Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Embryo Loss”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed1987

[Embryotoxic and teratogenic effects of Pharmachim's lincomycin hydrochloride].

Tested was the teratogenic and embryotoxic action of linkomycin hydrochloride with both placental and nonplacental animals. It was found that when applied twice, orally, to albino rats on the 4th day of pregnancy at the rate of 250 mg/kg body mass (=5 ED50), and once to chick embryos at 50 mg per egg the antibiotic raised the percent of pre- and postimplantation loss of embryos. In a series of applications (oral) from the 3rd up to the 19th day at 50 mg/kg body mass to rats as well as in a single application to chick embryos at 10, 20, and 50 mg per egg linkomycin showed no teratogenic effects.

Abnormalities, Drug-Induced↗
PubMed1994

An improved method for preparing whole specimens from bovine preimplantation embryos: A technique note.

A method was devised to prevent loss of whole embryos during fixation. Specimens were prepared in a chamber saturated with fixative vapors consisting of 3 : 1 (v/v) 96%. ethanol/glacial acetic acid. Good quality specimens were obtained after fixation for at least 24 but not more than 72 h. After staining, specimens could be preserved for 3 to 4 d by storage in the fixation chamber, in 45% aqueous acetic acid vapor. Using the method suggested in this paper prevents loss of early embryos during fixation and allows storage of specimens for longer than usual time while maintaining the quality of the specimen.

Journal Article↗
PubMed1984

Cell death of motoneurons in the chick embryo spinal cord. IX. The loss of motoneurons following removal of afferent inputs.

The primary aim of this study was to clarify the role of supraspinal, propriospinal, and primary sensory afferents in motoneuron (MN) development in the lateral motor column (LMC) of the lumbar spinal cord of the chick embryo. For this purpose three types of operations were carried out on embryonic day (E) 2. (1) The spinal cord was transected at the cervical (C-gap) or at the thoracic (T-gap) level so as to eliminate supraspinal and/or propriospinal inputs to the lumbar cord. (2) The entire lumbar neural crest was removed (NCR) in order to eliminate primary sensory inputs arising from the dorsal root ganglia (DRG). (3) A combined operation of T-gap and lumbar NCR was performed. The numbers of MNs in the LMC of the lumbar spinal cord were counted in embryos sacrificed between E10 and E18. The number of MNs on E10, when naturally occurring neuron death is almost complete, was not changed following either operation 1 or 2 described above. However, by E16, when naturally occurring neuron death is over, these same deafferented groups had 20 to 25% fewer MNs than did controls. Thus, the removal of either descending or sensory (DRG) afferents results in a significant increased loss of MNs that appears to take place only during the final stages of natural neuronal death or later. By contrast, the removal of both sources of input (T-gap + NCR) results in an additional 37% loss of MNs by E10 compared to controls. Thus, in this group deafferentation significantly increases cell loss during the major period of naturally occurring MN death (E5 to E10). No further loss of MNs occurs in this group after E10. Chronic treatment of deafferented embryos with curare from E6 to E9 or from E10 to E14 prevented the naturally occurring MN loss during these stages but was without effect on the increased cell loss induced by deafferentation. These results imply that the cellular mechanisms involved in target- versus afferent-regulated cell death are different. Collectively, these results indicate that the regulation of MN numbers is more complicated than previously thought. Both targets and afferents appear to be involved in controlling the survival of this population of neurons during the period of naturally occurring MN death.

Animals↗
PubMed2004

Receptor tyrosine phosphatase psi is required for Delta/Notch signalling and cyclic gene expression in the presomitic mesoderm.

Segmentation in vertebrate embryos is controlled by a biochemical oscillator ('segmentation clock') intrinsic to the cells in the unsegmented presomitic mesoderm, and is manifested in cyclic transcription of genes involved in establishing somite polarity and boundaries. We show that the receptor protein tyrosine phosphatase psi (RPTPpsi) gene is essential for normal functioning of the somitogenesis clock in zebrafish. We show that reduction of RPTPpsi activity using morpholino antisense oligonucleotides results in severe disruption of the segmental pattern of the embryo, and loss of cyclic gene expression in the presomitic mesoderm. Analysis of cyclic genes in RPTPpsi morphant embryos indicates an important requirement for RPTPpsi in the control of the somitogenesis clock upstream of or in parallel with Delta/Notch signalling. Impairing RPTPpsi activity also interferes with convergent extension during gastrulation. We discuss this dual requirement for RPTPpsi in terms of potential functions in Notch and Wnt signalling.

Animals↗
PubMed1994

Cryopreservation of immature mouse oocytes.

Mouse oocytes enclosed in cumulus cells were isolated from antral follicles at the germinal vesicle (GV) stage. They were stored in straws at -196 degrees C by a conventional mouse embryo freezing method using dimethylsulphoxide (1.5 M) as the cryoprotectant. Overall survival assessed after removal of the cumulus cells was 93% (299/320). A significantly greater proportion of fresh oocytes remained arrested at the GV stage during culture (11 versus 1%), but the rate of maturation to metaphase II was not significantly different between frozen and fresh oocytes (83 versus 74%). The rate of fertilization in vitro was similar for frozen and fresh oocytes matured in vitro (70 versus 81%) but significantly less than with mature ovulated oocytes (96%). Fertilization of frozen and fresh oocytes arrested after germinal vesicle breakdown was similar (77 versus 95%). No evidence of parthenogenetic activation was found in the different groups after overnight incubation of metaphase II oocytes. Implantation was similar for embryos derived from fresh and frozen GV-stage oocytes matured in vitro and mature ovulated oocytes, but the loss of embryos after implantation was significantly higher in the in-vitro matured groups (frozen, 40% and fresh, 46% versus 24%). The overall survival of oocytes frozen at the GV stage was 27%. This compares favourably with the estimated overall survival of mature oocytes cryopreserved by a similar procedure. We conclude that the increased post-implantation loss is due to suboptimal conditions for maturation in vitro rather than freezing injury.

Animals↗
PubMed1989

Cell loss in bisected mouse, sheep and cow embryos.

The purpose of this experiment was to determine the loss of cells during the splitting of embryos. The experiment was carried out on early, middle and late stage mouse blastocysts as well as on late stage sheep and cow blastocysts. The embryos were bisected with a metal mioroscalpel. Manipulation of the embryos was done in phosphate buffered saline (PBS) solution with 20% fetal calf serum (FCS) at +37 degrees C or in PBS solution free of Ca(++) and Mg(++) ions. To determine the number of cells present, intact embryos and demi-embryos were placed in acridine orange solution and examined under a fluorescent microscope. The average number of cells in early, middle and late stage mouse blastocysts was 39.4, 54.1 and 71.9, respectively. The loss of cells caused by splitting was 6.4, 7.6 and 9.9, respectively. The average number of cells in late stage sheep blastocysts was 115.3 and in late stage cow blastocysts it was 138.5. In sheep and cows, the loss of cells due to splitting the embryos in a PBS solution free of Ca(++) and Mg(++) ions did not differ from that observed in a PBS solution with 20% FCS. Similarly, bisection carried out at +37 degrees C did not result in lower cell losses, than that done at room temperature.

Journal Article↗
PubMed1998

Mammalian male and female germ cells express a germ cell-specific Y-Box protein, MSY2.

Here we report the isolation and characterization of mouse testicular cDNAs encoding the mammalian homologue of the Xenopus germ cell-specific nucleic acid-binding protein FRGY2 (mRNP3+4), hereafter designated MSY2. MSY2 is a member of the Y box multigene family of proteins; it contains the cold shock domain that is highly conserved among all Y box proteins and four basic/aromatic islands that are closely related to the other known germline Y box proteins from Xenopus, FRGY2, and goldfish, GFYP2. Msy2 undergoes alternative splicing to yield alternate N-terminal regions upstream of the cold shock domain. Although MSY2 is a member of a large family of nucleic acid-binding proteins, Southern blotting detects only a limited number of genomic DNA fragments, suggesting that Msy2 is a single copy gene. By Northern blotting and immunoblotting, MSY2 appears to be a germ cell-specific protein in the testis. Analysis of Msy2 mRNA expression in prepubertal and adult mouse testes, and in isolated populations of germ cells, reveals maximal expression in postmeiotic round spermatids, a cell type with abundant amounts of stored messenger ribonucleoproteins. In the ovary, MSY2 is present exclusively in diplotene-stage and mature oocytes. MSY2 is maternally inherited in the one-cell-stage embryo but is not detected in the late two-cell-stage embryo. This loss of MSY2 is coincident with the bulk degradation of maternal mRNAs in the two-cell embryo.

Alternative Splicing↗
PubMed2004

Gain- and loss-of-function in chick embryos by electroporation.

It remained very difficult to manipulate gene expression in chick embryos until the advent of in ovo electroporation which enabled the induction of both gain-of-function, and recently loss-of-function, of a gene of interest at a specific developmental stage. Gain-of-function by electroporation is so effective that it has become widely adopted in developmental studies in the chick. Recently, it became possible to induce loss-of-function by introducing an siRNA expression vector by electroporation. In this review, the methods of electroporation for gain-of-function and for loss-of-function by siRNA are discussed.

Animals↗
PubMed2005

Exogenous gibberellins inhibit coffee (Coffea arabica cv. Rubi) seed germination and cause cell death in the embryo.

The mechanism of inhibition of coffee (Coffea arabica cv. Rubi) seed germination by exogenous gibberellins (GAs) and the requirement of germination for endogenous GA were studied. Exogenous GA(4+7) inhibited coffee seed germination. The response to GA(4+7) showed two sensitivity thresholds: a lower one between 0 and 1 microM and a higher one between 10 and 100 microM. However, radicle protrusion in coffee seed depended on the de novo synthesis of GAs. Endogenous GAs were required for embryo cell elongation and endosperm cap weakening. Incubation of coffee seed in exogenous GA(4+7) led to loss of embryo viability and dead cells were observed by low temperature scanning microscopy only when the endosperm was surrounding the embryo. The results described here indicate that the inhibition of germination by exogenous GAs is caused by factors that are released from the endosperm during or after its weakening, causing cell death in the embryo and leading to inhibition of radicle protrusion.

Cell Death↗
PubMed2000

Suppression of decidual cell response induced by tributyltin chloride in pseudopregnant rats: a cause of early embryonic loss.

In our previous studies, tributyltin chloride (TBTCl) at doses of 16.3 mg/kg and above caused implantation failure (preimplantation embryonic loss) and postimplantation embryonic loss in rats following administration on gestational day (GD) 0 through GD 3 and GD 4 through GD 7, respectively. This study was designed to assess the effects of TBTCl on uterine function as a cause of early embryonic loss in pseudopregnant rats. TBTCl was given orally to pseudopregnant rats at doses of 4.1, 8.1, 16.3 and 32.5 mg/kg on pseudopregnant day (PPD) 0 to PPD 3 or 8.1, 16.3, 32.5 and 65.1 mg/kg on PPD 4 to PPD 7. The decidual cell response was induced by bilateral scratch trauma on PPD 4. The uterine weight on PPD 9 served as an index of uterine decidualization. Uterine weight and serum progesterone levels on PPD 9 were significantly decreased after administration of TBTCl at doses of 16.3 mg/kg and above on PPD 0 to PPD 3 or PPD 4 to PPD 7. Administration of TBTCl at doses of 8.1 mg/kg and above on PPD 0 to 3 also significantly decreased serum progesterone levels on PPD 4. TBTCl had no effect on ovarian weight and number of corpora lutea. It can be concluded that TBTCl suppresses the uterine decidual cell response and decreases progesterone levels, and these effects are responsible for early embryonic loss due to TBTCl exposure.

Animals↗
PubMed1993

Increased reproductive losses in cattle infected with bovine pestivirus around the time of insemination.

Unmated heifers seronegative to bovine pestivirus were used to investigate the effects on conception and embryo-fetal survival of pestivirus infection around the time of artificial insemination. The reproductive performances of three groups were compared; the control group did not become infected during pregnancy, group 1 heifers were infected by contact with a persistently infected cow and calf four days after insemination and group 2 heifers were infected intranasally nine days before insemination. Conception rates and embryo-fetal survival were monitored by serial serum progesterone assays, transrectal ultrasonography and manual palpation of the uterus. The conception rates (determined 20 days after insemination) of 60 per cent (nine of 15) and 44 per cent (eight of 18) for groups 1 and 2 were lower than the 79 per cent (11 of 14) achieved by the control group. The group 1 heifers subsequently experienced significant embryo-fetal loss, resulting in a pregnancy rate (determined 77 days after insemination) of 33 per cent (five of 15), significantly lower than the control group's 79 per cent (11 of 14). The pregnancy rate of the group 2 heifers (39 per cent, seven of 18) was also significantly lower than that of the controls, largely as a result of the group's poor conception rate. All the heifers diagnosed pregnant 275 days after insemination were induced to calve. No persistently infected calves were born.

Animals↗
PubMed1985

Legal abortion: limits and contributions to human life.

The traditional approach to abortion has been to regard it as disposing of human life, even when it is justifiable to induce abortion in accordance with legal and ethical principles. Contraception as distinct from abortion has never been so treated even though, in some respects, the biological processes involved in contraception and abortion raise similar issues. This is particularly so when contraception is by an intrauterine device or a postcoital technique which can prevent implantation rather than fertilization. Modern evidence shows that abortion is not only a loss of human life, but--paradoxically--is also a biological condition of human life. An unavoidably high rate of spontaneous loss of embryos has been shown to arise in the course of natural reproduction, due either to failure of implantation or to loss, such as the 'vanishing twin' of children born in single births. More common than the vanishing twin is spontaneous loss after implantation. Planned embryonic loss in artificial reproduction duplicates rather than defies nature. Further, sociological perceptions indicate that the availability of reliable prenatal diagnosis, especially of genetic conditions, and of induced abortion to terminate dysgenic life, may free couples to conceive and bear healthy children they would otherwise not have conceived. Moreover, prenatal diagnosis, for example by amniocentesis, may increasingly permit maternal or fetal treatment and so encourage the continuation of a pregnancy which might otherwise have been terminated.

Abortion, Illegal↗
PubMed1996

The Drosophila smoothened gene encodes a seven-pass membrane protein, a putative receptor for the hedgehog signal.

Smoothened (smo) is a segment polarity gene required for correct patterning of every segment in Drosophila. The earliest defect in smo mutant embryos is loss of expression of the Hedgehog-responsive gene wingless between 1 and 2 hr after gastrulation. Since smo mutant embryos cannot respond to exogenous Hedgehog (Hh) but can respond to exogenous Wingless, the smo product functions in Hh signaling. Smo acts downstream of or in parallel to Patched, an antagonist of the Hh signal. The smo gene encodes an integral membrane protein with characteristics of G protein-coupled receptors and shows homology to the Drosophila Frizzled protein. Based on its predicted physical characteristics and on its position in the Hh signaling pathway, we suggest that smo encodes a receptor for the Hh signal.

Animals↗
PubMed2000

Embryo freezing after intracytoplasmic sperm injection.

This study reports on the safety and efficiency of the cryopreservation of human embryos obtained after intracytoplasmic sperm injection. For this, we evaluated the morphological survival, the capacity of the surviving embryo to develop further in vitro and in vivo. After freezing-thawing embryos obtained after ICSI, 40% of the embryos do not survive the cryopreservation procedure. After selective transfer of further cleaving frozen-thawed embryos, pregnancy loss was 31% (subclinical pregnancy rate of 13% and miscarriage rate of 18%). As a result the livebirth rate per transferred embryos and per thawed embryo was 7 and 3% respectively. Obstetric outcome as well as further follow-up of the children born indicate that cryopreservation of ICSI embryos is a safe procedure, long term follow-up of the children born however is still warranted.

Cryopreservation↗
PubMed2005

Endometrial tumor necrosis factor alpha (TNFalpha) is a likely mediator of early luteal phase mifepristone-mediated negative effector action on the preimplantation embryo.

Cytokines and growth factors are important mediators of progesterone-regulated endometrial receptivity and embryo development. Early luteal phase administration of a potent antiprogestin-like mifepristone to the rhesus monkey results in endometrial desynchrony, loss of embryo viability and implantation failure. In the present study, administration of mifepristone (2 mg/kg body weight, s.c.) on day 2 after ovulation resulted in a significant increase (P < 0.01) in the level of tumor necrosis factor alpha (TNFalpha) in glandular and vascular compartments of endometrium, and in endometrial secretion and luminal fluid on day 6 after ovulation in the rhesus monkey. There was an associated lag in embryonic development, characterized by delayed mitochondrial maturity, poorly developed junctional complexes, a relative absence of intra-cytoplasmic filaments and a high degree of intra-cellular degenerative features. Exposure of TNFalpha (0, 0.5, 5, 50 ng/ml) to preimplantation stage mouse embryos in vitro showed a dose-dependent arrest in growth and development at both morula and blastocyst stages along with ultra-structural features of degeneration similar to those observed in embryos collected from early luteal phase mifepristone-treated monkeys. The de novo synthesized and released proteins in terms of trichloroacetic acid precipitable 35S by morulae and blastocysts in vitro showed a marked depression following exposure to TNFalpha compared with control embryos. Based on the above observation and the fact that preimplantation stage embryos express receptors for TNFalpha, we suggest that increased levels of TNFalpha in endometrial and luminal compartments around the time of uterine receptivity following early luteal phase administration of mifepristone adversely affect the growth and viability of preimplantation stage embryos.

Animals↗
PubMed1998

What is a preclinical pregnancy loss?

PURPOSE: To evaluate the contribution of embryo quality to preclinical loss rates after in vitro fertilization (IVF)/embryo transfer (ET) pregnancy, multiple gestation, and clinical loss rates were compared to preclinical pregnancy loss rates over a 3-year period. METHODS: The pregnancy outcomes after 1675 fresh ETs from 1994 to 1997 were studied. While establishment of a clinical pregnancy confirms uterine receptivity, multiple gestation rates reflect embryo quality. Because the majority of clinical losses are chromosomally abnormal, clinical loss rates serve as another indicator of embryo quality. RESULTS: The overall preclinical pregnancy loss rate was 5% (78/1675) of ETs and 17% (78/472) of pregnancies. During the 3-year period the pregnancy rates per ET increased from 19 to 36% (P < 0.0001), multiple gestation rates increased from 21 to 48% (P < 0.008), clinical loss rates decreased from 20 to 6% (P < 0.0001), and preclinical pregnancy loss rates remained unchanged from 13 to 19% (P = 0.1). CONCLUSIONS: Preclinical pregnancy loss more likely reflects abnormalities in uterine receptivity rather than embryo quality. If recurrent preclinical pregnancy loss occurs after IVF/ET, evaluation for abnormalities of uterine receptivity should be performed.

Abortion, Spontaneous↗
PubMed1983

Inhibitory influence of uterine secretions on mouse blastocysts decreases at the time of blastocyst activation.

Uterine flushings from artificially 'pseudopregnant', pseudopregnant and pregnant mice and those with 'diapausing' embryos were tested for their effect on [3H]uridine incorporation by mouse blastocysts. An inhibitor of [3H]uridine incorporation was detected in the uterine fluid of the mice with diapausing embryos and the activity of the inhibitor was significantly reduced 6.25 h after an injection of oestrogen. This reduction of the inhibitory activity was dependent on the presence of blastocysts in utero, since a similar reduction did not occur in uterine fluids of pseudopregnant mice. The results support the suggestion that 'delayed' implantation in mice is caused by the presence of inhibitors of blastocyst metabolism and that activation, after an increase in oestradiol, is due to an embryo-dependent loss of activity of the inhibitors.

Animals↗