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Query: UMLS:C0029713 (immaturity)
4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sperm morphology was studied in 302 extensively managed Zebu bulls (aged 1.5-9 years), classified as sound (n=166) or unsound (n=136) for breeding, under field conditions in the dry tropics of Costa Rica. Single semen samples were collected by electro-ejaculation and fixed in formol-saline solution immediately after collection. Sperm morphology was determined in the field on wet smears using a microscope equipped with phase-contrast optics, and further determined in the laboratory on air-dried smears stained with carbol-fuchsin. The frequencies of sperm abnormalities (such as abnormal acrosome, head, neck, mid-piece, tail, and presence of cytoplasmic droplets) were recorded as a percentage of the total number of counted spermatozoa (400 cells). Zebu bulls considered unsound for breeding showed a higher mean prevalence (p < 0.05) of knobbed acrosomes (4.0 versus 0.9%), head defects [specifically, nuclear invaginations and heads with abnormal shapes and sizes (27.6 versus 4.0%)], abnormal tails (11.2 versus 4.7%), and proximal droplets (8.4 versus 1.6%), compared with bulls considered sound for breeding. In these latter bulls, the abnormality most commonly seen was the presence of single bent tails with an entrapped cytoplasmic droplet (3.0 +/- 3.7%). Young Zebu bulls (i.e. bulls under 2 years of age) showed a higher percentage of missing acrosomes, and proximal cytoplasmic droplets, than older sires (12.1 versus 2.4%, and 23.9 versus 3.6%, respectively; p < 0.05), interpreted as an indication of low ejaculation frequency and sexual immaturity, respectively. Bulls with a long scrotum and soft testicular consistency (TC) at palpation showed higher percentages of abnormal sperm heads in the ejaculate than bulls with a normal scrotal length (SL) and a normal TC (32.7 versus 12.8% and 30.7 versus 10.3%, respectively; p < 0.05). In addition, Zebu bulls with a scrotal circumference (SC) < or = 30 cm showed a higher prevalence of proximal cytoplasmic droplets than bulls whose SC was > 30 cm (9.8 versus 2.6%, p < 0.05). A higher mean percentage of abnormally sized and shaped heads, especially undeveloped and narrow at the base, was more frequently found in stained smears than in unstained samples (26.0 versus 9.9%, p < 0.05), which clearly underlines the importance of using both stained and wet smears when assessing sperm head morphology. However, for a quick assessment of sperm morphology under field, tropical conditions, phase-contrast microscopy provides useful information for the spermiogramme evaluation.
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PMID:Assessment of sperm morphology in zebu bulls, under field conditions in the tropics. 1132 62

Previously, a relationship has been found between diminished cellular maturity of human spermatozoa and low-level expression of the testis-specific chaperone protein, HspA2. Because HspA2 is a component of the synaptonemal complex in rodents, and assuming that this is also the case in men, it was postulated that the frequency of chromosomal aneuploidies would be higher in immature versus mature spermatozoa. This question was examined in spermatozoa from semen and from 80% Percoll pellets (enriched for mature spermatozoa) of the same ejaculate in 10 oligozoospermic men. Immature spermatozoa with retained cytoplasm, which signifies spermiogenetic arrest, were identified by immunocytochemistry. Using fluorescence in-situ hybridization (FISH), approximately 7000 sperm nuclei were evaluated in each of the 20 fractions (142 086 spermatozoa in all) using centromeric probes for the X, Y and 17 chromosomes. The proportions of immature spermatozoa were 45.4 +/- 3.4 versus 26.6 +/- 2.2% in the two semen versus the Percoll groups (medians: 48.2 versus 25%, P < 0.001, n = 300 spermatozoa per fraction, total 6000 spermatozoa). There was also a concomitant decline in total disomy, total diploidy and total aneuploidy frequencies in the 80% Percoll versus semen fractions (0.17 versus 0.54%, 0.14 versus 0.26% and 0.31 versus 0.81% respectively, P < 0.001 in all comparisons). The mean decline of aneuploidies was 2.7-fold. With regard to the hypothesis that aneuploidies are related to sperm immaturity, there was a close correlation between the incidence of immature spermatozoa and disomies (r = 0.7, P < 0.001) but no correlation with diploidies (r = 0.03), indicating that disomies originate primarily in immature spermatozoa. It is suggested that the common factor underlying sperm immaturity and aneuploidies is the diminished expression of HspA2. In addition, the lack of this chaperone may also cause diminished cellular transport of proteins, such as DNA-repair enzymes or of the retention of cytoplasm that is extruded from normally maturing spermatozoa during spermiogenesis.
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PMID:FISH assessment of aneuploidy frequencies in mature and immature human spermatozoa classified by the absence or presence of cytoplasmic retention. 1138 94

Electron microscopy is a valuable tool in understanding not only the presence but also the nature of sperm malformation causing human infertility. In the past, we have examined patients affected by severe teratospermia concomitant with andrological pathologies such as varicocele, cryptorchidism, and infection. In particular, we have demonstrated that, in the case of varicocele, a combination of different phenotypic defects typical of immature spermatozoa is present. This general study was carried out on 2000 infertile men who presented for sperm analysis at our laboratory over the course of 10 years. The ejaculate of all of them was examined by electron microscopy, statistically evaluated by a formula created by us (J of Andrology, 1995), and cytogenetically checked by fluorescence microscopy techniques. First of all, this study concerned the techniques of assisted reproduction, i.e. intracytoplasmic sperm injection (ICSI), partial zona disruption (PZD), and in vitro fertilization (IVF). The conclusion was that the evaluation of the sperm quality of males attempting artificial insemination must concern not only motility or staining characteristics but mainly submicroscopical and molecular properties. Moreover, the effect of follicle stimulating hormone (FSH) treatment on human sperm quality has been evaluated by our group testing the ultrastructure and the function of spermatozoa before and after the therapy. Using the sperm as an andrological monitor, it seems that the therapeutic effect of FSH depends on the type of sperm affections. In particular, phenotypic defects as apoptosis and immaturity can be corrected by FSH treatment. More recently, we approached the problem of genotypic sperm infertility. We demonstrated that some very peculiar defects, detected by electron microscopy, show a hereditary transmission having a genetic basis. In fact, they are much more frequent in consanguineous patients, and are clearly related to different degrees of consanguinity. Frequently, chromosomal translocations have sometimes been found correlated to these defects.A consequence of these demonstrations is that most of the present sperm defects are phenotypic and can be submitted to surgical or pharmaceutical cares, but others have genetic origin and cannot be corrected by surgical or pharmaceutical treatment. These malformations are transmitted to the offspring by techniques of assisted fertilization.
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PMID:Recent advances in human sperm pathology. 1202 Jul 79

We investigated the histopathological effects of excess L-cysteine on the male rat reproductive tract during sexual maturation. Male 6-week-old Sprague-Dawley rats were injected intraperitoneally daily with L-cysteine, 1,000 mg/kg body weight, for 1, 2, 3, and 4 weeks. L-Cysteine-treated rats developed sperm granulomas in the epididymides at an incidence of 0% (0/6), 50% (3/6), 83% (5/6), and 100% (6/6) in rats examined at study weeks 1, 2, 3, and 4, respectively. These sperm granulomas were unilateral or bilateral, and most frequently involved the proximal cauda region of the epididymides. Interestingly, small ducts, indicative of immaturity, were seen frequently in L-cysteine-treated rats. These findings suggest that the maturation of epididymides in L-cysteine-treated rats might be delayed. Additionally, dilated ducts and interstitial edema, suggestive of an increase in intraluminal pressure, were seen often in the epididymides of L-cysteine-treated rats. Labeling spermatozoa and epithelial cells with monobromobimane indicated no influence of the thiol-disulfide status of L-cysteine to the epididymides. The testes and prostate glands also showed no effects, suggesting that inhibited epididymis maturation was not a result of hormonal deficiencies. We speculate that defective development of the ducts might result in aberrant fluid flow, leading to ductal rupture in the epididymides. In that case, sperm granulomas might form around leaked spermatozoa.
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PMID:Development of sperm granulomas in the epididymides of L-cysteine-treated rats. 1274 15

Disorders of testicular function may have their origins in fetal or early life as a result of abnormal development or proliferation of Sertoli cells. Failure of Sertoli cells to mature, with consequent inability to express functions capable of supporting spermatogenesis, is a prime example. In a similar way, failure of Sertoli cells to proliferate normally at the appropriate period in life will result in reduced production of spermatozoa in adulthood. This review focuses on the control of proliferation of Sertoli cells and functional maturation, and is motivated by concerns about 'testicular dysgenesis syndrome' in humans, a collection of common disorders (testicular germ-cell cancer, cryptorchidism, hypospadias and low sperm counts) which are hypothesized to have a common origin in fetal life and to reflect abnormal function of Sertoli (and Leydig) cells. The timing of proliferation of Sertoli cells in different species is reviewed, and the factors that govern the conversion of an immature, proliferating Sertoli cell to a mature, non-proliferating cell are discussed. Protein markers of maturity and immaturity of Sertoli cells in various species are reviewed and their usefulness in studies of human testicular pathology are discussed. These markers include anti-Mullerian hormone, aromatase, cytokeratin-18, GATA-1, laminin alpha5, M2A antigen, p27(kip1), sulphated glycoprotein 2, androgen receptor and Wilms' tumour gene. A scheme is presented for characterization of Sertoli-cell only tubules in the adult testis according to whether or not there is inherent failure of maturation of Sertoli cells or in which the Sertoli cells have matured but there is absence, or acquired loss, of germ cells. Functional 'de-differentiation' of Sertoli cells is considered. It is concluded that there is considerable evidence to indicate that disorders of maturation of Sertoli cells may be a common underlying cause of human male reproductive disorders that manifest at various life stages. This recognition emphasizes the important role that animal models must play to enable identification of the mechanisms via which failure of proliferation and maturation of Sertoli cells can arise, as this failure probably occurs in fetal life.
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PMID:Proliferation and functional maturation of Sertoli cells, and their relevance to disorders of testis function in adulthood. 1277 99

The essence of fertilization is the union and mingling of male and female genomes. Therefore it is not surprising that microsurgical deposition of a single spermatozoon in an oocyte (ICSI) results in the development of normal offspring. Poorly motile or structurally aberrant spermatozoa, which are unable to fertilize under ordinary conditions, are not necessarily genomically abnormal. This is the reason why normal offspring are obtained after ICSI using such spermatozoa. At present, ICSI is most successful in humans and mice, but there is no reason to believe that ICSI does not work in other animal species as well. Injection of round spermatids into oocytes (ROSI) works routinely in the mouse, but it is controversial in humans. While some investigators have claimed successes, many others have reported complete failure. There must be several reasons for this, including the difficulty of distinguishing true spermatids from other small cells. Insufficient oocyte activation following ROSI and the functional immaturity of the centrosome could also be responsible for this. In mice, it is possible to obtain normal offspring by injection of primary or secondary spermatocytes into oocytes. The nucleus of a spermatocyte undergoes meiotic division(s) within the oocyte's cytoplasm before a haploid sperm pronucleus unites with an oocyte's haploid pronucleus. However, only a few of the produced zygotes have developed into fertile offspring. There are many hurdles to clear before ROSI and spermatocyte injection becomes efficient and medically safe methods for assisted fertilization.
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PMID:Fertilization and developmental initiation of oocytes by injection of spermatozoa and pre-spermatozoal cells. 1610 Oct 32

The sperm 'round head' defect, also known as globozoospermia, is an uncommon alteration of sperm morphology generally characterised by 100% round headed sperm totally lacking an acrosome. This alteration is a genetic sperm defect as demonstrated by analysing the incidence of these alterations in a population of infertile men showing a history of consanguinity and cases belonging to the same family. Ultrastructural characteristics and meiotic segregation in spermatozoa from two patients affected by 'round head' sperm defect were investigated. The sperm quality was examined by light and transmission electron microscopy (TEM) and fluorescence in situ hybridization (FISH) analysis was performed in order to investigate the meiotic behavior of chromosomes namely gonosomes and chromosome 18. TEM analysis, mathematically elaborated, clearly diagnosed the 'round head' genetic sperm defect and highlighted at the same time the presence of other phenotypic alterations belonging to pathologies such as immaturity, apoptosis and necrosis. It is possible to hypothesize that round headed sperm could be a 'weak phenotype' allowing the sperm pathologies to overlap with a sperm defect of genetic origin, further compromising fertilizing potential. FISH analysis revealed a positive correlation between globozoospermia and higher disomies of sex chromosomes and diploidies suggesting a higher risk of creating an aneuploid embryo after intracytoplasmic sperm injection.
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PMID:'Round head' sperm defect. Ultrastructural and meiotic segregation study. 1661 73

A fluorescent assay was used to reveal the presence of lipid peroxidation (LPO) in spermatozoa from individuals with genitourinary infections (GI). The incidence of LPO was compared with sperm pathologies (apoptosis, immaturity, necrosis) evaluated by transmission electron microscopy (TEM) and motility. A C11-BODIPY(581/591) probe was used to detect and localize LPO in sperm from 34 individuals. The sperm morphological characteristics were studied by TEM and the results were mathematically assessed. Using the LPO percentage we divided the patients into four groups. Group 1 included ten patients with GI with almost normal progressive motility, a very low percentage of LPO and sperm pathology values that were not far from the standard ranges. Group 2 had eleven infected patients showing reduced motility, LPO of 10 to 20% and sperm pathologies that were just out of normal range. Group 3 included 6 infected patients with progressive motility < or =22%, low levels of LPO with a higher percentage of apoptosis and necrosis. Group 4 had 7 patients showing normal semen parameters, without GI, LPO ranged from 0% to 1% and a normal incidence of sperm pathologies. In all groups, LPO was inversely correlated with sperm motility and directly correlated with low semen quality. However, the LPO percentage was low in Group 3, in which sperm necrosis, concomitant with GI, was the predominant pathology. C11-BODIPY(581/591) is a useful labeling method for quantifying and localizing LPO in spermatozoa from patients with GI. The detection of LPO could be questionable in cases of sperm necrosis because in this pathology the plasma membrane is often disrupted and the lipidic probe is unable to intercalate within the phospholipidic bilayer.
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PMID:Lipid peroxidation in human spermatozoa from men with genitourinary infections. 1844 48

Data on reproductive physiology from the Eurasian lynx (Lynx lynx) are still scarce. The lynx is protected under Swedish hunting legislation. All lynx that are found dead or that are culled at hunting are to be sent to the Swedish National Veterinary Institute. In this study, we examined reproductive organs from 55 male lynx collected during the years 2002-2005. Age, body weight, testicular weight and volume, production of spermatozoa, and sperm viability were evaluated. The majority of the animals (39) had been killed in February and March, which is during the hunting season. The ages varied between 6 months and 17 years, body weight between 3.6 and 25.5 kg, and mean testes weight between 0.16 and 3.16 g. The gonadosomatic index was low compared with other species (approximately 0.02% in mature males). Mean testes weight differed significantly between males <12 months of age and all other age groups but did not differ between males of 18-23 months and older males. Spermatozoa could be collected but had lost most of their viability. Seven of 10 males of 18-23 months were fertile, as defined by the production of spermatozoa while no males < or =15 months of age were fertile. Adherence of the prepuce to the penis and absence of penile spines were associated with immaturity. The results indicate that most males are fertile during the reproductive season of their second year.
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PMID:Reproductive maturation in the male Eurasian lynx (Lynx lynx): a study on 55 reproductive organs collected from carcasses during 2002-2005. 1914 19

We analysed ejaculated spermatozoa from five infertile men with different balanced reciprocal translocations to contribute to the study of meiotic segregation of chromosomes 18, X and Y and also to evaluate sperm morphology by transmission electron microscopy (TEM) analysis. Conventional lymphocyte karyotype analyses highlighted different reciprocal balanced translocations: t(12;13), t(4;9), t(X;8), t(8;10) and t(3;16). Semen analysis was performed by light and TEM. Fluorescence in situ hybridization was performed directly on sperm nuclei using centromeric probes for chromosomes 18, X and Y. The carriers of the balanced reciprocal translocations considered in the present study showed a very similar pattern of sperm pathologies: diffused presence of apoptosis and immaturity. All patients showed meiotic segregation derangements, highlighted by the presence of sperm diploidies and sex chromosome disomies particularly related to the failure of the first meiotic division. However, an increased incidence of chromosome 18 aneuploidy was detected in spermatozoa from t(X;8) and t(8;10) carriers. We have also reported values from sex chromosomes such as t(X;8), although the X chromosome was involved in translocation. Since patients with reciprocal translocations and spermatogenetic impairment are candidates for intracytoplasmic sperm injection cycles, the study of sperm parameters, and particularly of the level of aneuploidy rates, would provide better information for couples at risk and would contribute to the data in the literature for a better understanding of the effects of chromosomal rearrangement on the whole meiotic process and, in particular, on chromosomes not involved in translocation.
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PMID:18, X, Y aneuploidies and transmission electron microscopy studies in spermatozoa from five carriers of different reciprocal translocations. 1934 51


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