Academic literature on the topic 'Human fetal testis development'

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Journal articles on the topic "Human fetal testis development"

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Waters, Brenda, and Thomas Trainer. "Development of the Human Fetal Testis." Fetal and Pediatric Pathology 16, no. 1 (January 1, 1996): 9–23. http://dx.doi.org/10.3109/15513819609168658.

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Waters, Brenda L., and Thomas D. Trainer. "DEVELOPMENT OF THE HUMAN FETAL TESTIS." Pediatric Pathology & Laboratory Medicine 16, no. 1 (February 1, 1996): 9–23. http://dx.doi.org/10.1080/107710496175840.

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Waters, Brenda. "DEVELOPMENT OF THE HUMAN FETAL TESTIS." Fetal and Pediatric Pathology 16, no. 1 (February 1, 1996): 9–23. http://dx.doi.org/10.1080/713601130.

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O'Shaughnessy, Peter J., and Paul A. Fowler. "Development of the human fetal testis." Annales d'Endocrinologie 75, no. 2 (May 2014): 48–53. http://dx.doi.org/10.1016/j.ando.2014.03.009.

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Waters, Brenda L., and Thomas D. Trainer. "Development of the Human Fetal Testis." Pediatric Pathology & Laboratory Medicine 16, no. 1 (January 1996): 9–23. http://dx.doi.org/10.1080/15513819609168658.

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Huang, Xiaoyan, Jun Zhang, Li Lu, Lanlan Yin, Min Xu, Youqun Wang, Zuomin Zhou, and Jiahao Sha. "Cloning and expression of a novel CREB mRNA splice variant in human testis." Reproduction 128, no. 6 (December 2004): 775–82. http://dx.doi.org/10.1530/rep.1.00036.

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Identification of genes specifically expressed in adult and fetal testis is important in furthering our understanding of testis development and function. In this study, a novel human transcript, designated human testis cAMP-responsive element-binding protein (htCREB), was identified by hybridization of adult and fetal human testis cDNA probes with a human cDNA microarray containing 9216 clones. The htCREB transcript (GenBank Accession no. AY347527) was expressed at 2.35-fold higher levels in adult human testes than in fetal testes. Sequence and ntBLAST analyses against the human genome database indicated that htCREB was a novel splice variant of human CREB. RT-PCR-based tissue distribution experiments demonstrated that the htCREB transcript was highly expressed in adult human testis and in healthy sperm, but not in testes from patients with Sertoli cell-only syndrome. Taken together, these results suggest that the htCREB transcript is chiefly expressed in germ cells and is most likely involved in spermatogenesis.
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Mitchell, R. T., P. T. K. Saunders, A. J. Childs, C. Cassidy-Kojima, R. A. Anderson, W. H. B. Wallace, C. J. H. Kelnar, and R. M. Sharpe. "Xenografting of human fetal testis tissue: a new approach to study fetal testis development and germ cell differentiation." Human Reproduction 25, no. 10 (August 3, 2010): 2405–14. http://dx.doi.org/10.1093/humrep/deq183.

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Mitchell, Rod T., Philippa T. K. Saunders, Andrew J. Childs, Claire Cassidy-Kojima, Richard A. Anderson, W. Hamish B. Wallace, Chris J. H. Kelnar, and Richard M. Sharpe. "Xenografting of Human Fetal Testis Tissue: A New Approach to Study Fetal Testis Development and Germ Cell Differentiation." Obstetrical & Gynecological Survey 66, no. 1 (January 2011): 21–22. http://dx.doi.org/10.1097/ogx.0b013e3182168278.

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Niederberger, Craig. "Re: Xenografting of Human Fetal Testis Tissue: A New Approach to Study Fetal Testis Development and Germ Cell Differentiation." Journal of Urology 186, no. 1 (July 2011): 245. http://dx.doi.org/10.1016/s0022-5347(11)60337-6.

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Kilcoyne, Karen R., and Rod T. Mitchell. "Effect of environmental and pharmaceutical exposures on fetal testis development and function: a systematic review of human experimental data." Human Reproduction Update 25, no. 4 (March 14, 2019): 397–421. http://dx.doi.org/10.1093/humupd/dmz004.

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Abstract BACKGROUND Overall, the incidence of male reproductive disorders has increased in recent decades. Testicular development during fetal life is crucial for subsequent male reproductive function. Non-genomic factors such as environmental chemicals, pharmaceuticals and lifestyle have been proposed to impact on human fetal testicular development resulting in subsequent effects on male reproductive health. Whilst experimental studies using animal models have provided support for this hypothesis, more recently a number of experimental studies using human tissues and cells have begun to translate these findings to determine direct human relevance. OBJECTIVE AND RATIONALE The objective of this systematic review was to provide a comprehensive description of the evidence for effects of prenatal exposure(s) on human fetal testis development and function. We present the effects of environmental, pharmaceutical and lifestyle factors in experimental systems involving exposure of human fetal testis tissues and cells. Comparison is made with existing epidemiological data primarily derived from a recent meta-analysis. SEARCH METHODS For identification of experimental studies, PubMed and EMBASE were searched for articles published in English between 01/01/1966 and 13/07/2018 using search terms including ‘endocrine disruptor’, ‘human’, ‘fetal’, ‘testis’, ‘germ cells’, ‘testosterone’ and related search terms. Abstracts were screened for selection of full-text articles for further interrogation. Epidemiological studies involving exposure to the same agents were extracted from a recent systematic review and meta-analysis. Additional studies were identified through screening of bibliographies of full-texts of articles identified through the initial searches. OUTCOMES A total of 25 experimental studies and 44 epidemiological studies were included. Consistent effects of analgesic and phthalate exposure on human fetal germ cell development are demonstrated in experimental models, correlating with evidence from epidemiological studies and animal models. Furthermore, analgesic-induced reduction in fetal testosterone production, which predisposes to the development of male reproductive disorders, has been reported in studies involving human tissues, which also supports data from animal and epidemiological studies. However, whilst reduced testosterone production has been demonstrated in animal studies following exposure(s) to a variety of environmental chemicals including phthalates and bisphenol A, these effects are not reproduced in experimental approaches using human fetal testis tissues. WIDER IMPLICATIONS Direct experimental evidence for effects of prenatal exposure(s) on human fetal testis development and function exists. However, for many exposures the data is limited. The increasing use of human-relevant models systems in which to determine the effects of environmental exposure(s) (including mixed exposures) on development and function of human tissues should form an important part of the process for assessment of such exposures by regulatory bodies to take account of animal–human differences in susceptibility.
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Dissertations / Theses on the topic "Human fetal testis development"

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Mitchell, Roderick T. "Germ cell development in the human and marmoset fetal testis and the origins of testicular germ cell tumours." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4818.

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Normal germ cell development in the human testis is crucial for subsequent fertility and reproductive health. Disruption of testis development in fetal life can result in deleterious health consequences such as testicular dysgenesis syndrome (TDS), which includes disorders, such as cryptorchidism, hypospadias, infertility and testicular germ cell tumours (TGCT). A rat model of TDS in which rats are exposed to phthalates in utero has been validated, but does result in the development of TGCT. In humans, TGCTs result from transformation of pre-neoplastic carcinoma in-situ (CIS) cells and these CIS cells are believed to arise from human fetal germ cells during their transition from gonocyte to spermatogonia, based on their morphology and protein expression profile. It has been proposed asynchronous differentiation of germ cells in the human fetal testis may predispose fetal germ cells to become CIS cells. Studying the development of these tumours in humans is difficult because of their fetal origins and prolonged duration from initiation of impaired development to invasive disease. For this reason the use of relevant animal models that can mimic normal and abnormal germ cell development may provide new insight into how TGCT develop. The Common Marmoset monkey, a New World primate exhibits many similarities to the human in terms of reproductive biology and could represent such a model. This thesis aimed to further characterise the origins of CIS cells in the human testis by investigating the protein expression profile of CIS cells in patients with TGCT and comparing them to established markers of human fetal germ cell types using immunohistochemistry and immunofluorescence. Quantification of the various subpopulations of CIS and proliferation within these populations was performed. The thesis also investigated the Common Marmoset monkey as a potential model of normal testis and germ cell development by comparing the differentiation and proliferation profile of germ cells with those of the human during fetal and early postnatal life. During the present studies methods were successfully developed that enabled us to use testicular xenografts to recapitulate normal development of immature testes from marmoset and human. This involved grafting pieces of testis tissue subcutaneously under the dorsal skin of immunodeficient mice and retrieving them several weeks later to investigate their development during the grafting period. Xenografts using tissue from fetal, neonatal and juvenile marmosets were performed in addition to testes from first and second trimester human fetuses. Finally the present studies aimed to use the marmoset and the xenografting approach as systems in which to examine the effects of gonadotrophin suppression and phthalate treatment on germ cell differentiation and proliferation, with particular attention to the potential for development of CIS and TGCT. Heterogeneous phenotypes of CIS cells were identified, mostly consistent with those seen in the normal human fetal testis, however some of these CIS cells did not exhibit the same phenotype as germ cells identified in normal fetal testes. In addition it was shown that some of the proteins considered to be ‘classical’ markers of CIS cells, such as the pluripotent transcription factor OCT4, were not expressed in a proportion of the CIS cells. The proliferation index of CIS cells is also significantly higher in those subpopulations with the most ‘undifferentiated’ phenotype (i.e. OCT4+/VASA-). The present studies have generated novel data showing that the marmoset is a good model of fetal and neonatal germ cell development, with similarities to the human in terms of an asynchronous and prolonged period of differentiation and proliferation of germ cells from gonocyte to spermatogonia. This feature is also common to the human, but not a characteristic of the rodent. Fetal, neonatal and pre-pubertal germ cell development can be re-capitulated by xenografting tissue from marmoset and human testes into nude mouse hosts. Human fetal testis grafts produced testosterone and were responsive to hCG stimulation. First trimester human testis xenografts that have not developed fully formed seminiferous cords prior to grafting can complete the process of cord formation whilst grafted in host mice. In addition, germ cells in fetal human and marmoset xenografts can differentiate and proliferate in a similar manner to that seen in the intact non-grafted testis. In the intact neonatal marmoset, suppression of gonadotrophins resulted in a 30% decrease in proliferation, however differentiation of gonocytes is not affected. In-utero treatment of neonatal marmosets with mono-n-butyl phthalate was associated with unusual ‘gonocyte’ clusters, however, di-n-butyl phthalate treatment of mice carrying fetal marmoset xenografts resulted in no visible effects on germ cell differentiation or proliferation and did not result in the development of CIS or TGCT. In conclusion, this thesis has shown that there are many subpopulations of CIS cells of which many have not been previously described. These subpopulations have different characteristics, such as variable proliferation rates and this may indicate the potential for progression or invasiveness. These subpopulations have similar protein expression phenotypes to normal human fetal germ cells although the present studies have identified some CIS cells with phenotypes that are not found in the normal human testis. This thesis has demonstrated that the marmoset is a comparable model to the human in terms of asynchronous fetal germ cell development, which may predispose this species to the development of CIS/TGCT. In addition to the use of intact marmosets, these studies have also demonstrated for the first time that testis xenografting provides a comparable system for testis cord formation, germ cell differentiation and proliferation in fetal/postnatal marmosets and fetal human testis. In addition the marmoset and xenografting models have indicated that phthalates may have minor effects on testis development in the human and marmoset but do not result in CIS or TGCT. These model systems are suitable for further investigation of normal and disrupted testis development.
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Muczynski, Vincent. "Polluants environnementaux et développement du testicule foetal humain : effets et mécanismes des phtalates." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00631554.

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Au cours des dernières décennies, nous avons progressivement vu augmenter un certain nombre d'anomalies de la fonction de reproduction masculine dans les pays industrialisés. Ces constatations ont fait émerger l'hypothèse selon laquelle certains polluants de notre environnement pourraient altérer le développement du testicule fœtal et ainsi être responsables de ces anomalies. Parmi les composants incriminés se trouvent les phtalates, largement répandus dans l'environnement. Ces composés ont été décrits comme reprotoxiques, ils altèrent le développement de la lignée germinale dans différentes espèces et entraînent une diminution de la production de testostérone chez le rat. Toutefois, très peu de données sont disponibles quant à leurs effets chez l'Homme. Dans cette étude, nous avons analysé les effets d'un phtalate, le MEHP, sur le développement du testicule fœtal humain au premier trimestre de la grossesse, dans un modèle de culture organotypique qui permet le maintien des différentes structures de l'organe. Nous avons tout d'abord démontré que le MEHP (10-4M) n'altère pas la production de testostérone du testicule fœtal humain, contrairement aux résultats décrits chez le rat. En revanche, nous avons montré que l'exposition au MEHP entraîne une rapide diminution du nombre de cellules germinales par apoptose. A la suite de ces résultats, nous avons testé l'effet de doses plus faibles de MEHP afin de se placer à des concentrations de phtalates ayant été mesurées dans les liquides biologiques. Nous avons ainsi démontré que les cellules germinales du testicule fœtal humain sont altérées suite à l'exposition à des doses de MEHP de 10-5M. Enfin, dans la 3ème partie de ce travail, nous nous sommes intéressés aux mécanismes d'action des phtalates. Différentes études, notamment dans le foie, démontrent l'implication des récepteurs nucléaires dans les effets de ces composés. Il nous a donc semblé important de rechercher leur implication dans les effets des phtalates sur le testicule fœtal. Nous avons démontré que LXRα est très certainement impliqué ces effets puisque l'expression des ARNm de ce récepteur est augmentée. Par ailleurs, ce récepteur nucléaire contrôle deux voies métaboliques, la synthèse de cholestérol et la synthèse des acides gras qui semblent toutes deux modulées par les phtalates dans le testicule fœtal humain. Enfin, nous avons montré que l'implication de ces voies métaboliques est commune entre la gonade mâle et la gonade femelle, sans pour autant que l'effet sur les cellules germinales mâles ai pu être mis en évidence dans l'ovaire fœtal. En conclusion, cette étude a contribué à caractériser les effets des phtalates sur la mise en place des fonctions de reproduction chez le fœtus humain. Nous avons également pu mettre en évidence un nouveau mécanisme de ces composés, impliquant la superfamille des récepteurs nucléaires ainsi que la synthèse du cholestérol et des acides gras.
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Yuen, Ka Chun. "Epigenetics of human fetal and placental development." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/35689.

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Dysregulation of placental and fetal epigenetics can affect gene expression patterns, including the parent-of-origin dependent expression in imprinted genes. While defects of imprinted genes have been implicated in some adverse pregnancy outcomes, little is currently known about the role of epigenetics in regulating normal or pathological human pregnancy and development. The objective of this thesis is to provide fundamental DNA methylation profiles of human fetal and placental development so as to offer insights into the etiology of human disease and adverse pregnancy outcomes. Taking advantage of the unbalanced parental genomic constitutions in triploidies, 45 novel imprinted genes were identified by comparing the genome-wide DNA methylation profiles between 10 diandries and 10 digynies. A comparison of DNA methylation profiles between placentas of different gestations and other somatic tissues showed tissue-specific and gestational age-specific DNA methylation changes in many imprinted genes. To gain insight into the genomic pattern of tissue-specific methylation, DNA methylation profile was evaluated in 5 somatic tissues (brain, kidney, lung, muscle and skin) from eight normal second-trimester fetuses. Tissue-specific differentially methylated regions (tDMRs) were identified in 195 loci, suggesting that tissue-specific methylation is established early in the second trimester. Importantly, only 17% of the identified fetal tDMRs were found to maintain this same tissue-specific methylation in adult tissues, implicating an extensive epigenetic reprogramming between fetus and adult. Besides intra-individual differences, there is also substantial DNA methylation variation between individuals. While many sites show a continuous pattern of DNA methylation variation between different placentas, WNT2, TUSC3 and EPHB4 were identified to have epipolymorphisms at their promoter region. The methylation status at the TUSC3 promoter showed an association with preeclampsia, suggesting a role of DNA methylation change in adverse pregnancy outcomes. A further investigation of DNA methylation profiles in 26 placentas from preeclampsia, IUGR and control subjects showed 34 loci were hypomethylated in the early-onset preeclamptic placentas, with TIMP3 having a potential of being a biomarker for the disorder. These results provided comprehensive DNA methylation profiles for both normal and abnormal fetal and placental tissues, which contribute to the biological and clinical aspects of the pathogenesis of fetal and placental disorders.
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Tieppo, Paola. "The development of human fetal γδ thymocytes." Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/303402.

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γδ T cells are unconventional T cells that that can recognize infected and transformed cells via their γẟ TCR, thus promoting different immune responses. In addition, several studies showed that γδ T cells are important in the protection against different pathogens in early life, such as human cytomegalovirus (CMV). The diversity of the γδ TCR repertoire is mainly generated in the complementarity determining region 3 (CDR3) where V(D)J recombination takes place. One of the main players in the junctional diversity is the terminal-deoxynucleotidyl-transferase (TdT) enzyme responsible for the random template-independent nucleotide addition at the junction of the joining gene segments.In the mouse model it is established that during development, especially before birth, innate γδ T cell subsets are generated in waves and their generation depends on the type of hematopoietic stem and precursor cells (HSPC). These γδ T cells express a semi-invariant γδ TCR and can acquire a functional program already in the thymus. In human, in contrast, the idea of γδ T cells as innate-like lymphocytes is questioned by recent works showing that the γδ TCR repertoire of human pediatric thymuses and of term-delivery cord blood is highly diverse. Here, by analyzing in detail human fetal and post-natal thymi, we observed striking differences between fetal and post-natal γδ thymocytes at the γδ TCR repertoire and functional level. In contrast to post-natal γδ thymocytes, fetal γδ thymocytes were functionally programmed, expressed low levels of TdT and were highly enriched for invariant/public CMV-reactive CDR3 sequences (TRGV8-TRJP1-CATWDTTGWFKIF, TRDV2-TRDD3-CACDTGGY, and TRDV1-TRDD3-CALGELGD). The rearrangements of these invariant sequences were driven by short-homology repeats at the end of the involved gene segments, as it was observed in the mouse. In addition, we investigated the role of HSPC in the generation of this invariant γδ thymocytes by using an in vitro T cell development system and we showed that only fetal HSPC could generate γδ T cells enriched for the same specific features that were found in the ex-vivo fetal γδ thymocytes. Moreover, we showed that the RNA-binding protein Lin28b, highly expressed in fetal γδ T cells, reprogrammed the term delivery HSPC towards the generation of γδ T cells resembling to their fetal counterpart.In conclusion, we show that the human fetal thymus generates, in a HSPC- and Lin28b-dependent manner, innate invariant γδ T cells with programmed effector functions that might provide protection to the fetus during congenital infections, such as against CMV.
Doctorat en Sciences biomédicales et pharmaceutiques (Pharmacie)
info:eu-repo/semantics/nonPublished
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Jobling, Matthew S. "Fetal germ cell development in the rat testis and the impact of di (n-Butyl) phthalate exposure." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4803.

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During gonad development and fetal life, the germ cells (GC) undergo a range of different developmental processes necessary for correct postnatal gametogenesis and the production of the next generation. If these fetal events are disrupted by genetic or environmental factors, there could be severe consequences that may not present until adulthood. This is of particular importance in relation to human testicular GC tumours (TGCT), the most common cancer of young men, as TGCT is thought to arise from fetal GCs that have failed to differentiate normally during development and thus persist into adulthood, eventually becoming tumourigenic. TGCT is one of several related disorders of male reproductive health thought to comprise a Testicular Dysgenesis Syndrome (TDS), in which faulty testis development in fetal life may predispose to the development of cryptorchidism, hypospadias, reduced sperm count and TGCT. Currently there is no accepted animal model for TGCT, but some insight into human TDS has been gained through the use of a rat model using in utero Di (n-Butyl) Phthalate (DBP) exposure to induce cryptorchidism, hypospadias, low sperm count and reduced fertility (but not TGCT). However, a previous study suggested that DBP exposure can disrupt GC differentiation, resulting in significantly reduced GC number prior to birth and postnatal consequences. This thesis has been directed at investigating the normal process of GC development in the fetal rat and how this is altered by DBP exposure; such understanding may give insights into the origins of human TGCT by showing how and when disruption of normal fetal GC differentiation can occur. The first objective was to characterise GC development in both the rat testis and ovary to understand the normal events that occur between embryonic day (e)13.5 and e21.5, as most data in the literature is based on the mouse. Analysis by immunohistochemical, stereological and mRNA expression indentified that during this time period, a GC will undergo a dynamic sequence of changes involving migration, proliferation followed by differentiation (manifested by loss of specific protein markers), whilst undergoing germ-line specific remethylation. Whilst whole gonad development is vastly different between testes and ovaries, GC development was broadly the same with only minor differences up to the point where GCs in the ovary enter meiosis. Having established the normal process of GC development in the fetal rat testis, the effects of in utero DBP exposure was then investigated. DBP exposure reduced GC number at all ages investigated even after only 24 hours of exposure and simultaneously prolonged GC proliferation. As apoptosis was unaltered by DBP exposure, the consistent reduction in GC number was suggested to be due to an initial reduction in GC number that does not recover to control levels. GC differentiation was assessed by the expression and localization of specific protein markers (OCT4, DMRT1 and DAZL). The pattern of expression of OCT4 and DMRT1 was altered by DBP exposure. GCs in DBP exposed animals also showed a delay in disaggregation from within the centre of seminiferous cords. These results suggested that a delay in GC differentiation was occurring with DBP exposure. This delay in GC development persisted into early postnatal life, following cessation of DBP exposure. Thus at postnatal day (D)6, GC specific re-expression of DMRT1, GC migration to the basal lamina and resumption of GC proliferation all showed a delay. DBP also induced an increase in the presence of multinucleated gonocytes. DNA methylation in the fetal rat testis was also investigated as a mechanism that could be disrupted by DBP exposure. DNA methylation of GCs increased during the last week of fetal life by global methylation of the GC genome and the increased expression of DNA methyl transferases. No effect of DBP exposure was detected. Inhibition of methylation by 5-aza-2’deoxycytidine was then investigated as a way to block GC differentiation in fetal rat testes and this resulted in a similar transient delay in GC differentiation but was perinatally lethal to the fetus. Bisulphite sequencing of the OCT4 promoter was also performed but proved inconclusive. Methylation patterns may be being altered by DBP exposure, but such changes could not be identified in this thesis. To complement the in vivo DBP exposure studies, an in vitro testis explant system using e14.5 testes was investigated. These in vitro testis explants showed some GC effects with MBP, the active metabolite of DBP, and also suggested a novel role for Hedgehog signalling in GC survival in the fetal rat testis. The studies in this thesis have characterised several aspects of fetal GC development in the rat and identified which of these are affected by DBP exposure, resulting in a delay in GC development. As DBP exposure delays but does not block GC differentiation, this may explain why TGCT is not induced in the DBP exposure rat model for TDS.
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Willerton, Louise. "Gene expression in mouse testis during development." Thesis, Connect to electronic version, 2003. http://theses.gla.ac.uk:82/theses/available/etd-07042003-142909/.

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Thesis (Ph. D.)--University of Glasgow, 2003.
Ph. D. thesis submitted to the Faculty of Veterinary Medicine, University of Glasgow, 2003. Includes bibliographical references. Electronic version also available via Glasgow University e-Theses service.
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Jeffery, Nathan. "Fetal development and evolution of the human cranial base." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392131.

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Conliffe, Phyllis R. (Phyllis Rowena). "Effects of maternal diabetes on fetal development in rats." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39344.

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The mechanisms underlying the high incidence of fetal abnormalities including fetal lung immaturity during maternal diabetes are not fully understood. Utilizing streptozotocin-diabetic rats as the model, I have examined the role of fetal hyperglycemia and hyperinsulinemia and other factors on fetal adrenal and lung functions in culture. Insulin and glucose did not alter fetal adrenal and lung cell proliferation and adrenal corticosterone output. On the other hand, a novel protein-bound, low molecular weight non-proteinaceous cytotoxic factor was detected in the serum of diabetic animals. In addition, a novel protein with cytostatic activity was found in fetal lungs, the concentration of which increased during diabetes. Partial amino acid sequence and Western Blot analysis revealed this protein to be similar to histone H2B. An extra-nuclear role is suggested for this protein because it appears to be present in the microsomal fraction of fetal lungs. It is concluded that fetal lung immaturity during diabetes may be contributed by cytotoxic and cytostatic factors contained in the serum and fetal lungs, respectively.
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Feichtinger, Julia. "Development of a bioinformatic analytical approach to identify novel human cancer testis gene candidates." Thesis, Bangor University, 2012. https://research.bangor.ac.uk/portal/en/theses/development-of-bioinfirmatic-analytical-approach-to-identify-novel-human-cancer-testis-gene-candidates(09065b27-9fc0-49df-a9eb-fb7ef8aab878).html.

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The identification of tumour antigens (TAs) represents an ongoing challenge to the development of novel cancer diagnostic, prognostic and therapeutic strategies. A group of proteins, the cancer testis (CT) antigens are promising targets for such clinical applications. Their encoding genes show expression restricted to the immunologically privileged testes but their expression is also found in cells with a cancerous phenotype. To facilitate and automate the identification of novel CT genes, bioinformatic analytical pipelines based on publicly available microarray and expressed sequence tag (EST) data were developed and implemented as web tools to support wider application. Human germline-associated datasets were generated and the developed screening pipelines were subsequently used to analyse these datasets, leading to the identification of a. novel cohort of meiosis-speci fic genes, the meiCT genes that exhibit t he characteristics of CT genes and may have oncogenic features. In general, frequent germline gene expression found in cancer could reflect a soma-to-germline transformation occurring in human cells in the course of the development of cancer. The expression of germline-specific genes, in particular of meiotic genes, could lead to the production of proteins that cause oncogenic events and thus contribute to tumorigenesis and to the acquisition of tumour characteristics.
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Ask, Björnberg Karolin. "Mercury exposure during early human development /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-224-1/.

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Books on the topic "Human fetal testis development"

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Bhattacharya, Niranjan, and Phillip G. Stubblefield, eds. Human Fetal Growth and Development. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-14874-8.

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Hutson, John M. Descent of testis. London: E. Arnold, 1992.

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Life before birth: The challenges of fetal development. New York: W.H. Freeman, 1996.

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Peavey, Mary C., and Sarah K. Dotters-Katz. Ultrasound of Mouse Fetal Development and Human Correlates. First edition. | Boca Raton : CRC Press, 2021. | Series: Reproductive medicine and assisted reproductive techniques series: CRC Press, 2021. http://dx.doi.org/10.1201/9781315114736.

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1940-, Hopkins Brian, and Johnson Scott P. 1959-, eds. Prenatal development of postnatal functions. Westport, Conn: Praeger Publishers, 2005.

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Human blastogenesis: Formation of the extraembryonic cavities. Basel: Karger, 1987.

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Color atlas of life before birth: Normal fetal development. Chicago, Ill: Year Book Medical Publishers, 1990.

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Barker, D. J. P. (David James Purslove), Moffett Ashley, and Thornburg Kent L, eds. The placenta and human developmental programming. Cambridge: Cambridge University Press, 2011.

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9

A colour atlas of life before birth: Normal fetal development. London: Wolfe, 1990.

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Lenhoff, Howard M. Conception to birth: Human reproduction, genetics, and development. Dubuque, Iowa: Kendall/Hunt Pub. Co., 1989.

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Book chapters on the topic "Human fetal testis development"

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Kos, Marina, and Tanja Leniček. "The Fetal Human Testis." In Atlas on the Human Testis, 55–68. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2763-5_5.

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Huff, Dale S., and Chrystalle Katte Carreon. "Testis." In Color Atlas of Human Fetal and Neonatal Histology, 129–46. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11425-1_10.

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Rousseau, François, Colin Studholme, Renaud Jardri, and Moriah E. Thomason. "In Vivo Human Fetal Brain Analysis Using MR Imaging." In Fetal Development, 407–27. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22023-9_20.

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Mulder, Eduard J. H., and Gerard H. A. Visser. "Fetal Behavior: Clinical and Experimental Research in the Human." In Fetal Development, 87–105. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22023-9_5.

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Bhattacharya, Niranjan, and Phillip G. Stubblefield. "Fetal Growth." In Human Fetal Growth and Development, 3–9. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-14874-8_1.

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Jost, Alfred, and Solange Magre. "Endocrine Cytodifferentiation of the Rat Fetal Testis." In Endocrine and Biochemical Development of the Fetus and Neonate, 3–10. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-9567-0_1.

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Nistal, Manuel, and Pilar González-Peramato. "Disorders of Sex Development." In Atlas on the Human Testis, 265–80. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2763-5_18.

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Zaninović, Nikica, and Peter N. Schlegel. "MicroTESE and Embryo Development." In Atlas on the Human Testis, 7–21. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2763-5_2.

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Hepper, Peter G. "Observing the Fetus’ Behavior to Assess Health: The Behavior of the Human Fetus in Response to Maternal Alcohol Consumption." In Fetal Development, 317–30. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22023-9_16.

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Jurić-Lekić, Gordana, Marta Himelreich, Marta Lekić, Đurđica Grbeša, and Floriana Bulić-Jakuš. "Early Development of the Human Testis." In Atlas on the Human Testis, 37–53. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2763-5_4.

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Conference papers on the topic "Human fetal testis development"

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Fu, Luoyu, Peiqi Yi, Zikun Gao, and Yan Gan. "Design and Research of Flexible Wearable Medical Testing Equipment for Pregnant Women." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001478.

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Pregnant women, as a special group, bear the mission of nurturing and continuing human life. Pregnant women need to experience psychological and physiological changes in the tenth month of pregnancy. In the special "post-epidemic era", it is hard and unsafe for pregnant women to go to the hospital regularly for birth check-up. In order to make pregnant women have a better prenatal experience, our team wants to design a wearable device, which can monitor the fetal heart rate and the frequency of fetal movement, so that pregnant women can also realize routine detection of the fetal condition at home, and protect the growth health and safety of the fetus. In this design, questionnaire interview, literature search and collaborative story telling are used to deeply understand the pain points of pregnant women's antenatal examination, the development status of wearable devices for pregnant women at home and abroad, pregnant women's preferences and so on. Then, determine the product use process, product functional structure and product packaging. This design adopts cutting-edge technologies such as flexible sensors, and combines ergonomics and kansei engineering. The product obtains the data and information of pregnant women and fetuses, and then through sorting and analysis, the results are intuitively transmitted to pregnant women, pregnant women's relatives or doctors in the matching APP, so that users can clearly obtain the health data of pregnant women in real time. Realize early warning of physical abnormalities of infants and mothers, early warning and early treatment, so as to better protect the safety and health of pregnant women and fetuses during pregnancy. After the usability test, the interviewed pregnant women thought that the design had a certain effect.
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Yalcin, Huseyin C., Huseyin E. Salman, and Reema Y. Kamal. "Assessment of Human Fetal Left Heart Hemodynamics during Prenatal Development." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0086.

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The hemodynamic forces and wall shear stresses (WSS) play an important role during the fetal heart development. Abnormal levels of flow-driven shear stress can deteriorate the proper functioning of the cells responsible for the growth and remodeling of the heart and lead to congenital heart defects (CHDs). Hypoplastic left heart syndrome (HLHS) is a critical CHD with severely underdeveloped left ventricle and responsible for 25-40% of all neonatal cardiac deaths. To characterize the main differences between the healthy and HLHS fetal hearts in terms of morphology, flow behavior, and WSS levels, will help to understand the mechanobiological development of the human fetal hearts. The comparison of healthy and HLHS fetal hearts is important to understand the embryonic development of HLHS. Computational fluid dynamics (CFD) modeling is performed to elucidate the flow behavior and WSS levels in the heart chambers. First, the model geometries are generated using the medical images. Then, the flow domain is discretized in spatial and time domains for solving the governing fluid flow equations. Inlet flow conditions are determined using the Doppler ultrasound velocity measurements. The analyses cover the range of gestational week 16 and week 34. HLHS hearts have higher peak flow rates at the valves compared to the control hearts. The turbulent activity in the left side of the heart is higher than the right side. For the control hearts, there is a balance between the left and right sides of the heart, which is preserved during the development. The ratio of the cross-sectional area between the left and right sides of the heart is about 57.5% to 42.5% for the control hearts. HLHS significantly reduces the cross-sectional area of the left side of the heart. For HLHS hearts, the ratio between the left and right sides becomes about 30% to 70%. The average WSS levels significantly increase at the left side of the HLHS hearts. This study indicates the critical importance of the altered inflow hemodynamics during the human fetal heart development. CFD analysis can be used to predict the initiation and growth of CHDs. The presence of CHDs significantly changes the biomechanical environment in the fetal hearts.
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Bobrova, Yu O. "The Development of a Remote Fetal Activity Monitoring System." In 2018 Third International Conference on Human Factors in Complex Technical Systems and Environments (ERGO). IEEE, 2018. http://dx.doi.org/10.1109/ergo.2018.8443852.

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Lin, N., C. Liu, I. V. Yang, L. A. Maier, D. L. Demeo, S. Ye, M. H. Cruse, et al. "Sex-Specific Differences in MicroRNA Expression During Human Fetal Lung Development." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5264.

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Ouyang, Austin, Qiaowen Yu, Virendra Mishra, Lina Chalak, Tina Jeon, Muraleedharan Sivarajan, Greg Jackson, Nancy Rollins, Shuwei Liu, and Hao Huang. "Structural development of human brain white matter from mid-fetal to perinatal stage." In SPIE Medical Imaging, edited by Barjor Gimi and Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2082418.

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RENESME, L., F. Lesage, D. P. Cook, S. Zhong, S. M. Hänninen, O. Carpén, I. Mižíková, and B. Thébaud. "A single-cell atlas of human fetal lung development between 14 and 19 weeks of gestation." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.145.

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Dodson, Reuben B., Kendall S. Hunter, and Virginia L. Ferguson. "Elastic Properties of the Human Umbilical Cord in Preeclampsia." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53673.

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Maternal diseases of pregnancy have been found to detrimentally affect the fetal circulatory system, with consequences lasting well into adulthood. In 1995, Barker introduced the idea that major disorders of adult life (including coronary heart disease, hypertension, stroke and diabetes) arise not only through an interaction between factors in our lifestyle, such as a high-fat diet, obesity and smoking, and a genetically determined susceptibility but also through development in utero [1]. Epidemiological evidence continues to support the notion that adult cardiovascular disease (CVD) has fetal origins [2–5].
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Hassan, H. J., A. Leonardi, C. Chelucci, R. Guerriero, P. M. Mannucci, and C. Peschle. "EXPRESSION IN ONTOGENESIS OF HUMAN BLOOD COAGULATION FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644610.

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We have analyzed the expression of several blood coagulation factors (IX, VIII, X, fibrinogen chains) and inhibitors (antithrombin III, protein C) in human embryonic and fetal livers, obtained from legal abortions at 6-11 week post-conception. The age was established by morphologic staging and particularly crown-rump lenght measurement.Total cellular RNA was isolated from partially purified hepatocytes or total liver homogenate using the guanidine isothiocyanate method. Poly(A)+ RNA was selected by oligodT cellulose chromatography. The size and the number of the embryonic and fetal transcripts are equivalent to those observed in adult liver, as evaluated by Northern blot analysis of total or poly(A)+ RNA hybridized to human cDNA probes.The level of coagulation factor transcripts in embryonic and fetal liver was evaluated by dot hybridization of total RNA (0.5-10 ug), as compared to RNA extracted from normal adult liver biopsies. The expression of blood coagulation factors in embryos is generally reduced for all factors, but at a different degree. In 5-11 wk liver, the level of factor IX is 5-10% of that observed in adults, while fibrinogen, protein C, antithrombin III RNA level rises from 25 to 50% and factor X is expressed at a level comparable to that observed in adult liver.We conclude that during these stages of development blood coagulation factors are expressed according to three different time, curves, possibly due to the effect of different types of regulatory mechanisms.
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Leasure, Jeremi, Roza Mahmoodian, Sorin Siegler, Franco Capaldi, and Nancy Pleshko. "Fourier Transform Infrared Spectroscopic Assessment of Changes in Composition of Proteoglycans and Collagen in Developing Human Fetal Tarsal Bones." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-67862.

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The proteoglycan and collagen composition of cartilage is known to change during fetal and postnatal development. The current report represents the first attempt to semi-quantitatively determine the changes in the composition of developing human fetal cartilage. Human fetal talus bones were obtained from late 2nd and 3rd trimester specimen. Fetal bones are comprised of an intramembranous tissue commonly referred to as cartilage anlagen. During maturation the anlagen develops an ossific nucleus. Fourier Transform Infrared Spectroscopy (FT-IRS) and Fourier Transform Infrared Imaging Spectroscopy (FT-IRIS) were used to assess the changes in composition relating to tissues main constituents, collagen (COL) and proteoglycan (PG). FT-IRS was used to obtain average values of composition across the entire anterior-posterior length of each bone. Relative percent composition values of COL and PG were calculated by multivariate least-squares analysis of model compound spectral features associated with COL (Amide I spectral absorbance) and PG (C-O-C sugar absorbance). It was shown that PG/Amide I values decreases from 4.9 +/−3.4 to 2.9 +/−3.2 over development. These values were translated to a relative percent compositional drop of PG from 49.9% +/−16.2% to 36.4% +/−8.1%. FT-IRIS was used to observe the spatial changes in composition from the subchondral region to the articulating surfaces. Collagen was observed to be distributed away from the articulating surfaces with increase in development. Proteoglycans were observed to have uniform concentrations with a marked decrease in PG across developmental stages. A noticeable benchmark in development is the ossific nucleus which was absent in the 2nd trimester. The findings of the current study demonstrate that cartilage anlage contains approximately triple the amount of proteoglycan in the 2nd trimester as compared to that previously reported in hyaline articular cartilage. The proteoglycan decreases over development, resulting in double the proteoglycan in the 3rd trimester as compared to previously reported adult values. No site-specific, macroscopic (FT-IRS), differences in PG content were found while microscopic assessment (FT-IRIS) observed heterogeneity with marked changes in PG content.
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Knutsen, Andrew K., Jason E. Hill, Jeffrey J. Neil, Terrie E. Inder, and Philip V. Bayly. "Quantification of Cortical Surface Convolution in the Developing Ferret and Human Infant." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205716.

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The human cerebral cortex undergoes folding from the 5th fetal month into the first post-natal year. Disturbances of folding have serious and lasting consequences, but the mechanism is not well understood. Van Essen [1] has hypothesized that axonal tension between strongly interconnected regions draws them together and induces outward folds. However, no direct measurements have confirmed this theory. As measures of shape, cortical curvature and sulcal depth changes during development can help provide insight into underlying mechanisms of growth.
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Reports on the topic "Human fetal testis development"

1

Beach, Brian, Joseph Ferrie, and Martin Saavedra. Fetal Shock or Selection? The 1918 Influenza Pandemic and Human Capital Development. Cambridge, MA: National Bureau of Economic Research, June 2018. http://dx.doi.org/10.3386/w24725.

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