scholarly journals Male infertility in Northeast China: a cytogenetic study of 135 patients with non-obstructive azoospermia and severe oligozoospermia

2011 ◽  
Vol 29 (1) ◽  
pp. 83-87 ◽  
Author(s):  
Zhi-Bo Zhang ◽  
Yu-Ting Jiang ◽  
Xin Yun ◽  
Xiao Yang ◽  
Rui-Xue Wang ◽  
...  
Keyword(s):  
Male Infertility ◽  
Northeast China ◽  
Cytogenetic Study ◽  
Obstructive Azoospermia ◽  
Severe Oligozoospermia

scholarly journals Multicenter study of genetic abnormalities associated with severe oligospermia and non-obstructive azoospermia

2017 ◽  
Vol 46 (1) ◽  
pp. 107-114 ◽  
Author(s):  
Chong Xie ◽  
Xiangfeng Chen ◽  
Yulin Liu ◽  
Zhengmu Wu ◽  
Ping Ping
Keyword(s):  
Genetic Testing ◽  
Male Infertility ◽  
Multicenter Study ◽  
Chromosomal Abnormalities ◽  
Eastern China ◽  
Genetic Defects ◽  
Obstructive Azoospermia ◽  
Assisted Reproductive Technique ◽  
Severe Oligozoospermia ◽  
Genetic Abnormalities

Objective * Chong Xie, Xiangfeng Chen, and Yulin Liu contributed equally to this work. Genetic defects are identified in nearly 20% of infertile males. Determining the frequency and types of major genetic abnormalities in severe male infertility helps inform appropriate genetic counseling before assisted reproductive techniques. Methods Cytogenetic results of 912 patients with non-obstructive azoospermia (NOA) and severe oligozoospermia (SOS) in Eastern China were reviewed in this multicenter study from January 2011 to December 2015. Controls were 215 normozoospermic men with offspring. Results Among all patients, 22.6% (206/912) had genetic abnormalities, including 27.3% (146/534) of NOA patients and 15.9% (60/378) of SOS patients. Chromosomal abnormalities (all autosomal) were detected in only 1.9% (4 /215) of controls. In NOA patients, sex chromosomal abnormalities were identified in 25.8% (138/534), of which 8% (43/534) had a 47,XXY karyotype or its mosaic; higher than the SOS group prevalence (1.1%; 4/378). The incidence of Y chromosome microdeletions was lower in the SOS group (13.2%; 50/378) than in the NOA group (17.8%; 95/534). Conclusions The high prevalence of genetic abnormalities in our study indicates the importance of routine genetic testing in severe male infertility diagnosis. This may help determine the choice of assisted reproductive technique and allow specific pre-implantation genetic testing to minimize the risk of transmitting genetic defects.

scholarly journals Cryopreservation Benefits in Cryptozoospermia, Severe Oligozoospermia and Non-Obstructive Azoospermia in Male Infertility

OALib ◽  
2021 ◽  
Vol 08 (02) ◽  
pp. 1-9
Author(s):  
Aya Al-Ibraheemi ◽  
Noureddine Louanjli ◽  
Mohamed Zarqaoui ◽  
Mohamed Ennaji ◽  
Wassym R. Senhaji ◽  
...  
Keyword(s):  
Male Infertility ◽  
Obstructive Azoospermia ◽  
Severe Oligozoospermia

Detection Y Chromosome Microdeletions Among Iraq Population in Infertile Patients with Azoospermia and Severe Oligospermia

2019 ◽  
Vol 9 (02) ◽  
Author(s):  
Samah A Hammood ◽  
Alaauldeen S M AL-Sallami ◽  
Saleh M Al-Khafaji
Keyword(s):  
Y Chromosome ◽  
Karyotype Analysis ◽  
Semen Analysis ◽  
Obstructive Azoospermia ◽  
Severe Oligozoospermia ◽  
Infertile Men ◽  
Y Chromosome Microdeletions ◽  
Detailed Evaluation ◽  
Health Organization ◽  
Infertile Patients

Objective: To detection of microdeletions of Y chromosome and study the frequency of microdeletions in infertile men with non-obstructive azoospermia or severe oligozoospermia(Middle Euphrates center)in Iraq population. Material and methods: 153 males were included in the study, the casesweredivided into groups according to the infertility etiology and semen analysis according to Word health organization, the frequencies and the characteristicsof Y chromosome microdeletions were investigated in groups. Multiplex PCR was applied to detect the microdeletions. Results:Y chromosome microdeletion was detected in 42 (40.7%) of 153 cases ,Microdeletions in azoospermia showed more frequently detected 28 (52.8%), followed by severe oligospermia 14 (28 %),Microdeletions in the AZFc region were the most common 12 (22.64%), followed by AZFb 11(20.75%) and AZFa 5(9.43%) in azoospermia compared to severe oligospermisAZFc 6 (12%) AZFb 4 (8 %) and AZFa 4 (8%). Conclusion: Y chromosome microdeletions were detected quite frequently in certain infertility subgroups. Therefore, detailed evaluation of an infertile man by physical examination, semen analysis, hormonal evaluationsand when required, karyotype analysis may predict the patients for whom Y chromosome microdeletionanalysis is necessary and also prevent cost increases. Recommendation: This study emphasizes that analysis of microdeletions should be carried out for all patients with idiopathic azoospermia and severe oligospermia who are candidates for intracytoplasmic sperm injection

scholarly journals Cellular Therapy via Spermatogonial Stem Cells for Treating Impaired Spermatogenesis, Non-Obstructive Azoospermia

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1779
Author(s):  
Nesma E. Abdelaal ◽  
Bereket Molla Tanga ◽  
Mai Abdelgawad ◽  
Sahar Allam ◽  
Mostafa Fathi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Male Infertility ◽  
Cellular Therapy ◽  
Antihypertensive Drugs ◽  
Testicular Biopsy ◽  
Testicular Tissue ◽  
Spermatogonial Stem Cells ◽  
Obstructive Azoospermia ◽  
Promising Alternative ◽  
Major Health Problem

Male infertility is a major health problem affecting about 8–12% of couples worldwide. Spermatogenesis starts in the early fetus and completes after puberty, passing through different stages. Male infertility can result from primary or congenital, acquired, or idiopathic causes. The absence of sperm in semen, or azoospermia, results from non-obstructive causes (pretesticular and testicular), and post-testicular obstructive causes. Several medications such as antihypertensive drugs, antidepressants, chemotherapy, and radiotherapy could lead to impaired spermatogenesis and lead to a non-obstructive azoospermia. Spermatogonial stem cells (SSCs) are the basis for spermatogenesis and fertility in men. SSCs are characterized by their capacity to maintain the self-renewal process and differentiation into spermatozoa throughout the male reproductive life and transmit genetic information to the next generation. SSCs originate from gonocytes in the postnatal testis, which originate from long-lived primordial germ cells during embryonic development. The treatment of infertility in males has a poor prognosis. However, SSCs are viewed as a promising alternative for the regeneration of the impaired or damaged spermatogenesis. SSC transplantation is a promising technique for male infertility treatment and restoration of spermatogenesis in the case of degenerative diseases such as cancer, radiotherapy, and chemotherapy. The process involves isolation of SSCs and cryopreservation from a testicular biopsy before starting cancer treatment, followed by intra-testicular stem cell transplantation. In general, treatment for male infertility, even with SSC transplantation, still has several obstacles. The efficiency of cryopreservation, exclusion of malignant cells contamination in cancer patients, and socio-cultural attitudes remain major challenges to the wider application of SSCs as alternatives. Furthermore, there are limitations in experience and knowledge regarding cryopreservation of SSCs. However, the level of infrastructure or availability of regulatory approval to process and preserve testicular tissue makes them tangible and accurate therapy options for male infertility caused by non-obstructive azoospermia, though in their infancy, at least to date.

Decreased expression of DNA methyltransferases in the testes of patients with non-obstructive azoospermia leads to changes in global DNA methylation levels

2019 ◽  
Vol 31 (8) ◽  
pp. 1386 ◽  
Author(s):  
Fatma Uysal ◽  
Gokhan Akkoyunlu ◽  
Saffet Ozturk
Keyword(s):  
Dna Methylation ◽  
Male Infertility ◽  
De Novo ◽  
Biological Effects ◽  
Testicular Biopsy ◽  
Round Spermatid ◽  
Dna Methyltransferases ◽  
Global Dna Methylation ◽  
Obstructive Azoospermia ◽  
Spermatogenic Cells

DNA methylation plays key roles in epigenetic regulation during mammalian spermatogenesis. DNA methyltransferases (DNMTs) function in de novo and maintenance methylation processes by adding a methyl group to the fifth carbon atom of the cytosine residues within cytosine–phosphate–guanine (CpG) and non-CpG dinucleotide sites. Azoospermia is one of the main causes of male infertility, and is classified as obstructive (OA) or non-obstructive (NOA) azoospermia based on histopathological characteristics. The molecular background of NOA is still largely unknown. DNA methylation performed by DNMTs is implicated in the transcriptional regulation of spermatogenesis-related genes. The aim of the present study was to evaluate the cellular localisation and expression levels of the DNMT1, DNMT3A and DNMT3B proteins, as well as global DNA methylation profiles in testicular biopsy samples obtained from men with various types of NOA, including hypospermatogenesis (hyposperm), round spermatid (RS) arrest, spermatocyte (SC) arrest and Sertoli cell-only (SCO) syndrome. In the testicular biopsy samples, DNMT1 expression and global DNA methylation levels decreased gradually from the hyposperm to SCO groups (P<0.05). DNMT3A expression was significantly decreased in the RS arrest, SC arrest and SCO groups compared with the hyposperm group (P<0.05). DNMT3B expression was significantly lower in the RS arrest and SCO groups than in the hyposperm group (P<0.05). Although both DNMT1 and DNMT3A were localised in the cytoplasm and nucleus of the spermatogenic cells, staining for DNMT3B was more intensive in the nucleus of spermatogenic cells. In conclusion, the findings suggest that significant changes in DNMT expression and global DNA methylation levels in spermatogenic cells may contribute to development of male infertility in the NOA groups. Further studies are needed to determine the molecular biological effects of the altered DNMT expression and DNA methylation levels on development of male infertility.

scholarly journals Testis-Specific SEPT12 Expression Affects SUN Protein Localization and is Involved in Mammalian Spermiogenesis

2019 ◽  
Vol 20 (5) ◽  
pp. 1163 ◽  
Author(s):  
Chung-Hsin Yeh ◽  
Ya-Yun Wang ◽  
Shi-Kae Wee ◽  
Mei-Feng Chen ◽  
Han-Sun Chiang ◽  
...  
Keyword(s):  
Male Infertility ◽  
Nuclear Membrane ◽  
Sperm Count ◽  
Protein Localization ◽  
Cancer Cell Line ◽  
Structural Defects ◽  
Preimplantation Embryos ◽  
Severe Oligozoospermia ◽  
Vitro Fertilization

Male infertility is observed in approximately 50% of all couples with infertility. Intracytoplasmic sperm injection (ICSI), a conventional artificial reproductive technique for treating male infertility, may fail because of a severe low sperm count, immotile sperm, immature sperm, and sperm with structural defects and DNA damage. Our previous studies have revealed that mutations in the septin (SEPT)-coding gene SEPT12 cause teratozoospermia and severe oligozoospermia. These spermatozoa exhibit morphological defects in the head and tail, premature chromosomal condensation, and nuclear damage. Sperm from Sept12 knockout mice also cause the developmental arrest of preimplantation embryos generated through in vitro fertilization and ICSI. Furthermore, we found that SEPT12 interacts with SPAG4, a spermatid nuclear membrane protein that is also named SUN4. Loss of the Spag4 allele in mice also disrupts the integration nuclear envelope and reveals sperm head defects. However, whether SEPT12 affects SPAG4 during mammalian spermiogenesis remains unclear. We thus conducted this study to explore this question. First, we found that SPAG4 and SEPT12 exhibited similar localizations in the postacrosomal region of elongating spermatids and at the neck of mature sperm through isolated murine male germ cells. Second, SEPT12 expression altered the nuclear membrane localization of SPAG4, as observed through confocal microscopy, in a human testicular cancer cell line. Third, SEPT12 expression also altered the localizations of nuclear membrane proteins: LAMINA/C in the cells. This effect was specifically due to the expression of SEPT12 and not that of SEPT1, SEPT6, SEPT7, or SEPT11. Based on these results, we suggest that SEPT12 is among the moderators of SPAG4/LAMIN complexes and is involved in the morphological formation of sperm during mammalian spermiogenesis.

A modern view of male infertility

1994 ◽  
Vol 6 (1) ◽  
pp. 93 ◽  
Author(s):  
SJ Silber
Keyword(s):  
Male Infertility ◽  
Y Chromosome ◽  
Obstructive Azoospermia ◽  
Male Factor Infertility ◽  
Male Factor ◽  
Sperm Retrieval ◽  
Modern Approach ◽  
Vitro Fertilization ◽  
Defective Spermatogenesis

It is archaic to view male factor infertility today separately from in vitro fertilization (IVF) and treatment of the female partner. Oligoasthenozoospermia may be an inherited condition (most likely on the Y chromosome), and is refractory to any treatment of the male including hormones and varicocelectomy. IVF technology is the only justifiable approach for achieving a pregnancy in these couples. The reasons for this view and the suggested modern approach to couples with oligoasthenozoospermia are outlined in this review. However, obstructive azoospermia is different as it can be successfully corrected with microsurgery in over 90% of men. When it cannot be corrected, as in congenital absence of vas, microsurgical sperm retrieval combined with IVF can still be highly effective in producing pregnancy with sperm from the husband. The most important arena for research into male infertility in the next decade will be to map out the deletions on the Y chromosome that might result in defective spermatogenesis, and which probably cause most cases of non-obstructive male factor infertility.

The CFTR gene: male infertility and assisted conception

1999 ◽  
Vol 7 (2) ◽  
pp. 155-160 ◽  
Author(s):  
S Kulshrestha ◽  
A Makrigiannakis ◽  
P Patrizio
Keyword(s):  
Male Infertility ◽  
Vas Deferens ◽  
Cftr Gene ◽  
Obstructive Azoospermia ◽  
Male Factor Infertility ◽  
Assisted Conception ◽  
Male Factor ◽  
Fertility Treatments ◽  
Bilateral Absence ◽  
Testicular Failure

Approximately 30–40% of couples seeking fertility treatments have male factor infertility. Their dysfunctions include azoospermia, oligozoospermia, asthenozoospermia and teratozoospermia. Those with azoospermia represent about 25% of the total, and of these about 30% have an obstructive process while the remaining have either primary or secondary testicular failure. In the obstructive azoospermia group, 25% of males have congenital bilateral absence of the vas deferens (CBAVD).

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