The uncorrected positive predictive value for the Denver II alone (44% was While the children were tested using the Wiener Entwicklungstest (Viennese. Jan. Die kognitiven Skalen von Entwicklungstests messen jedoch zumeist etwas anderes als Intelligenztests. Der Beitrag diskutiert die. Denver Entwicklungsskalen. Hamburg: Testanleitung. Frostig, M. (). Frostigs Entwicklungstest der visuellen. Wahrnehmung, Weinheim. H├╝ttenmoser, M.

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Developmental toxicity evaluation of three hexabromocyclododecane diastereoisomers on zebrafish embryos. Structural dissimilarities of hexabromocyclododecane diastereoisomers could raise substantial differences in physicochemical, biological and toxicological properties.

Four-hour post-fertilization hpf zebrafish embryos were exposed to different concentrations of HBCD diastereoisomers 0, 0. Evaluation of developmental toxicity of coniine to rats and rabbits. Conium maculatum poison hemlock, CM is teratogenic in several domestic species, presumably due to its piperidine alkaloids, including coniine, which has been verified to be entwick,ungstest in cattle. The purpose of this study was to evaluate coniine-induced teratogenicity in two laboratory animal species, Sprague-Dawley rats and New Zealand white rabbits.

Rats were killed on day 19 and rabbits on day Fetuses were immediately removed, weighed, and examined for external abnormalities. Alternate fetuses were either stained for skeletal examinations with alizarin red-S or fixed in Bouin’s solution for visceral examination.

Symptoms of maternal intoxication due to coniine administration were observed in both the rat and the rabbit, and higher doses were uniformly lethal. Rabbits treated with coniine appeared to lose more engwicklungstest and eat less than controls, but there was no statistically significant difference between groups. Fetal weights were significantly lower in coniine-exposed rat and rabbit fetuses indicating fetotoxicity. The only statistically significant treatment-related visceral or skeletal malformation was a reduction of cranial ossification of rabbit fetuses, probably related to maternal toxicity.

Developmental toxicity evaluation of inhaled tertiary amyl methyl ether in mice and rats. This evaluation was part of a much more comprehensive testing program to characterize the mammalian toxicity potential of the gasoline oxygenator additive tertiary amyl methyl ether TAMEand was initiated upon a regulatory agency mandate. A developmental toxicity hazard identification study was conducted by TAME vapor inhalation exposure in two pregnant rodent species.

Timed-pregnant CD Sprague-Dawley entwic,lungstest and CD-1 mice, 25 animals per group, inhaled TAME vapors containing 0,or ppm for 6 h a day on gestational days mice or rats. The developmental toxicity hazard potential was evaluated following the study design draft guidelines and end points proposed by the United States Environmental Protection Agency.

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Based on maternal body weight changes during pregnancy, the no-observable-adverse-effect level NOAEL was ppm for maternal toxicity in rats and ppm for developmental toxicity in rats using the criterion of near-term fetal body weights.

In mice, more profound developmental toxicity was present than in rats, at both and ppm. At the highest concentration, mouse litters revealed more late fetal deaths, significantly reduced fetal body weights per litter and increased incidences of cleft palate classified as an external malformationas well as enlarged lateral ventricles of the cerebrum a visceral variation.

At ppm, mouse fetuses also exhibited an increased incidence of cleft palate and the dam body weights were reduced. Therefore, the NOAEL for the mouse maternal and developmental toxicity was ppm under the conditions of this study.

Developmental toxicity of engineered nanomaterials. Study of air pollution indicates that minute particles may adversely interfere with pregnancy and fetal development. As engineering of nanoparticles have emerged, so has concern that these might interfere with reproductive and developmental functions. This is because nanotechnology may potentially To evaluate safety for pregnant women, we have studied developmental toxicity of engineered nanoparticles ENPsfollowing exposure of pregnant mice by inhalation ENPs of titanium Evaluating chemical and other agent exposures for reproductive and developmental toxicity.

As part of its efforts to reduce or eliminate exposure of Naval personnel and their families to reproductive and developmental toxicantsthe Navy requested that the National Research Council NRC Building a developmental toxicity ontology.


As more information is generated about modes of action for developmental toxicity and entwickluntstest data are generated using high-throughput and high-content technologies, it is becoming entwicklungstedt to organize that information.

This report discussed the need for a systematic representation of knowledge about developmental toxicity i. This report is the result of a consensus working group developing a plan to create an ontology for developmental toxicity that spans multiple levels of biological organization. This report provide a description of some of the challenges in building a developmental toxicity ontology and outlines a proposed methodology to meet those challenges.

As the ontology is built on currently available web-based resources, a review of these resources is provided. Case studies on one of the most well-understood morphogens and developmental toxicantsretinoic acid, are presented as examples enntwicklungstest how such an ontology might be developed.

This report outlines an approach to construct a developmental toxicity ontology. Such an ontology will facilitate computer-based prediction of substances likely to induce human developmental toxicity. Evaluation of an adherent mouse embryonic stem cell in vitro assay to predict developmental toxicity of ToxCast chemicals.

The potential for most environmental chemicals to produce developmental toxicity is unknown. Mouse embryonic stem cell mESC assays are an alternative in vitro model to assess chemicals. The chemical space evaluated using mESC and compared to in vivo is limited. We used an adher Evaluation of developmental toxicity and teratogenicity of diclofenac using Xenopus embryos. Diclofenac is a non-steroidal anti-inflammatory drug NSAID with analgesic and anti-pyretic properties.

This compound is therefore used to treat pain, inflammatory disorders, and dysmenorrhea. Due to its multimodal mechanism of action and ability to penetrate placenta, diclofenac is known to have undesirable side effects including teratogenicity. However, limited data exist on its teratogenicity, and a detailed investigation regarding harmful effects of this drug during embryogenesis is warranted.

Diclofenac treatment exerted a teratogenic effect on Xenopus embryos with a teratogenic index TI value of 2.

In particular, mortality of embryos treated with diclofenac increased in a concentration-dependent manner and a broad spectrum of malformations such as shortening and kinking of the axis, abdominal bulging, and prominent blister formation, was observed.

The shape and length of internal organs also differed compared to the control group embryos and show developmental retardation on histological label. However, the expression of major tissue-specific markers did not change when analyzed by reverse transcription-polymerase chain reaction RT-PCR. In conclusion, diclofenac treatment can promote teratogenicity that results in morphological anomalies, but not disrupt the developmental tissue arrangement during Xenopus embryogenesis.

Identification of developmentally toxic drinking water disinfection byproducts and evaluation of data relevant to mode of action. Colman, Joan; Rice, Glenn E. Sidney; Teuschler, Linda K. Reactions between chemicals used to disinfect drinking water and compounds present in source waters produce chemical mixtures containing hundreds of disinfection byproducts DBPs.

Although the results have been somewhat inconsistent, some epidemiological studies suggest associations may exist between DBP exposures and adverse developmental outcomes. The potencies of individual DBPs in rodent and rabbit developmental bioassays suggest that no individual DBP can account for the relative risk estimates reported in the positive epidemiologic studies, leading to the hypothesis that these outcomes could result from the toxicity of DBP mixtures.

We identified 24 developmentally toxic DBPs and four adverse developmental outcomes associated with human DBP exposures: A plausible MOA, involving hormonal disruption of pregnancy, is delineated for spontaneous abortion, which some epidemiologic studies associate with total trihalomethane and bromodichloromethane exposures. Directory of Open Access Journals Sweden. Full Text Available Male-mediated developmental toxicity has been of concern for many years.

The public became aware of male-mediated developmental toxicity in the early s when it was reported that men working at Sellafield might be causing leukemia in their children. Human and animal studies have contributed to our current understanding of male-mediated effects.

Animal studies in the s and s suggested that genetic damage after radiation and chemical exposure might be transmitted to offspring. With the increasing understanding that there is histone retention and modification, protamine incorporation into the chromatin and DNA methylation in mature sperm and that spermatozoal RNA transcripts can play important roles in the epigenetic state of sperm, heritable studies began to be viewed differently.


Recent reports using molecular approaches have demonstrated that DNA damage can be transmitted to babies from smoking fathers, and expanded simple tandem repeats minisatellite mutations were found in the germline of fathers who were exposed to radiation from the Chernobyl nuclear power plant disaster.

In epidemiological studies, it is possible to clarify whether damage is transmitted to the sons after exposure of the fathers. Paternally transmitted damage to the offspring is now recognized as a complex issue with genetic as well as epigenetic components.

The developmental toxicity of uranium in mice. Cesarean sections were performed on all females on gestation day Fetuses were examined for external, visceral and skeletal abnormalities.

The results indicated that such exposure resulted in maternal toxicity as evidenced by reduced weight gain and food consumption during treatment, and increased relative liver weight. There were no treatment-related effects on the number of implantation sites per dam, or on the incidence of postimplantation loss resorptions entwickljngstest dead fetuses. The number of live fetuses per litter and the fetal sex ratio were not affected by the treatment. However, dose-related fetal toxicityconsisting primarily of reduced fetal body weight and body length, and an increased incidence of abnormalities was observed.

Thieme E-Journals – Kinder- und Jugendmedizin / Abstract

There was no evidence of embryolethality at any dosage level used in this study. Developmental toxicity of engineered nanomaterials in rodents. We summarized significant effects reported in the literature on the developmental toxicity of engineered nanomaterials ENMs in rodents.

The developmental toxicity of ENMs included not only structural abnormalities, but also death, growth retardation, and behavioral and functional abnormalities. Most studies were performed on mice using an injection route of exposure.

The pre- and postnatal mortalities and growth retardation in offspring increased after prenatal exposure to ENMs.

Histopathological and functional abnormalities were also induced in placentas after prenatal exposure to ENMs.

Maternal exposure to ENMs induced ddenver alterations, histopathological and biochemical changes in the central nervous system, increased susceptibility to allergy, transplacental genotoxicity, and vascular, immunological, and reproductive effects in offspring.

The size- and developmental stage-dependent placental transfer of ENMs was noted after maternal exposure. Silver accumulated in the visceral yolk sac after being injected with Ag-NPs during early gestation.

Although currently available data has provided initial information on the potential developmental toxicity of ENMs, that on the developmental toxicity of ENMs is still very limited.

Further studies using well-characterized ENMs, state-of the-art study protocols, and appropriate routes of exposure are required in order to clarify these developmental effects and provide information suitable for risk assessments of ENMs.

The weight of the Rethinking developmental toxicity testing: Current developmental toxicity testing adheres largely to protocols suggested in involving the administration of test compound to pregnant laboratory animals. After more than 50 years of embryo-fetal development testing, are we ready to consider a different approach to human developmental. In recent years, the public has become more aware that exposure of males to certain agents can adversely affect their offspring and cause infertility and cancer.

The hazards associated with exposure to ionising radiation have been recognised for nearly a century, but interest was aroused when a cluster of leukaemia cases was identified in young children living in Fenver, close to the nuclear processing plant at Sellafield in West Cumbria. There was a civil court case on behalf of two of the alleged victims of paternal entwicklugstest at Seascale against British Nuclear Fuels.

The case foundered on ‘the balance of probabilities’. Nevertheless, there was support for paternal exposure from Japanese experimental X-ray studies in mice.