Database : MEDLINE
Search on : Fetal and Resorption [Words]
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[PMID]: 29363057
[Au] Autor:Abdulrazzaq YM; Shafiullah M; Kochyil J; Padmanabhan R; Bastaki SMA
[Ad] Address:Department of Pediatrics, College of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates. yousef@uaeu.ac.ae.
[Ti] Title:Ameliorative effects of supplemental folinic acid on Lamotrigine-induced fetal malformations in the mouse.
[So] Source:Mol Cell Biochem;, 2018 Jan 23.
[Is] ISSN:1573-4919
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Data from our previous work indicate that Lamotrigine (LTG) is teratogenic in the mouse. In the present study, we attempted to determine the possible protective effects of exogenous folate on LTG-induced fetal anomalies in TO mouse. Experiment I entailed administering 4mg/kg of folinic acid (FA) and (25mg/kg) of LTG intraperitoneally three times on gestation day (GD) 8 to a group of mice; other groups were a group that received similar volumes of saline, a group that received LTG and Saline, a group that received FA and saline. Experiment 2 involved administering groups of mice with daily 3 doses FA (or proportionate volume of saline) on GD 5 through 10 and either 3 doses of saline on GD8, or 3 doses of LTG on GD8. Maternal plasma concentrations of FA, vitamin B12 and homocysteine were determined an hour after the last injection from one-half of all animals. The other half were allowed to go to term (GD18) when they were euthanized and their fetuses were examined for visceral and skeletal malformations. A high incidence of resorption, abortion, embryolethality, congenital malformations, and intrauterine growth restriction (IUGR), was observed in the LTG-treated group. Folic acid and B12 levels were decreased and homocysteine concentration increased significantly in LTG groups. Mice receiving LTG with FA had normal levels of folate, Vitamin B12 and homocysteine levels, and the fetuses had fewer birth defects similar to the controls which were given saline only. Supplemental FA ameliorated to a great extent the LTG-induced embryonic resorption and malformations and restored the FA status.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180124
[Lr] Last revision date:180124
[St] Status:Publisher
[do] DOI:10.1007/s11010-018-3285-0

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[PMID]: 29179165
[Au] Autor:Hasegawa T; Amizuka N
[Ad] Address:Developmental Biology and Hard Tissue, Faculty of Dental Medicine, Hokkaido University,Japan.
[Ti] Title:[Bone remodeling and modeling/mini-modeling.]
[So] Source:Clin Calcium;27(12):1713-1722, 2017.
[Is] ISSN:0917-5857
[Cp] Country of publication:Japan
[La] Language:jpn
[Ab] Abstract:Modeling, adapting structures to loading by changing bone size and shapes, often takes place in bone of the fetal and developmental stages, while bone remodeling-replacement of old bone into new bone-is predominant in the adult stage. Modeling can be divided into macro-modeling(macroscopic modeling)and mini-modeling(microscopic modeling). In the cellular process of mini-modeling, unlike bone remodeling, bone lining cells, i.e., resting flattened osteoblasts covering bone surfaces will become active form of osteoblasts, and then, deposit new bone onto the old bone without mediating osteoclastic bone resorption. Among the drugs for osteoporotic treatment, eldecalcitol(a vitamin D3 analog)and teriparatide(human PTH[1-34])could show mini-modeling based bone formation. Histologically, mature, active form of osteoblasts are localized on the new bone induced by mini-modeling, however, only a few cell layer of preosteoblasts are formed over the newly-formed bone, and accordingly, few osteoclasts are present in the region of mini-modeling. In this review, histological characteristics of bone remodeling and modeling including mini-modeling will be introduced.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180123
[Lr] Last revision date:180123
[St] Status:In-Process
[do] DOI:CliCa171217131722

  3 / 4490 MEDLINE  
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[PMID]: 29317300
[Au] Autor:Salek Farrokhi A; Zarnani AH; Moazzeni SM
[Ad] Address:Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Electronic address: A.Salek@modares.ac.ir.
[Ti] Title:Mesenchymal stem cells therapy protects fetuses from resorption and induces Th2 type cytokines profile in abortion prone mouse model.
[So] Source:Transpl Immunol;, 2018 Jan 06.
[Is] ISSN:1878-5492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The imbalance of Th1/Th2 cytokines is well known in recurrent spontaneous abortion (RSA) mouse model. Mesenchymal stem cells (MSCs) possess potent immunoregulatory properties that could modulate the Th1 cytokine responses in benefit of Th2 types. In this study, we aimed to analyze the local and systemic balance of Th1/Th2 cytokines following MSCs therapy. Syngeneic adipose derived MSCs were administered to abortion prone mice during the implantation window. The abortion rate was determined and IL-4, IL-6, IL-12, IL-2, IFN-γ and GM-CSF gene expression was evaluated by Real-Time-PCR in decidual and placental tissues of pregnant mice at day 13.5 of pregnancy. Splenocytes of pregnant mice were co-cultured with mitomycin C treated paternal splenocytes and IL-2, IL-4, IL-10 and IFN-γ cytokines were measured in co-cultures supernatants by ELISA method. Proliferation response of female splenocytes to paternal antigens was also evaluated using the CFSE method. Our results showed a significant reduction in abortion rate following MSCs administration in abortion prone mice. We also observed a significant down-regulation of IL-2 and IFN-γ as well as up-regulation of IL-4 and IL-10 production from pregnant mouse splenocytes following MSCs therapy along with a significant reduction of splenocytes proliferation against paternal antigens. Our findings revealed that MSCs therapy increased the IL-4, IL-6, IL-10 and GM-CSF and at the same time decreased the IL-12, IL-2 and IFN-γ gene expression at feto-maternal interface. Here, we showed that MSCs therapy could modulate the systemic as well as local Th1/Th2 cytokines production along with protection of fetus from resorption in abortion prone mice. The fine balance of Th1/Th2 cytokine response could be considered as one of the possible mechanisms for fetal protection following MSCs therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180116
[Lr] Last revision date:180116
[St] Status:Publisher

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[PMID]: 29305462
[Au] Autor:Yockey LJ; Jurado KA; Arora N; Millet A; Rakib T; Milano KM; Hastings AK; Fikrig E; Kong Y; Horvath TL; Weatherbee S; Kliman HJ; Coyne CB; Iwasaki A
[Ad] Address:Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
[Ti] Title:Type I interferons instigate fetal demise after Zika virus infection.
[So] Source:Sci Immunol;3(19), 2018 Jan 05.
[Is] ISSN:2470-9468
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Zika virus (ZIKV) infection during pregnancy is associated with adverse fetal outcomes, including microcephaly, growth restriction, and fetal demise. Type I interferons (IFNs) are essential for host resistance against ZIKV, and IFN-α/ receptor (IFNAR)-deficient mice are highly susceptible to ZIKV infection. Severe fetal growth restriction with placental damage and fetal resorption is observed after ZIKV infection of type I IFN receptor knockout ( ) dams mated with wild-type sires, resulting in fetuses with functional type I IFN signaling. The role of type I IFNs in limiting or mediating ZIKV disease within this congenital infection model remains unknown. In this study, we challenged dams mated with sires with ZIKV. This breeding scheme enabled us to examine pregnant dams that carry a mixture of fetuses that express ( ) or do not express IFNAR ( ) within the same uterus. Virus replicated to a higher titer in the placenta of than within the concepti. Yet, rather unexpectedly, we found that only fetuses were resorbed after ZIKV infection during early pregnancy, whereas their littermates continue to develop. Analyses of the fetus and placenta revealed that, after ZIKV infection, IFNAR signaling in the conceptus inhibits development of the placental labyrinth, resulting in abnormal architecture of the maternal-fetal barrier. Exposure of midgestation human chorionic villous explants to type I IFN, but not type III IFNs, altered placental morphology and induced cytoskeletal rearrangements within the villous core. Our results implicate type I IFNs as a possible mediator of pregnancy complications, including spontaneous abortions and growth restriction, in the context of congenital viral infections.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180106
[Lr] Last revision date:180106
[St] Status:In-Data-Review

  5 / 4490 MEDLINE  
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[PMID]: 29193867
[Au] Autor:Clark RL; Edwards TL; Longo M; Kinney J; Walker DK; Rhodes J; Clode SA; Rckle T; Wells T; Andenmatten N; Huber AC
[Ad] Address:Artemis Pharmaceutical Research, Jacksonville, Florida.
[Ti] Title:Improved safety margin for embryotoxicity in rats for the new endoperoxide artefenomel (OZ439) as compared to artesunate.
[So] Source:Birth Defects Res;, 2017 Nov 28.
[Is] ISSN:2472-1727
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Combination medicines including an artemisinin are the mainstay of antimalarial therapy. Artemisinins are potent embryotoxicants in animal species due to their trioxane moiety. METHODS: As part of its development, the new synthetic trioxolane antimalarial artefenomel (OZ439) was tested in rat whole embryo culture and in rat embryo-fetal toxicity studies with dosing throughout organogenesis or with a single dose on Gestational Day (GD) 12. The single-dose studies included groups treated with artesunate to allow a direct comparison of the embryotoxicity of the two antimalarials and included toxicokinetics hematology and histological examination of embryos. In addition, the distribution of artefenomel-related material in plasma was determined after the administration of C-artefenomel. RESULTS: Artefenomel and artesunate showed similar patterns of embryotoxicity including cardiovascular defects and resorption with a steep dose-response. They both also caused a depletion of circulating embryonic erythroblasts both in vitro and in vivo and decreases in maternal reticulocyte count. However, artefenomel was ∼250-fold less potent than the active metabolite of artesunate (dihydroartemisinin) as an embryotoxicant in vitro. The safety margin (based on AUC) for artefenomel administered on GD 12 was approximately 100-fold greater than that for artesunate. Also, unlike artesunate, artefenomel was not a selective developmental toxicant. CONCLUSIONS: The lesser embryotoxicity of artefenomel is likely linked to its original design which included two blocking side groups that had been introduced to lower the reactivity with ferrous iron. Our data support the hypothesis that artefenomel's improved safety margin is linked to a lower potential for inhibiting heme biosynthesis in embryonic erythroblasts.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171201
[Lr] Last revision date:171201
[St] Status:Publisher
[do] DOI:10.1002/bdr2.1170

  6 / 4490 MEDLINE  
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[PMID]: 29168595
[Au] Autor:Huang CH; Huang ZW; Ho FM; Chan WH
[Ad] Address:Department of Obstetrics and Gynecology, Taoyuan General Hospital, Ministry of Health & Welfare, Taoyuan City 33004, Taiwan.
[Ti] Title:Berberine impairs embryonic development in vitro and in vivo through oxidative stress-mediated apoptotic processes.
[So] Source:Environ Toxicol;, 2017 Nov 23.
[Is] ISSN:1522-7278
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Berberine, an isoquinoline alkaloid isolated from several traditional Chinese herbal medicines, has been shown to suppress growth and induce apoptosis in some tumor cell lines. However, berberine has also been reported to attenuate H O -induced oxidative injury and apoptosis. The basis for these ambiguous effects of berberine-triggering or preventing apoptosis-has not been well characterized to date. In the current investigation, we examined whether berberine exerts cytotoxic effects on mouse embryos at the blastocyst stage and affects subsequent embryonic development in vitro and in vivo. Treatment of blastocysts with berberine (2.5-10 M) induced a significant increase in apoptosis and a corresponding decrease in trophectoderm cell number. Moreover, the implantation success rate of blastocysts pretreated with berberine was lower than that of their control counterparts. Pretreatment with berberine was also associated with increased resorption of postimplantation embryos and decreased fetal weight. In an animal model, intravenous injection of berberine (2, 4, or 6 mg/kg body weight/d) for 4 days resulted in apoptosis of blastocyst cells and early embryonic developmental injury. Berberine-induced injury of mouse blastocysts appeared to be attributable to oxidative stress-triggered intrinsic apoptotic signaling processes that impaired preimplantation and postimplantation embryonic development. Taken together, our results clearly demonstrate that berberine induces apoptosis and retards early preimplantation and postimplantation development of mouse embryos, both in vitro and in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171123
[Lr] Last revision date:171123
[St] Status:Publisher
[do] DOI:10.1002/tox.22515

  7 / 4490 MEDLINE  
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[PMID]: 29142173
[Au] Autor:Furukawa S; Tsuji N; Kobayashi Y; Yamagishi Y; Hayashi S; Abe M; Kuroda Y; Kimura M; Hayakawa C; Sugiyama A
[Ad] Address:Biological Research Laboratories, Nissan Chemical Industries, Ltd.
[Ti] Title:Effect of dibutyltin on placental and fetal toxicity in rat.
[So] Source:J Toxicol Sci;42(6):741-753, 2017.
[Is] ISSN:1880-3989
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:In order to elucidate the effect of chorioallantoic and yolk sac placenta on the embryonic/fetal toxicity in dibutyltin dichloride (DBTCl)-exposed rats, we examined the histopathological changes and the tissue distribution of dibutyltin in the placentas and embryos. DBTCl was orally administered to the groups at doses of 0 mg/kg during gestation days (GD)s 7-9 (control group) and 20 mg/kg during GDs 7-9 (GD7-9 treated group), and GDs 10-12 (GD10-12 treated group). The total fetal mortality was increased, and malformations characterized by craniofacial dysmorphism were detected in the GD7-9 treated group. The embryonic/fetal weight and placental weight showed a decrease in both DBTCl-treated groups. Histologically, some embryos on GD 9.5 in the GD7-9 treated group underwent apoptosis without any changes of yolk sac. In the laser ablation-inductively coupled plasma-mass spectrometry analysis (LA-ICP-MS), tin was detected in the embryo, allantois, yolk sac, ectoplacental cone and decidual mass surrounding the conceptus on GD 9.5 in the GD7-9 treated group. Thus, it is considered that the embryo in this period is specifically sensitive to DBTCl-induced apoptosis, compared with other parts. The chorioallantoic placentas in both DBTCl-treated groups showed the developmental delay and hypoplasia in the fetal parts of placenta, resulting from apoptosis and mitotic inhibition. Thus, it was speculated that the DBTCl-induced malformations and fetal resorption resulted from the apoptosis in the embryo caused by the direct effect of DBTCl. The DBTCl-induced lesions in the chorioallantoic placenta were a non-specific transient developmental retardation in the fetal parts of placenta, leading to intrauterine growth retardation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[St] Status:In-Process
[do] DOI:10.2131/jts.42.741

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[PMID]: 29138679
[Au] Autor:Hussain T; Tan B; Liu G; Murtaza G; Rahu N; Saleem M; Yin Y
[Ad] Address:National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture Chinese Academy of Sciences, Changsha, Hunan 410125, China.
[Ti] Title:Modulatory Mechanism of Polyphenols and Nrf2 Signaling Pathway in LPS Challenged Pregnancy Disorders.
[So] Source:Oxid Med Cell Longev;2017:8254289, 2017.
[Is] ISSN:1942-0994
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Early embryonic loss and adverse birth outcomes are the major reproductive disorders that affect both human and animals. The LPS induces inflammation by interacting with robust cellular mechanism which was considered as a plethora of numerous reproductive disorders such as fetal resorption, preterm birth, teratogenicity, intrauterine growth restriction, abortion, neural tube defects, fetal demise, and skeletal development retardation. LPS-triggered overproduction of free radicals leads to oxidative stress which mediates inflammation via stimulation of NF- B and PPAR transcription factors. Flavonoids, which exist in copious amounts in nature, possess a wide array of functions; their supplementation during pregnancy activates Nrf2 signaling pathway which encounters pregnancy disorders. It was further presumed that the development of strong antioxidant uterine environment during gestation can alleviate diseases which appear at adult stages. The purpose of this review is to focus on modulatory properties of flavonoids on oxidative stress-mediated pregnancy insult and abnormal outcomes and role of Nrf2 activation in pregnancy disorders. These findings would be helpful for providing new insights in ameliorating oxidative stress-induced pregnancy disorders.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1711
[Cu] Class update date: 171117
[Lr] Last revision date:171117
[St] Status:In-Process
[do] DOI:10.1155/2017/8254289

  9 / 4490 MEDLINE  
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[PMID]: 29086601
[Au] Autor:Zhang Y; Wu J; Feng X; Wang R; Chen A; Shao L
[Ad] Address:a Department of Stomatology , Nanfang Hospital, Southern Medical University , 1838 North Guangzhou Road, Guangzhou 510515 , PR China.
[Ti] Title:Current understanding of the toxicological risk posed to the fetus following maternal exposure to nanoparticles.
[So] Source:Expert Opin Drug Metab Toxicol;, 2017 Oct 31.
[Is] ISSN:1744-7607
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: With the broad use of nanotechnology, the number and variety of nanoparticles that humans can be exposed to has further increased. Consequently, there is growing concern about the potential effect of maternal exposure to various nanoparticles during pregnancy on a fetus. However, the nature of this risk is not fully known. Areas covered: In this review, materno-fetal transfer of nanoparticles through the placenta is described. Both prenatal and postnatal adverse effects, such as fetal resorption, malformation and injury to various organs in mice exposed to nanoparticles are reviewed. The potential mechanisms of toxicity are also discussed. Expert opinion: The toxicology and safe application of recently developed nanoparticles has attracted much attention in the past few years. Although many studies have demonstrated the toxicology of nanoparticles in various species, only a small number of studies have examined the effect on a fetus after maternal exposure to nanoparticles. This is particularly important, because the developing fetus is especially vulnerable to the toxic effects of nanoparticles during fetal development due to the unique physical stage of the fetus. Nanoparticles may directly or indirectly impair fetal development and growth after maternal exposure to nanoparticles.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171031
[Lr] Last revision date:171031
[St] Status:Publisher
[do] DOI:10.1080/17425255.2018.1397131

  10 / 4490 MEDLINE  
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[PMID]: 29032167
[Au] Autor:Traesel GK; de Lima FF; Dos Santos AC; Souza RIC; Cantadori DT; Kretschmer CR; Navarini VJ; Oesterreich SA
[Ad] Address:Faculty of Health Sciences, Federal University of Grande Dourados, Dourados, Mato Grosso do Sul, Brazil. Electronic address: giselitraesel@gmail.com.
[Ti] Title:Evaluation of embryotoxic and teratogenic effects of the oil extracted from Caryocar brasiliense Cambess pulp in rats.
[So] Source:Food Chem Toxicol;110:74-82, 2017 Dec.
[Is] ISSN:1873-6351
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The objective of this study was to evaluate the maternal, embryotoxic and teratogenic effects of Caryocar brasiliense pulp oil (OPCB), oil widely used in Brazilian cuisine and traditional medicine. Pregnant Wistar female rats were used in this study for three treatment groups (250, 500 and 1000mg/kg/day) and a control group. The OPCB was administered orally throughout the period of organogenesis of females (6th until the 15th day of gestation). The pregnant females were gross necropsied on d20, followed by maternal and fetus examination, to evaluate the teratogenicity, reproductive and developmental performance of OPCB. The results showed there was no significant statistical difference in the ponderal evolution of the pregnant females, as well as in the behavioral, hematological, biochemical or histopathological data, indicating the absence of maternal toxicity of the oil. The mean number of corpora lutea, implantation and resorption sites, as well as all calculated reproductive rates, also remained statistically similar between the groups, indicating low embryotoxic effects of the tested plant specie. In fetal examination, external anomalies and skeletal abnormalities were observed in all treated and control groups. The NOAEL for maternal toxicity and embryo/fetal development for the OPCB administered by gavage, was 1000mg/kg/bw/day.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[St] Status:In-Process


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