Cycloaddition between nitrogen-doped graphene (6π-component) and benzene (4π-component): a theoretical approach using density functional theory with vdW-DF correction.

The interaction between nitrogen-doped graphene defects (N3V1 and N4V2 pyridinic, and N3V1 and N3V3 pyrrolic) and benzene have been investigated by applying density functional theory (DFT), together with the vdW-DF correction. We discovered that only the N3V3 pyrrolic defect is a reactive site (6π-component), forming a cycloadduct with benzene (4π-component) that has energy barriers below 154.38 kJ mol-1 (1.60 eV). The conduction and valence bands (HOMO and LUMO) for N3V3 form a degenerate pair of orbitals at the gamma point, with the same ionization potential (IP) and electron affinity (EA). Likewise, inspection of the orbital symmetries for both systems confirms that these must undergo concerted reactions based on the Woodward and Hoffmann principles of orbital symmetry, with the appropriate orbital occupancies. This is the first time that substitutionally doped graphene has been demonstrated to participate as a 6π-component for cycloaddition reactions with benzene.

Novel biochar and hydrochar for the adsorption of 2-nitrophenol from aqueous solutions: An approach using the PVSDM model.

Two new adsorbents, namely avocado-based hydrochar and LDH/bone-based biochar, were developed, characterized, and applied for adsorbing 2-nitrophenol. The pore volume and surface diffusion model (PVSDM) was numerically solved for different geometries and applied to interpret the adsorption decay curves. Both adsorbents presented interesting textural and physicochemical characteristics, which achieved maximum adsorption capacities of 761 mg/g for biochar and 562 mg/g for hydrochar. The adsorption equilibrium data were well fitted by Henry isotherm. Besides, thermodynamic investigation revealed endothermic adsorption with the occurrence of electrostatic interactions. PVSDM predicted the adsorption decay curves for different adsorbent geometries at different initial concentrations of 2-nitrophenol. The surface diffusion was the main intraparticle mass transport mechanism. Furthermore, the external mass transfer and surface diffusion coefficients increased with the increase of 2-nitrophenol concentration.

Changes to the dissociation barrier of H2 due to buckling induced by a chemisorbed hydrogen on a doped graphene surface.

An effectiveway of enhancing hydrogen storage on adsorbent materials can be induced by the hydrogen spill-over mechanism, although to date there is no general consensus which satisfactorily explains the mechanism. In this work, a possible reaction path to explain hydrogen adsorption is shown. Density-functional calculations were used to study the dissociation of molecular hydrogen near to a stressed region, as a consequence of chemisorbed hydrogen at the graphene-nitrogen surface. We found that as a result of the buckling induced by the chemisorbed hydrogen, the dissociation barrier of molecular hydrogen diminished by 0.84 eV. The chemisorbed hydrogen is the final state in the spill-over mechanism on a graphene-nitrogen decorated with palladium clusters. This effect helps to create hydrogen nanoislands that may change the diffusion and detrapping of H. An electronic structure analysis suggests that these systems occasionally present metallic or semiconductor behavior. Graphical Abstract Hydrogen dissociation and adsorption process via buckling defect.

Retinoic Acid Modulates PTGDR Promoter Activity.

BACKGROUND AND OBJECTIVE: Vitamin A has been linked to the development of allergic diseases although its role is not fully understood, Retinoic acid (RA), a metabolite of Vitamin A, has been previously associated with the prostaglandin pathway, and PTGDR, a receptor of PGD2, has been proposed as a candidate gene in allergy and asthma. Considering the role of PTGDR in allergy, the goal of this study was to analyze the effect of RA on the activation of the promoter region of the PTGDR gene. METHODS: A549 lung epithelial cells were transfected with 4 combinations of genetic variants of the PTGDR promoter and stimulated with all-trans RA (ATRA); luciferase assays were performed using the Dual Luciferase Reporter System, and real-time quantitative polymerase chain reaction was used to measure the expression of PTGDR, CYP26A1, RARA, RARB, RARG, and RXRA in basal A549 cell cultures and after ATRA treatment. We also performed an in silico analysis. RESULTS: After ATRA treatment increased expression of CYP26A1 (12-fold) and RARB (4-fold) was detected. ATRA activated PTGDR promoter activity in transfected cells (P<.001) and RA response element sequences were identified in silico in this promoter region. CONCLUSIONS: RA modulated PTGDR promoter activity. Differential response to RA and to new treatments based on PTGDR modulation could depend on genetic background in allergic asthmatic patients.

Analysis of FOXP3 gene in children with allergy and autoimmune diseases

BACKGROUND: Allergy and autoimmunity are important immunological entities underlying chronic diseases in children. In some cases both entities develop simultaneously in the same patient. FOXP3 gene codes for a transcription factor involved in regulation of the immune system. Considering that regulatory T cells are involved in controlling immunological disease development, and the relevant role of FOXP3 in this kind of T cells, the objective of this study was to analyse the FOXP3gene in the most prevalent autoimmune diseases and/or allergies in childhood in a European population. METHODS: A total of 255 Caucasian individuals, 95 controls and 160 patients diagnosed with allergic, autoimmune or both diseases were included in this study. The molecular analysis of FOXP3 was performed by DNA sequencing following the recommendations for quality of the European Molecular Genetics Quality Network. Genomic DNA was extracted from peripheral blood of all participants and was amplified using the polymerase chain reaction. After the visualisation of the amplified fragments by agarose gel-electrophoresis, they were sequenced. RESULTS: Thirteen different polymorphisms in FOXP3 gene were found, seven of which had not been previously described. The mutated allele of SNP 7340C>T was observed more frequently in the group of male children suffering from both allergic and autoimmune diseases simultaneously (p = 0.004, OR = 16.2 [1.34-195.15]). CONCLUSIONS: In this study we identified for first time genetic variants of FOXP3 that are significantly more frequent in children who share allergic and autoimmune diseases. These variants mainly affect regulatory sequences that could alter the expression levels of FOXP3 modifying its function including its role in Treg cells

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Analysis of FOXP3 gene in children with allergy and autoimmune diseases.

BACKGROUND: Allergy and autoimmunity are important immunological entities underlying chronic diseases in children. In some cases both entities develop simultaneously in the same patient. FOXP3 gene codes for a transcription factor involved in regulation of the immune system. Considering that regulatory T cells are involved in controlling immunological disease development, and the relevant role of FOXP3 in this kind of T cells, the objective of this study was to analyse the FOXP3 gene in the most prevalent autoimmune diseases and/or allergies in childhood in a European population. METHODS: A total of 255 Caucasian individuals, 95 controls and 160 patients diagnosed with allergic, autoimmune or both diseases were included in this study. The molecular analysis of FOXP3 was performed by DNA sequencing following the recommendations for quality of the European Molecular Genetics Quality Network. Genomic DNA was extracted from peripheral blood of all participants and was amplified using the polymerase chain reaction. After the visualisation of the amplified fragments by agarose gel-electrophoresis, they were sequenced. RESULTS: Thirteen different polymorphisms in FOXP3 gene were found, seven of which had not been previously described. The mutated allele of SNP 7340C>T was observed more frequently in the group of male children suffering from both allergic and autoimmune diseases simultaneously (p=0.004, OR=16.2 [1.34-195.15]). CONCLUSIONS: In this study we identified for first time genetic variants of FOXP3 that are significantly more frequent in children who share allergic and autoimmune diseases. These variants mainly affect regulatory sequences that could alter the expression levels of FOXP3 modifying its function including its role in Treg cells.

Retinoic acid modulates PTGDR promoter activity

Background and Objective: Vitamin A has been linked to the development of allergic diseases although its role is not fully understood, Retinoic acid (RA), a metabolite of Vitamin A, has been previously associated with the prostaglandin pathway, and PTGDR, a receptor of PGD2, has been proposed as a candidate gene in allergy and asthma. Considering the role of PTGDR in allergy, the goal of this study was o analyze the effect of RA on the activation of the promoter region of the PTGDR gene. Methods: A549 lung epithelial cells were transfected with 4 combinations of genetic variants of the PTGDR promoter and stimulated with all-trans RA (ATRA); luciferase assays were performed using the Dual Luciferase Reporter System, and real-time quantitative polymerase chain reaction was used to measure the expression of PTGDR, CYP26A1, RARA, RARB, RARG , and RXRA in basal A549 cell cultures and after ATRA treatment. We also performed an in silico analysis. Results: After ATRA treatment increased expression of CYP26A1 (12-fold) and RARB (4-fold) was detected. ATRA activated PTGDR promoter activity in transfected cells (P<.001) and RA response element sequences were identified in silico in this promoter region. Conclusions: RA modulated PTGDR promoter activity. Differential response to RA and to new treatments based on PTGDR modulation could depend on genetic background in allergic asthmatic patients (AU)

Introducción y Objetivo: La vitamina A se ha relacionado con el desarrollo de las enfermedades alérgicas, si bien su papel no se comprende en su totalidad. El ácido retinoico, un metabolito de la vitamina A, se ha asociado previamente con la ruta de las prostaglandinas. Además, PTGDR, uno de los receptores de PGD2, se ha propuesto como un gen candidato en la alergia y el asma. Considerando el papel de PTGDR en la alergia, el objetivo de este estudio fue analizar el efecto del ácido retinoico sobre la activación de la región promotora del gen PTGDR. Métodos: Se utilizó la línea celular A549 de epitelio de pulmón. Las células fueron transfectadas con cuatro combinaciones de las variantes génicas de PTGDR y fueron estimuladas con ácido retinoico todo-trans (ATRA). Los ensayos de Luciferasa se llevaron a cabo mediante el sistema Dual Luciferase Reporter System. Se realizaron análisis de RT-qPCR para medir la expresión basal de PTGDR, CYP26A1, RARA, RARB, RARG y RXRA de los cultivos de A549 tras el tratamiento con ATRA. Se realizaron también análisis bioinformáticos. Resultados: Se encontraron diferencias significativas en la actividad promotora entre las variantes haplotípicas tras la transfección en la línea celular A549. Tras el tratamiento con ATRA se detectó un incremento de la expresión de CYP26A1 (12 veces) y RARB (4 veces). El ácido retinoico activó la actividad promotora de PTGDR en las células transfectadas (p<0,001). Se identificaron secuencias de Elementos de Respuesta a Ácido Retinoico (RARE) in silico en la región promotora de PTGDR. Conclusiones: El ácido retinoico modula la actividad promotora de PTGDR . Esto podría explicar las diferencias en los efectos del ácido retinoico y en las respuestas a los nuevos tratamientos de la enfermedad alérgica basados en la modulación del receptor PTGDR (AU)

Genome-wide association studies (GWAS) and their importance in asthma

Asthma is a complex disease determined by the interaction of different genes and environmental factors. The first genetic investigations in asthma were candidate gene association studies and linkage studies. In recent years research has focused on association studies that scan the entire genome without any prior conditioning hypothesis: the so-called genome-wide association studies (GWAS). The first GWAS was published in 2007, and described a new locus associated to asthma in chromosome 17q12-q21, involving the ORMDL3, GSDMB and ZPBP2 genes (a description of the genes named in the manuscript are listed in Table 1). None of these genes would have been selected in a classical genetic association study since it was not known they could be implicated in asthma. To date, a number of GWAS studies in asthma have been made, with the identification of about 1000 candidate genes. Coordination of the different research groups in international consortiums and the application of new technologies such as new generation sequencing will help discover new implicated genes and improve our understanding of the molecular mechanisms underlying the disease

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Genome-wide association studies (GWAS) and their importance in asthma.

Asthma is a complex disease determined by the interaction of different genes and environmental factors. The first genetic investigations in asthma were candidate gene association studies and linkage studies. In recent years research has focused on association studies that scan the entire genome without any prior conditioning hypothesis: the so-called genome-wide association studies (GWAS). The first GWAS was published in 2007, and described a new locus associated to asthma in chromosome 17q12-q21, involving the ORMDL3, GSDMB and ZPBP2 genes (a description of the genes named in the manuscript are listed in Table 1). None of these genes would have been selected in a classical genetic association study since it was not known they could be implicated in asthma. To date, a number of GWAS studies in asthma have been made, with the identification of about 1000 candidate genes. Coordination of the different research groups in international consortiums and the application of new technologies such as new generation sequencing will help discover new implicated genes and improve our understanding of the molecular mechanisms underlying the disease.

Implications of cytokine genes in allergic asthma

Asthma is a complex disease involving numerous mediator molecules and effector cells, in combination with a range of environmental determining factors. Cytokines play a key role in the physiopathological mechanisms of asthma; the study of the structure, regulation and variations of the genes that encode for these molecules is therefore crucial. Cytokines have extremely diverse roles, and exert effects both as activators and inhibitors of the innate and adaptive immune response. Certain modifications in the expression or structure of these molecules, resulting from the presence of polymorphisms, may give rise to deregulation of the mentioned effects, and therefore to a predisposition to develop concrete asthma phenotypes

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Implications of cytokine genes in allergic asthma.

Asthma is a complex disease involving numerous mediator molecules and effector cells, in combination with a range of environmental determining factors. Cytokines play a key role in the physiopathological mechanisms of asthma; the study of the structure, regulation and variations of the genes that encode for these molecules is therefore crucial. Cytokines have extremely diverse roles, and exert effects both as activators and inhibitors of the innate and adaptive immune response. Certain modifications in the expression or structure of these molecules, resulting from the presence of polymorphisms, may give rise to deregulation of the mentioned effects, and therefore to a predisposition to develop concrete asthma phenotypes.

The prostaglandin D2 receptor (PTGDR) gene in asthma and allergic diseases

The prostaglandin D2 receptor (PTGDR) gene has been associated to asthma and related phenotypes by linking and association studies. Functional studies involving animal models and other expression studies based on in vitro cell models also point to a possible role of polymorphisms in the promoter region, in the differential binding of transcription factors, and thus in PTGDR expression, which appear to be associated to the development of asthma or of susceptibility to the disease

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The prostaglandin D2 receptor (PTGDR) gene in asthma and allergic diseases.

The prostaglandin D2 receptor (PTGDR) gene has been associated to asthma and related phenotypes by linking and association studies. Functional studies involving animal models and other expression studies based on in vitro cell models also point to a possible role of polymorphisms in the promoter region, in the differential binding of transcription factors, and thus in PTGDR expression, which appear to be associated to the development of asthma or of susceptibility to the disease.

Tamoxifen favoured the rat sensorial cortex regeneration after a penetrating brain injury.

A penetrating brain injury produces a glial scar formed by astrocytes, oligodendrocytes, microglia and NG2 cells. Glial scar is a barrier preventing the extent of damage but it has deleterious effects in the regeneration of the axons. Estradiol and tamoxifen reduce gliosis and have neuroprotective effects in the hippocampus and the spinal cord. We evaluated the proliferation of glia and the electrocorticogram in the sensorial cortex in a brain injury model. At seven days post-injury, estradiol, tamoxifen and estradiol plus tamoxifen reduced the number of resident and proliferative NG2 and reactive astrocyte vimentin+ cells. Estradiol and tamoxifen effects on NG2 cells could be produced by the classical oestrogen receptors found in these cells. The glial scar was also reduced by tamoxifen. At thirty days post-injury, the amount of resident and proliferative astrocytes increased significantly, except in the estradiol plus tamoxifen group, whilst the oligodendrocytes proliferation in the glial scar was reduced in treated animals. Tamoxifen promotes the survival of FOX-3+ neurons in the injured area and a recovery in the amplitude of electrocorticogram waves. At thirty days, estradiol did not favour the survival of neurons but produced a greater number of reactive astrocytes. In contrast, the number of oligodendrocytes was reduced. Tamoxifen could favour brain repair promoting neuron survival and adjusting glial cell number. It seems to recover adequate neural communication.

Tryptase: Genetic and functional considerations

Tryptase is one of the main proteases located in the secretory granules of the mast cells, and is released through degranulation. It is therefore assumed to play an important role in inflammatory and allergic processes. Four genes are known to encode for these enzymes, with different alleles that give rise to different types of tryptases. The term "tryptase" generally refers to beta-tryptase, which in vivo is a heterotetramer, possessing a structure of vital importance for enabling drug and substrate access to the active site of the molecule. Tryptase has been reported to possess antagonistic functions, since it plays an important role both in inflammatory phenomena and as a protector against infection. In allergic processes it is associated to bronchial hyperresponsiveness in asthmatic patients, where PAR-2 is of great importance as an airway receptor. Lastly, the genes that encode for tryptase are highly polymorphic and complex. As a result, it is important to establish a relationship between genotype and phenotype in disorders such as asthma, and to identify mutations that are presumably of pharmacological relevance(AU)

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Genetic association study in nasal polyposis.

BACKGROUND AND OBJECTIVES: Nasal polyposis (NP) is a chronic inflammatory disease of the upper airways with a variable clinical course and unknown pathogenesis that often coexists with other conditions. Considering the possibility of genetic predisposition, we decided to analyze whether polymorphisms in LTC4S, CYSLTR1, PTGDR, and NOS2A were associated with NP. METHODS: The study population comprised 486 Caucasian individuals. Polyposis and aspirin intolerance were diagnosed following the recommendations of the European Position Paper on Rhinosinusitis and Nasal Polyps. Genotypes were determined using polymerase chain reaction amplification and direct sequencing. RESULTS: The -444A > C LTC4S polymorphism was significantly associated with NP and atopy (P = .033) and with NP and atopic asthma, (P =.012). In addition, a significant association was found when the (CCTTT) repetition of the NOS2A gene was present more than 14 times in patients with NP and asthma (P = .034), in patients with polyposis and intolerance to nonsteroidal anti-inflammatory drugs (P = .009), and in patients with the aspirin triad (P = .005). The PTGDR diplotype CCCT/CCCC (-613CC, -549CC, -441CC and -197TC) was more frequent in patients with NP (P = .043), NP with asthma (P = .013), and the aspirin triad (P = .041). CONCLUSIONS: NP was associated with specific polymorphisms only when it occurred with related phenotypes. Our results suggest that this genetic background plays a more relevant role in the development of the associated clinical features of nasal polyposis than in simple polyposis.

Tryptase: genetic and functional considerations.

Tryptase is one of the main proteases located in the secretory granules of the mast cells, and is released through degranulation. It is therefore assumed to play an important role in inflammatory and allergic processes. Four genes are known to encode for these enzymes, with different alleles that give rise to different types of tryptases. The term "tryptase" generally refers to ß-tryptase, which in vivo is a heterotetramer, possessing a structure of vital importance for enabling drug and substrate access to the active site of the molecule. Tryptase has been reported to possess antagonistic functions, since it plays an important role both in inflammatory phenomena and as a protector against infection. In allergic processes it is associated to bronchial hyperresponsiveness in asthmatic patients, where PAR-2 is of great importance as an airway receptor. Lastly, the genes that encode for tryptase are highly polymorphic and complex. As a result, it is important to establish a relationship between genotype and phenotype in disorders such as asthma, and to identify mutations that are presumably of pharmacological relevance.

Incontinencia urinaria de esfuerzo en la mujer. Comparación de la técnica de Raz y de la técnica de Bologna / Comparison of Raz bladder neck suspension and the Bologna procedure for the treatment of urinary stress incontinence

Nuestra situación es la de comparar las complicaciones y los resultados sobre la incontinencia de esfuerzo de 2 técnicas de suspensión cervicouretral: la técnica de Raz y la técnica de Bologna. Se ha evaluado retrospectivamente a 199 pacientes que se han beneficiado de un tratamiento de incontinencia urinaria de esfuerzo, bien mediante la técnica de Bologna (grupo 1, 99 pacientes), bien por la técnica de Raz (grupo 2, 100 pacientes). Los datos clínicos preoperatorios, los parámetros urodinámicos y las complicaciones postoperatorias se han comparado en cada uno de los 2 grupos. El margen entre el tratamiento de la incontinencia urinaria y la recidiva se ha comparado con los 2 grupos por un test logarítmico. Se fabricó un modelo multivariante con la ayuda de un modelo de Cox, a fin de exponer los parámetros explicativos del fracaso quirúrgico. La duración de la curación en el grupo 1 es significativamente más larga que en el grupo 2 (p = 0,00001). La mediana de duración del intervalo libre sin incontinencia (éxito) es de 51 meses en el grupo 1 y de 21 meses en el 2 (p = 0,00001). La frecuencia de las complicaciones operatorias (lesión vesical y hemorragia) y postoperatorias (hemorrágicas, infecciosas y embólicas) no difieren en los 2 grupos. El análisis multivariante según el modelo de Cox muestra que la única variable preoperatoria explicativa de las recidivas es la técnica de colposuspensión realizada: Raz y Bologna. Después de este estudio comparativo, la técnica de Bologna debe preferirse a la de Raz para tratar los pacientes con IUE por el hecho de la presencia de suficiente pared vaginal anterior para confeccionar las cinchas vaginales. Si tal no es el caso, la técnica de Raz, tal y como nosotros la habíamos practicado, se debe abandonar en beneficio de otros métodos de colposuspensión (AU)

The aim of this study was to evaluate and compare perioperative morbidity and the long-term results of Raz colposuspension and the Bologna procedure in the treatment of urinary stress incontinence in women. Data from 199 women who underwent either the Bologna procedure (group 1; n = 99) or Raz colposuspension (group 2; n =100) for urinary stress incontinence were retrospectively analyzed. Preoperative clinical data, urodynamic parameters and postoperative complications were compared between the two groups. Logarithmic analysis was used to compare time to recurrence of stress incontinence between the two groups. Multivariate analysis using a Cox proportional hazards regression model was performed to identify possible outcome predictors. The success rate was significantly higher in group 1 than in group 2 (p = 0.00001). The median incontinence- free interval was 51 months in group 1 and was 21 months in group 2 (p = 0.00001). No differences were found between the two groups in the frequency of intraoperative complications (inadvertent cystotomy, hemorrhage) and postoperative complications (hemorrhagic, infectious and embolic complications). Multivariate analysis using the Cox regression model showed that the only variable correlated with the surgical cure rate was the type of surgical anti-incontinence procedure adopted: Bologna or Raz (p = 0.00001). The results of this study indicate that the Bologna procedure should be preferred over Raz colposuspension in the treatment of urinary stress incontinence when sufficient anterior vaginal tissue is available to create vaginal bands. When this is not the case, Raz colposuspension, as performed in the present study, should be abandoned in favor of other colposuspension methods (AU)

Liposarcoma de mama / Liposarcoma of the breast

El liposarcoma de mama es una lesión rara, pudiendo afectar a la mujer de 45 a 55 años de promedio de edad y que presenta las características clínicas y radiológicas de una lesión benigna. Aportamos en este trabajo el caso de una paciente de 52 años bajo tratamiento hormonal sustitutivo de la menopausia, en la cual una exploración rutinaria de mama individual descubrió un nódulo duro. La exéresis de este nódulo y su análisis anatomopatológico han permitido el diagnóstico de un liposarcoma de mama. Después de dos años de la intervención la evolución después de realizar solamente cirugía es satisfactoria. Más allá del carácter poco frecuente de esta patología, el caso subraya la posibilidad del diagnóstico precoz de este tipo de tumor, gracias a los exámenes mamográficos de vigilancia del tratamiento hormonal sustitutivo de la menopausia, así como el excelente pronóstico después de practicar solo cirugía

Liposarcoma of the breast is an unfrequent tumor that can be found in 45-55-year- old women, ussually with benign clinical and radiological characteristics. We report the case of a 52 –year- old patient treated with menopausal hormonal replacement therapy, for whom mammografic screening revealed a solid tumor. Lumpectomy was perfomed and histology reported liposarcoma of the breast. Two years after surgery alone no relapse was observed. Our case report underlines the possibility of discovering this type of tumor by means on mammographic examination performed during menopausal hormonal replacement therapy. It suggest good prognosis after surgery alone

Síndrome de Kartagener e infertilidad / Kartagener´s syndrome e infertility

Las disquinesias ciliares primitivas son etiologías raras de esterilidad primaria en caso del hombre (prevalencia 1/ 6000 a 1/ 40000). El síndrome de Kartagener es una entidad particular entre esta disquinesias ciliares primitivas. Se transmite según un modo autosómico recesivo. Se distingue por la asociación de un situs inverso, poliposis naso-sinusal y de una dilatación de los bronquios. Esta inmovilidad ciliar esta en el origen de numerosas infecciones broncopulmonares, sinusales y en el hombre, de infertilidad. Describiendo la observación de una pareja en la cual el hombre es portador de este síndrome, son analizados los orígenes genéticos de esta disquinesia y discutidas las diferentes opiniones observadas en la literatura

Primary ciliary dyskinesia is a rare etiology of sterility in man (prevalence betwen 1/ 6000 and 1/ 40000). Kartagener’s syndrome is an autosomal recessive disorder, characterized by total or parcial dysfunction of the ciliary or flagellated cells. This syndrome associates situs inversus, sinusitis, bronchiectasis and occasionally sterility in males. We report a case of inmotile cilia syndrome with male infertility and compare the data with four other couples reported in the literature. The difficulty is to select and alive sperm cell for ICSI