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• W2014511280 abstract "In this report, we describe 10 male cases of complex chromosome rearrangements (CCRs) with fertility problems: seven of them showed impairment of spermatogenesis, oligoasthenoteratozoospermia or azoospermia; in the other three cases, recurrent abortions were observed. The CCRs were characterized by conventional fluorescence in situ hybridization (FISH) and multicolor FISH methods as well as by the routine G-banding technique. CCRs found in three cases with recurrent abortions were double two-way exchanges, which were the simplest forms of CCRs; three oligoastenoteratozoospermic cases were double two-way exchanges or three-way exchanges. However, the CCRs in four azoospermic cases were much more complicated forms of CCRs. From our results and a review of the literature, we conclude that the complexity of CCRs might affect the severity of spermatogenetic impairment rather than the number of chromosomes involved or the location of breakpoints. In this report, we describe 10 male cases of complex chromosome rearrangements (CCRs) with fertility problems: seven of them showed impairment of spermatogenesis, oligoasthenoteratozoospermia or azoospermia; in the other three cases, recurrent abortions were observed. The CCRs were characterized by conventional fluorescence in situ hybridization (FISH) and multicolor FISH methods as well as by the routine G-banding technique. CCRs found in three cases with recurrent abortions were double two-way exchanges, which were the simplest forms of CCRs; three oligoastenoteratozoospermic cases were double two-way exchanges or three-way exchanges. However, the CCRs in four azoospermic cases were much more complicated forms of CCRs. From our results and a review of the literature, we conclude that the complexity of CCRs might affect the severity of spermatogenetic impairment rather than the number of chromosomes involved or the location of breakpoints. Complex chromosome rearrangements (CCRs) are structural aberrations involving at least three chromosomes with three or more chromosomal breakpoints (1Pai G.S. Thomas G.H. Mahoney W. Migeon B.R. Complex chromosome rearrangements. Report of a new case and literature review.Clin Genet. 1980; 18: 436-444Crossref PubMed Scopus (115) Google Scholar). CCRs are very rare events in the human population: to date about 160 patients with CCRs have been reported in the literature, although this number will likely increase owing to the application of cytogenetic techniques (2Ergul E. Liehr T. Mrasek K. Sazci A. A de novo complex chromosome rearrangement involving three chromosomes (2, 13, and 18) in an oligospermic male.Fertil Steril. 2009; 92 (e9–e12): 391Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar). CCRs have been classified into three major categories: [1] three-way exchanges, which are the most common category, in which three segments from three chromosomes break off, translocate, and unite; [2] more complicated CCRs, or rearrangements with more than one breakpoint per chromosome, that is, additional insertions or inversions and hence production of even more complicated meiotic configurations leading to additional possibilities of unbalanced segregation; and [3] double two-way exchanges, the simplest CCR, in which there is a coincidence of two separate simple translocations (3Kausch K. Haaf T. Khler J. Schmid M. Complex chromosomal rearrangement in a woman with multiple miscarriages.Am J Med Genet. 1988; 31: 415-420Crossref PubMed Scopus (53) Google Scholar). CCRs can also be divided into two groups, familial and de novo (4Voullaire L.E. Webb G.C. Complex chromosome rearrangements involving chromosomes 1;3 and 2;3 in two abnormal children.Clin Genet. 1988; 34: 313-320Crossref PubMed Scopus (6) Google Scholar). Most familial cases have a normal phenotype with apparently balanced rearrangements (5Lespinasse J. North M.O. Paravy C. Brunel M.J. Malzac P. Blouin J.L. A balanced complex chromosomal rearrangement (BCCR) in a family with reproductive failure.Hum Reprod. 2003; 18: 2058-2066Crossref PubMed Scopus (20) Google Scholar). In contrast, half of de novo CCRs, which are apparently balanced, are associated with multiple structural anomalies as well as mental retardation (6Coco R. Rahn M.I. Estanga P.G. Antonioli G. Solari A.J. A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.Hum Reprod. 2004; 19: 2784-2790Crossref PubMed Scopus (29) Google Scholar). Carriers of CCRs are at risk of conceptions with various anomalies and reproductive failure owing to abnormal segregation of the derivative chromosome or meiotic failure. Female carriers with CCRs have been identified after having malformed babies or repeated abortions (7Batista D.A. Pai G.S. Stetten G. Molecular analysis of a complex chromosomal rearrangement and a review of familial cases.Am J Med Genet. 1994; 53: 255-263Crossref PubMed Scopus (103) Google Scholar). Most males with CCRs have shown infertility problems resulting from hypospermatogenesis or spermatogenic failure, and there have been several reports of CCRs in males with oligozoospermia or azoospermia (2Ergul E. Liehr T. Mrasek K. Sazci A. A de novo complex chromosome rearrangement involving three chromosomes (2, 13, and 18) in an oligospermic male.Fertil Steril. 2009; 92 (e9–e12): 391Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar, 6Coco R. Rahn M.I. Estanga P.G. Antonioli G. Solari A.J. A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.Hum Reprod. 2004; 19: 2784-2790Crossref PubMed Scopus (29) Google Scholar, 8Bartels I. Starke H. Argyriou L. Sauter S.M. Zoll B. Liehr T. An exceptional complex chromosomal rearrangement (CCR) with eight breakpoints involving four chromosomes (1;3;9;14) in an azoospermic male with normal phenotype.Eur J Med Genet. 2007; 50: 133-138Crossref PubMed Scopus (28) Google Scholar). However, males with CCRs do not always show infertility or subfertility phenotypes (9Cai T. Yu P. Tagle D.A. Lu D. Chen Y. Xia J. A de novo complex chromosomal rearrangement with a translocation 7;9 and 8q insertion in a male carrier with no infertility.Hum Reprod. 2001; 16: 59-62Crossref PubMed Scopus (21) Google Scholar). We assessed the relationship between CCRs and spermatogenetic failure in 10 phenotypically normal males with CCRs who were referred to the Genetics Laboratory of CHA Gangnam Medical Center from 2002 to 2009 owing to fertility problems. Sexual development was apparently normal in all 10 patients. These patients were evaluated by chromosome analysis and histological examination as well as by basic laboratory tests such as hormone and sperm assays. Chromosome abnormalities were characterized by fluorescent in situ hybridization (FISH) and multicolor FISH (M-FISH) as well as by routine G-banding. This study was approved by the Institutional Review Board of CHA Gangnam Medical Center. Conventional cytogenetic studies were performed on lymphocytes from phytohemagglutinin-stimulated peripheral blood cultures. GTG-banded chromosomes were obtained according to a standard protocol, and 20 metaphases were examined and karyotyped using the CytoVision System version 3.6 (Applied Imaging, Thunderland, UK). Chromosomal abnormalities were described according to the International System for Human Cytogenetic Nomenclature 2009. Chromosomal abnormalities identified by conventional chromosome analysis were initially reevaluated by conventional FISH using Vysis whole chromosome painting probes (Abbott Molecular Inc. Chicago, IL). Two patients were evaluated by M-FISH and FISH using Vysis locus-specific identifier probes. M-FISH was performed using the 24 XCyte multicolor probe kit (Metasystems, Altlussheim, Germany). All FISH procedures were performed according to the manufacturer’s protocols. FISH signals were analyzed using a Zeiss AXIO Imager A2 fluorescent microscope with the Isis FISH imaging system version 5.3 (Metasystems). Patients were also evaluated for microdeletions of azoospermic factor (AZF) regions on the long arm of the Y chromosome. Genomic DNAs were extracted from peripheral blood using the QIAamp DNA blood Midi kit (Qiagen, Hilden, Germany). The DAZ gene family (DAZ1, 2, 3, and 4) and sequences-tagged sites in the AZF regions (AZFb, AZFc: sY117, sY127, sY143, sY134, sY138, sY152, sY153, sY147, sY149, sY269, sY157, and sY158) were analyzed by polymerase chain reaction (PCR), performed as described elsewhere (10Nakashima M. Koh E. Namiki M. Yoshida A. Multiplex sequence-tagged site PCR for efficient screening of microdeletions in Y chromosome in infertile males with azoospermia or severe oligozoospermia.Arch Androl. 2002; 48: 351-358Crossref PubMed Scopus (15) Google Scholar, 11de Vries J.W. Hoffer M.J. Repping S. Hoovers J.M. Leschot N.J. van der Veen F. Reduced copy number of DAZ genes in subfertile and infertile men.Fertil Steril. 2002; 77: 68-75Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar). The PCR products were electrophoresed on 2% agarose gels and visualized under ultraviolet light. The testicular biopsies were performed by a urologist, after approval by patients, to search for male gametes. Paraffin-embedded specimens were sectioned and stained with a standard hematoxylin and eosin staining method. The specimens underwent meticulous histological evaluation as well as a thorough examination to collect male gametes of any stage. Photomicrographs were taken using a digital microscope (Coolscope, Nikon, Tokyo, Japan). Hormone profiles and semen analyses of the seven males with spermatogenetic defects are shown in Supplementary Table 1. The level of testosterone was detected to be slightly below the normal range (2.45–18.36 ng/mL) in only one patient. Otherwise, no hormonal abnormalities were uncovered. Three patients (numbers 1, 4, and 9) were diagnosed with oligoastenoteratozoospermia (OAT) and four (numbers 6, 7, 8, and 10) with azoospermia, whereas the other three had recurrent abortions (RA). RA was defined as three or more clinically recognized pregnancy losses before 20 weeks from the last menstrual period. The AZF region deletions were not detected in the seven patients with spermatogenetic defects. For azoospermic males, histological examinations were performed. According to the histopathologic criteria (12Hendin B.N. Patel B. Levin H.S. Thomas A.J. Agarwal A. Identification of spermatozoa and round spermatids in the ejaculates of men with spermatogenic failure.Urology. 1998; 51: 816-819Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar), specimens can be classified into five groups: normal, hypospermatogenesis, maturation arrest, Sertoli cells only, and tubular fibrosis. Histopathologic examination of patient 6 showed that he had no germ cells and was defined as having Sertoli cells only (Supplementary Fig. 1A), whereas examination of the three other azoospermic males (numbers 7, 8, and 10) showed no evidence of mature sperm, with all germ cells in the seminiferous tubules showing maturation arrest (Supplementary Fig. 1B). Patients 1 and 9 tried to get pregnant with intracytoplasmic sperm injection and preimplantation genetic diagnosis using blastomeres biopsies, but both patients failed to achieve pregnancy. Results of karyotype analyses in all 10 patients are summarized in Supplementary Table 2. Three-way exchanges (group 1) were identified in two patients (numbers 8 and 9); double two-way exchanges or two independent abnormalities (a two-way exchange plus an inversion), which are categorized as group 3, were identified in five (numbers 1–5); and group 2 CCRs were identified in three (numbers 6, 7, and 10). All three patients referred for RA had group 3 CCRs. In contrast, of the seven patients with spermatogenetic defects, two were classified as group 1, three as group 2, and only two as group 3. The CCRs in the patients 7 and 10, were characterized using M-FISH methods. M-FISH confirmed the routine G-bands and FISH results in patient 7 (Supplementary Fig. 2). In case 10, however, the 16q24-16qter region on der(6Coco R. Rahn M.I. Estanga P.G. Antonioli G. Solari A.J. A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.Hum Reprod. 2004; 19: 2784-2790Crossref PubMed Scopus (29) Google Scholar) chromosome identified by the TelVysion 16q probe was not fully identified by M-FISH (Supplementary Fig. 3). We also performed routine checkup of the female partner for infertility, especially when RA was the main outcome, including chromosomal analyses. The karyotypes of all three females with RA were 46,XX, and the hormone profiles and clinical findings of the other seven women showed no abnormalities. In the present study, all 10 of our patients with CCR showed reproductive impairments, either RA or spermatogenetic failure, with seven (70%) also showing spermatogenetic impairment. In a female carrier of CCR, chromosomal malsegregations during gametogenesis result in abnormal conceptions, with most of these spontaneously aborted. In contrast to female CCR carriers, the male CCR carriers often show impaired spermatogenesis, resulting in oligo- or azoospermia. The association between CCR and spermatogenesis is not fully understood. In all three of our patients with RA, the CCRs belonged to group 3 CCR, whereas most of the CCRs found in azoospermic males were group 1 or 2. These findings indicate that an increase in the number of breakpoints and more complex structural rearrangements have more severe consequences for gametogenesis. Testicular biopsy results in the four azoospermic males showed maturation arrest in three patients (numbers 7, 8, and 10) and Sertoli cells only in one patient (number 6). The latter patient also showed bilateral varicoceles. Varicoceles, leading to ischemic damage to testicular tissue, have been found to result in impaired sperm quality and reduction in quantity (13Gat Y. Zukerman Z. Chakraborty J. Gornish M. Varicocele, hypoxia and male infertility. Fluid mechanics analysis of the impaired testicular venous drainage system.Hum Reprod. 2005; 20: 2614-2619Crossref PubMed Scopus (110) Google Scholar). Although a comparatively less complex chromosomal rearrangement (involving two chromosomes with four breakpoints), the serious clinical outcome in patient 6 may be due to the combination of chromosomal rearrangement and varicoceles. In the other three azoospermic patients, most spermatogenesis was arrested at the level of spermatocytes, mainly at the late pachytene stage, with only a few cells being early spermatids. There were no mature spermatozoa. The possible mechanisms of spermatogenetic failure in males with CCR have suggested that the number of breakpoints in the autosomes involved in the structural rearrangement is very numerous, increasing the probability of asynapsis as well as of pachytene checkpoint activation. This results in a considerable reduction in the number of postmeiotic cells, including spermatozoa production (14Oliver-Bonet M. Ko E. Martin R.H. Male infertility in reciprocal translocation carriers: the sex body affair.Cytogenet Gen Res. 2005; 111: 343-346Crossref PubMed Scopus (32) Google Scholar, 15Turner J.M. Mahadevaiah S.K. Fernandez-Capetillo O. Nussenzweig A. Xu X. Deng C. et al.Silencing of unsynapsed meiotic chromosomes in the mouse.Nat Genet. 2005; 37: 41-47PubMed Google Scholar). Moreover, the few spermatocytes that escape pachytene apoptosis are unable to deal with a pentavalent and one univalent in the metaphase I spindle and die before anaphase (6Coco R. Rahn M.I. Estanga P.G. Antonioli G. Solari A.J. A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.Hum Reprod. 2004; 19: 2784-2790Crossref PubMed Scopus (29) Google Scholar). Although we did not examine the synaptonemal complexes in any of our azoospermic patients, they may be more complex than those found in individuals with the three-way CCR, or else they failed. Most CCRs were identified using routine cytogenetic analyses, and M-FISH was widely used for confirmation of the G-banding results. However, as shown in one of our patients (number 10), subtle rearrangements could not be identified by either of these methods. In this patient, the der (6Coco R. Rahn M.I. Estanga P.G. Antonioli G. Solari A.J. A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.Hum Reprod. 2004; 19: 2784-2790Crossref PubMed Scopus (29) Google Scholar) chromosome identified by the locus-specific probe could not be fully identified by either G-banding or M-FISH, indicating that, in addition to M-FISH, conventional FISH using locus-specific probes still remains crucial for the detailed identification of cryptic chromosomal rearrangements. Other than the complexity of rearrangements, gene defects or microdeletions in the long arm of the Y-chromosome, the most common cause of oligo- or azoospermia, may have caused spermatogenetic impairment in our patients, Yq microdeletions were excluded. If the specific breakpoints are associated with spermatogenetic impairment, those regions may contain genes involved in spermatogenesis or chromosomal segregation. We therefore reviewed the chromosomal breakpoints presented in the literature about male cases with a CCR and reproductive failure (Fig. 1) (2Ergul E. Liehr T. Mrasek K. Sazci A. A de novo complex chromosome rearrangement involving three chromosomes (2, 13, and 18) in an oligospermic male.Fertil Steril. 2009; 92 (e9–e12): 391Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar, 6Coco R. Rahn M.I. Estanga P.G. Antonioli G. Solari A.J. A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.Hum Reprod. 2004; 19: 2784-2790Crossref PubMed Scopus (29) Google Scholar, 8Bartels I. Starke H. Argyriou L. Sauter S.M. Zoll B. Liehr T. An exceptional complex chromosomal rearrangement (CCR) with eight breakpoints involving four chromosomes (1;3;9;14) in an azoospermic male with normal phenotype.Eur J Med Genet. 2007; 50: 133-138Crossref PubMed Scopus (28) Google Scholar, 16Salahshourifar I. Shahrokhshahi N. Tavakolzadeh T. Beheshti Z. Gourabi H. Complex chromosomal rearrangement involving chromosomes 1, 4 and 22 in an infertile male: case report and literature review.J Appl Genet. 2009; 50: 69-72Crossref PubMed Scopus (11) Google Scholar, 17Chandley A.C. Edmond P. Christie S. Gowans L. Fletcher J. Frackiewicz A. et al.Cytogenetics and infertility in man. I. Karyotype and seminal analysis: results of a five-year survey of men attending a subfertility clinic.Ann Hum Genet. 1975; 39: 231-254Crossref PubMed Scopus (165) Google Scholar, 18Gorski J.L. Kistenmacher M.L. Punnett H.H. Zackai E.H. Emanuel B.S. Reproductive risks for carriers of complex chromosome rearrangements: analysis of 25 families.Am J Med Genet. 1988; 29: 247-261Crossref PubMed Scopus (72) Google Scholar, 19Johannisson R. Lhrs U. Passarge E. Pachytene analysis in males heterozygous for a familial translocation (9;12;13)(q22;q22;q32) ascertained through a child with partial trisomy 9.Cytogenet Cell Genet. 1988; 47: 160-166Crossref PubMed Scopus (42) Google Scholar, 20Joly-Helas G. de La Rochebrochard C. Mousset-Simon N. Moirot H. Tiercin C. Romana S.P. et al.Complex chromosomal rearrangement and intracytoplasmic sperm injection: a case report.Hum Reprod. 2007; 22: 1292-1297Crossref PubMed Scopus (21) Google Scholar, 21Joseph A. Thomas I.M. A complex rearrangement involving three autosomes in a phenotypically normal male presenting with sterility.J Med Genet. 1982; 19: 375-377Crossref PubMed Scopus (31) Google Scholar, 22Lee I.W. Su M. Hsu C. Lin Y. Chen P. Kuo P. Constitutional complex chromosomal rearrangements in azoospermic men: case report and literature review.Urology. 2006; 68 (e5–e8): 1343PubMed Google Scholar, 23Rodriguez M.T. Martin M.J. Abrisqueta J.A. A complex balanced rearrangement involving four chromosomes in an azoospermic man.J Med Genet. 1985; 22: 66-67Crossref PubMed Scopus (35) Google Scholar, 24Saadallah N. Hulten M. A complex three breakpoint translocation involving chromosomes 2, 4, and 9 identified by meiotic investigations of a human male ascertained for subfertility.Hum Genet. 1985; 71: 312-320Crossref PubMed Scopus (60) Google Scholar, 25Salahshourifar I. Gilani M.A. Vosough A. Tavakolzadeh T. Tahsili M. Mansori Z. et al.De novo complex chromosomal rearrangement of 46, XY, t(3;16;8)(p26;q13;q21.2) in a non-obstructive azoospermic male.J Appl Genet. 2007; 48: 93-94Crossref PubMed Scopus (9) Google Scholar, 26Siffroi J.P. Benzacken B. Straub B. Le Bourhis C. North M.O. Curotti G. et al.Assisted reproductive technology and complex chromosomal rearrangements: the limits of ICSI.Mol Hum Reprod. 1997; 3: 847-851Crossref PubMed Scopus (36) Google Scholar, 27Sills E.S. Kim J.J. Witt M.A. Palermo G.D. Non-obstructive azoospermia and maturation arrest with complex translocation 46, XY, t(9;13;14)(p22;q21.2;p13) is consistent with the Luciani-Guo hypothesis of latent aberrant autosomal regions and infertility.Cell Chromosome. 2005; 4: 2Crossref PubMed Scopus (16) Google Scholar, 28Walker S. Howard P.J. Hunter D. Familial complex autosomal translocations involving chromosomes 7, 8, and 9 exhibiting male and female transmission with segregation and recombination.J Med Genet. 1985; 22: 484-491Crossref PubMed Scopus (29) Google Scholar). Several breakpoints on chromosomes 4q, 5q, 7q, 9p, and 14q have been frequently reported in males with RA, whereas breakpoints on chromosomes 3, 4q, 11q, 12q, and 13q have been reported to be related to spermatogenetic failure. We found, however, that the breakpoints were generally randomly distributed. Although any breakpoints may include genes or gene regions related to spermatogenesis, no particular breakpoint had a decisive effect on spermatogenetic failure. In conclusion, the complexity of chromosomal rearrangements in patients with CCRs plays a role in male factor infertility and affects the spermatogenetic process rather than the number of chromosomes involved or the location of breakpoints. To corroborate this conclusion, further studies with larger sample sizes and using an advanced technique, such as array-based comparative genomic hybridization, to characterize the breakpoints in detail are required. The authors thank Professor Kyung-Ah Lee for the contribution to the histological examination and the staff of the Genetics Laboratory of CHA Gangnam Medical Center for cytogenetic analyses. Tabled 1Clinical findings of males with CCRs diagnosed at CHA medical center (2002–2009).Semen analysisCaseAge at diagnosisHeight, cmWeight, kgFSH, mIU/mLLH, mIU/mLT, ng/mLVolume, mLpHConcentration, ×106/mLMotility, %Morphology, % with normal formViability, %Leukocytes/HPFNotes133183832.28.019—16—Amorphos head, 40%2353304321.65.35.235.62.520<1250.1Amorphous head, most common529633172683.52.96.364.98.2————1Immotile sperm 8/10 μL after centrifuge736165485.94.62.220.18.6————1.3840176785.42.75.233.07.5————1934172766.03.04.42.48.1528541—Amorphous, elongated, vacuole head, each 14%1033170789.45.93.24.27.2—————Note: Blank columns represent not analyzed. Normal ranges of hormonal profiles: FSH (1.1–13.5 mIU/mL), LH (0.4–5.7 mIU/mL), T (2.45–18.36 ng/mL). Open table in a new tab Note: Blank columns represent not analyzed. Normal ranges of hormonal profiles: FSH (1.1–13.5 mIU/mL), LH (0.4–5.7 mIU/mL), T (2.45–18.36 ng/mL). Tabled 1Summary of the results of studies of males with CCRs.CaseKaryotypeAZF and DAZTesticular biopsyP146,XY,inv(3)(p21:q11.2),t(6:22)(q22:q13)NDP246,XY,t(4:5)(q31.3:q32),t(5:11)(q15:p15)P345,XY,t(5:8)(q22:p23),der(13:14)(q10,q10)P445,XY,t(3:9)(q24:q21.2),der(13:14)(q10:q10)NDP546,XY,inv(1)(p13:q21)t(17:22)(p11:p11)P646,XY,der(3)(14pter::3q10→3qter),der(14)(3pter→3p11.1::14q21→14p11::14q21→14qter)NDSertoli cell onlyP746,XY,der(1)(9qter→9q22::1p32→1qter),der(4)(1pter→1p32::13q32→13q14::4p14→4qter),der(9)(9pter→9q22::4p14→4pter),der(13)(13pter→13q14::13q32→13qter)NDMaturation arrestP846,XY,t(2:19:22)(q11.2:p13.2:p11.2)NDMaturation arrestP946,XY,t(2:7:4)(q31;q34;q33)NDP1046,XY,der(3)(3pter→3p23::3q25.3→3p11.1::6q27→6qter),der(6)(6pter→6q27::16q24→16qter),der(12)(12pter→12q24.3::3q25.3→3qter),der(16)(16pter→16q24::3p11.1→3p23::12q24.3→12qter)NDMaturation arrestNote: ND = no deletion. Open table in a new tab Note: ND = no deletion." @default.
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• W2014511280 title "Complex chromosomal rearrangements in infertile males: complexity of rearrangement affects spermatogenesis" @default.
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