; Jose Luis Royo Tel +34 952131531; +34 952136655Email engel@uma.es; jlroyo@uma.esPurpose: Tryptophan is the only precursor of serotonin, the hormone which helps regulate key human functions such as appetite, memory, mood, and sexual behavior. Connections have been identified between serotonin system dysfunction and the molecular etiology and treatment of mood disorders in a wide range of studies. Proposals have been put forward to co-administer tryptophan supplementation together with serotonin reuptake inhibitors in major depression patients, and also to exploit the sub-therapeutic depressive status in healthy populations. The reported responses, however, have been very dissimilar and this uneven effect may largely be explained by interindividual genetic differences.Materials and Methods: We studied mood change in 138 healthy subjects using both Goldberg’s General Health Questionnaire and the Profile of Mood States Questionnaire to determine the effects of a daily supplementation of 1g of tryptophan or placebo. Buccal DNA samples were provided and TPH1 (rs1800532), MAOA (rs3788862 and rs979605), MAOB (rs3027452), and COMT (rs6269 and rs4680) variants were genotyped.Results: MAOB rs3027452 was equally associated with tryptophan supplementation efficacy in the depression subscales of both questionnaires (ΔT-Score.D; ΔT-Score.TMD and ΔPOMS.D p-values < 0.01).Conclusion: Here we provide evidence that tryptophan supplementation has an uneven effect on mood improvement in the general population.Keywords: tryptophan, serotonin, 5-HT, mood, pharmacogenetics, monoamine oxidase

Published
2021

7. A Functional Pipeline of Genome-Wide Association Data Leads to Midostaurin as a Repurposed Drug for Alzheimer’s Disease

Author

Esteban-Martos, Alvaro, primary, Brokate-Llanos, Ana Maria, additional, Real, Luis Miguel, additional, Melgar-Locatelli, Sonia, additional, de Rojas, Itziar, additional, Castro-Zavala, Adriana, additional, Bravo, Maria Jose, additional, Mañas-Padilla, Maria del Carmen, additional, García-González, Pablo, additional, Ruiz-Galdon, Maximiliano, additional, Pacheco-Sánchez, Beatriz, additional, Polvillo, Rocío, additional, Rodriguez de Fonseca, Fernando, additional, González, Irene, additional, Castilla-Ortega, Estela, additional, Muñoz, Manuel J., additional, Rivera, Patricia, additional, Reyes-Engel, Armando, additional, Ruiz, Agustin, additional, and Royo, Jose Luis, additional

Published
2023
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8. Monoamino oxidase alleles correlate with the presence of essential hypertension among hypogonadic patients

Author

José Luis Royo, Daniel Castellano‐Castillo, Maximiliano Ruiz‐Galdon, María Molina‐Vega, Fernando Cardona, Francisco J. Tinahones, José C. Fernández‐García, and Armando Reyes‐Engel

Subjects
hypertension, hypogonadism, MAOA, MAOB, Genetics, QH426-470
Abstract

Abstract Background Monoamine oxidase (MAO) activity has been traditionally implicated in blood pressure through its effects on biogenic amine levels such as catecholamines, serotonin, and dopamine. Nowadays, this role is considered relegated to side‐effects such as orthostatic hypotension and/or hypertensive crisis derived from MAO‐inhibitory treatments in patients with psychiatric disease. Methods In the present work we have found an association between a polymorphic variant of MAOB gene and arterial hypertension in obese hypogonadic patients. The study cases comprised a series of 219 nondiabetic males with a body mass index ≥30 kg/m2 and aged

Published
2020
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9. Moderate exercise reveals the influence of ACTN3 R577X and ACE I/D polymorphisms on physical performance in non-athlete active subjects

Author

Alvero-Cruz, Jose Ramón, primary, Alarcón-Martín, Emilio, additional, García-Romero, Jerónimo, additional, Ruiz-Galdon, Maximiliano, additional, Carrillo-Albornoz-Gil, Margarita, additional, Polvillo, Rocío, additional, González, Irene, additional, Reyes-Engel, Armando, additional, and Royo, José Luis, additional

Published
2023
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10. Profiling the Influence of Gene Variants Related to Folate-Mediated One-Carbon Metabolism on the Outcome of In Vitro Fertilization (IVF) with Donor Oocytes in Recipients Receiving Folic Acid Fortification

Author

Rodriguez-Wallberg, Arturo Reyes Palomares, Maximiliano Ruiz-Galdon, Kui Liu, Armando Reyes-Engel, and Kenny A.

Subjects
one-carbon metabolism, IVF, ART, embryo viability, folic acid, MTHFR, ABCB1, BHMT, SHMT1, gene polymorphism, oocyte donation
Abstract

Nutritional status and gene polymorphisms of one-carbon metabolism confer a well-known interaction that in pregnant women may affect embryo viability and the health of the newborn. Folate metabolism directly impacts nucleotide synthesis and methylation, which is of increasing interest in the reproductive medicine field. Studies assessing the genetic influence of folate metabolism on IVF treatments have currently been performed in women using their own oocytes. Most of these patients seeking to have a child or undergoing IVF treatments are advised to preventively intake folate supplies that restore known metabolic imbalances, but the treatments could lead to the promotion of specific enzymes in specific women, depending on their genetic variance. In the present study, we assess the influence of candidate gene variants related to folate metabolism, such as Serine Hydroxymethyltransferase 1 SHMT1 (rs1979276 and rs1979277), Betaine-Homocysteine S-Methyltransferase BHMT (rs3733890), Methionine synthase reductase MTRR (rs1801394), Methylenetetrahydrofolate reductase MTHFR (rs1801131 and rs1801133), methionine synthase MTR (rs12749581), ATP Binding Cassette Subfamily B Member 1 ABCB1 (rs1045642) and folate receptor alpha FOLR1 (rs2071010) on the success of IVF treatment performed in women being recipients of donated oocytes. The implication of such gene variants seems to have no direct impact on pregnancy consecution after IVF; however, several gene variants could influence pregnancy loss events or pregnancy maintenance, as consequence of folic acid fortification.

Published
2022
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11. Profiling the Influence of Gene Variants Related to Folate-Mediated One-Carbon Metabolism on the Outcome of In Vitro Fertilization (IVF) with Donor Oocytes in Recipients Receiving Folic Acid Fortification

Author

Palomares, Arturo Reyes, Ruiz-Galdon, Maximiliano, Liu, Kui, Reyes-Engel, Armando, and Rodriguez-Wallberg, Kenny A

Subjects
gene polymorphism, Genotype, BHMT, Fertilization in Vitro, 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase, Polymorphism, Single Nucleotide, folic acid, Adenosine Triphosphate, Pregnancy, Humans, Folate Receptor 1, Methylenetetrahydrofolate Reductase (NADPH2), Glycine Hydroxymethyltransferase, Nucleotides, ABCB1, one-carbon metabolism, SHMT1, Carbon, Ferredoxin-NADP Reductase, Betaine-Homocysteine S-Methyltransferase, IVF, MTHFR, oocyte donation, Oocytes, embryo viability, Female, ART
Abstract

Nutritional status and gene polymorphisms of one-carbon metabolism confer a well-known interaction that in pregnant women may affect embryo viability and the health of the newborn. Folate metabolism directly impacts nucleotide synthesis and methylation, which is of increasing interest in the reproductive medicine field. Studies assessing the genetic influence of folate metabolism on IVF treatments have currently been performed in women using their own oocytes. Most of these patients seeking to have a child or undergoing IVF treatments are advised to preventively intake folate supplies that restore known metabolic imbalances, but the treatments could lead to the promotion of specific enzymes in specific women, depending on their genetic variance. In the present study, we assess the influence of candidate gene variants related to folate metabolism, such as Serine Hydroxymethyltransferase 1 SHMT1 (rs1979276 and rs1979277), Betaine-Homocysteine S-Methyltransferase BHMT (rs3733890), Methionine synthase reductase MTRR (rs1801394), Methylenetetrahydrofolate reductase MTHFR (rs1801131 and rs1801133), methionine synthase MTR (rs12749581), ATP Binding Cassette Subfamily B Member 1 ABCB1 (rs1045642) and folate receptor alpha FOLR1 (rs2071010) on the success of IVF treatment performed in women being recipients of donated oocytes. The implication of such gene variants seems to have no direct impact on pregnancy consecution after IVF; however, several gene variants could influence pregnancy loss events or pregnancy maintenance, as consequence of folic acid fortification.

Published
2022

12. Profiling the Influence of Gene Variants Related to Folate-Mediated One-Carbon Metabolism on the Outcome of In Vitro Fertilization (IVF) with Donor Oocytes in Recipients Receiving Folic Acid Fortification

Author

Arturo Reyes, Palomares, Maximiliano, Ruiz-Galdon, Kui, Liu, Armando, Reyes-Engel, and Kenny A, Rodriguez-Wallberg

Subjects
Glycine Hydroxymethyltransferase, Genotype, Nucleotides, Fertilization in Vitro, 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase, Polymorphism, Single Nucleotide, Carbon, Ferredoxin-NADP Reductase, Adenosine Triphosphate, Folic Acid, Betaine-Homocysteine S-Methyltransferase, Pregnancy, Oocytes, Humans, Female, Folate Receptor 1, Methylenetetrahydrofolate Reductase (NADPH2)
Abstract

Nutritional status and gene polymorphisms of one-carbon metabolism confer a well-known interaction that in pregnant women may affect embryo viability and the health of the newborn. Folate metabolism directly impacts nucleotide synthesis and methylation, which is of increasing interest in the reproductive medicine field. Studies assessing the genetic influence of folate metabolism on IVF treatments have currently been performed in women using their own oocytes. Most of these patients seeking to have a child or undergoing IVF treatments are advised to preventively intake folate supplies that restore known metabolic imbalances, but the treatments could lead to the promotion of specific enzymes in specific women, depending on their genetic variance. In the present study, we assess the influence of candidate gene variants related to folate metabolism, such as Serine Hydroxymethyltransferase 1

Published
2022

17. Moderate exercise reveals the influence of ACTN3 R577X and ACE I/D polymorphisms on physical performance in non-athlete active subjects

Author

Jose Ramón Alvero-Cruz, Emilio Alarcón-Martín, Jerónimo García-Romero, Maximiliano Ruiz-Galdon, Margarita Carrillo-Albornoz-Gil, Rocío Polvillo, Irene González, Armando Reyes-Engel, and José Luis Royo

Subjects
Polymorphism, Genetic, Genotype, Genetics, Humans, Actinin, General Medicine, Peptidyl-Dipeptidase A, Physical Functional Performance, Exercise
Abstract

Genome variations contribute to the vast majority of interindividual differences and may decisively influence sports capability. This study was conceived as a means of finding out when exactly polymorphisms start being physically discriminative. The polymorphisms we studied were two of the best characterized ones: ACE I/D and ACTN3 R577X. These germline variants were determined in a cohort of 200 healthy volunteers from the university environment who underwent a series of physical evaluations that included a Cooper test, a 20-meter sprint test and a vertical jump test. Initially, no statistical association was found because the genetic effect was masked by those subjects with sedentary lifestyles. But when only physically active volunteers were considered, the ACE and ACTN3 genotypes were found to have an impact on heart rate after the Cooper test (p-value = 0.033 and 0.032 respectively) and ACTN3 was found to correlate with the total distance covered in the same test (p-value = 0.051). This can therefore be considered a paradigmatic example in which the environment might hide the genetic effect, with genotypic differences arising only upon training.

Published
2023
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19. Maob rs3027452 modifies mood improvement after tryptophan supplementation

Author

Armando Reyes-Engel, Maximiliano Ruiz-Galdón, Irene Gonzalez, Jose Luis Royo, and Rocio Polvillo

Subjects
medicine.medical_specialty, Serotonin, Population, 5-HT, International Journal of General Medicine, 030204 cardiovascular system & hematology, Profile of mood states, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Mood, medicine, education, Original Research, education.field_of_study, TPH1, business.industry, Monoamine oxidase, Tryptophan, General Medicine, medicine.disease, Endocrinology, Mood disorders, Pharmacogenetics, 030220 oncology & carcinogenesis, Monoamine oxidase B, business, rs4680
Abstract

© 2021 Gonzalez et al., [Purpose]: Tryptophan is the only precursor of serotonin, the hormone which helps regulate key human functions such as appetite, memory, mood, and sexual behavior. Connections have been identified between serotonin system dysfunction and the molecular etiology and treatment of mood disorders in a wide range of studies. Proposals have been put forward to co-administer tryptophan supplementation together with serotonin reuptake inhibitors in major depression patients, and also to exploit the sub-therapeutic depressive status in healthy populations. The reported responses, however, have been very dissimilar and this uneven effect may largely be explained by interindividual genetic differences., [Materials and Methods]: We studied mood change in 138 healthy subjects using both Goldberg’s General Health Questionnaire and the Profile of Mood States Questionnaire to determine the effects of a daily supplementation of 1g of tryptophan or placebo. Buccal DNA samples were provided and TPH1 (rs1800532), MAOA (rs3788862 and rs979605), MAOB (rs3027452), and COMT (rs6269 and rs4680) variants were genotyped., [Results]: MAOB rs3027452 was equally associated with tryptophan supplementation efficacy in the depression subscales of both questionnaires (ΔT-Score.D; ΔT-Score.TMD and ΔPOMS.D p-values < 0.01)., [Conclusion]: Here we provide evidence that tryptophan supplementation has an uneven effect on mood improvement in the general population.

Published
2021

20. Influence of high homocysteine and low folate plasmatic levels in medium-term prognosis after acute coronary syndromes

Author

García-Pinilla, José Manuel, Espinosa-Caliani, Salvador, Gómez-Doblas, Juan José, Jiménez-Navarro, Manuel, Gaitán, María J., Muñoz-Morán, Encarnación, Cabrera-Bueno, Fernando, Hernández-García, José M., Ortega-Jiménez, María Victoria, Ruiz-Galdón, Maximiliano, Reyes-Engel, Armando, and de Teresa-Galván, Eduardo

Published
2007
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25. Effects of SHBG rs1799941 Polymorphism on Free Testosterone Levels and Hypogonadism Risk in Young Non-Diabetic Obese Males

Author

Jose Luis Royo, Maximiliano Ruiz-Galdón, Armando Reyes-Engel, Juan J Álvarez-Millán, María Isabel Queipo-Ortuño, José Carlos Fernández-García, Daniel Castellano-Castillo, Francisco J. Tinahones, Pablo Cabezas-Sanchez, María Molina-Vega, Lidia Sánchez-Alcoholado, Ana Martínez-Escribano, and Fernando Cardona

Subjects
medicine.medical_specialty, obesity, lcsh:Medicine, 030209 endocrinology & metabolism, 030204 cardiovascular system & hematology, Article, polymorphism, 03 medical and health sciences, 0302 clinical medicine, Sex hormone-binding globulin, Internal medicine, Genotype, medicine, hypogonadism, Allele, SHBG, rs1799941, free testosterone, Free testosterone, biology, business.industry, lcsh:R, General Medicine, medicine.disease, Obesity, Endocrinology, Increased risk, biology.protein, business, Non diabetic
Abstract

Introduction: Obesity has been associated with increased risk of presenting hypogonadism. Free testosterone (FT) is the fraction of testosterone that carries out the biological function of testosterone, and is determined from total testosterone (TT) and sex-hormone binding globulin (SHBG) levels. We aimed to study the SHBG polymorphism rs1799941 in a cohort of young non-diabetic obese males to unravel the possible implication of this polymorphism in obesity-related hypogonadism. Methodology: 212 young (&lt, 45 years) non-diabetic obese (BMI &ge, 30 kg/m2) males participated in this study. Subjects were classified according to TT and FT levels in: Eugonadal (n = 55, TT &gt, 3.5 ng/mL and FT &ge, 70 pg/mL, EuG), normal FT hypogonadism (n = 40, TT &lt, 3.5 and FT &ge, normal FT HG) and hypogonadism (n = 117, TT &lt, 3.5 ng/mL and TL &lt, HG). The SHBG rs1799941 polymorphism (GG/GA/AA) was analyzed using the Taqman Open Array (Applied biosystem). Results: The rs1799941 frequencies were different among the groups. Higher proportion of the allele (A) was found in HG, compared to EuG and normal FT HG. Among the genotypes, the rare homozygous (AA) were found in the normal FT HG group and higher levels of serum SHBG and lower of FT were observed. The presence of the allele A was related (according to lineal regression models) to an increased of SHBG levels ((GA) &beta, = 3.28, (AA) &beta, = 12.45) and a decreased of FT levels ((GA) &beta, = &minus, 9.19, 18.52). The presence of the allele (A) increased the risk of presenting HG compared to normal FT HG (OR = 2.54). Conclusions: The rs1799941 of the SHBG gene can partially determine the presence of obesity-related hypogonadism in young non-diabetic males and whether these subjects have normal FT HG.

Published
2019

26. Monoamino oxidase alleles correlate with the presence of essential hypertension among hypogonadic patients

Author

Maximiliano Ruiz-Galdón, Jose Luis Royo, Fernando Cardona, María Molina-Vega, José Carlos Fernández-García, Francisco J. Tinahones, Armando Reyes-Engel, and Daniel Castellano-Castillo

Subjects
0301 basic medicine, Adult, Male, medicine.medical_specialty, hypertension, lcsh:QH426-470, Monoamine oxidase, MAOB, Blood Pressure, 030105 genetics & heredity, Essential hypertension, Polymorphism, Single Nucleotide, Body Mass Index, 03 medical and health sciences, Orthostatic vital signs, Internal medicine, Genetics, medicine, Humans, hypogonadism, Eunuchism, Testosterone, MAOA, Allele, Molecular Biology, Monoamine Oxidase, Genetics (clinical), business.industry, Original Articles, medicine.disease, lcsh:Genetics, 030104 developmental biology, Endocrinology, Blood pressure, Original Article, Monoamine oxidase B, business, Body mass index
Abstract

Background Monoamine oxidase (MAO) activity has been traditionally implicated in blood pressure through its effects on biogenic amine levels such as catecholamines, serotonin, and dopamine. Nowadays, this role is considered relegated to side‐effects such as orthostatic hypotension and/or hypertensive crisis derived from MAO‐inhibitory treatments in patients with psychiatric disease. Methods In the present work we have found an association between a polymorphic variant of MAOB gene and arterial hypertension in obese hypogonadic patients. The study cases comprised a series of 219 nondiabetic males with a body mass index ≥30 kg/m2 and aged, Male hypogonadism is a disorder in which the testes are not functional or there is a genetic inability of the hypothalamus to secrete normal amounts of GnRH. The masculine sexual characteristics are not developed and can bring a wide range of clinical manifestations. We have found an association between a polymorphic variant of MAOB gene and arterial hypertension in obese hypogonadic patients.

Published
2019

30. Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states

Author

Jose Luis Royo, Armando Reyes-Engel, Rocio Polvillo, Maximiliano Ruiz-Galdón, and Irene Gonzalez

Subjects
Male, Emotions, Anger, Behavioral neuroscience, Synaptic Transmission, Behavioral Neuroscience, 0302 clinical medicine, Surveys and Questionnaires, mood state, Medicine, Depression (differential diagnoses), media_common, Original Research, HTR2A, education.field_of_study, 05 social sciences, Healthy Volunteers, Goldberg, Receptor, Serotonin, 5-HT1A, MAO, Anxiety, Female, Monoamine oxidase B, medicine.symptom, Clinical psychology, Adult, OPRM1, Genotype, media_common.quotation_subject, Population, Psychological Techniques, 050105 experimental psychology, 03 medical and health sciences, Sex Factors, Humans, 0501 psychology and cognitive sciences, POMS, education, Students, Monoamine Oxidase, Polymorphism, Genetic, business.industry, Mood state, Oxytocin receptor, Neurosecretory Systems, COMT, Mood, BDNF, Vesicular Monoamine Transport Proteins, SLC18A1, business, 030217 neurology & neurosurgery
Abstract

© The Author(s)., [Objective]: From an evolutionary perspective, emotions emerged as rapid adaptive reactions that increase survival rates. Current psychobiology includes the consideration that genetic changes affecting neuroendocrine and neurotransmission pathways may also be affecting mood states. Following this hypothesis, abnormal levels of any of the aminergic neurotransmitters would be of considerable importance in the development of a pathophysiological state. [Materials and Methods]: A total of 668 students from the School of Medicine of the University of Malaga (Average = 22.41 ± 3; 41% men) provided self‐report measures of mood states using POMS and GHQ‐28 questionnaires and buccal cells for genotyping 19 polymorphisms from 14 selected neurotransmitter pathways genes (HTR1A; HTR2A; HTR2C; HTR3B; TPH1; SLC18A1; SLC18A2; COMT; MAOA; MAOB) and neuroendocrine system (AVPR1B; OPRM1; BDNF; OXTR). [Results]: MAOA rs3788862 genotype correlates with decreasing levels of Tension among females (beta = −0.168, p‐value = 0.003) but it is neutral among males in this subscale. On the contrary, it correlates with lower GHQ‐28 depression scores among males (beta = −0.196, p‐value = 0.008). Equivalently, SLC18A1 and HTR2A variants correlated with anger and vigor scores, only among males. From the neuroendocrine system, OPRM1 rs1799971 correlated increasing levels of female's Anxiety, depression and Social Dysfunction scores. [Conclusion]: Our findings suggest that these polymorphisms contribute to define general population mood levels, although exhibiting a clear sexual dimorphism.

Published
2019

32. Effects of SHBG rs1799941 Polymorphism on Free Testosterone Levels and Hypogonadism Risk in Young Non-Diabetic Obese Males

Author

Castellano-Castillo, Daniel, primary, Royo, José Luis, additional, Martínez-Escribano, Ana, additional, Sánchez-Alcoholado, Lidia, additional, Molina-Vega, María, additional, Queipo-Ortuño, María Isabel, additional, Ruiz-Galdon, Maximiliano, additional, J. Álvarez-Millán, Juan, additional, Cabezas-Sanchez, Pablo, additional, Reyes-Engel, Armando, additional, Tinahones, Francisco J., additional, Cardona, Fernando, additional, and Fernandez-Garcia, José C., additional

Published
2019
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33. Genetic polymorphisms in folate pathway enzymes, DRD4 and GSTM1 are related to temporomandibular disorder

Author

Mayor-Olea Alvaro, Aguado Lidia, Perez-Nevot Beatriz, Palomares Arturo R, Lendinez Ana M, Aneiros-Guerrero Angel, Ruiz-Galdon Maximiliano, and Reyes-Engel Armando

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Temporomandibular disorder (TMD) is a multifactorial syndrome related to a critical period of human life. TMD has been associated with psychological dysfunctions, oxidative state and sexual dimorphism with coincidental occurrence along the pubertal development. In this work we study the association between TMD and genetic polymorphisms of folate metabolism, neurotransmission, oxidative and hormonal metabolism. Folate metabolism, which depends on genes variations and diet, is directly involved in genetic and epigenetic variations that can influence the changes of last growing period of development in human and the appearance of the TMD. Methods A case-control study was designed to evaluate the impact of genetic polymorphisms above described on TMD. A total of 229 individuals (69% women) were included at the study; 86 were patients with TMD and 143 were healthy control subjects. Subjects underwent to a clinical examination following the guidelines by the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD). Genotyping of 20 Single Nucleotide Polymorphisms (SNPs), divided in two groups, was performed by multiplex minisequencing preceded by multiplex PCR. Other seven genetic polymorphisms different from SNPs (deletions, insertions, tandem repeat, null genotype) were achieved by a multiplex-PCR. A chi-square test was performed to determine the differences in genotype and allelic frequencies between TMD patients and healthy subjects. To estimate TMD risk, in those polymorphisms that shown significant differences, odds ratio (OR) with a 95% of confidence interval were calculated. Results Six of the polymorphisms showed statistical associations with TMD. Four of them are related to enzymes of folates metabolism: Allele G of Serine Hydoxymethyltransferase 1 (SHMT1) rs1979277 (OR = 3.99; 95%CI 1.72, 9.25; p = 0.002), allele G of SHMT1 rs638416 (OR = 2.80; 95%CI 1.51, 5.21; p = 0.013), allele T of Methylentetrahydrofolate Dehydrogenase (MTHFD) rs2236225 (OR = 3.09; 95%CI 1.27, 7.50; p = 0.016) and allele A of Methionine Synthase Reductase (MTRR) rs1801394 (OR = 2.35; 95CI 1.10, 5.00; p = 0.037). An inflammatory oxidative stress enzyme, Gluthatione S-Tranferase Mu-1(GSTM1), null allele (OR = 2.21; 95%CI 1.24, 4.36; p = 0.030) and a neurotransmission receptor, Dopamine Receptor D4 (DRD4), long allele of 48 bp-repeat (OR = 3.62; 95%CI 0.76, 17.26; p = 0.161). Conclusions Some genetic polymorphisms related to folates metabolism, inflammatory oxidative stress, and neurotransmission responses to pain, has been significantly associated to TMD syndrome

Published
2011
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36. Human genetic selection on the MTHFR 677C>T polymorphism

Author

Rodríguez Alfonso, Gaitán María, Jiménez Ana J, Palomares Arturo R, Callejón Gonzalo, Mayor-Olea Álvaro, Ruiz Maximiliano, and Reyes-Engel Armando

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background The prevalence of genotypes of the 677C>T polymorphism for the MTHFR gene varies among humans. In previous studies, we found changes in the genotypic frequencies of this polymorphism in populations of different ages, suggesting that this could be caused by an increase in the intake of folate and multivitamins by women during the periconceptional period. The aim was to analyze changes in the allelic frequencies of this polymorphism in a Spanish population, including samples from spontaneous abortions (SA). Methods A total of 1305 subjects born in the 20th century were genotyped for the 677C>T polymorphism using allele specific real-time PCR with Taqman® probes. A section of our population (n = 276) born in 1980–1989 was compared with fetal samples (n = 344) from SA of unknown etiology from the same period. Results An increase in the frequency of the T allele (0.38 vs 0.47; p < 0.001) and of the TT genotype (0.14 vs 0.24; p < 0.001) in subjects born in the last quarter of the century was observed. In the 1980–1989 period, the results show that the frequency of the wild type genotype (CC) is about tenfold lower in the SA samples than in the controls (0.03 vs 0.33; p < 0.001) and that the frequency of the TT genotype increases in the controls (0.19 to 0.27) and in the SA samples (0.20 to 0.33 (p < 0.01)); r = 0.98. Conclusion Selection in favor of the T allele has been detected. This selection could be due to the increased fetal viability in early stages of embryonic development, as is deduced by the increase of mutants in both living and SA populations.

Published
2008
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37. Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states

Author

González, Irene, Polvillo Hernández, Rocío, Ruiz‐Galdón, Maximiliano, Reyes‐Engel, Armando, Royo, José Luis, González, Irene, Polvillo Hernández, Rocío, Ruiz‐Galdón, Maximiliano, Reyes‐Engel, Armando, and Royo, José Luis

Abstract

[Objective]: From an evolutionary perspective, emotions emerged as rapid adaptive reactions that increase survival rates. Current psychobiology includes the consideration that genetic changes affecting neuroendocrine and neurotransmission pathways may also be affecting mood states. Following this hypothesis, abnormal levels of any of the aminergic neurotransmitters would be of considerable importance in the development of a pathophysiological state. [Materials and Methods]: A total of 668 students from the School of Medicine of the University of Malaga (Average = 22.41 ± 3; 41% men) provided self‐report measures of mood states using POMS and GHQ‐28 questionnaires and buccal cells for genotyping 19 polymorphisms from 14 selected neurotransmitter pathways genes (HTR1A; HTR2A; HTR2C; HTR3B; TPH1; SLC18A1; SLC18A2; COMT; MAOA; MAOB) and neuroendocrine system (AVPR1B; OPRM1; BDNF; OXTR). [Results]: MAOA rs3788862 genotype correlates with decreasing levels of Tension among females (beta = −0.168, p‐value = 0.003) but it is neutral among males in this subscale. On the contrary, it correlates with lower GHQ‐28 depression scores among males (beta = −0.196, p‐value = 0.008). Equivalently, SLC18A1 and HTR2A variants correlated with anger and vigor scores, only among males. From the neuroendocrine system, OPRM1 rs1799971 correlated increasing levels of female's Anxiety, depression and Social Dysfunction scores. [Conclusion]: Our findings suggest that these polymorphisms contribute to define general population mood levels, although exhibiting a clear sexual dimorphism.

Published
2019

38. Direct quantification of HIV-1 RNA in human plasma by free solution capillary electrophoresis (FSCE)

Author

Fernandez-Arcas, Nieves, Dieguez-Lucena, Jose L., Garcia-Villanova, Javier, Pena, Jose, Morell-Ocana, Miguel, and Reyes-Engel, Armando

Subjects
RNA -- Measurement, HIV (Viruses) -- Reproduction, Electrophoresis -- Usage, Health
Abstract

Free solution capillary electrophoresis may be an effective alternative for measuring HIV RNA levels in blood. The technique was used on blood samples from 15 healthy volunteers and 10 people with HIV infection. Four were in the initial stage of the infection and 6 were chronically infected but asymptomatic. The 4 people with acute HIV infection had peaks on electrophoresis corresponding to HIV RNA levels of 1.08-1.71 x 10(super)8. No electrophoretic peaks were visible from samples provided by the 6 asymptomatic patients or the 15 healthy volunteers.

Published
1996

40. Sperm count and motility are quantitatively affected by functional polymorphisms of HTR2A, MAOA and SLC18A

Author

Maximiliano Ruiz-Galdón, Ana M. Lendínez, Jose-Luis Royo, Armando Reyes-Engel, Arturo Reyes-Palomares, and Miriam Cortés-Rodriguez

Subjects
0301 basic medicine, Male, endocrine system, Genotype, Rs6313, Biology, Asthenozoospermia, Male infertility, Andrology, 03 medical and health sciences, 0302 clinical medicine, Polymorphism (computer science), medicine, Humans, Receptor, Serotonin, 5-HT2A, Monoamine Oxidase, Sperm motility, 030219 obstetrics & reproductive medicine, Polymorphism, Genetic, Sperm Count, Obstetrics and Gynecology, medicine.disease, Sperm, 030104 developmental biology, Reproductive Medicine, Case-Control Studies, Vesicular Monoamine Transport Proteins, Sperm Motility, Developmental Biology, SNP array
Abstract

Spermatozoa and neurones share similar membrane characteristics and features. Associations of multiple polymorphisms traditionally related to neurotransmission were investigated. Infertile men were grouped into controls with normospermia (n = 182) and idiopathic infertile men with asthenozoospermia (n = 103), and analysed as a case-control study and as a quantitative association of each genotype. Ten neurotransmission-associated genetic variants were mapped by SNP analysis using quantitative polymerase chain reaction with TaqMan probes. Men with HTR2A rs6313 had a higher risk of asthenozoospermia (OR = 2.14; P = 0.04). MAOA rs3788862 G carriers displayed an increased risk of asthenozoospermia (OR = 2.29; P = 0.02). The SLC18A1 rs1390938 G allele was more frequent among such cases (0.75 versus 0.87; P < 0.01 and P < 0.01 for Armitage trend test); for SLC18A1 rs2270641 P = 0.02 (case-control frequency) and P = 0.01 (Armitage trend test). MAOA rs3788862 was correlated with sperm motility (Spearman ρ = 0.14; P = 0.02); SLC18A1 rs1390938 was correlated with sperm count and motility (Spearman ρ = 0.20; P < 0.01). Gene polymorphisms of HTR2A, MAOA and SLC18A1, related to neurotransmission, are individually associated with asthenozoospermia through variation in sperm count and motility, without detectable allelic or genotype interaction.

Published
2017

41. Fetal alpha 5-reductase Val89Leu mutation is associated with late miscarriage

Author

Ana M. Lendínez, Beatriz Pérez-Nevot, Armando Reyes-Engel, Jose Luis Royo, Maximiliano Ruiz-Galdón, Miriam Cortés, Ana José Jiménez, and Arturo Reyes-Palomares

Subjects
medicine.medical_specialty, Spontaneous pregnancy loss, Population, Single-nucleotide polymorphism, Miscarriage, Polymorphism, Single Nucleotide, 03 medical and health sciences, 0302 clinical medicine, Aromatase, Fetus, 3-Oxo-5-alpha-Steroid 4-Dehydrogenase, Internal medicine, medicine, CYP19A1, Humans, education, Testosterone, education.field_of_study, 030219 obstetrics & reproductive medicine, business.industry, ESR1, Case-control study, Estrogen Receptor alpha, Obstetrics and Gynecology, Membrane Proteins, Odds ratio, medicine.disease, Abortion, Spontaneous, Endocrinology, Reproductive Medicine, 030220 oncology & carcinogenesis, Dihydrotestosterone, SRD5A2, Case-Control Studies, business, Developmental Biology, medicine.drug
Abstract

The present study was undertaken to determine the role of different polymorphisms affecting the testosterone/oestrogen pathway in miscarriage. Alpha 5-reductase (SRD5A2) rs523349 and rs9282858, cytochrome P450 aromatase (CYP19A1) rs4646, rs10046 and rs2236722 and oestrogen receptor (ESR1) rs9340799, rs2234693 and rs6932902 polymorphisms were selected. The case group consisted of 94 samples of formalin-fixed and paraffin-embedded fetal tissue from a miscarriage at ≤24 weeks. The control group comprised a population of 331 young healthy subjects. Only those single nucleotide polymorphisms (SNPs) fitting the Hardy-Weinberg equilibrium (n = 4) and euploid miscarriage samples (n = 67) were included for downstream analysis. Interestingly, SRD5A2 rs523349 (Val89Leu) was significantly associated with the risk of undergoing miscarriage after Bonferroni correction (odds ratio = 11.245, P < 2.2 × 10-9). Moreover, when Mantel-Cox regression analysis was performed, we observed that the effect was significantly constrained to the second trimester (P = 0.024, log rank). These results are compatible with an imbalance of testosterone/dihydrotestosterone, associated with a higher risk of miscarriage, especially in late pregnancy.

Published
2017

44. Reproductive (epi)genetics

Author

C. Lynch, N. Tee, H. Rouse, A. Gordon, L. Sati, C. Zeiss, B. Soygur, I. Bassorgun, E. Goksu, R. Demir, J. McGrath, M. L. Groendahl, L. Thuesen, A. N. Andersen, A. Loft, J. Smitz, T. Adriaenssens, J. Vikesa, R. Borup, E. Mersy, N. Kisters, M. V. E. Macville, J. J. M. Engelen, S.-E. N. N. Consortium, P. P. C. A. Menheere, J. P. Geraedts, A. B. C. Coumans, S. G. M. Frints, T. Aledani, S. Assou, S. Traver, O. Ait-ahmed, H. Dechaud, S. Hamamah, E. Mizutani, N. Suzumori, C. Sugiyama, Y. Hattori, T. Sato, H. Ando, Y. Ozaki, M. Sugiura-Ogasawara, M. Wissing, S. G. Kristensen, C. Y. Andersen, A. L. Mikkelsen, T. Hoest, A. Velthut-Meikas, J. Simm, M. Metsis, A. Salumets, S. Palini, L. Galluzzi, S. De Stefani, M. Primiterra, D. Wells, M. Magnani, C. Bulletti, P. H. Vogt, P. Frank-Herrmann, U. Bender, T. Strowitzki, B. Besikoglu, P. Heidemann, L. Wunsch, M. Bettendorf, L. Jelinkova, S. Vilimova, M. Kosarova, P. Sebek, E. Volemanova, M. Kruzelova, J. Civisova, L. Svobodova, V. Sobotka, T. Mardesic, C. van de Werken, M. A. Santos, C. Eleveld, J. S. E. Laven, E. B. Baart, L. Y. Pylyp, L. A. Spinenko, V. D. Zukin, J. Perez-Sanz, R. Matorras, J. Arluzea, J. Bilbao, N. Gonzalez-Santiago, N. Yeh, A. Koff, A. Barlas, Y. Romin, K. Manova-Todorova, C. D. l. Hoz, A. L. Mauri, A. M. Nascimento, L. D. Vagnini, C. G. Petersen, J. Ricci, F. C. Massaro, M. Cavagna, A. Pontes, J. B. A. Oliveira, R. L. R. Baruffi, J. G. Franco, E. X. Wu, S. Ma, M. Parriego, M. Sole, M. Boada, B. Coroleu, A. Veiga, G. Kakourou, M. Poulou, C. Vrettou, A. Destouni, J. Traeger-Synodinos, E. Kanavakis, A. N. Yatsenko, A. P. Georgiadis, M. M. McGuire, M. Zorrilla, K. D. Bunce, D. Peters, A. Rajkovic, M. Olszewska, M. Kurpisz, A. Z. A. Gilbertson, C. S. Ottolini, M. C. Summers, K. Sage, A. H. Handyside, A. R. Thornhill, D. K. Griffin, M. K. Chung, J. W. Kim, J. H. Lee, H. J. Jeong, M. H. Kim, M. J. Ryu, S. J. Park, H. Y. Kang, H. S. Lee, B. Zimmermann, M. Banjevic, M. Hill, P. Lacroute, M. Dodd, S. Sigurjonsson, P. Lau, D. Prosen, N. Chopra, A. Ryan, M. Hall, S. McAdoo, Z. Demko, B. Levy, M. Rabinowitz, A. Vereczeky, Z. S. Kosa, S. Savay, M. Csenki, L. Nanassy, B. Dudas, Z. S. Domotor, D. Debreceni, A. Rossi, J. R. Alegretti, J. Cuzzi, M. Bonavita, M. Tanada, P. Matunaga, P. Fettback, M. B. Rosa, V. Maia, P. Hassun, E. L. A. Motta, M. Piccolomini, C. Gomes, B. Barros, M. Nicoliello, T. Criscuolo, E. Miyadahira, D. Montjean, M. Benkhalifa, I. Berthaut, J. F. Griveau, K. Morcel, A. Bashamboo, K. McElreavey, C. Ravel, C. Rubio, L. Rodrigo, E. Mateu, A. Mercader, V. Peinado, P. Buendia, M. Milan, A. Delgado, N. Al-Asmar, L. Escrich, I. Campos-Galindo, S. Garcia-Herrero, M. E. Poo, P. Mir, C. Simon, A. Reyes-Engel, M. Cortes-Rodriguez, A. Lendinez, B. Perez-Nevot, A. R. Palomares, M. R. Galdon, A. Ruberti, M. G. Minasi, A. Biricik, A. Colasante, D. Zavaglia, E. Iammarrone, F. Fiorentino, E. Greco, N. Demir, S. Ozturk, B. Sozen, R. Morales, B. Lledo, J. A. Ortiz, J. Ten, J. Llacer, R. Bernabeu, M. Nagayoshi, A. Tanaka, I. Tanaka, H. Kusunoki, S. Watanabe, S. G. Temel, C. Beyazyurek, G. C. Ekmekci, F. Aybar, C. Cinar, S. Kahraman, S. Nordqvist, K. Karehed, H. Akerud, M. Gultomruk, P. Tulay, N. Findikli, E. Yagmur, G. Karlikaya, U. Ulug, M. Bahceci, M. F. Bargallo, M. R. Arevalo, M. M. Salat, I. V. Barbat, J. T. Lopez, M. E. Algam, A. B. Boluda, G. C. de Oya, E. N. Tolmacheva, A. A. Kashevarova, N. A. Skryabin, I. N. Lebedev, E. Semaco, A. Belo, M. Riboldi, L. Luz, N. Nobrega, R. Mazetto, J. A. Alegretti, M. Bibancos, P. Serafini, J. Neupane, M. Vandewoestyne, B. Heindryckx, T. Deroo, Y. Lu, S. Ghimire, S. Lierman, C. Qian, D. Deforce, P. De Sutter, T. Viloria, J. M. Martinez-Jabaloyas, M. Gil-Salom, A. Capalbo, N. Treff, D. Cimadomo, X. Tao, K. Ferry, F. M. Ubaldi, L. Rienzi, R. T. Scott, N. Katzorke, H. P. Vogt, A. Hehr, C. Gassner, B. Paulmann, Z. Kowalzyk, M. Klatt, S. Krauss, D. Seifert, B. Seifert, U. Hehr, M. Lobascio, M. T. Varricchio, P. Rubino, S. Bono, R. P. Cotarelo, L. Spizzichino, A. Colicchia, P. Giannini, M. Suhorutshenko, and K. Rosenstein-Tamm

Subjects
Genetics, Reproductive Medicine, Rehabilitation, Obstetrics and Gynecology, Biology
Published
2013
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45. Changes in CDKN2D,TP53, and miR125a expression: potential role in the evaluation of human amniotic fluid-derived mesenchymal stromal cell fitness

Author

Carmen Benito, Jose Maria Miranda-Sayago, Nieves Fernández-Arcás, Antonio Alonso, Armando Reyes-Engel, and I. Narbona

Subjects
Stromal cell, Cell Survival, Cellular differentiation, Biology, Regenerative Medicine, Regenerative medicine, Cell therapy, microRNA, Cell Adhesion, Genetics, Humans, RNA, Messenger, Cyclin-Dependent Kinase Inhibitor p19, Cells, Cultured, Cell Proliferation, Oligonucleotide Array Sequence Analysis, Regulation of gene expression, Mesenchymal stem cell, Computational Biology, Cell Differentiation, Mesenchymal Stem Cells, Cell Biology, Amniotic Fluid, Embryonic stem cell, Cell biology, MicroRNAs, Gene Expression Regulation, Immunology, Tumor Suppressor Protein p53
Abstract

Human amniotic fluid-derived mesenchymal stromal cells (hAMSC) have become one of the main cell populations used in regenerative medicine and for the study of various clinical disorders. These cells have a great capacity for proliferation and differentiation and do not form teratomas when transplanted into animal models, and their stemness seems to be between embryonic cells and adult mesenchymal cells. Before their use in cell therapy, they must be cultured and expanded in vitro, but the effect this process has on their fitness, a determining factor for the success or failure of cell therapy, is unknown. We undertook a follow-up of gene and microRNAs (miRNAs) expression using microarray of hAMSC for the first 15 passages. Significant changes were noted in the expression of various mRNAs and miRNAs, particularly down-regulation of TP53, increased expression of hsa-miR-125a and up-regulation of CDKN2D . The variations in TP53 and hsa-miR-125a may act as an indicator of the stemness of the hAMSC, whereas CDKN2D may indicate the begging of early senescence process in a p53-independent mechanism. The genes described in this study will help evaluate the fitness of hAMSC, thus guaranteeing their biological quality for use in regenerative medicine.

Published
2012
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46. TRANSLATIONAL RESEARCH

Author

E. M. Rosenbluth, L. M. Wells, A. E. Sparks, B. J. Van Voorhis, A. Reyes-Palomares, A. R. Palomares, M. A. Medina, M. Ruiz Galdon, A. Reyes Engel, I. Stanghellini, D. Luiselli, M. C. Magli, M. Lang, G. Romeo, A. P. Ferraretti, L. Gianaroli, O. Gun Eryilmaz, E. Sarikaya, S. Yilmaz, A. Avci, C. Ozogul, S. Barun, M. Genc, C. Kitsou, I. Kosmas, D. Peschos, A. Euaggelou, L. Lazaros, T. Stefos, H. Tournaye, S. Prapa, N. Prapas, Y. Prapas, K. Zikopoulos, I. Georgiou, K. Loewke, F. Moussavi, M. Maddah, J. Conaghan, K. Ivani, V. Suraj, A. Chen, S. Shen, R. Dittrich, I. Hoffmann, J. Kunzel, L. Lotz, A. Mueller, C. Reissmann, T. Hildebrandt, J. Hakl, N. Unluhan, P. G. Oppelt, M. W. Beckmann, G. Huszar, N. Geerts, J. McGrath, K. Vanderlick, O. Pohl, J. P. Gotteland, E. Bestel, V. Sinai Talaulikar, and I. Manyonda

Subjects
Reproductive Medicine, Rehabilitation, Obstetrics and Gynecology
Published
2012
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47. POSTER VIEWING SESSION - EARLY PREGNANCY

Author

T. Kamijo, P. Milart, K. Wojcik, P. Szkodziak, S. Wozniak, P. Czuczwar, T. Paszkowski, H. Landolsi, M. T. Yacoubi, W. Stita, M. Gribaa, S. Hmissa, N. Molenaar, N. H. van Besouw, E. A. P. Steegers, W. Visser, P. de Kuiper, R. de Krijger, N. Exalto, R. Lagrand, S. P. Kaandorp, C. H. M. Mellink, M. van Wely, E. J. W. Redeker, A. C. Knegt, M. Goddijn, C. Vidal, J. Giles, M. Meseguer, J. L. Zuzuarregui, E. Bosch, A. Pellicer, D. Schust, M. Sugimoto, J. Sugimoto, A. D. Reus, M. D. Stephenson, R. R. Krijger de, F. M. Dunne van, C. Exacoustos, E. Vaquero, A. Di Giovanni, V. Romeo, N. Lazzarin, D. Arduini, S. Brahem, M. Mehdi, F. Atig, H. Ghedir, S. Ibala, M. Ajina, A. Saad, C. Chang, H. Wang, S. Huang, S. Pai, Y. Soong, E. Papanikolaou, G. Pantos, G. Grimbizis, E. Bili, N. Polyzos, K. Karastefanou, P. Humaidan, S. Esteves, B. Tarlatzis, K. McNamee, A. Topping, R. G. Farquharson, F. Dawood, M. Ruiz Galdon, A. M. Lendinez, A. R. Palomares, F. Martinez, B. Perez-Nevot, A. Jimenez Fernandez, A. Reyes-Engel, J. A. Horcajadas, R. F. Savaris, V. Kovac, M. Reljic, V. Vlaisavljevic, A. Colicchia, I. Pergolini, B. Gilio, M. R. Rampini, P. Alfano, D. Marconi, C. Verlengia, E. Alviggi, J. Bellver, F. Cruz, M. C. Martinez, J. Ramirez, J. Ferro, N. Garrido, J. K. Brown, K. B. Lauer, N. F. Inglis, H. O. D. Critchley, A. W. Horne, H. Samli, B. Cetinkaya Demir, A. Ozgoz, M. A. Atalay, G. Uncu, Y. Yan, M. A. Cai-hong, Q. I. A. O. Jie, C. H. E. N. Xin-na, C. H. E. Weimar, A. Kavelaars, B. Gellersen, J. J. Brosens, J. M. T. de Vreeden-Elbertse, C. J. Heijnen, N. S. Macklon, J. C. Castillo, M. Dolz, O. Caballero, L. Abad, J. Perez-Panades, F. Bonilla-Musoles, W. Eggert - Kruse, S. Scholz, I. Klopsch, and T. Strowitzki

Subjects
medicine.medical_specialty, Reproductive Medicine, biology, business.industry, Rehabilitation, biology.protein, Physical therapy, Obstetrics and Gynecology, Medicine, Early pregnancy factor, Session (computer science), business
Published
2011
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48. POSTER VIEWING SESSION - REPRODUCTIVE (EPI) GENETICS

Author

B. Acar-Perk, J. Weimer, K. Koch, A. Salmassi, N. Arnold, L. Mettler, A. G. Schmutzler, C. S. Ottolini, D. K. Griffin, A. H. Handyside, M. C. Summers, A. R. Thornhill, D. Montjean, M. Benkhalifa, P. Cohen-Bacrie, J. P. Siffroi, J. Mandelbaum, I. Berthaut, A. Bashamboo, C. Ravel, K. McElreavey, A. Ao, X. Y. Zhang, A. Yilmaz, J. T. Chung, E. Demirtas, W. Y. Son, M. Dahan, W. Buckett, H. Holzer, S. L. Tan, A. Perheentupa, M. Vierula, N. Jorgensen, N. E. Skakkebaek, S. Chantot-Bastaraud, J. Toppari, L. Muzii, M. C. Magli, L. Gioia, M. Mattioli, A. P. Ferraretti, L. Gianaroli, I. Koscinski, E. Elinati, C. Fossard, P. Kuentz, Z. Kilani, A. Demirol, T. Gurgan, F. Schmitt, J. Velez de la Calle, N. Iqbal, N. Louanjli, M. Pasquier, F. Carre-Pigeon, J. Muller, C. Barratt, S. Viville, C. Magli, C. Grugnetti, E. Castelletti, B. Paviglianiti, L. Pepas, P. Braude, J. Grace, V. Bolton, Y. Khalaf, T. El-Toukhy, I. Galeraud-Denis, H. Bouraima, L. Sibert, N. Rives, S. Carreau, F. Janse, L. M. de With, B. C. J. M. Fauser, C. B. Lambalk, J. S. E. Laven, A. J. Goverde, J. C. Giltay, V. De Leo, L. Governini, A. Quagliariello, M. A. Margollicci, P. Piomboni, A. Luddi, H. Miyamura, H. Nishizawa, S. Ota, M. Suzuki, A. Inagaki, H. Egusa, S. Nishiyama, T. Kato, I. Nakanishi, T. Fujita, Y. Imayoshi, A. Markoff, I. Yanagihara, Y. Udagawa, H. Kurahashi, B. Alvaro Mercadal, R. Imbert, I. Demeestere, A. De Leener, Y. Englert, S. Costagliola, A. Delbaere, E. Velilla, A. Colomar, E. Toro, S. Chamosa, J. Alvarez, M. Lopez-Teijon, S. Fernandez, Y. Hosoda, A. Hasegawa, N. Morimoto, Y. Wakimoto, Y. Ito, S. Komori, L. Sati, C. Zeiss, R. Demir, J. McGrath, S. Y. Ku, Y. J. Kim, Y. Y. Kim, H. J. Kim, K. E. Park, S. H. Kim, Y. M. Choi, S. Y. Moon, A. Minor, V. Chow, S. Ma, E. Martinez Mendez, M. Gaytan, A. Linan, A. Pacheco, M. San Celestino, C. Nogales, M. Ariza, D. Cernuda, F. Bronet, A. M. Lendinez Ramirez, A. R. Palomares, B. Perez-Nevot, V. Urraca, A. Ruiz Martin, A. Reche, M. Ruiz Galdon, A. Reyes-Engel, N. R. Treff, X. Tao, D. Taylor, B. Levy, K. M. Ferry, R. T. Scott Jr., S. Vasan, K. K. Acharya, B. Vasan, R. Yalaburgi, K. K. Ganesan, S. C. Darshan, C. H. Neelima, P. Deepa, B. Akhilesh, D. Sravanthi, K. S. Sreelakshmi, H. Deepti, J. H. van Doorninck, C. Eleveld, M. van der Hoeven, E. Birnie, E. A. P. Steegers, R. J. Galjaard, I. M. van den Berg, F. Fiorentino, L. Spizzichino, S. Bono, A. Biricik, G. Kokkali, L. Rienzi, F. M. Ubaldi, E. Iammarrone, A. Gordon, K. Pantos, E. Oitmaa, A. Tammiste, S. Suvi, M. Punab, M. Remm, A. Metspalu, A. Salumets, L. Rodrigo, P. Mir, A. Cervero, E. Mateu, A. Mercader, C. Vidal, J. Giles, J. Remohi, A. Pellicer, J. Martin, C. Rubio, H. Mozdarani, S. Moghbeli Nejad, M. Behmanesh, A. Alleyasin, H. Ghedir, S. Ibala-Romdhane, O. Mamai, S. Brahem, H. Elghezal, M. Ajina, M. Gribaa, A. Saad, M. C. Martinez, V. Peinado, M. Milan, N. Al-Asmar, P. Buendia, A. Delgado, L. Escrich, B. Amorocho, C. Simon, L. Petrussa, H. Van de Velde, N. De Munck, M. De Rycke, S. Altmae, J. A. Martinez-Conejero, F. J. Esteban, M. Ruiz-Alonso, A. Stavreus-Evers, J. A. Horcajadas, B. Bug, G. Raabe-Meyer, U. Bender, J. Zimmer, B. Schulze, P. H. Vogt, T. Laisk, M. Peters, V. Grabar, A. Feskov, E. Zhilkova, N. Sugawara, M. Maeda, T. Seki, T. Manome, R. Nagai, Y. Araki, I. Georgiou, L. Lazaros, N. Xita, A. Chatzikyriakidou, A. Kaponis, N. Grigoriadis, E. Hatzi, I. Grigoriadis, N. Sofikitis, K. Zikopoulos, M. Gunn, P. R. Brezina, A. Benner, L. Du, W. G. Kearns, X. Shen, C. Zhou, Y. Xu, Y. Zhong, Y. Zeng, G. Zhuang, M. C. Gunn, K. Richter, P. Andreeva, I. Dimitrov, M. Konovalova, S. Kyurkchiev, A. Shterev, A. Daser, E. Day, H. Turley, A. Immesberger, T. Haaf, T. Hahn, P. H. Dear, M. Schorsch, J. Don, N. Golan, T. Eldar, and R. Yaverboim

Subjects
03 medical and health sciences, medicine.medical_specialty, 030219 obstetrics & reproductive medicine, 0302 clinical medicine, Reproductive Medicine, business.industry, Rehabilitation, medicine, Obstetrics and Gynecology, Medical physics, Session (computer science), business
Published
2011
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49. Andrology (Male Fertility, Spermatogenesis)

Author

Y. Matsumoto, S. Goto, H. Hashimoto, S. Kokeguchi, M. Shiotani, H. Okada, P. Cohen - Bacrie, A. Hazout, S. Belloc, J. De Mouzon, Y. Menezo, M. Dumont, A. M. Junca, M. Cohen-Bacrie, S. Alvarez, F. Olivennes, N. Prisant, M. Weltin, W. Geissler, C. Clussmann, T. Strowitzki, W. Eggert-Kruse, Y. Endou, Y. Fjii, H. Motoyama, F. Q. Quintana, Z. L. Zaloa Larreategui, I. P. Iratxe Penalba, S. O. Sara Ortega, M. M. Monica Martin, G. Q. Guillermo Quea, J. S. Jose Serna, M. G. Showell, J. Brown, A. Yazdani, M. T. Stankiewicz, R. J. Hart, C. Zumoffen, M. J. Munuce, A. Caille, S. Ghersevich, A. M. Lendinez, B. Perez-Nevot, A. R. Palomares, A. Serrano Garballo, A. Rodriguez, A. Reche, A. Mayor-Olea, M. Ruiz-Galdon, A. Reyes-Engel, J. Mendiola, N. Jorgensen, A. M. Andersson, A. M. Calafat, J. B. Redmon, E. Z. Drobnis, C. Wang, A. Sparks, S. W. Thurston, F. Liu, S. H. Swan, A. C. Tarasconi, B. V. Tarasconi, D. V. Tarasconi, E. M. V. Silva, Y. Fujii, I. Crha, J. Pribyl, P. Skladal, J. Zakova, P. Ventruba, M. Pohanka, G. De La Fuente, A. Pacheco, J. A. G. Velasco, A. Requena, A. Pacheco Castro, M. San Celestino Carchenilla, R. Salvanes, A. Arnanz, C. Balmori, A. Pellicer, J. A. Garcia-Velasco, T. Ishikawa, M. Fujisawa, S. Kranz, K. Hersemeyer, A. Hentrich, H. R. Tinneberg, L. Konrad, L. Simon, D. Lutton, J. McManus, S. E. M. Lewis, S. Rubio, P. Simon Sanjurjo, S. Lewis, J. Buzzi, A. Valcarcel, E. Lombardi, R. Oses, V. Rawe, E. Young, A. Magendzo, S. Lizama, G. Duque, A. Mackenna, A. Monqaut, C. Zavaleta, G. Lopez, R. Lafuente, M. Brassesco, R. Condorelli, S. La Vignera, S. La Rosa, N. Barone, E. Vicari, S. Bellanca, R. D'Agata, A. E. Calogero, M. Enciso, M. Iglesias, I. Galan, A. Gosalvez, J. Gosalvez, M. Curaba, J. Poels, A. Van Langendonckt, J. Donnez, C. Wyns, M. Garcez, M. Salvador, E. B. Pasqualotto, D. P. A. F. Braga, E. Borges, F. F. Pasqualotto, T. Aoki, R. C. S. Figueira, L. G. L. Maldonado, A. Iaconelli, R. Frassini, J. Mandelli, A. S. Setti, S. S. Cortezzi, M. Di Mauro, N. Burrello, J. Kashir, C. Jones, C. Young, M. Ruas, P. Grasa, K. Rietdorf, E. Heytens, B. Heindryckx, S. Y. Yoon, R. A. Fissore, C. M. Deane, D. Nikiforaki, S. T. Tee, P. de Sutter, J. Parrington, K. Coward, L. Visser, G. H. Westerveld, S. K. M. van Daalen, F. van der Veen, M. P. Lombardi, S. Repping, S. Cubillos, S. Sanchez, J. Pedraza, G. Charria, H. Aparicio, A. Gongora, F. Caldino, S. Cuneo, J. P. Ou, W. E. Zhao, Y. F. Liu, Y. W. Xu, C. Q. Zhou, N. Al-Asmar Pinar, V. Peinado, J. Gruhn, M. Susiarjo, M. Gil-Salom, J. M. Martinez-Jabaloyas, J. Remohi, C. Rubio, T. Hassold, N. Al-Asmar, L. Rodrigo, T. J. Hassold, M. Bungum, N. Forsell, A. Giwercman, I. Amiri, N. Sheikh, R. Najafi, M. Godarzi, M. Farimani, H. Makukh, M. Tyrkus, D. Zastavna, A. Nakonechnuy, S. S. Khayat, L. V. Schileiko, L. F. Kurilo, S. Garcia-Herrero, N. Garrido, J. A. Martinez-Conejero, L. Romany, M. Meseguer, B. Dorphin, M. Lefevre, C. Gout, P. Oger, C. Yazbeck, N. Rougier, S. De Stefani, V. Scala, S. Benedetti, M. C. Tagliamonte, E. Zavagnini, S. Palini, C. Bulletti, F. Canestrari, N. Subiran, F. M. Pinto, M. L. Candenas, E. Agirregoitia, J. Irazusta, E. M. Cha, J. H. Lee, I. H. Park, K. H. Lee, M. H. Kim, M. S. Jensen, C. Rebordosa, A. M. Thulstrup, G. Toft, H. T. Sorensen, J. P. Bonde, T. B. Henriksen, J. Olsen, L. Bosco, M. Speciale, M. Manno, N. Amireh, M. C. Roccheri, E. Cittadini, P. Wu, Y. M. Lee, H. W. Chen, C. R. Tzeng, J. Llacer, J. Ten, B. Lledo, A. Rodriguez-Arnedo, R. Morales, R. Bernabeu, A. Garcia-Peiro, J. Martinez-Heredia, M. Oliver-Bonet, J. Ribas, C. Abad, M. J. Amengual, J. Navarro, J. Benet, C. Moutou, N. Gardes, J. C. Nicod, N. Becker, M. P. Bailly, I. Galland, O. Pirello, C. Rongieres, C. Wittemer, S. Viville, W. Elmahaishi, B. Smith, A. Doshi, P. Serhal, J. C. Harper, C. Rennemeier, U. Kammerer, J. Dietl, P. Staib, K. Elgmati, M. Nomikos, M. Theodoridou, B. Calver, K. Swann, F. A. Lai, I. Georgiou, L. Lazaros, N. Xita, A. Kaponis, N. Plachouras, E. Hatzi, K. Zikopoulos, F. Ferfouri, P. Clement, D. Molina Gomes, M. Albert, M. Bailly, R. Wainer, J. Selva, F. Vialard, T. Takisawa, K. Usui, T. Kyoya, Y. Shibuya, H. Hattori, Y. Sato, M. Ota, K. Kyono, P. C. Chiu, K. K. Lam, C. L. Lee, M. K. Chung, V. W. Huang, W. S. O, F. Tang, P. C. Ho, W. S. Yeung, C. H. Kim, J. Y. Lee, S. H. Kim, C. S. Suh, Y. K. Shin, Y. J. Kang, J. H. Jung, C. Y. Cha, E. S. Hwang, T. Mukaida, M. Nagaba, K. Takahashi, D. Elkaffash, M. Sedrak, I. Huhtaniemi, T. Abdel-Al, D. Younan, N. G. Cassuto, D. Bouret, I. Hammoud, Y. Barak, S. Seshadri, M. Bates, G. Vince, D. I. Jones, M. Ben Khalifa, D. Montjean, P. Cohen-Bacrie, F. X. Aubriot, M. Cohen, E. Boudjema, M. C. Magli, A. Crippa, B. Baccetti, A. P. Ferraretti, L. Gianaroli, T. Singer, Q. V. Neri, J. C. Hu, R. Maggiulli, Z. Kollman, E. Rauch, P. N. Schlegel, Z. Rosenwaks, G. D. Palermo, B. Zorn, B. Skrbinc, E. Matos, B. Golob, M. Pfeifer, J. Osredkar, E. Sabanegh, R. K. Sharma, A. Thiyagarajan, A. Agarwal, G. Robin, F. Boitrelle, F. Marcelli, C. Marchetti, V. Mitchell, D. Dewailly, J. M. Rigot, N. Rives, A. Perdrix, A. Travers, J. P. Milazzo, N. Mousset-Simeon, B. Mace, A. Jakab, Z. Molnar, M. Benyo, I. Levai, Z. Kassai, A. Ihan, A. Kopitar, M. Kolbezen, D. Vaamonde, M. E. Da Silva-Grigoletto, J. M. Garcia-Manso, R. Vaamonde-Lemos, S. C. Oehninger, G. Walis, D. Monahan, E. Ermolovich, E. Fadlon, A. Abu Elhija, M. Abu Elhija, E. Lunenfeld, M. Huleihel, M. Costantini-Ferrando, J. C. Y. Hu, J. G. Alvarez, E. Velilla, M. Lopez-Teijon, C. Lopez-Fernandez, H. G. Tempest, F. Sun, E. Ko, P. Turek, R. H. Martin, M. T. Zomeno-Abellan, A. Ramirez, A. Gutierrez-Adan, J. C. Martinez, J. Landeras, J. Ballesta, M. Aviles, M. Ganaiem, S. Binder, A. Meinhardt, L. Sousa, A. Grangeia, F. Carvalho, M. Sousa, A. Barros, C. Sifer, N. Sermondade, E. Hafhouf, C. Poncelet, B. Benzacken, R. Levy, J. P. Wolf, L. Crisol, F. Aspichueta, M. L. Hernandez, A. Exposito, R. Matorras, M. B. Ruiz-Larrea, J. I. Ruiz-Sanz, S. Jallad, F. Atig, H. Ben Amor, A. L. I. Saad, A. Kerkeni, M. Ajina, A. L. I. Othmane, I. Koscinski, L. Ladureau, F. Scarselli, V. Casciani, M. Lobascio, M. G. Minasi, P. Rubino, A. Colasante, L. Arizzi, K. Litwicka, E. Iammarrone, S. Ferrero, C. Mencacci, G. Franco, D. Zavaglia, Z. P. Nagy, E. Greco, S. Ohgi, M. Takahashi, C. Kishi, K. Suga, A. Yanaihara, L. W. Chamley, A. Wagner, and A. N. Shelling

Subjects
Andrology, Reproductive Medicine, Phospholipase C, Point mutation, Rehabilitation, Obstetrics and Gynecology, Identification (biology), Biology, Sperm, Gene, Molecular biology
Published
2010
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50. Posters * Reproductive Genetics (PGD/PGS)

Author

A. Crippa, M. C. Magli, F. Robles, A. Capoti, A. P. Ferraretti, L. Gianaroli, A. Gallina, E. Bonaparte, M. Moretti, G. M. Colpi, F. Nerva, G. Contalbi, L. Vacalluzzo, S. Tabano, F. R. Grati, G. Gazzano, S. M. Sirchia, G. Simoni, M. Miozzo, A. Handyside, A. Gabriel, A. R. Thornhill, E. Clemente, C. Reitter, N. Affara, D. K. Griffin, M. Macek, P. Feldmar, H. Kluckova, M. Hrehorcak, J. Diblik, P. Paulasova, M. Turnovec, S. Vilimova, L. Fontes, L. Haddad, E. Borges, A. Iaconelli, D. P. A. F. Braga, A. M. Vianna-Morgante, A. Komsky, E. Kasterstein, D. Komarovsky, O. Bern, B. Maslansky, T. Kaplan, A. Raziel, S. Friedler, Y. Gidoni, I. Ben-Ami, R. Ron-El, D. Strassburger, R. Maggiulli, D. Monahan, Q. V. Neri, J. C. Y. Hu, Z. Rosenwaks, G. D. Palermo, C. Beyazyurek, G. C. Ekmekci, H. A. Tac, N. Ajredin, O. Verlinsky, F. Fiorentino, S. Kahraman, M. Camp, L. Hesters, M. Le Lorc'h, R. Frydman, S. Romana, N. Frydman, J. Perez Sanz, R. Matorras, J. Arluzea, Y. Romin, J. Bilbao, N. Gonzalez-Santiago, K. Manova-Todorova, A. Koff, J. M. Rivera-Pomar, C. de la Hoz-Torres, L. Xanthopoulou, H. Ghevaria, A. Mantzouratou, P. Serhal, A. Doshi, J. D. Delhanty, Y. Ye, Y. Qian, F. Jin, S. Munne, C. Gutierrez, C. Wagner, D. Hill, K. Wiemer, J. Fischer, B. Kaplan, H. Danzer, M. Surrey, M. Opsahl, B. Hladikova, A. Sobek, E. Tkadlec, K. Kyselova, M. Nichi, R. C. S. Figueira, A. S. Setti, S. S. Colturato, C. Rubio, J. Domingo, L. Rodrigo, A. Mercader, M. J. De los Santos, T. Pehlivan, E. Bosch, M. Fernandez, C. Simon, J. Remohi, A. Pellicer, B. Perez-Nevot, A. M. Lendinez, A. R. Palomares, M. Polo, A. Rodriguez, A. Reche, M. Ruiz-Galdon, A. Reyes-Engel, E. A. H. Knauff, H. M. Blauw, K. Kok, C. Wijmenga, B. C. J. M. Fauser, L. Franke, A. Paffoni, V. Paracchini, S. Ferrari, L. Restelli, D. A. Coviello, C. Scarduelli, M. Seia, G. Ragni, N. Aoyama, Y. Takehara, S. Kawachiya, T. Kuroda, N. Kawasaki, R. Yamadera, T. Suzuki, K. Kato, O. Kato, Q. H. Xu, Z. G. Zhang, P. Zhou, Z. L. Wei, D. K. Huang, Q. Xing, Y. X. Cao, P. Fauque, M. A. Ripoche, J. Tost, L. Journot, P. Jouannet, D. Vaiman, L. Dandolo, H. Jammes, A. Hellani, A. Elsheikh, K. K. Abuamero, S. Elakoum, F. Martinez, E. Perez de la Blanca, O. Koutna, T. Cepelak, and A. J. R. Sobek

Subjects
Genetics, 03 medical and health sciences, 030219 obstetrics & reproductive medicine, 0302 clinical medicine, Reproductive Medicine, Rehabilitation, Obstetrics and Gynecology, Biology
Published
2010
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