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PubMed1976

Rib anomalies in myelodysplasia. An approach to embryologic inference.

An embryologic teratogenic mechanism is reconstructed by utilizing the distribution of anomalous ribs in children with lumbosacral myelomeningocele. This methodology may help to coalesce information from experimental models of teratogenesis and from descriptive human embryology. It provides an approach to deductive reasoning about human structural anomalies based on dynamic embryonic models of teratogenesis. Availability of a developmental time scale, based for example on the distribution of defective ribs, may be useful in the study of other teratogenic and developmental processes.

Abnormalities, Multiple↗
PubMed1998

An ovarian teratoma in a cat.

A 5-month-old, intact female, domestic shorthaired cat was presented for evaluation of abdominal distension. Abdominal radiographs revealed a midabdominal mass that contained multiple, irregular, mineralized opacities. The mass was surgically removed, and an ovariohysterectomy performed. The mass was located at the tip of the left uterine horn and was covered partially by haired skin. Histologically, the mass was diagnosed as a mature ovarian teratoma based on the presence of well-differentiated somatic structures derived from three primary embryonal germ-cell layers. Germ-cell tumor classification and feline ovarian teratomas are reviewed.

Animals↗
PubMed1995

Cloche, an early acting zebrafish gene, is required by both the endothelial and hematopoietic lineages.

Endothelial and hematopoietic cells appear synchronously on the extra-embryonic membranes of amniotes in structures known as blood islands. This observation has led to the suggestion that these two ventral lineages share a common progenitor. Recently, we have shown in the zebrafish, Danio rerio, that a single cell in the ventral marginal zone of the early blastula can give rise to both endothelial and blood cells as well as to other mesodermal cells (Stainier, D. Y. R., Lee, R. K. and Fishman, M. C. (1993). Development 119, 31-40; Lee, R. K. K., Stainier, D. Y. R., Weinstein, B. M. and Fishman, M. C. (1994). Development 120, 3361-3366). Here we describe a zebrafish mutation, cloche, that affects both the endothelial and hematopoietic lineages at a very early stage. The endocardium, the endothelial lining of the heart, is missing in mutant embryos. This deletion is selective as evidenced by the presence of other endothelial cells, for example those lining the main vessels of the trunk. Early cardiac morphogenesis proceeds normally even in the absence of the endocardium. The myocardial cells form a tube that is demarcated into chambers, beats rhythmically, but exhibits a reduced contractility. This functional deficit is likely due to the absence of the endocardial cells, although it may be a direct effect of the mutation on the myocardial cells. Cell transplantation studies reveal that the endothelial defect, i.e. the endocardial deletion, is a cell-autonomous lesion, consistent with the possibility that cloche is part of a signal transduction pathway. In addition, the number of blood cells is greatly reduced in cloche mutants and the hematopoietic tissues show no expression of GATA-1 or GATA-2, two key hematopoietic transcription factors that are first expressed during early embryogenesis. These results show that cloche is involved in the genesis and early diversification of the endothelial and blood lineages, possibly by affecting a common progenitor cell population.

Animals↗
PubMed1999

Gli3 is required for Emx gene expression during dorsal telencephalon development.

Dentate gyrus and hippocampus as centers for spatial learning, memory and emotional behaviour have been the focus of much interest in recent years. The molecular information on its development, however, has been relatively poor. To date, only Emx genes were known to be required for dorsal telencephalon development. Here, we report on forebrain development in the extra toes (Xt(J)) mouse mutant which carries a null mutation of the Gli3 gene. This defect leads to a failure to establish the dorsal di-telencephalic junction and finally results in a severe size reduction of the neocortex. In addition, Xt(J)/Xt(J) mice show absence of the hippocampus (Ammon's horn plus dentate gyrus) and the choroid plexus in the lateral ventricle. The medial wall of the telencephalon, which gives rise to these structures, fails to invaginate during embryonic development. On a molecular level, disruption of dorsal telencephalon development in Xt(J)/Xt(J) embryos correlates with a loss of Emx1 and Emx2 expression. Furthermore, the expression of Fgf8 and Bmp4 in the dorsal midline of the telencephalon is altered. However, expression of Shh, which is negatively regulated by Gli3 in the spinal cord, is not affected in the Xt(J)/Xt(J) forebrain. This study therefore implicates Gli3 as a key regulator for the development of the dorsal telencephalon and implies Gli3 to be upstream of Emx genes in a genetic cascade controlling dorsal telencephalic development.

Animals↗
PubMed2002

Hedgehog is required for murine yolk sac angiogenesis.

Blood islands, the precursors of yolk sac blood vessels, contain primitive erythrocytes surrounded by a layer of endothelial cells. These structures differentiate from extra-embryonic mesodermal cells that underlie the visceral endoderm. Our previous studies have shown that Indian hedgehog (Ihh) is expressed in the visceral endoderm both in the visceral yolk sac in vivo and in embryonic stem (ES) cell-derived embryoid bodies. Differentiating embryoid bodies form blood islands, providing an in vitro model for studying vasculogenesis and hematopoiesis. A role for Ihh in yolk sac function is suggested by the observation that roughly 50% of Ihh(-/-) mice die at mid-gestation, potentially owing to vascular defects in the yolk sac. To address the nature of the possible vascular defects, we have examined the ability of ES cells deficient for Ihh or smoothened (Smo), which encodes a receptor component essential for all hedgehog signaling, to form blood islands in vitro. Embryoid bodies derived from these cell lines are unable to form blood islands, and express reduced levels of both PECAM1, an endothelial cell marker, and alpha-SMA, a vascular smooth muscle marker. RT-PCR analysis in the Ihh(-/-) lines shows a substantial decrease in the expression of Flk1 and Tal1, markers for the hemangioblast, the precursor of both blood and endothelial cells, as well as Flt1, an angiogenesis marker. To extend these observations, we have examined the phenotypes of embryo yolk sacs deficient for Ihh or SMO: Whereas Ihh(-/-) yolk sacs can form blood vessels, the vessels are fewer in number and smaller, perhaps owing to their inability to undergo vascular remodeling. Smo(-/-) yolk sacs arrest at an earlier stage: the endothelial tubes are packed with hematopoietic cells, and fail to undergo even the limited vascular remodeling observed in the Ihh(-/-) yolk sacs. Our study supports a role for hedgehog signaling in yolk sac angiogenesis.

Animals↗
PubMed2002

Three cases of ovarian epidermoid cysts in cattle.

Three cases of bovine, ovarian epidermoid cysts were diagnosed as unilateral benign lesions in three out of 1,971 cows at slaughter. A stratified, cornifying, and squamous epithelium without associated skin adnexal structures or tissues from other embryonic tissue layers lined the cysts. The cysts were small, usually multiple, and contained keratin debris. Macroscopically, they resembled abscesses. These are benign, congenital lesions that are a separate entity from dermoids and teratomas, and they appear to have a higher incidence in cattle with Bos indicus breeding.

Animals↗
PubMed2005

Gene knockouts that cause female infertility: search for novel contraceptive targets.

The gene knockout technology has revolutionized the fertility/infertility field. It has revealed several essential previously undiscovered molecules, new insights and novel mechanisms involved in steps of the fertility cascade in females. Using database and literature search, knockouts of at least 83 genes were discovered that demonstrated an effect on fertility of female mice. These effects ranged from abnormality in reproductive structure, ovarian function, oocyte, fertilization, embryonic and fetal development, implantation and pregnancy to delivery. However, only a few of these knockout of genes such as encoding oocyte glycoprotein coat comprised of zona pellucida (ZP) 1, ZP2 and ZP3 and oocute plasma membrane specific proteins showed a specific and exclusive target infertility effect without concomitant effects on the non-reproductive organ system. These molecules will provide novel targets of contraception including contraceptive vaccine development.

Animals↗
PubMed2000

CB1 cannabinoid receptor-mediated cell migration.

Recent studies have suggested that cell migratory responses are often mediated by G(i) protein-coupled receptors. Because it is known that CB1 cannabinoid receptors are coupled to pertussis toxin-sensitive G proteins, we proposed that CB1 may mediate cell migration. To test this hypothesis, modified Boyden chamber assays were used to investigate cell migration mediated by CB1 cannabinoid receptors. HU-210, WIN55212-2, and anandamide, three cannabinoid agonists with distinct chemical structures, induced migration of human embryonic kidney 293 cells stably transfected with human CB1 gene, but not 293 cells transfected with an empty expression vector. These migratory responses were concentration-dependent. The EC(50) values for HU-210, WIN55212-2, and anandamide were 0.19 +/- 0.04, 12. 2 +/- 1.4, and 39.9 +/- 3.7 nM, respectively. The maximal migration index for HU-210, WIN55212-2, and anandamide were 8.9 +/- 1.6, 9.5 +/- 1.6, and 8.8 +/- 1.3, respectively. Pretreating cells with 100 ng/ml pertussis toxin eliminated the cannabinoid agonist-induced cell migration. SR141716A, a selective antagonist for CB1, inhibited the cannabinoid agonist-induced migratory responses in a concentration-dependent manner. Checkerboard analysis demonstrated that anandamide-induced cell migrations are due to chemotaxis as well as chemokinesis. Furthermore, anandamide-induced migratory responses were inhibited, in a concentration-dependent manner, by PD098059, an inhibitor of mitogen-activated protein kinase activation, but not by 8-bromoadenosine-3',5'-cyclic monophosphate, a cell-permeable cAMP analog. These data demonstrate that cannabinoid agonists are able to induce chemotaxis and chemokinesis, and that these migratory responses are mediated by G protein-coupled, CB1 cannabinoid receptors. In addition, these data suggest that activation of mitogen-activated protein kinase plays an important role, whereas inhibition of adenylate cyclase is probably not involved in the cell migration mediated by CB1.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Three-dimensional ultrasound with surface rendering for the study of fetal small parts.

The purpose of this article is to report that the use of three-dimensional (3D) ultrasound with surface rendering offers advantage in fetal small parts evaluation. Compared with two-dimensional (2D) ultrasonography, three-dimensional ultrasonography provides a better spatial vision of the surface and anatomic boundary of different embryonal and fetal organs and structures. Visualization of an embryo or fetus in all space planes with surface rendering allows a more detailed evaluation of external fetal structures that could easily be missed with 2D ultrasonography. The advent of 3D ultrasound has dramatically improved clinical prenatal diagnosis of small parts anomalies. We anticipate that 3D ultrasonography will be used more widely in obstetrics.

Female↗
PubMed2004

Neuroblastoma: a disease requiring a multitude of imaging studies.

Neuroblastoma stands out among pediatric solid tumors because of its relative frequency, intriguing natural history, prognostic biologic features, and therapeutic challenges. It is the most common extracranial pediatric solid tumor and the most common neoplasm in infancy; >90% of the approximately 600 cases diagnosed annually in the United States are in children < or = 5 y old. Screening programs of infants show that many cases escape detection because of spontaneous regression or maturation into benign lesions. Origin from precursors of the sympathetic nervous system accounts for (a) primary sites in adrenal glands and in paraspinal locations from neck to pelvis and (b) high urinary levels of catecholamines in >90% of cases. This embryonal neoplasm often encases vascular structures and, unlike most solid cancers, usually presents with substantial metastatic disease (bone, bone marrow, lymph nodes, liver; spread to lung or brain is rare). Hence, defining disease status requires CT (or MRI), bone scan, metaiodobenzylguanidine (MIBG) scan, bone marrow tests, and urine catecholamine measurements. The natural history is strikingly variable but is largely predictable from clinical and biologic features. The latter are critical for distinguishing low-risk (90% survival) from high-risk ( approximately 25%-30% survival) subsets, allowing identification of patients who, despite a favorable clinical profile (e.g., localized tumor), are likely to develop lethal metastatic disease, versus patients who have an ominous clinical profile (e.g., widespread disease) but are likely to survive, sometimes with little or no cytotoxic therapy.

Antineoplastic Agents↗
PubMed2004

[Gene expression of extracellular-signal regulated protein kinase 5 and their MAPKK in fetal skin hypertrophic scars].

OBJECTIVE: To explore the change of gene expression of extracellular-signal regulated protein kinase 5 (ERK5) and its upstream signaling molecule (MEK5) in fetal skin of differentially developmental stages and hypertrophic scars. METHODS: After morphological characteristics of skin of different developmental stages and hypertrophic scars were detected with pathological methods, gene expression of ERK5 and MEK5 was examined with reverse transcription-polymerase chain reaction analysis (RT-PCR). RESULTS: In early gestational fetal skin, genes of ERK5 and MEK5 were strongly expressed, while in late gestational skin and children skin, the expression of ERK5 and MEK5 was apparently decreased (P < 0.05). In normal skin, the level of gene expression of ERK5 was lower. In proliferative hypertrophic scars, mRNA content of this gene was apparently increased. In mature scars, the content of this gene transcript was 3.2 times the normal skin. In contrast, the levels of MEK5 transcript in normal skin and hypertrophic scars of various phases showed no substantial changes (P > 0.05). CONCLUSION: ERKS medicating signaling pathway might be involved in regulating cutaneous development at the embryonic stage and determining cutaneous structure ad function. The increase of gene transcription of ERK5 and MEK5 in younger fetal skin might be a reason for rapid proliferation of the skin cells and scraless healing of skin. The activation of ERK5 gene expression in hypertrophic scars versus normal skin might be one of the mechanisms controlling the formation of hypertrophic scars, in which the role of MEK5 needed to be further studied.

Child↗
PubMed1990

Teratogenically induced fetal anomalies.

A variety of infectious and physical agents, maternal diseases and altered metabolic states, and drugs and chemicals have been shown to cause postnatal structural or functional disabilities when embryonic or fetal exposure occurs during human pregnancy. These disabilities are potentially preventable through public education and awareness. Health-care providers must be equipped to collect relevant data regarding exposures of concern from their pregnant patients, locate and evaluate pertinent current teratology information resources, and sensitively counsel these women regarding the associated potential teratogenic risks. Comprehensive care of the patient exposed to a human teratogen may also include discussion of prenatal diagnostic procedures and other pregnancy management options.

Abnormalities, Drug-Induced↗
PubMed1986

Appearance of a unique cell type in the fusion sites of facial processes.

The contact sites between the medial and lateral nasal processes during the period of facial formation of the mouse embryo were examined by light and electron microscopy. Characteristic superficial cells were observed at the transitional regions between the surface ectoderms and the nasal epithelia at the end of the isthmus, where the initial contact of the opposing nasal processes took place. At the later stage the contact sites extended to the bottom of the ravine formed by the two nasal processes, where the superficial cells always seemed to bridge the area between the nasal processes. These superficial cells had a large, clear nucleus and abundant cytoplasm as well as the common structural features characteristic of the embryonic cells. These cells were also observed on the surface near the contact site in the presumptive fusion area. These observations suggest that these superficial cells play a critical role in the epithelial adhesion of the medial and lateral nasal processes throughout the fusion.

Animals↗
PubMed1986

Distribution of stage-specific neurite-associated proteins in the developing murine nervous system recognized by a monoclonal antibody.

A monoclonal antibody, 4D7, obtained with embryonic rat brain as an immunogen, recognizes an epitope on 3 protein species of 150-160, 100-110, and 80 kDa, present in mouse and rat brain during the fetal period. Vital immunostaining of dissociated cultures of fetal forebrain indicates that the antigen is localized largely on the external plasma membrane of a subpopulation of neurites. Immunocytochemistry reveals that the distribution of the antigen in vivo is restricted to the nervous system. Immunoreactivity is concentrated primarily in the pathways of a limited set of CNS and PNS axon systems during early stages of their development, as delineated by staining with the neurofilament antibody, C2. Depending on the particular axon system, immunoreactivity with 4D7 persists only for one to several days of prenatal or perinatal development. In the spinal cord, stage-specific-neurite-associated proteins (SNAP) expression occurs first along motor axon pathways on embryonic day (E) 10 and then within the nerve trunks of dorsal root ganglia and the commissural fiber system on E11. Immunoreactivity is detectable among most cranial nerves starting in the interval from E11 to E13. Within the brain, the onset of SNAP expression within several discrete axon tracts occurs in the interval E14-16, including the lateral olfactory tract, anterior commissure, corpus callosum, fasciculus retroflexus, and fornix. Immunoreactivity within the embryonic intermediate zones of some structures matches the location of certain other axon systems. Sites of 4D7 staining which do not correspond to the location of axon populations include the internal portion of the external granular layer of the postnatal cerebellum and the cortex of the reeler mutant mouse. The predominant localization of the 4D7 antigen among axon systems and its precisely regulated spatio-temporal pattern of expression are consistent with the possibility that the SNAP antigens play a significant role in the early stages of growth of axonal tracts in vivo.

Animals↗
PubMed1983

[Embryonal carcinoma and vitelline tumor of the mediastinum. Diagnostic and prognostic value of alpha-fetoprotein levels. A propos of 5 cases].

Five cases are reported of embryonal carcinoma with a vitelline structure more or less predominating. The presentation was of an anterior mediastinal tumour occurring in young men and in three cases there was mediastinal obstruction. The clinical examination, in particular testicular examination, was negative. In each case the level of the alpha-fetoprotein was greater than 1,000 micrograms/l, even post-operatively. The alpha-fetoprotein and HCG-beta should be measured systematically in all cases of anterior mediastinal tumour occurring in young subjects, and would enable a more frequent identification of tumours with difficult histology. The serum levels reflected the changes noted clinically and radiologically. Polychemotherapy bases around cis platinum led to a significant but transitory regression of the tumours. Radiotherapy was ineffective. Surgery was never totally curative.

Adult↗
PubMed1983

The regeneration of skeletal muscle fibers following injury: a review.

Regeneration is a unique adaptation of skeletal muscle that occurs in response to injury. Following direct trauma or disease, regeneration results in restoration, to some degree, of the original structure and function of the muscle. Our purpose is to summarize the main features of the regeneration of skeletal muscle fibers and entire muscles with an emphasis on aspects of regeneration that may be important to the understanding and treatment of sports injuries. The regeneration of skeletal muscle is compared structurally and functionally with its embryonic development. The free muscle graft is used as a model to illustrate the integration of regenerating muscle with the rest of the body. Finally, the breakdown and regeneration of skeletal muscle fibers are discussed in relation to local anesthetics, sports injuries, and disease.

Anesthetics, Local↗
PubMedDate not supplied

Collagen substrates for cytogenetic studies of domestic animal embryos.

A technique of cell culture on collagen substrate is proposed for cytogenetic studies on domestic animal embryos. The embryonic cells sampled by biopsy or micromanipulation grow on collagen coated cover slips in Leighton tubes with Ham's F12 medium, supplemented with 20 percent fetal calf serum. This method may be used to study the embryonic karyotype induced by a structural abnormality, as well as the karyotype of domestic animal embryos before transfer.

Animals↗
PubMed1981

Control of globin gene expression in mouse yolk sac erythroid cells.

In the present paper are reported results from our laboratory and data of the literature on the structure and the expression of embryonic globin genes in mouse fetuses. The following aspects are presented: 1. Erythropoiesis and synthesis of globin chains in fetal mice. 2. The transcriptional and post-transcriptional control of embryonic globin gene expression. 3. The chromosomal location and organization of mouse embryonic globin genes.

Animals↗