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Journal articles on the topic 'Mice embryology; mice genetics'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Juriloff, D. M., T. M. Gunn, M. J. Harris, D. G. Mah, M. K. Wu, and S. L. Dewell. "Multifactorial genetics of exencephaly in SELH/Bc mice." Teratology 64, no. 4 (2001): 189–200. http://dx.doi.org/10.1002/tera.1064.

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2

Gabriel, George C., Hisato Yagi, Xinxiu Xu, and Cecilia W. Lo. "Novel Insights into the Etiology, Genetics, and Embryology of Hypoplastic Left Heart Syndrome." World Journal for Pediatric and Congenital Heart Surgery 13, no. 5 (September 2022): 565–70. http://dx.doi.org/10.1177/21501351221102961.

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Hypoplastic left heart syndrome (HLHS) is a relatively rare severe congenital heart defect (CHD) closely linked to other left ventricular outflow tract (LVOT) lesions including bicuspid aortic valve (BAV), one of the most common heart defects. While HLHS, BAV, and other LVOT lesions have a strong genetic underpinning, their genetic etiology remains poorly understood. Findings from a large-scale mouse mutagenesis screen showed HLHS has a multigenic etiology and is genetically heterogenous, explaining difficulties in identifying the genetic causes of HLHS. In Ohia mice, HLHS shows incomplete penetrance. Some mice exhibited small LV with normal aorta, and others a normal LV with hypoplastic aorta, indicating the LV hypoplasia is not hemodynamically driven. In Ohia mutants, HLHS was found to have a digenic modular construction, with mutation in a chromatin modifier causing the small LV phenotype and mutation in Pcdha9 causing the aorta/aortic valve hypoplasia. The Pcdha9 mutation alone can cause BAV, and in the human genome two common deletion copy number variants spanning PCDHA7-10 are associated with BAV. Hence the digenic etiology of HLHS can account for the close association of HLHS, a rare CHD, with BAV, one of the most common CHD. Functional analysis of Ohia HLHS heart tissue showed severe mitochondrial dysfunction in the small LV, while the normal size RV is also affected but milder, suggesting possible role in vulnerability of surgically palliated HLHS patients to heart failure. These findings suggest insights into the genetics of HLHS may yield new therapies for improving outcome for patients with HLHS.

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3

Naruse, Ichiro, and Yoshiro Kameyama. "Fetal laser surgery in genetic Polydactyly mice." Teratology 41, no. 6 (June 1990): 731–35. http://dx.doi.org/10.1002/tera.1420410610.

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4

Ruetten, Hannah, Kyle A. Wegner, Helen L. Zhang, Peiqing Wang, Jaskiran Sandhu, Simran Sandhu, Jacquelyn Morkrid, et al. "Insight and Resources From a Study of the “Impact of Sex, Androgens, and Prostate Size on C57BL/6J Mouse Urinary Physiology." Toxicologic Pathology 47, no. 8 (October 29, 2019): 1038–42. http://dx.doi.org/10.1177/0192623319877867.

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The purpose of this symposium report is to summarize information from a session 3 oral presentation at the Society of Toxicologic Pathology Annual Symposium in Raleigh, North Carolina. Mice are genetically tractable and are likely to play an important role in elucidating environmental, genetic, and aging-related mechanisms of urinary dysfunction in men. We and others have made significant strides in developing quantitative methods for assessing mouse urinary function and our collaborators recently showed that aging male mice, like men, develop urinary dysfunction. Yet, it remains unclear how mouse prostate anatomy and histology relate to urinary function. The purpose of this report is to share foundational resources for evaluating mouse prostate histology and urinary physiology from our recent publication “Impact of Sex, Androgens, and Prostate Size on C57BL/6J Mouse Urinary Physiology: Functional Assessment.” We will begin with a review of prostatic embryology in men and mice, then move to comparative histology resources, and conclude with quantitative measures of rodent urinary physiology.

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5

Mei, Hua, Cara Walters, Richard Carter, and William H. Colledge. "Gpr54−/− mice show more pronounced defects in spermatogenesis than Kiss1−/− mice and improved spermatogenesis with age when exposed to dietary phytoestrogens." REPRODUCTION 141, no. 3 (March 2011): 357–66. http://dx.doi.org/10.1530/rep-10-0432.

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Mice with mutations in the kisspeptin signaling pathway (Kiss1−/− or Gpr54−/−) have low gonadotrophic hormone levels, small testes, and impaired spermatogenesis. Between 2 and 7 months of age, however, the testes of the mutant mice increase in weight and in Gpr54−/− mice, the number of seminiferous tubules containing spermatids/spermatozoa increases from 17 to 78%. In contrast, the Kiss1−/− mice have a less severe defect in spermatogenesis and larger testes than Gpr54−/− mice at both 2 and 7 months of age. The reason for the improved spermatogenesis was investigated. Plasma testosterone and FSH levels did not increase with age in the mutant mice and remained much lower than in wild-type (WT) mice. In contrast, intratesticular testosterone levels were similar between mutant and WT mice. These data indicate that age-related spermatogenesis can be completed under conditions of low plasma testosterone and FSH and that intratesticular testosterone may contribute to this process. In addition, however, when the Gpr54−/− mice were fed a phytoestrogen-free diet, they showed no age-related increase in testes weight or improved spermatogenesis. Thus, both genetic and environmental factors are involved in the improved spermatogenesis in the mutant mice as they age although the mice still remain infertile. These data show that the possible impact of dietary phytoestrogens should be taken into account when studying the phenotype of mutant mice with defects in the reproductive axis.

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6

McFarlane, L., V. Truong, J. S. Palmer, and D. Wilhelm. "Novel PCR Assay for Determining the Genetic Sex of Mice." Sexual Development 7, no. 4 (2013): 207–11. http://dx.doi.org/10.1159/000348677.

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7

Suto, J. "Genetic analysis of inferior nurturing ability in RR mice." Reproduction 123, no. 1 (January 1, 2002): 52–58. http://dx.doi.org/10.1530/reprod/123.1.52.

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8

Astrof, Sophie, Andrew Kirby, Kerstin Lindblad-Toh, Mark Daly, and Richard O. Hynes. "Heart development in fibronectin-null mice is governed by a genetic modifier on chromosome four." Mechanisms of Development 124, no. 7-8 (August 2007): 551–58. http://dx.doi.org/10.1016/j.mod.2007.05.004.

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9

Vieira, A. R. "Oral Clefts and Syndromic Forms of Tooth Agenesis as Models for Genetics of Isolated Tooth Agenesis." Journal of Dental Research 82, no. 3 (March 2003): 162–65. http://dx.doi.org/10.1177/154405910308200303.

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Genetic defects responsible for tooth agenesis are only now beginning to be uncovered. MSX1 and PAX9 have been associated with tooth agenesis in mice and humans, but interestingly for humans, these genes are associated with specific missing teeth. Mouse models also show that specific genes contribute to the development of specific types of teeth. A precise description of the phenotype specifying which teeth are missing has become fundamental. Mendelian segregation can be identified in families with tooth agenesis, but heterogenous or multiple genes may be responsible for the development of specific types of teeth agenesis in humans. Data from animal models are still very complex, and the human embryology is still poorly understood. Oral clefts and syndromic forms of tooth agenesis may be the best models for isolated tooth agenesis. In the future, a precise description of the missing teeth in syndromes involving tooth agenesis may be useful.

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10

Tuffrey, M., F. Alexander, C. Woods, and D. Taylor-Robinson. "Genetic susceptibility to chlamydial salpingitis and subsequent infertility in mice." Reproduction 95, no. 1 (May 1, 1992): 31–38. http://dx.doi.org/10.1530/jrf.0.0950031.

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11

Fröhlich, Carolin, Jens Ehrhardt, Diana Krüger, Dominika Trojnarska, Marek Zygmunt, and Damián Oscar Muzzio. "Pregnancy status alters IL-21-mediated effects on murine B lymphocytes." Reproduction 159, no. 3 (March 2020): 351–59. http://dx.doi.org/10.1530/rep-19-0407.

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A favorable outcome of pregnancy depends greatly on an adequate balance of immune protection and fetal tolerance at the fetomaternal interface. IL-21 is a pro-inflammatory cytokine associated with altering immune responses in autoimmune diseases. IL-21 has pleiotropic functions, including induction of Th17 T cells, inhibition of Treg development, and modulation of antibody responses of B lymphocytes. Genetic polymorphisms of IL21 have been associated to poor pregnancy outcomes. However, the mechanism of IL-21 actions needs further evaluation. Here, we postulate that IL-21 affects splenic B cell function during pregnancy and shapes immune responses. We show that splenic B cells from CBA/J × BALB/c mice with favorable pregnancy outcome expressed lower IL21R levels than in CBA/J × DBA/2J mice, a mouse model for immune-induced bad pregnancy outcome. As a consequence, B cells from CBA/J × BALB/c mice reacted less sensitively to IL-21 than B cells from non-pregnant mice (NPM) or from CBA/J × DBA/2J mice. Also, LPS-induced apoptotic rates were altered in NPM and CBA/J × DBA/2J but not in CBA/J × BALB/c mice. This is accompanied by improved survival of B cells that produce the anti-inflammatory cytokine IL-10 upon stimulation with LPS. We also observed lower numbers of CD4+CXCR5+Bcl-6+ follicular T-helper cells (Tfh) in normal pregnant mice, compared to non-pregnant and mice with disturbed pregnancies. Our data indicate that alterations of the Tfh/IL-21/IL-10 axis may have important influence on pregnancy outcome.

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12

Gunn, T. M., D. M. Juriloff, and M. J. Harris. "Further genetic studies of the cause of exencephaly in SELH mice." Teratology 45, no. 6 (June 1992): 679–86. http://dx.doi.org/10.1002/tera.1420450613.

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13

Lundberg, Yunxia Wang, Michael J. Wing, Wanfen Xiong, Jian Zhao, and Richard H. Finnell. "Genetic dissection of hyperthermia-induced neural tube defects in mice." Birth Defects Research Part A: Clinical and Molecular Teratology 67, no. 6 (June 2003): 409–13. http://dx.doi.org/10.1002/bdra.10044.

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14

Spearow, J. L. "Characterization of genetic differences in hormone-induced ovulation rate in mice." Reproduction 82, no. 2 (March 1, 1988): 799–806. http://dx.doi.org/10.1530/jrf.0.0820799.

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15

Kusanagi, Takao, and James R. Miller. "Genetic analysis of spontaneous and induced palatal slit in C57BL/6 mice." Teratology 32, no. 1 (August 1985): 125–32. http://dx.doi.org/10.1002/tera.1420320117.

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16

Kappen, C., A. Neubüser, R. Balling, and R. Finnell. "Molecular basis for skeletal variation: insights from developmental genetic studies in mice." Birth Defects Research Part B: Developmental and Reproductive Toxicology 80, no. 6 (2007): 425–50. http://dx.doi.org/10.1002/bdrb.20136.

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17

Harris, M. J., and D. M. Juriloff. "Mini-review: toward understanding mechanisms of genetic neural tube defects in mice." Teratology 60, no. 5 (November 1999): 292–305. http://dx.doi.org/10.1002/(sici)1096-9926(199911)60:5<292::aid-tera10>3.0.co;2-6.

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18

Vaz, B., F. El Mansouri, X. Liu, and T. Taketo. "Premature ovarian insufficiency in the XO female mouse on the C57BL/6J genetic background." Molecular Human Reproduction 26, no. 9 (July 7, 2020): 678–88. http://dx.doi.org/10.1093/molehr/gaaa049.

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Abstract In humans, all but 1% of monosomy 45.X embryos die in utero and those who reach term suffer from congenital abnormalities and infertility termed Turner’s syndrome (TS). By contrast, XO female mice on various genetic backgrounds show much milder physical defects and normal fertility, diminishing their value as an animal model for studying the infertility of TS patients. In this article, we report that XO mice on the C57BL/6J (B6) genetic background showed early oocyte loss, infertility or subfertility and high embryonic lethality, suggesting that the effect of monosomy X in the female germline may be shared between mice and humans. First, we generated XO mice on either a mixed N2(C3H.B6) or B6 genetic background and compared the number of oocytes in neonatal ovaries; N2.XO females retained 45% of the number of oocytes in N2.XX females, whereas B6.XO females retained only 15% of that in B6.XX females. Second, while N2.XO females were as fertile as N2.XX females, both the frequency of delivery and the total number of pups delivered by B6.XO females were significantly lower than those by B6.XX females. Third, after mating with B6 males, both N2.XO and B6.XO females rarely produced XO pups carrying paternal X chromosomes, although a larger percentage of embryos was found to be XO before implantation. Furthermore, B6.XO females delivered 20% XO pups among female progeny after mating with C3H males. We conclude that the impact of monosomy X on female mouse fertility depends on the genetic background.

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19

Liu, Jianmin, Sherry L. Ball, Yuan Yang, Pinchao Mei, Lei Zhang, Haining Shi, Henry J. Kaminski, Vance P. Lemmon, and Huaiyu Hu. "A genetic model for muscle–eye–brain disease in mice lacking protein O-mannose 1,2-N-acetylglucosaminyltransferase (POMGnT1)." Mechanisms of Development 123, no. 3 (March 2006): 228–40. http://dx.doi.org/10.1016/j.mod.2005.12.003.

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20

Everett, Clare A., Catherine A. Auchincloss, Matthew H. Kaufman, Catherine M. Abbott, and John D. West. "Genetic influences on ovulation of primary oocytes in LT/Sv strain mice." Reproduction 128, no. 5 (November 2004): 565–71. http://dx.doi.org/10.1530/rep.00325.

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A high proportion of LT/Sv strain oocytes arrest in meiotic metaphase I (MI) and are ovulated as diploid primary oocytes rather than haploid secondary oocytes. (Mus musculus castaneus × LT/SvKau)F1 × LT/SvKau backcross females were analysed for the proportion of oocytes that arrested in MI and typed by PCR for a panel of microsatellite DNA sequences (simple sequence repeat polymorphisms) that differed between strain LT/SvKau and M. m. castaneus. This provided a whole genome scan of 86 genetic markers distributed over all 19 autosomes and the X chromosome, and revealed genetic linkage of the MI arrest phenotype to markers on chromosomes 1 and 9. Identification of these two chromosomal regions should facilitate the identification of genes involved in mammalian oocyte maturation and the control of meiosis.

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21

Biggers, John D., and Virginia E. Papaioannou. "Water-escape time in adult mice derived from manipulated preimplantation embryos." Journal of In Vitro Fertilization and Embryo Transfer 8, no. 6 (December 1991): 352–60. http://dx.doi.org/10.1007/bf01133028.

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22

Jaroszynski, L., A. Dev, M. Li, A. Meinhardt, D. G. de Rooij, Christian Mueller, Detlef Böhm, et al. "Asthenoteratozoospermia in mice lacking testis expressed gene 18 (Tex18)." MHR: Basic science of reproductive medicine 13, no. 3 (January 5, 2007): 155–63. http://dx.doi.org/10.1093/molehr/gal107.

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23

Kotlarska, Magdalena, Dawid Winiarczyk, Wiesława Florek, Marta Ziętek, Jolanta Pęczkowicz-Szyszka, Adrian Mateusz Stankiewicz, Rafał Radosław Starzyński, et al. "Blastomere removal affects homeostatic control leading to obesity in male mice." Reproduction 161, no. 1 (January 2021): 61–72. http://dx.doi.org/10.1530/rep-20-0253.

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Preimplantation embryos are particularly vulnerable to environmental perturbations, including those related to assisted reproductive technologies. Invasive embryo manipulations, such as blastomere biopsy, are applied worldwide in clinical settings for preimplantation genetic testing. Mouse models have previously shown that blastomere biopsy may be associated with altered phenotypes in adult offspring. The aim of the present study was to investigate the specific contribution of blastomere removal to the physiological, behavioral, and molecular regulators of energy homeostasis, as compared to sham manipulation (re-introducing the blastomere into the embryo after its removal) and in vitro culture. Mice derived from 8-cell embryos subjected to blastomere removal displayed: (i) higher body weight and adiposity, (ii) increased food intake and sucrose preference, (iii) decreased time of immobility in the tail suspension test, and (iv) resistance to weight loss after social isolation or following 3 days of physical exercise – compared to mice derived from sham biopsy or from in vitro-cultured embryos. Mice generated after blastomere removal also had increased circulating leptin and leptin gene expression in adipose tissue, as well as increased ghrelin receptor gene expression in the hypothalamus, compared to control mice. The effects of blastomere biopsy on offspring phenotype were sexually dimorphic, with females not being affected. These results indicate that blastomere deprivation, rather than other perturbations of the blastomere biopsy procedure, programs male embryos to develop physiological, behavioral, and molecular dysregulation of energy homeostasis, leading to postnatal obesity.

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24

Papaioannou, Virginia E. "Salome Gluecksohn-Waelsch. 6 October 1907—7 November 2007." Biographical Memoirs of Fellows of the Royal Society 67 (August 14, 2019): 153–71. http://dx.doi.org/10.1098/rsbm.2019.0024.

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Salome Gluecksohn-Waelsch was a pioneer in establishing the field of mammalian developmental genetics, bringing together experimental embryology and genetics at a time when the role of genes in development was far from accepted. She studied in Germany in the 1930s with the renowned experimental embryologist Hans Spemann and then moved to New York City where she spent her entire professional career at Columbia University and the Albert Einstein College of Medicine of Yeshiva University. Her career was remarkable not only for its longevity—she continued experiments well into her 90s—but also for ushering in new ways of approaching developmental biology in mammals. In her studies of the T -complex in mice, she made use of naturally occurring mutations as nature's own experiments that allowed the investigation of the normal role of the genes in the events of morphogenesis. In her later work with the albino chromosomal deletions, she extended her studies to the genetics of physiological traits. Throughout the decades that saw a blossoming of the entire field of genetics, Salome Gluecksohn-Waelsch's work tackling some of the most perplexing problems in mammalian genetics firmly established the mouse as model organism, not only for studying development, but also for the eventual application of molecular biology techniques to development. Her published work is a beautifully coherent and rigorous opus, for which she received many honours. Her influence on a generation of geneticists, developmental biologists and the field of developmental genetics was profound. The life of Salome Gluecksohn–Waelsch spanned a century that suffered the destructive upheaval of two world wars but also saw phenomenal progress in the sciences, including embryology and genetics. At the start of Salome's career, these two fields were far apart and developmental genetics was barely a concept. Along with a few other pioneers, Salome was instrumental in establishing that genes actually had roles in development and in founding the field of mammalian developmental genetics. Her career laid the ground work for the eventual integration of genetic and developmental studies through molecular biology. Salome Gluecksohn–Waelsch published under four different names at different stages of her life and career: Salome Glücksohn, Salome Gluecksohn–Schoenheimer, Salome Gluecksohn–Waelsch, and Salome G. Waelsch. Among her colleagues and friends, she was almost universally known as Salome and so for the purpose of this biographical memoir, I have chosen to refer to her by her first name, out of friendship and respect.

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25

Lorente, Mar, Claudia Pérez, Carmen Sánchez, Mary Donohoe, Yang Shi, and Miguel Vidal. "Homeotic transformations of the axial skeleton of YY1 mutant mice and genetic interaction with the Polycomb group gene Ring1/Ring1A." Mechanisms of Development 123, no. 4 (April 2006): 312–20. http://dx.doi.org/10.1016/j.mod.2006.02.003.

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26

Rulli, Susana B., and Ilpo Huhtaniemi. "What have gonadotrophin overexpressing transgenic mice taught us about gonadal function?" Reproduction 130, no. 3 (September 2005): 283–91. http://dx.doi.org/10.1530/rep.1.00661.

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The two gonadotrophins, follicle-stimulating hormone and luteinising hormone, are pivotal regulators of the development and maintenance of normal fertility by maintaining testicular and ovarian endocrine function and gametogenesis. Too low gonadotrophin secretion, i.e. hypogonadotrophic hypogonadism, is a common cause of infertility. But there are also physiological and pathophysiological conditions where gonadotrophin secretion and/or action are either transiently or chronically elevated, such as pregnancy, pituitary tumours, polycystic ovarian syndrome, activating gonadotrophin receptor mutations, perimenopause and menopause. These situations can be either the primary or secondary cause of infertility and gonadal pathologies in both sexes. Also the role of gonadotrophins as tumour promoters is possible. Recently, the possibility to combine information from genetically modified mice and human phenotypes in connection with mutations of gonadotrophin or gonadotrophin receptor genes has elucidated many less well known mechanisms involved in dysregulation of gonadotrophin function. Among the genetically modified mouse models, transgenic mice with gonadotrophin hypersecretion have been developed during the last few years. In this review, we describe the key findings on transgenic mouse models overexpressing gonadotrophins and present their possible implications in related human pathologies. In addition, we provide examples of genetic mouse models with secondary effects on gonadotrophin production and, consequently, on gonadal function.

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27

Garratt, Michael, Roslyn Bathgate, Simon P. de Graaf, and Robert C. Brooks. "Copper-zinc superoxide dismutase deficiency impairs sperm motility and in vivo fertility." REPRODUCTION 146, no. 4 (October 2013): 297–304. http://dx.doi.org/10.1530/rep-13-0229.

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Oxidative stress, overproduction of reactive oxygen species (ROS) in relation to defence mechanisms, is considered to be a major cause of male infertility. For protection against the deleterious effects of ROS, animals have a variety of enzymatic antioxidants that reduce these molecules to less reactive forms. The physiological role of these antioxidantsin vivohas been explored extensively through genetic inhibition of gene expression; surprisingly, many of these animals remain fertile in spite of increased oxidative stress. Copper-zinc superoxide dismutase-deficient (Sod1−/−) male mice are one such example for whichin vivofertility has been repeatedly reported as normal, although examination of fertility has consisted of simply pairing animals of the same strain and checking for litters. This is a fairly low criterion by which to assess fertility. Herein, we show thatSod1-deficient males have zero fertilisation success in sperm competition trials that pit them against wild-type males of an otherwise identical genetic background and are almost completely infertile when mated singly with females of a different genotype. We also show that various aspects of sperm motility and function are impaired inSod1-deficient mice. Testing the breeding capabilities of mice under more ecologically relevant conditions and with females of different genotypes may help reveal additional physiological causes of infertility.

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28

Morishima, Masae, Hiroshi Yasui, Masahiko Ando, Makoto Nakazawa, and Atsuyoshi Takao. "Influence of genetic and maternal diabetes in the pathogenesis of visceroatrial heterotaxy in mice." Teratology 54, no. 4 (October 1996): 183–90. http://dx.doi.org/10.1002/(sici)1096-9926(199610)54:4<183::aid-tera2>3.0.co;2-2.

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29

Neel, James V. "Changing perspectives on the genetic doubling dose of ionizing radiation for humans, mice, andDrosophila." Teratology 59, no. 4 (April 1999): 216–21. http://dx.doi.org/10.1002/(sici)1096-9926(199904)59:4<216::aid-tera5>3.0.co;2-o.

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30

Eo, J., H. Shin, S. Kwon, H. Song, K. M. Murphy, and H. J. Lim. "Complex ovarian defects lead to infertility in Etv5-/- female mice." Molecular Human Reproduction 17, no. 9 (April 8, 2011): 568–76. http://dx.doi.org/10.1093/molehr/gar021.

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31

Srivastav, Archana, Bendangla Changkija, Kunal Sharan, Geet Kumar Nagar, and Falgun W. Bansode. "Influence of antifertility agents Dutasteride and Nifedipine on CatSper gene level in epididymis during sperm maturation in BALB/c mice." Reproduction 155, no. 4 (April 2018): 347–59. http://dx.doi.org/10.1530/rep-17-0664.

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Calcium (Ca2+) signaling is critical for successful fertilization. In spermatozoa, capacitation, hyperactivation of motility and the acrosome reaction are all mediated by increases in intracellular Ca2+ through CatSper (sperm-specific cation channel). The CatSper channel complex contains four pore-forming α subunits (CatSper1–4) and five accessory subunits called β, δ, ε, γ and ζ. Genetic deletion of any of the four CatSper genes in mice results in loss of hyperactivated motility and male infertility. Despite their vital role in male fertility, almost very little is known about influence of antifertility agents on CatSper gene expression in epididymis and epididymal spermatozoa. Therefore, we performed quantitative real-time qPCR analysis for CatSper expression in the epididymis and epididymal sperm of BALB/c mice after treatment with Dutasteride (DS), a dual 5-α reductase inhibitor and Nifedipine (NF) a calcium channel blocker as positive control. We observed that treatment with antifertility agents Dutasteride and Nifedipine induced significant decreases in the caput and cauda epididymal sperm counts, motility and fertility which could partly be attributed to alteration in the normal morphology of the sperm associated with downregulation/upregulation of CatSper mRNAs in epididymis and epididymal spermatozoa of male BALB/c mice. These can be explained on the basis of interference with mechanisms affecting calcium ion signaling resulting in changes in intracellular calcium required for sperm activity, finally affecting sperm maturation and fertility of male BALB/c mice. These studies provide some novel avenues for developing new male contraceptives in future.

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32

Berger, T., C. C. Calvert, and G. E. Bradford. "Reduced male reproductive capacity in mice with high genetic potential for post-weaning growth." Reproduction 87, no. 1 (September 1, 1989): 33–38. http://dx.doi.org/10.1530/jrf.0.0870033.

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33

Condon-Mahony, Mary, J. W. Edward Wortham, and Barbara Shirley. "Utilization of embryos from previously superovulated mice in an in vivo fertilization system." Journal of In Vitro Fertilization and Embryo Transfer 2, no. 4 (December 1985): 236–38. http://dx.doi.org/10.1007/bf01201804.

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34

Mori, Chisato, Hisashi Hashimoto, Kazumasa Hoshino, Aisaku Fukuda, Yoichi Noda, and Takahide Mori. "Influences of prolactin upon spermatogenesis and spermatozoa during in vitro fertilization in mice." Journal of In Vitro Fertilization and Embryo Transfer 5, no. 2 (April 1988): 61–66. http://dx.doi.org/10.1007/bf01130660.

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35

Fukuda, Aisaku, Yoichi Noda, Takahide Mori, Chisato Mori, Hisashi Hashimoto, and Kazumasa Hoshino. "Effects of prolactin on gametes and zygotes during in vitro fertilization in mice." Journal of In Vitro Fertilization and Embryo Transfer 5, no. 1 (February 1988): 25–30. http://dx.doi.org/10.1007/bf01138866.

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36

Kumar, T. Rajendra. "What have we learned about gonadotropin function from gonadotropin subunit and receptor knockout mice?" Reproduction 130, no. 3 (September 2005): 293–302. http://dx.doi.org/10.1530/rep.1.00660.

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A number of biochemical and physiological studies elucidated the roles of pituitary and placental glycoprotein hormones. Advances in the past two decades in manipulating the mouse genome by random or site-specific mutagenesis have heralded a new dimension to our understanding of the biology of gonadotropins. It is now possible to model many human reproductive disorders involving gonadotropins/gonadotropin-signaling in the mouse. Mutant mice selectively lacking either FSH or LH or their cognate receptors have been generated. The gonadotropin ligand and the corresponding receptor knockout mice mostly phenocopy each other. Analyses with these genetic models confirmed earlier physiological studies; in addition they also revealed novel roles for gonadotropins previously unrecognized. While FSH action seems dispensable for male but not female fertility, absence of LH causes infertility in both the sexes. While Sertoli cell number and germ cell carrying capacity of the Sertoli cells in compromised in FSH mutants, both somatic and germ cell lineages are affected in the LH mutants resulting in complete male infertility. FSH mutant females demonstrate a preantral stage block in folliculogenesis and FSH alone is not sufficient to promote full folliculogenesis in the absence of LH. Pre-ovulatory stage follicles do not form and most of the follicles undergo apoptosis in the absence of LH. Many extra-gonadal phenotypes have been described for the receptor knockout mice and whether these bear any resemblances to those in patients with similar inactivating mutations in the receptors for FSH and LH remains an open question. Thus the in vivo models will continue to have a significant impact in understanding gonadotropin physiology and pathophysiology and serve as novel genetic tools to study signaling mechanisms in the gonads.

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Betts, D. H., and B. Kalionis. "Viable iPSC mice: a step closer to therapeutic applications in humans?" Molecular Human Reproduction 16, no. 2 (December 1, 2009): 57–62. http://dx.doi.org/10.1093/molehr/gap101.

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Li, Xiangyun, Wei Wei, Jun Yong, Qing Jia, Yuansong Yu, and Keqian Di. "The genetic heterozygosity and fitness of tetraploid embryos and embryonic stem cells are crucial parameters influencing survival of mice derived from embryonic stem cells by tetraploid embryo aggregation." Reproduction 130, no. 1 (July 2005): 53–59. http://dx.doi.org/10.1530/rep.1.00667.

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The aim of this paper was to determine whether the genetic background of tetraploid embryos contributed to the survival of mice derived from embryonic stem (ES) cells by tetraploid embryo complementation. Twenty-five newborns were produced by aggregation of hybrid ES cells and tetraploid embryos with different genetic backgrounds. These newborns were entirely derived from ES cells judged by microsatellite DNA (A specific sequence of DNA bases or nucleotides that contains mono, di, tri or tetra repeats) and coat colour phenotype and germline transmission. Fifteen survived to adulthood while seven died of respiratory failure. All newborns were derived from outbred or hybrid tetraploid aggregates and no newborns were from the inbreds. Our results demonstrate that the genetic heterozygosity, fitness of tetraploid embryos and fitness of ES cells are crucial parameters influencing survival of mice derived from ES cells by tetraploid embryo aggregation. In addition, this method represents a simple and efficient procedure for immediate generation of targeted mouse mutants from genetically modified ES cell clones, in contrast to the standard protocol, which involves the production of chimeras and several breeding steps.

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Quinn, Jane C., John D. West, and M. H. Kaufman. "Genetic background effects on dental and other craniofacial abnormalities in homozygous small eye ( Pax6 Sey /Pax6 Sey ) mice." Anatomy and Embryology 196, no. 4 (September 23, 1997): 311–21. http://dx.doi.org/10.1007/s004290050100.

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Hall, J. L., M. J. Harris, and D. M. Juriloff. "Effect of multifactorial genetic liability to exencephaly on the teratogenic effect of valproic acid in mice." Teratology 55, no. 5 (May 1997): 306–13. http://dx.doi.org/10.1002/(sici)1096-9926(199705)55:5<306::aid-tera2>3.0.co;2-x.

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41

Elia, E. M., D. Belgorosky, M. Faut, S. Vighi, C. Pustovrh, D. Luigi, and A. B. Motta. "The effects of metformin on uterine tissue of hyperandrogenized BALB/c mice." Molecular Human Reproduction 15, no. 7 (May 29, 2009): 421–32. http://dx.doi.org/10.1093/molehr/gap033.

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42

Kang, H. J., S. J. Hwang, J. A. Yoon, J. H. Jun, H. J. Lim, T. K. Yoon, and H. Song. "Activation of peroxisome proliferators-activated receptor (PPAR ) promotes blastocyst hatching in mice." Molecular Human Reproduction 17, no. 10 (April 20, 2011): 653–60. http://dx.doi.org/10.1093/molehr/gar030.

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43

Hardy, Christopher M., Gavin Clydesdale, and Karen J. Mobbs. "Development of mouse-specific contraceptive vaccines: infertility in mice immunized with peptide and polyepitope antigens." Reproduction 128, no. 4 (October 2004): 395–407. http://dx.doi.org/10.1530/rep.1.00276.

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Mouse-specific immunocontraceptive peptides have been identified in mouse proteins with key roles in reproduction from sequence comparisons to other species and tested for efficacy as immunocontraceptive antigens. Peptides were derived from granulocyte-macrophage colony-stimulating factor (GMCSF), the placental 27 kDa heat-shock protein (HSP), leukemia inhibitory factor receptor (LIFR), oviduct glycoprotein (OGP), proliferin (PLF), prolactin (PRL), sperm protein SP56 and mouse zona pellucida subunits 1 and 3 (ZP1, ZP3). Fertility of female BALB/c mice was reduced after immunization with several peptides either conjugated to a carrier protein or in the form of recombinant polyepitopes. The most effective conjugated peptides (SP56, GMCSF and PRL) induced peptide-specific serum antibodies and reduced fertility by 50%. Fertility of mice was also reduced after immunization with polyepitope antigens containing up to five different peptides fused to maltose-binding protein, but antibodies were not produced against all the encoded peptides. The most effective polyepitope antigen (containing PLF, SP56, ZP1 and ZP3 peptides) reduced fertility by 50% but induced only SP56 and ZP1 antibodies. We demonstrate that lack of antibody response to a given peptide epitope (ZP3) can be overcome if repeated copies are used in the polyepitope antigen construct, but the effect varies between mouse strains. We conclude that infertility induced in mice with a range of peptide-based vaccines is dependent on antigen formulation and genetic factors but does not necessarily correlate with peptide-specific antibody levels. In light of these results, strategies to improve the efficacy of peptide-based antifertility vaccines are discussed.

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Pellicer, Antonio, Abraham Lightman, and Alan H. DeCherney. "The effect of prefreeze in vitro culturing on the success of embryo freezing in mice." Journal of In Vitro Fertilization and Embryo Transfer 6, no. 3 (June 1989): 176–79. http://dx.doi.org/10.1007/bf01130784.

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Nelson, J. F., K. Karelus, L. S. Felicio, and T. E. Johnson. "Genetic influences on oestrous cyclicity in mice: evidence that cycle length and frequency are differentially regulated." Reproduction 94, no. 1 (January 1, 1992): 261–68. http://dx.doi.org/10.1530/jrf.0.0940261.

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Ferrero, H., A. Corachán, A. Quiñonero, C. Bougeret, P. Pouletty, A. Pellicer, and F. Domínguez. "Inhibition of KIF20A by BKS0349 reduces endometriotic lesions in a xenograft mouse model." Molecular Human Reproduction 25, no. 9 (July 31, 2019): 562–71. http://dx.doi.org/10.1093/molehr/gaz044.

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Abstract Several studies have suggested a possible etiological association between ovarian endometriosis and ovarian cancer. Evidence has shown that KIF20A overexpression might confer a malignant phenotype to ovarian tumors by promoting proliferation and inhibiting apoptosis. However, no data about the role of KIF20A in endometriosis have been described. In this study, the human endometrium (n = 4) was transfected by mCherry adenovirus and intraperitoneally implanted in mice. Subsequently, mice were divided in three groups (n = 8/group) that were treated with Vehicle, BKS0349 (KIF20A-antagonist) or cabergoline (dopamine receptor agonist) for 21 days. mCherry-labeled endometriotic lesions were monitored over time using the IVIS Imaging System. Mice were sacrificed 72 h after the last administration; proliferation was evaluated by immunohistochemistry and apoptosis by TUNEL. CCND1 gene expression (G1 phase-related gene) was measured by qRT-PCR. A significant reduction in mCherry-fluorescent signal was observed in the BKS0349 group after treatment ended (D24) compared with D0 (P-value = 0.0313). Moreover, the mCherry signal on D24 showed a significant decrease in the BKS0349 group compared with controls (P-value = 0.0303), along with significant size reduction of endometriotic lesions observed in the BKS0349 group compared with control on D24 (P-value = 0.0006). Functional studies showed a significant reduction in proliferating cells in the BKS0349-treated group compared with controls (P-value = 0.0082). In addition, CCND1 expression was decreased in the BKS0349 group compared with control (P-value = 0.049) at D24 and a significant increase in apoptotic cells among endometriotic lesions in BKS0349-treated mice was observed compared with control (P-value = 0.0317). Based on these findings, we concluded that BKS0349 induces apoptosis and inhibits cell proliferation, reducing endometriotic lesion size and suggesting KIF20A inhibition by BKS0349 as a novel therapeutic treatment for endometriosis.

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Chang, Wen-Lin, Lina Cui, Yanli Gu, Minghua Li, Qian Ma, Zeng Zhang, Jing Ye, Fangting Zhang, Jing Yu, and Yaoting Gui. "TBC1D20 deficiency induces Sertoli cell apoptosis by triggering irreversible endoplasmic reticulum stress in mice." Molecular Human Reproduction 25, no. 12 (October 21, 2019): 773–86. http://dx.doi.org/10.1093/molehr/gaz057.

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Abstract Male ‘blind sterile’ mice with the causative TBC1 domain family member 20 (TBC1D20) deficiency are infertile with excessive germ cell apoptosis and spermatogenesis arrest at the spermatid stage. Sertoli cells are characterised as ‘nurse cells’ essential for normal spermatogenesis, but the role and corresponding molecular mechanisms of TBC1D20 deficiency in Sertoli cells of mice are not clear to date. In the present study, the histopathology of the testis and Sertoli cell proliferation and apoptosis were determined, and the corresponding molecular mechanisms were investigated by western blotting. Our data showed that TBC1D20 exhibits a testis-abundant expression pattern, and its expression level is positively associated with spermatogenesis. TBC1D20 is assembled in the Golgi and endoplasmic reticulum and is widely expressed by various germ cell subtypes and Sertoli cells. TBC1D20 deficiency in Sertoli cells led to an excessive apoptosis ratio and G1/S arrest. The increased apoptosis of TBC1D20-deficient Sertoli cells resulted from caspase-12 activation. TBC1D20-deficient Sertoli cells had an abnormal Golgi-endoplasmic reticulum structure, which led to endoplasmic reticulum stress, resulting in cell cycle arrest and excessive apoptosis. It suggested that TBC1D20 deficiency triggers irreversible endoplasmic reticulum stress resulting in G1/S arrest and excessive apoptosis in TBC1D20-deficient Sertoli cells, and TBC1D20 deficiency in Sertoli cells may also contribute to the infertility phenotype in ‘blind sterile’ male mice.

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Rodriguez-Sosa, Jose R., Robert A. Foster, and Ann Hahnel. "Development of strips of ovine testes after xenografting under the skin of mice and co-transplantation of exogenous spermatogonia with grafts." REPRODUCTION 139, no. 1 (January 2010): 227–35. http://dx.doi.org/10.1530/rep-09-0176.

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Xenografting of testicular tissue is an attractive new strategy for studying postnatal development of spermatogenesis and to preserve male genetics in large mammals. Typically, small cubes of immature testis (1 mm3) are grafted under the dorsal skin of immune-deficient mice. We attempted to increase the total number of seminiferous tubules in each xenograft with spermatogenesis by grafting flat strips of testis (∼9×5×1 mm) from ram lambs in immune-deficient mice. The percentage of grafts that survived and percentage of seminiferous tubules that developed spermatogenesis were the same as those reported after xenografting small cubes of lamb testis. Partially purified sheep spermatogonia were labeled with the fluorescent dye carboxy fluorescein diacetate succinyl diester and transplanted into the seminiferous tubules of one of the donor testis just before engraftment. The temporary label in the donor cells was detected for 4 weeks after xenografting, suggesting that co-engraftment of spermatogonia with testicular tissue may be a way to rapidly determine the effect of a specific gene on spermatogenesis. Finally, Sertoli cell lesions in xenografts of lamb testes were quantified, and their number and severity were found to increase, especially after grafts had been in place for 4 weeks. Although this coincided with the development of spermatogenesis, the extent of germ cell differentiation negatively correlated with severity of the lesions.

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Lu, Yong-qing, Xie-chao He, and Ping Zheng. "Decrease in expression of maternal effect geneMateris associated with maternal ageing in mice." Molecular Human Reproduction 22, no. 4 (January 14, 2016): 252–60. http://dx.doi.org/10.1093/molehr/gaw001.

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50

Tran, Tina N., Julianna Martinez, and John C. Schimenti. "A predicted deleterious allele of the essential meiosis gene MND1, present in ~ 3% of East Asians, does not disrupt reproduction in mice." Molecular Human Reproduction 25, no. 10 (August 8, 2019): 668–73. http://dx.doi.org/10.1093/molehr/gaz048.

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Abstract Infertility is a major health problem affecting ~15% of couples worldwide. Except for cases involving readily detectable chromosome aberrations, confident identification of a causative genetic defect is problematic. Despite the advent of genome sequencing for diagnostic purposes, the preponderance of segregating genetic variants complicates identification of culprit genetic alleles or mutations. Many algorithms have been developed to predict the effects of ‘variants of unknown significance’, typically single nucleotide polymorphisms (SNPs), but these predictions are not sufficiently accurate for clinical action. As part of a project to identify population variants that impact fertility, we have been generating clustered regularly interspaced short palindromic repeats-Cas9 edited mouse models of suspect SNPs in genes that are known to be required for fertility in mice. Here, we present data on a non-synonymous (amino acid altering) SNP (rs140107488) in the meiosis gene Mnd1, which is predicted bioinformatically to be deleterious to protein function. We report that when modeled in mice, this allele (MND1K85M), which is present at an allele frequency of ~ 3% in East Asians, has no discernable effect upon fertility, fecundity or gametogenesis, although it may cause sex skewing of progeny from homozygous males. In sum, assuming the mouse model accurately reflects the impact of this variant in humans, rs140107488 appears to be a benign allele that can be eliminated or de-prioritized in clinical genomic analyses of infertility patients.

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