Teratogens: An agent that causes the production of physical defects in the developing embryo.Veratrum: A plant genus of the family LILIACEAE with roots that contain VERATRUM ALKALOIDS used as emetics, parasiticides, antihypertensives. It is the main ingredient of Boicil.Abnormalities, Drug-Induced: Congenital abnormalities caused by medicinal substances or drugs of abuse given to or taken by the mother, or to which she is inadvertently exposed during the manufacture of such substances. The concept excludes abnormalities resulting from exposure to non-medicinal chemicals in the environment.Morning Sickness: Symptoms of NAUSEA and VOMITING in pregnant women that usually occur in the morning during the first 2 to 3 months of PREGNANCY. Severe persistent vomiting during pregnancy is called HYPEREMESIS GRAVIDARUM.Datura stramonium: A plant species of the genus DATURA, family SOLANACEAE, that contains TROPANES and other SOLANACEOUS ALKALOIDS.Senecio: A species of toxic plants of the Compositae. The poisonous compounds are alkaloids which cause cattle diseases, neoplasms, and liver damage and are used to produce cancers in experimental animals.Dichloroethylenes: Toxic chlorinated unsaturated hydrocarbons. Include both the 1,1- and 1,2-dichloro isomers. Both isomers are toxic, but 1,1-dichloroethylene is the more potent CNS depressant and hepatotoxin. It is used in the manufacture of thermoplastic polymers.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Embryo, Mammalian: The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes.Carcinogens: Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.Fetal Alcohol Spectrum Disorders: An umbrella term used to describe a pattern of disabilities and abnormalities that result from fetal exposure to ETHANOL during pregnancy. It encompasses a phenotypic range that can vary greatly between individuals, but reliably includes one or more of the following: characteristic facial dysmorphism, FETAL GROWTH RETARDATION, central nervous system abnormalities, cognitive and/or behavioral dysfunction, BIRTH DEFECTS. The level of maternal alcohol consumption does not necessarily correlate directly with disease severity.United States Indian Health Service: A division of the UNITED STATES PUBLIC HEALTH SERVICE that is responsible for the public health and the provision of medical services to NATIVE AMERICANS in the United States, primarily those residing on reservation lands.Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.Alcohol Drinking: Behaviors associated with the ingesting of alcoholic beverages, including social drinking.Alcoholic Intoxication: An acute brain syndrome which results from the excessive ingestion of ETHANOL or ALCOHOLIC BEVERAGES.Indians, North American: Individual members of North American ethnic groups with ancient historic ancestral origins in Asia.Genetics, Medical: A subdiscipline of human genetics which entails the reliable prediction of certain human disorders as a function of the lineage and/or genetic makeup of an individual or of any two parents or potential parents.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Congenital Abnormalities: Malformations of organs or body parts during development in utero.Medicare Part C: The Balanced Budget Act (BBA) of 1997 establishes a Medicare+Choice program under part C of Title XVIII, Section 4001, of the Social Security Act. Under this program, an eligible individual may elect to receive Medicare benefits through enrollment in a Medicare+Choice plan. Beneficiaries may choose to use private pay options, establish medical savings accounts, use managed care plans, or join provider-sponsored plans.Nurse Practitioners: Nurses who are specially trained to assume an expanded role in providing medical care under the supervision of a physician.Alcohol-Induced Disorders: Disorders stemming from the misuse and abuse of alcohol.Cellular Phone: Analog or digital communications device in which the user has a wireless connection from a telephone to a nearby transmitter. It is termed cellular because the service area is divided into multiple "cells." As the user moves from one cell area to another, the call is transferred to the local transmitter.Sphingosine: An amino alcohol with a long unsaturated hydrocarbon chain. Sphingosine and its derivative sphinganine are the major bases of the sphingolipids in mammals. (Dorland, 28th ed)Paclitaxel: A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.Databases, Factual: Extensive collections, reputedly complete, of facts and data garnered from material of a specialized subject area and made available for analysis and application. The collection can be automated by various contemporary methods for retrieval. The concept should be differentiated from DATABASES, BIBLIOGRAPHIC which is restricted to collections of bibliographic references.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Congresses as Topic: Conferences, conventions or formal meetings usually attended by delegates representing a special field of interest.Posters as Topic: Single or multi-sheet notices made to attract attention to events, activities, causes, goods, or services. They are for display, usually in a public place and are chiefly pictorial.Facial Asymmetry: Congenital or acquired asymmetry of the face.Diagnostic Techniques and Procedures: Methods, procedures, and tests performed to diagnose disease, disordered function, or disability.Craniofacial Abnormalities: Congenital structural deformities, malformations, or other abnormalities of the cranium and facial bones.Education, Graduate: Studies beyond the bachelor's degree at an institution having graduate programs for the purpose of preparing for entrance into a specific field, and obtaining a higher degree.Poaceae: A large family of narrow-leaved herbaceous grasses of the order Cyperales, subclass Commelinidae, class Liliopsida (monocotyledons). Food grains (EDIBLE GRAIN) come from members of this family. RHINITIS, ALLERGIC, SEASONAL can be induced by POLLEN of many of the grasses.Facial Bones: The facial skeleton, consisting of bones situated between the cranial base and the mandibular region. While some consider the facial bones to comprise the hyoid (HYOID BONE), palatine (HARD PALATE), and zygomatic (ZYGOMA) bones, MANDIBLE, and MAXILLA, others include also the lacrimal and nasal bones, inferior nasal concha, and vomer but exclude the hyoid bone. (Jablonski, Dictionary of Dentistry, 1992, p113)Toxicity Tests: An array of tests used to determine the toxicity of a substance to living systems. These include tests on clinical drugs, foods, and environmental pollutants.Neural Tube Defects: Congenital malformations of the central nervous system and adjacent structures related to defective neural tube closure during the first trimester of pregnancy generally occurring between days 18-29 of gestation. Ectodermal and mesodermal malformations (mainly involving the skull and vertebrae) may occur as a result of defects of neural tube closure. (From Joynt, Clinical Neurology, 1992, Ch55, pp31-41)Homicide: The killing of one person by another.Firearms: Small-arms weapons, including handguns, pistols, revolvers, rifles, shotguns, etc.Wounds, Gunshot: Disruption of structural continuity of the body as a result of the discharge of firearms.PhiladelphiaOvarian Neoplasms: Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.Suicide: The act of killing oneself.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Limb Deformities, Congenital: Congenital structural deformities of the upper and lower extremities collectively or unspecified.Valproic Acid: A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of voltage dependent sodium channels.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Sudden Infant Death: The abrupt and unexplained death of an apparently healthy infant under one year of age, remaining unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history. (Pediatr Pathol 1991 Sep-Oct;11(5):677-84)Infant Mortality: Postnatal deaths from BIRTH to 365 days after birth in a given population. Postneonatal mortality represents deaths between 28 days and 365 days after birth (as defined by National Center for Health Statistics). Neonatal mortality represents deaths from birth to 27 days after birth.Infant, Newborn: An infant during the first month after birth.Birth Weight: The mass or quantity of heaviness of an individual at BIRTH. It is expressed by units of pounds or kilograms.

2,3,7,8-Tetrachlorodibenzo-p-dioxin alters cardiovascular and craniofacial development and function in sac fry of rainbow trout (Oncorhynchus mykiss). (1/690)

Hallmark signs of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity in rainbow trout sac fry, are yolk sac edema, hemorrhage, craniofacial malformation, and growth retardation culminating in mortality. Our objective was to determine the role of cardiovascular dysfunction in the development of this toxicity. An embryotoxic TCDD dose (385 pg/g egg) caused a progressive reduction in blood flow in rainbow trout sac fry manifested first and most dramatically in the 1st and 2nd branchial arches and vessels perfusing the lower jaw. Blood flow was reduced later in the infraorbital artery and occipital vein of the head as well as segmental vessels and caudal vein of the trunk. Reduced perfusion occurred last in gill branchial arteries involved with oxygen uptake and the subintestinal vein and vitelline vein involved with nutrient uptake. Although heart rate throughout sac fry development was not affected, heart size at 50 days post-fertilization (dpf) was reduced far more than body weight or length, suggesting that the progressive circulatory failure caused by TCDD is associated with reduced cardiac output. Craniofacial development was arrested near hatch, giving rise to craniofacial malformations in which the jaws and anterior nasal structures were underdeveloped. Unlike the medaka embryo, in which TCDD causes apoptosis in the medial yolk vein, endothelial cell death was not observed in rainbow trout sac fry. These findings suggest a primary role for arrested heart development and reduced perfusion of tissues with blood in the early-life stage toxicity of TCDD in trout.  (+info)

AhR, ARNT, and CYP1A1 mRNA quantitation in cultured human embryonic palates exposed to TCDD and comparison with mouse palate in vivo and in culture. (2/690)

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is developmentally toxic in many species and induces cleft palate in the C57BL/6N mouse embryo. Palatogenesis in mouse and human embryos involves homologous processes at the morphological, cellular, and molecular levels. In organ culture, mouse and human palates respond similarly to TCDD. The present study quantitates the expression of AhR, ARNT, and CYP1A1 mRNA in human embryonic palates in organ culture. Palatal tissues were exposed to 1 x 10(-10), 1 x 10(-9), or 1 x 10(-8) M TCDD or control medium and sampled at 0, 2, 4, and 6 hours for quantitative RT-PCR using a synthetic RNA internal standard. Similar measurements of CYP1A1 gene expression were collected for mouse palates cultured in this model. In human palates, AhR expression correlated with ARNT and CYP1A1 mRNA expression. TCDD induction of CYP1A1 was time- and concentration-dependent. The expression of these genes presented a uniform and continuous distribution across the group of embryos, with no subset of either high or low expressors/responders. The ratio of AhR to ARNT was approximately 4:1. AhR mRNA increased during the culture period in both treated and control subjects; however, ARNT expression was relatively constant. TCDD did not alter either AhR or ARNT expression in a consistent dose- or time-related manner. Comparison of human and mouse data showed a high correlation across species for the induction of CYP1A1. Human embryos expressed approximately 350 times less AhR mRNA than the mouse, and in earlier studies it was shown that human palates required 200 times more TCDD to produce the same effects. When the morphological, cellular, and molecular responses to TCDD between mouse and human are compared, it seems highly unlikely that human embryos could be exposed to sufficient TCDD to achieve changes in palatal differentiation that would lead to cleft palate.  (+info)

RT-PCR quantification of AHR, ARNT, GR, and CYP1A1 mRNA in craniofacial tissues of embryonic mice exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin and hydrocortisone. (3/690)

C57BL/6N mouse embryos exposed to hydrocortisone (HC) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) develop cleft palate. An interaction between these agents produces clefts at doses which alone are not teratogenic. The glucocorticoid receptor (GR) and dioxin receptor (AhR) mediated these responses and their gene expression was altered by TCDD and/or HC in palates examined on gestation day (GD) 14 by Northern blot analysis and in situ hybridization. The present study quantifies AhR, AhR nuclear translocator (ARNT), and GR mRNA at 4, 12, 24, and 48 h after exposure (time 0 = dose administration at 8 A.M. on gestation day 12) on GD12 to TCDD (24 micrograms/kg), HC (100 mg/kg) or HC (25 mg/kg) + TCDD (3 micrograms/kg). The induction of CYP1A1 mRNA was also quantified at 2, 4, 6, 12, 24, and 48 h for control and TCDD-exposed samples. Total RNA was prepared from midfacial tissue of 4-6 embryos/litter at each time and dose. An RNA internal standard (IS) for each gene was synthesized, which included the gene's primer sequences separated by a pUC19 plasmid sequence. Reverse transcription-polymerase chain reaction (RT-PCR) was performed on total RNA + IS using a range of 5-7 IS concentrations across a constant level of total RNA. PCR products were separated in gels (mRNA and IS-amplified sequences differed by 30-50 bases), ethidium bromide-stained, imaged (Hamamatsu Photonics Systems, Bridgewater, NJ), and quantified with NIH Image. CYP1A1 mRNA was significantly induced in the TCDD-exposed samples at all time points examined (p = 0.005 at 2 h and 0.001 after 2 h). During palatal shelf outgrowth on GD12, AhR mRNA levels increased significantly and this was not affected by treatment with TCDD or HC + TCDD. A significant increase in GR was detected at 24 h (p < 0.05) and this was unaffected by any of the exposures. Expression of ARNT increased at 12 h (p < 0.001); however, treatment with HC or HC + TCDD blocked this increase (p < 0.05). At 24 h, the TCDD-treated embryos had significantly lower ARNT mRNA compared with controls (p < 0.001). The relative overall expression level of the genes was AhR > ARNT > GR. Within individuals, expression of AhR and/or ARNT was highly correlated with GR level. In conclusion, CYP1A1 mRNA was expressed in developing craniofacial tissue and was highly induced by TCDD exposure. AhR, ARNT, and GR mRNA are upregulated in early palatogenesis, although not on the same schedule. The TCDD-induced decrease in ARNT at 24 h after dosing and the HC and HC + TCDD-induced delay in upregulation of ARNT may affect the dynamics of heterodimer formation between AhR and ARNT. The changes in ARNT mRNA level could also affect availability of this transcriptional regulator to interact with other potential partners, and these effects, separately or in combination, may be involved in disruption of normal embryonic development.  (+info)

Amelioration of TCDD-induced teratogenesis in aryl hydrocarbon receptor (AhR)-null mice. (4/690)

The aryl hydrocarbon receptor (AhR) mediates many of the biological effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and transcriptional activation of genes encoding a number of xenobiotic metabolizing enzymes. Prenatal exposure of mice to TCDD causes severe alterations in embryo and fetal development, including hydronephrosis and cleft palate. However, the mechanisms underlying these effects are unclear. In this work, the teratogenicity of TCDD in AhR-null mice was evaluated to determine if this effect is mediated by the AhR. Homozygous wild-type (+/+) or AhR-null (-/-) female mice were mated with males of the same genotype overnight. On gestation day (GD)-10, mice were intubated orally with either corn oil (vehicle control) or 25 micrograms/kg TCDD. Fetuses were examined on GD18 for visceral and skeletal alterations. For non-TCDD-exposed litters, all developmental endpoints were comparable between genotypes, with the exception of a lower incidence of large interfrontal bones in (-/-) mice. For TCDD-exposed litters, (+/+) fetuses had a significantly greater incidence of cleft palate, hydronephrosis, small kidneys, tortuous ureters and greater dilation of the renal pelves and ureters compared to (-/-) fetuses. Interestingly, an increased resorption rate was observed in (-/-) fetuses exposed to TCDD. Results from this work demonstrate that fetal development per se is generally unaffected by the absence of the AhR or that other genes may have compensated for the loss of the AhR. More importantly, these data indicate that the AhR mediates TCDD-induced teratogenicity. Further, since a higher percentage of resorptions was observed in (-/-) litters from TCDD-treated dams, it is possible that AhR-independent mechanisms contribute to TCDD-induced developmental toxicity.  (+info)

Oxidized derivatives of 7-dehydrocholesterol induce growth retardation in cultured rat embryos: a model for antenatal growth retardation in the Smith-Lemli-Opitz syndrome. (5/690)

7-Dehydrocholesterol accumulates in fetuses affected by the Smith-Lemli-Opitz syndrome as a result of a deficit in the ultimate step of cholesterol synthesis catalyzed by Delta7 reductase. Rat embryos explanted at gestation day 10 and cultured for 48 h in the presence of the Delta7 reductase inhibitor AY 9944 were used as a model to discriminate between the beneficial effect of supplementation with cholesterol and the deleterious effect of supplementation with 7-dehydrocholesterol. Cholesterol supplementation in the form of mixed cholesterol/lecithin liposomes added to serum serving as the culture medium restores the growth of embryos which is markedly decreased in the presence of the inhibitor. 7-Dehydrocholesterol under identical conditions does not restore growth and impairs the beneficial effect of cholesterol added simultaneously. UV-photooxidation of 7-dehydrocholesterol-supplemented culture medium enhances its embryotoxicity, which suggests uptake by the embryo of toxic by-products formed from 7-dehydrocholesterol. By contrast photooxidation of cholesterol-supplemented culture medium does not induce embryotoxicity. alpha-Tocopherol reduces the toxicity of photooxidized 7-dehydrocholesterol supplementing the culture medium. We conclude that 7-dehydrocholesterol does not fulfill the cholesterol requirement of the developing embryos and exerts an additional embryotoxic effect probably via oxidized by-products. This could explain the antenatal growth retardation of SLOS by a blockage of the maternal compensatory cholesterol influx.  (+info)

Longitudinal limb deficiencies and the sclerotomes. An analysis of 378 dysmelic malformations induced by thalidomide. (6/690)

The pathogenesis of longitudinal reduction deformities of the limbs, or dysmelia, is still a matter of debate. Their morphological pattern was defined from a large collection of radiographs of children with dysmelia following the thalidomide disaster. We compared radiographs of 378 of these limbs with the sclerotomes which are areas of segmental sensory innervation of the limb skeleton defined by the radiation of referred pain. The pattern of dysmelia matched the sclerotomes closely in 279 limbs (73.5%). The principles of skeletal reduction in dysmelia are explained by the arrangement of the sclerotomes. The congruence between two separate and independent data sets shows that both patterns are expressions of the underlying segmental sensory innervation of the skeleton, and that the sensory nervous system is involved in the process of limb morphogenesis and teratogenesis.  (+info)

Expression cloning for arsenite-resistance resulted in isolation of tumor-suppressor fau cDNA: possible involvement of the ubiquitin system in arsenic carcinogenesis. (7/690)

Arsenic is a human carcinogen whose mechanism of action is unknown. Previously, this laboratory demonstrated that arsenite acts as a comutagen by interfering with DNA repair, although a specific DNA repair enzyme sensitive to arsenite has not been identified. A number of stable arsenite-sensitive and arsenite-resistant sublines of Chinese hamster V79 cells have now been isolated. In order to gain understanding of possible targets for arsenite's action, one arsenite-resistant subline, As/R28A, was chosen as a donor for a cDNA expression library. The library from arsenite-induced As/R28A cells was transfected into arsenite-sensitive As/S5 cells, and transfectants were selected for arsenite-resistance. Two cDNAs, asr1 and asr2, which confer arsenite resistance to arsenite-hypersensitive As/S5 cells as well as to wild-type cells, were isolated. asr1 shows almost complete homology with the rat fau gene, a tumor suppressor gene which contains a ubiquitin-like region fused to S30 ribosomal protein. Arsenite was previously shown to inhibit ubiquitin-dependent proteolysis. These results suggest that the tumor suppressor fau gene product or some other aspect of the ubiquitin system may be a target for arsenic toxicity and that disruption of the ubiquitin system may contribute to the genotoxicity and carcinogenicity of arsenite.  (+info)

Genetics of cortisone-induced cleft palate in the mouse-embryonic and maternal effects. (8/690)

Differences between mouse strains in frequency of embryonic, cortisone-induced cleft palate were examined. Probit analysis demonstrated a family of linear and parallel dose-response curves for different inbred and hybrid embryos. Since the differences between genotypes were not in the slopes of the response curves but rather in their location, it is proposed that the median effective dose (ED50) of cortisone required to induce cleft palate (or the tolerance) provides a more appropriate definition of the response trait and its difference that a frequency statement. The tolerance of C57BL/6J is dominant to that of A/J. A maternal effect of A/J relative to C57BL/6J dams caused a two-fold reduction in the embryonic tolerance of cortisone. Cortisone-induced cleft palate and mortality were separate response traits. In these and previous studies on cortisone- and other glucocorticoid-induced cleft palate in the mouse, the nature of the cleft-palate-response curve appeared to be the same for all glucocorticoids, and within-strain differences in tolerance could be used as measures of potency or bioassays for a particular effect of the glucocorticoids.  (+info)

  • Effects of Carcinogens, Mutagens, and Teratogens on Non-human Species (Aquatic Animals). (cdc.gov)
  • Studies were conducted of aquatic systems and organisms both under field and laboratory conditions to develop indicator, screening, and modeling capabilities for the detection and evaluation of carcinogens, mutagens, and teratogens. (cdc.gov)
  • American Journal of Medical Genetics Part C (Seminars in Medical Genetics) 157:201 - 208 (2011) A R T I C L E Case-Control Studies for Identifying Novel Teratogens MARTHA M. WERLER,* CAROL LOUIK, AND ALLEN A. MITCHELL The case-control study design offers an operationally efficient approach to measuring an association between an exposure and an outcome, especially when the outcome is rare, as is true for specific birth defects. (docme.ru)
  • BACKGROUND: Exposure of zebrafish embryos to a number of teratogens results in cyclopia, but little is known about the underlying molecular changes. (zfin.org)
  • CONCLUSIONS: These data suggest that each teratogen exposure leads to a unique set of molecular changes that underlie the single phenotype of cyclopia. (zfin.org)
  • I also focus on understanding how exposure to teratogens, such as alcohol, during gestation impacts the development of the precerebellar neurons. (strose.edu)
  • Instead, all teratogens studied produce a series of changes in the expression of gsc and six3b present in early axial development, as well as a later suppression of neural crest cell marker dlx3b. (zfin.org)
  • There is a developmental period of greater susceptibility to teratogens, which corresponds to the stages when most organs and systems are being formed. (conicyt.cl)
  • KARACHI: Toxically germ-infested unsafe drinking water is causing different form of disability among children globally, mainly caused by teratogens. (wordpress.com)
  • teratogens How to cite this article: Werler MM, Louik C, Mitchell AA. (docme.ru)
  • Thalidomide, mainly used for the treatment of leprosy, is a current teratogen in South America, and it is reasonable to assume that at present this situation is affecting many births in underdeveloped countries. (unifesp.br)
  • Some examples of environmental teratogens include radiation, infectious agents (such as chickenpox or syphilis), toxic metals (such as lead or mercury), chemical exposures, maternal conditions (i.e. obesity, hyperthyroidism, or iron deficiency), and of course ethanol, smoking, and both street drugs and prescription medications. (blogspot.com)
  • Currently, evaluation of potential developmental toxicants ( i.e. , teratogens) relies heavily on animal-based models which do not always adequately mimic human development. (rsc.org)
  • The deficiency of any research within the business of teratogen definitions might www.essay-company.com leave the question offered to become medicated just as only conjecture. (yourfinancedirectory.com)
  • As a baby grows in the womb, teratogens may affect parts of the baby's body as they are forming. (uhhospitals.org)
  • The Organization of Teratology Information Specialists ( OTIS ), the Teratology Society and the University of South Florida are pleased to announce the Human Teratogen Course which will be presented at the USF Center for Advanced Medical Learning and Simulation in Tampa, Florida, USA, between 24th and 26th February 2019. (entis-org.eu)
  • Many herbs used for these purposes are believed to be teratogens, substances that cause the development of abnormal structures in the embryo. (sisterzeus.com)
  • The meaning was first used at 1987 when Anne Campbell composed that the content"Teratogen Development" in the Journal of Obstetrics and Gynecology. (yourfinancedirectory.com)
  • This book reports the latest findings and provides the missing link between teratogens and autism spectrum disorder . (autismfallout.com)