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PubMed2000

Expression of the human poliovirus receptor/CD155 gene during development of the central nervous system: implications for the pathogenesis of poliomyelitis.

The gene for the human poliovirus receptor (hPVR/CD155) is the founding member of a new family of genes encoding proteins belonging to the immunoglobulin superfamily. To determine whether CD155 is expressed during mammalian development, we have made use of the previously characterized promoter of the CD155 gene and generated mice transgenic for a CD155 promoter-driven beta-galactosidase reporter gene. Expression of the reporter gene in transgenic embryos was observed during midgestation in anterior midline structures of the developing central nervous system and in the neuroretina. During that period, reporter gene expression appeared within the notochord and floor plate along the entire spinal cord reaching into the caudal diencephalon. In addition, transgene expression was observed in axonal projections emanating from retinal ganglion cells forming the optic nerve to reach the future region of the optic chiasm. Analysis of expression of CD155 during human embryonic development confirmed the distribution of reporter gene expression specified by CD155 promoter activity. The anatomical distribution of CD155 promoter activity during embryogenesis matches that of transacting factors previously identified to regulate transcription of the CD155 gene. Expression of CD155 within embryonic structures giving rise to spinal cord anterior horn motor neurons may explain the restrictive host cell tropism of poliovirus for this cellular compartment of the CNS.

Animals↗

PubMed1991

Liver-specific and position-effect expression of a retinol-binding protein-lacZ fusion gene (RBP-lacZ) in transgenic mice.

Transgenic mice carrying a liver-specific promoter fused to a nuclear-targeted lacZ reporter gene were generated. Three separate lines of mice showed liver expression in the adult and no expression elsewhere in the animal. These results show that a 1.7 kb 5'-flanking region in the retinol-binding protein gene contains necessary and sufficient transcriptional signals for expression in adult livers. A fourth line (R197) did not express the transgene in the liver; instead, constitutive lacZ expression was seen during postimplantation stages of development from Day 9.5 onwards and appeared to be associated with segmented structures including somites, branchial arches, and hindbrain rhombomeres until late fetal stages. The beta-galactosidase positive cells in R197 were later seen to give rise to facial and flank musculature, and to other region-specific subpopulations of the jaws, neocortex, and brain stem. Northern blot analysis for the host retinol-binding protein RNA transcript did not show overlapping tissue expression with the reporter gene and suggests that transgenic phenotype seen in segmented embryonic structures of R197 and other extra-hepatic sites is from novel cis-acting transcriptional specificity. RNase protection assays of the R197 mRNA indicate that the lacZ sequences are appropriately transcribed downstream of the RBP canonical TATA box, even though the RBP promoter is itself silent. This result would suggest host flanking sequences with enhancer activity may have either activated the lacZ reporter gene or cooperated with the RBP promoter to create novel region-specific transcription. Breeding experiments have so far failed to produce offsprings that are homozygous for the transgene, and mating of transgenic F1 siblings routinely produce reduced litter sizes. Embryos that are homozygous for the transgene appear to be unable to survive beyond the egg cylinder stages of development. Thus, disruption of the host genome by insertional mutation appears to be manifest at an earlier stage than when position-effect expression of the transgene is first apparent. These experiments demonstrate that the component parts of a transgene may be subject to differential activation or suppression by host genomic flanking sequences and that even a strong, tissue-specific promoter may be overridden by host genes.

Animals↗

PubMed1988

Comparison of a fixed and dynamic protocol for embryo replacement in an IVF/ET programme.

Implantation after embryo transfer is considered a major obstacle in terms of pregnancy rates after in-vitro fertilization. A flexible approach to the date of replacement, based on the fact that the most suitable embryonic structure for proper implantation is the four- to eight-cell embryo, has been studied. One-hundred-and-twenty patients with various aetiologies of infertility were stimulated with HMG or combined HMG and FSH, then treated by three different methods of embryo replacement. In group I embryos were replaced in mothers 48 h after ovum retrieval; in group II replacements were carried out 72 h after retrieval; and in group III replacements were related to embryonic cleavage development. Mean levels of oestradiol when HCG was given averaged 1301 +/- 121 pg/ml, 1016 +/- 96 pg/ml and 1182 +/- 101 pg/ml in the three groups, respectively. There was no significant difference in the average number of embryos transferred among the various groups. The pregnancy rates per transfer were 21.8, 24.2 and 38.7%, respectively (P less than 0.001). Although more investigation is required, a dynamic approach to embryo replacement might significantly improve pregnancy rates, because of improved interactions between the embryos and the uterus.

Chorionic Gonadotropin↗

PubMed1976

Simultaneous occurrence of melanotic neuroectodermal tumor and brain heterotopia in the oropharynx.

A case is described of heterotopic brain tissue with simultaneous occurrence of melanotic neuroectodermal tumor in the oropharynx of a 6-week-old infant. The melanotic neuroectodermal tumor was embedded within the heterotopic glial tissue. This coexistence leads us to speculate that a defect causing a pinching-off of both neural crest cap and medullary epithelium of neural tube might have taken place at, or before, the 25-30 somite stage. The displaced embryonic structures subsequently differentiated into glial tissue, choroid plexus, and melanotic neuroectodermal tumor. This observation may be interpreted as further support in favor of a neural crest origin of juvenile melanotic neuroectodermal tumor.

Brain↗

PubMed2000

tbx20, a new vertebrate T-box gene expressed in the cranial motor neurons and developing cardiovascular structures in zebrafish.

The T-box genes constitute a family of transcriptional regulator genes that have been implicated in a variety of developmental processes ranging from the formation of germ layers to the regionalization of the central nervous system. In this report we describe the cloning and expression pattern of a new T-box gene from zebrafish, which we named tbx20. tbx20 is an ortholog of two other T-box genes isolated from animals of different phyla - H15 of Drosophila melanogaster and tbx-12 of Caenorhabditis elegans, suggesting that the evolutionary origin of this gene predates the divergence between the protostomes and deuterostomes. During development, tbx20 is expressed in embryonic structures of both mesodermal and ectodermal origins, including the heart, cranial motor neurons, and the roof of the dorsal aorta.

Amino Acid Sequence↗

PubMed2005

Teratogen-induced apoptotic cell death: does the apoptotic machinery act as a protector of embryos exposed to teratogens?

Considerable evidence has been collected demonstrating that many teratogens induce apoptotic cell death in embryonic structures that turn out to be malformed in fetuses and newborns. Apoptosis is a genetically regulated process that is realized by the activation of death and pro-survival signaling cascades, and the interplay between these cascades determines whether the cell exposed to apoptotic stimuli dies or survives. Therefore, there is intense interest in understanding how the apoptotic machinery functions in embryos exposed to teratogens. However, the interpretation of the results obtained remains problematic. The main problem is that excessive embryonic cell death, regardless of its nature, if uncompensated for, ultimately leads to maldevelopment or embryonic death. Therefore, we can easily interpret results when the intensity of teratogen-induced cell death and the severity or incidence of teratogen-induced anomalies directly correlate with each other. However, when teratogen-induced cell death is not followed by the formation of anomalies, a usual explanation is that teratogen-induced apoptotic cell death contributes to the renewal of teratogen-targeted cell populations by promoting the removal of injured cells. It is clear that such an explanation leaves vague the role of the anti-apoptotic signaling mechanism (and, hence, the apoptotic machinery as a whole) with respect to protecting the embryo against teratogenic stress. In this review, we summarize the data from studies addressing the function of the apoptotic machinery in embryos exposed to teratogens, and then we discuss approaches to interpreting the results of these studies. We hypothesize that activation of a proapoptotic signaling in teratogen-targeted cell populations is a necessary condition for an anti-apoptotic signaling that counteracts the process of maldevelopment to be activated. If such a scenario is true, we need to modify our approaches to choosing molecular targets for studies addressing this topic.

Abnormalities, Drug-Induced↗

PubMed1997

Morphological changes of in-vitro-produced bovine blastocysts after vitrification, in-straw direct rehydration, and culture.

Morphological signs of injury and regeneration following vitrification and warming of bovine embryos were studied by light and electron microscopy. In-vitro-produced Day 7 expanded blastocysts (Day 0 = day of insemination) were vitrified by a two-step equilibration method using ethylene glycol and dimethyl sulphoxide as cryoprotectants. Thawing was performed by in-straw direct rehydration, followed by in vitro culture on a granulosa cell monolayer. Embryos were processed for transmission electron microscopy immediately after warming (0 hr) as well as after 4 hr or 24 hr of culture following warming. A control group of unfrozen embryos was also processed. At 0 hr after warming, except for a rapid collapse of the blastocoele, only minor changes were detectable by stereomicroscope. However, at the ultrastructural level, signs of extensive injury were seen, including a general distension or shrinkage of mitochondria, disintegration of cell adhesions between adjacent trophoblastic cells, and complete rupture of some cells. At 4 hr, stereomicroscopic investigation revealed collapsed blastocoele and a darkened granular appearance of the cell mass. At the ultrastructural level, signs of regeneration were also observable: cells with minor injuries were re-assembled in a central area forming a small blastocoele, cell adhesion structures were re-established, and damage of mitochondria was less severe. The majority of irreversibly damaged cells or cell debris was accumulated in the perivitelline space. At 24 hr, stereomicroscopic investigation of surviving blastocysts showed no signs of the previous injury. At the ultrastructural level, cellular debris in the perivitelline space and some degenerated cells in the blastocoele were the only signs of previous injuries. In conclusion, ultrastructural investigation revealed unexpectedly extensive damage followed by a rapid regeneration and reorganization of the embryonic structure.

Animals↗

PubMed1992

Decapentaplegic acts as a morphogen to organize dorsal-ventral pattern in the Drosophila embryo.

Zygotic expression of the Drosophila TGF beta family member decapentaplegic (dpp) is required for the development of the dorsal embryonic structures. By injecting dpp transcripts into young embryos, we find that 2- to 4-fold increases in the concentration of injected RNA elicit progressively more dorsal cell fates: only low levels of dpp permit development of ventral ectoderm, intermediate dpp levels drive dorsal epidermal development, and high dpp levels drive cells to differentiate as the most dorsal pattern element, the amnioserosa. Localized dpp RNA injections into embryos that lack all known maternal and zygotic dorsal-ventral polarity indicate that dpp can both define embryonic polarity and organize detailed patterning within the ectoderm. We infer that dpp acts as an extracellular morphogen and that the graded activity of dpp specifies the pattern of ectodermal cell fates in the Drosophila embryo.

Animals↗

PubMed2001

The forkhead transcription factor Foxf1 is required for differentiation of extra-embryonic and lateral plate mesoderm.

The murine Foxf1 gene encodes a forkhead transcription factor expressed in extra-embryonic and lateral plate mesoderm and later in splanchnic mesenchyme surrounding the gut and its derivatives. We have disrupted Foxf1 and show that mutant embryos die at midgestation due to defects in mesodermal differentiation and cell adhesion. The embryos do not turn and become deformed by the constraints of a small, inflexible amnion. Extra-embryonic structures exhibit a number of differentiation defects: no vasculogenesis occurs in yolk sac or allantois; chorioallantoic fusion fails; the amnion does not expand with the growth of the embryo, but misexpresses vascular and hematopoietic markers. Separation of the bulk of yolk sac mesoderm from the endodermal layer and adherence between mesoderm of yolk sac and amnion, indicate altered cell adhesion properties and enhanced intramesodermal cohesion. A possible cause of this is misexpression of the cell-adhesion protein VCAM1 in Foxf1-deficient extra-embryonic mesoderm, which leads to co-expression of VCAM with its receptor, alpha(4)-integrin. The expression level of Bmp4 is decreased in the posterior part of the embryo proper. Consistent with this, mesodermal proliferation in the primitive streak is reduced and somite formation is retarded. Expression of Foxf1 and the homeobox gene Irx3 defines the splanchnic and somatic mesodermal layers, respectively. In Foxf1-deficient embryos incomplete separation of splanchnic and somatic mesoderm is accompanied by misexpression of Irx3 in the splanchnopleure, which implicates Foxf1 as a repressor of Irx3 and as a factor involved in coelom formation.

Allantois↗

PubMed1977

[Vitelline components in teratomas and serum alpha-1 fetoprotein].

Serum alpha1-fetoprotein (AFP) had been determined in 31 patient with (mostly malignant) teratomas before or immediately after operation, and later in the evolution of 3 other cases with clinical evidence of recurrence or metastases. Without knowledge of these serum AFP levels, histological slides of the same 34 teratomas were reexamined, especially for the presence of yolk sac components. Two pure yolk sac tumors and 6 teratomas containing yolk sac structures were associated with serum AFP levels above 500 ng/ml. Teratomas without yolk sac structures were associated with normal serum AFP levels (i.e. 10-500 ng/ml) in 14 cases, and high serum levels (i.e. above 500 ng/ml) in one case. Histologic analysis of the 14 cases with slightly elevated AFP levels did not reveal tissue possibly responsible for the low but nevertheless abnormal AFP synthesis. High AFP levels, which are easily detectable by counter-current immunoelectrophoresis, are, however, highly specific for the yolk sac tumor or the yolk sac component of teratomas, and hence suggest that this extra-embryonic structure should be distinguished from other teratoma components.

Adolescent↗

PubMed1994

Homologs of the mouse Brachyury gene are involved in the specification of posterior terminal structures in Drosophila, Tribolium, and Locusta.

The Brachyury (T) gene is required for notochord differentiation in vertebrates. We have identified a Drosophila gene, the T-related gene (Trg), with high similarity to T within a stretch of approximately 200 amino acids, the DNA-binding domain of T. Trg is expressed throughout embryogenesis, first at the blastoderm stage in the hindgut primordium under the control of the terminal gap genes tll and hkb, and then until the end of embryogenesis in the differentiating hindgut. Drosophila embryos deficient for Trg do not form the hindgut, a phenotype that can be rescued by a Trg transgene. Thus, a common feature of T and Trg is their requirement in specifying the development of a single embryonic structure. Homologs of Trg are also expressed in the developing hindgut of Tribolium and Locusta embryos suggesting a highly conserved function of Trg in insects. This conservation and the high similarity of T and Trg raise the question of a common evolutionary origin of the hindgut of insects and the notochord of chordates.

Amino Acid Sequence↗

PubMed1986

Localization of radioactivity from 2-methoxy[1,2-14C]ethanol in maternal and conceptus compartments of CD-1 mice.

2-Methoxyethanol (ME) induces paw malformations in CD-1 mice when given by gavage on gestation day (gd) 11 (vaginal plug + day = gd 0). The distribution of radioactivity originating from 2-methoxy[1,2-14C]ethanol ([14C]ME) was examined by liquid scintillation spectrophotometry and whole body autoradiography in pregnant (gd 11) CD-1 mice from 5 min to 48 hr after oral administration. Each dam received either a trace dose of [14C]ME (0.92 mumol; 13 muCi) combined with an unlabeled teratogenic dose (187 mumol). By 5 min after the trace dose was administered, 14C had distributed throughout the maternal and conceptus compartments. Radioactivity in the maternal compartment was most concentrated in the liver, blood and gastrointestinal tract. Conceptus 14C was associated with the placenta, yolk sac, and embryonal structures such as limb buds, somites, and neuroepithelium. The concentration of blood 14C plateaued within 30 min after administration of the trace or combined trace/teratogenic dose. It remained stable for 1.5 hr and then gradually declined, reaching 2 to 10% of the maximal concentration by 48 hr. 14C content in the maternal liver, conceptuses, and embryos per se was always greater than that of the blood and was inversely related to ME dose at 6 hr but not 48 hr. At 6 hr after administration of the trace dose, 69% of total liver and 33% of embryonal 14C were acid insoluble. Tissue-specific interaction with [14C]ME was demonstrated by the distribution of acid insoluble radioactivity among various cellular components of the maternal liver and embryo. The findings indicate that the embryo is readily susceptible to blood borne ME and/or its metabolites. In addition, the chemical characteristics of the labeled molecule(s) apparently favored label incorporation into macromolecules by the liver and embryo.

Animals↗

PubMed2006

Maternal immunopotentiation affects caspase activation and NF-kappaB DNA-binding activity in embryos responding to an embryopathic stress.

PROBLEM: Increased embryonic resistance to teratogenic stresses as a result of maternal immunopotentiation is associated with a decrease in the intensity of teratogen-induced apoptosis in target embryonic structures. These findings suggest that this effect of maternal immunopotentiation might be realized through modification of the expression of molecules regulating the teratogen-induced apoptotic process. To examine this possibility, we evaluated caspases 3, 8 and 9 activation as well as nuclear factor (NF)-kappaB DNA-binding activity in the embryos of immunopotentiated mice exposed to cyclophosphamide (CP). METHODS OF STUDY: The rate of resorptions and the proportion of malformed fetuses in CP-treated mice were recorded on day 19 of pregnancy. Activity of caspases was tested in cytoplasmic extracts collected from the embryonic brain 24 hr after CP treatment using appropriate fluorometric kits, whereas NF-kappaB DNA-binding activity was evaluated in nuclear extracts using the electrophoretic mobility shift assay. RESULTS: As in our previous studies, immunopotentiated CP-treated females exhibited a lower rate of resorptions or fetuses with open eyes than their non-immunopotentiated counterparts. In parallel, we observed that maternal immunopotentiation normalized the CP-induced activation of the tested caspases as well as the CP-induced suppression of NF-kappaB DNA-binding activity. CONCLUSIONS: As caspases act as inducers of apoptosis, and NF-kappaB acts in CP-treated embryos as an apoptosis suppressor, the above results suggest that maternal immunopotentiation might affect embryonic sensitivity to embryopathic stresses via NF-kappaB- and caspases-associated pathways.

Animals↗

PubMed2004

Opposing regulation of cell proliferation by retinoic acid and the serotonin2B receptor in the mouse frontonasal mass.

Development of the frontonasal mass (FNM), branchial arches, heart, and limbs depends on neural crest-mediated epithelial-mesenchymal (E-M) interactions. Teratogenesis by retinoic acid (RA) or blockade of serotonergic (5-HT) signaling by the pan-5-HT(2) receptor antagonist, ritanserin, perturbs development of these embryonic structures. In both cases, resulting phenotypes include forebrain and olfactory placode anomalies, malformations of the face, eye and lens, as well as posterior neural tube and cardiac defects. Similar sites of malformations, together with the presence of RA response elements in the 5-HT(2B) receptor promoter, have led to the suggestion that a negative regulatory relationship may exist between RA and 5-HT(2)-mediated 5-HT signaling at sites of E-M interaction (Choi et al. 1997); however, another possibility is that RA and 5-HT act independently as opposing signals to regulate development of common embryonic targets. Together with recent evidence for opposite effects on chondrogenic differentiation in hindlimb micromass cultures (Bhasin et al. 2003a), results of the present study raise the possibility that these pathways may act as opposing signals for common targets in the mouse embryo. The RA receptors, co-factors and metabolic enzymes, and 5-HT(2B) receptors were found to be are coordinately expressed at sites of E-M interaction, including the FNM, in the embryonic day (E)10.5 mouse. Cell proliferation experiments using [(3)H]thymidine incorporation demonstrated that RA or activation of 5-HT(2B) receptors caused opposite effects in FNM explants, namely stimulation or inhibition of cell proliferation, respectively, 5-HT(2B) receptor activation did not appreciably alter patterning in FNM explants. While RA has been shown to regulate lateral patterning in the FNM (LaMantia et al. 2000), 5-HT(2B) receptor activation did not alter patterning in FNM explants. Quantification of 5-HT(2B) receptor transcripts by real-time PCR provided no evidence of negative regulation of 5-HT(2B) receptor expression by RA in FNM explants, although preliminary studies using in situ hybridization had suggested that this was a possibility in both explants and RA teratogenized embryos. Future studies using quantitative PCR may still show this to be the case in teratogenized embryos. Together with the finding of coordinate expression of 5-HT(2B )receptors and RA signaling molecules, results of the present study suggest that RA, and 5-HT mediated by 5-HT(2B )receptors, may act as opposing signals to regulate cell proliferation during craniofacial development in the mouse embryo.

Animals↗

PubMed2001

Zebrafish admp is required to restrict the size of the organizer and to promote posterior and ventral development.

Bone morphogenetic proteins (Bmps) and their roles during early dorsoventral patterning of the vertebrate embryo are well understood. The role and regulation of a more distant member of this family, the anti-dorsalizing morphogenetic protein (Admp), however, are less clear. Here, we report the isolation and characterization of zebrafish admp. Unlike other bmps, admp is exclusively expressed on the dorsal side. Expression starts at blastula stages in the region of the organizer, giving rise to anterior neuroectoderm and axial mesoderm. During the course of gastrulation, both the neuroectodermal and the mesodermal admp transcripts vanish in an anterior-posterior wave. The maintenance of admp expression is positively influenced by Nodal signaling and by Bozozok (Boz), an organizer-promoting homeodomain protein acting as a repressor of early bmp2b expression. Despite the positive effect of boz on admp expression, Boz and Admp have rather opposite effects on zebrafish patterning, as revealed in gain- and loss-of-function experiments. Upon overexpression, admp has Bmp-like activities causing a smaller organizer and enhanced ventral specification, very similar to the phenotype caused by the loss of boz function in mutant embryos. Antisense-based admp knockdown, on the other side, leads to an enlarged organizer and impaired ventral and posterior development, as observed in embryos after boz overexpression. This finding indicates that admp is required for the development of embryonic structures normally suppressed by organizer activities. The seeming discrepancy between the regulative and functional relationship of boz and admp is discussed, and models are proposed according to which Admp might be part of a negative feedback loop to pattern and confine the organizer region.

Animals↗

PubMed2001

Hensen's node.

With the 125th anniversary of the original description of Hensen's node in the rabbit coming up and with current research focused on the function of this pivotal embryonic structure, this article proposes a simplified use of terms for the gastrulation organizer in amniote embryos and reemphasizes the achievements of Victor Hensen (1835-1924) in embryology. A partial translation of Hensen's paper (originally published in German) is accompanied by a short historical introduction that concentrates on the framework of embryological research at Hensen's time and on the subsequent reception of his classic paper.

Amphibians↗

PubMed1996

A spinal cord fate map in the avian embryo: while regressing, Hensen's node lays down the notochord and floor plate thus joining the spinal cord lateral walls.

The spinal cord of thoracic, lumbar and caudal levels is derived from a region designated as the sinus rhomboidalis in the 6-somite-stage embryo. Using quail/chick grafts performed in ovo, we show the following. (1) The floor plate and notochord derive from a common population of cells, located in Hensen's node, which is equivalent to the chordoneural hinge (CNH) as it was defined at the tail bud stage. (2) The lateral walls and the roof of the neural tube originate caudally and laterally to Hensen's node, during the regression of which the basal plate anlage is bisected by floor plate tissue. (3) Primary and secondary neurulations involve similar morphogenetic movements but, in contrast to primary neurulation, extensive bilateral cell mixing is observed on the dorsal side of the region of secondary neurulation. (4) The posterior midline of the sinus rhomboidalis gives rise to somitic mesoderm and not to spinal cord. Moreover, mesodermal progenitors are spatially arranged along the rest of the primitive streak, more caudal cells giving rise to more lateral embryonic structures. Together with the results reported in our study of tail bud development (Catala, M., Teillet, M.-A. and Le Douarin, N.M. (1995). Mech. Dev. 51, 51-65), these results show that the mechanisms that preside at axial elongation from the 6-somite stage onwards are fundamentally similar during the complete process of neurulation.

Animals↗

PubMed1990

Experimental diabetes impairs rat embryo development during the preimplantation period.

Congenital malformations and early fetal losses are still the main complications of diabetic pregnancy. Whether the diabetic state affects the early embryo development during the preimplantation period is not known. To understand better the early steps of embryo growth, we collected the embryonic structures from the uterine horns of pregnant diabetic rats on day 5 of pregnancy. Diabetes was induced by streptozotocin (50 mg/kg) injection, 7, 14 or 21 days before mating. The morphological analysis revealed a lower rate of blastocysts (72% of all structures) and an increased rate of morulae (19.5%) in diabetic rats, compared to control animals (86.7 and 7.9% respectively). Hence, diabetic rats had fewer blastocysts (5.5 +/- 2.9 per rat) and more morulae (1.5 +/- 1.7) than control animals (7.2 +/- 2.7 and 0.66 +/- 1.2 respectively). Moreover, blastocysts from diabetic rats had fewer nuclei (26.9 +/- 7.3 per blastocyst) than blastocysts from control animals (31 +/- 6.1). In another set of experiments, subdiabetogenic doses of streptozotocin were administered. In rats injected with 25 mg/kg, neither the glycaemia, nor the morphological aspects of the embryos, nor the number of blastocyst nuclei differed from the control animals. In the animals receiving 35 mg/kg, the glycaemia was increased to approximately twice the control group value. However, the embryonic morphology and the nuclei counting of the blastocysts were similar to those of the fully diabetic group injected with 50 mg of streptozotocin. These results show that experimentally induced diabetes, even of a rather mild degree, affects the embryo development during the preimplantation period. The recovered embryos appear less mature and less developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗