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Results: 5

1.
Figure 2.

Figure 2. From: Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

Placental size of ThbdProPro embryos relative to controls. Each symbol represents a measurement from a single fetoplacental unit. All litters were analyzed at E9.5. Mean ratios and SDs are shown.

Rashmi Sood, et al. J Exp Med. 2007 May 14;204(5):1049-1056.
2.
Figure 1.

Figure 1. From: Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

Phenotype of ThbdProPro embryos in FVQQThbdPro+ mothers. (a, c, and e) ThbdPro+ littermates at E9.5, E12.5, and E18.5, respectively, of ThbdProPro embryos (b, d, and f). At E9.5, some ThbdProPro embryos are smaller (b). By E11.5, most ThbdProPro embryos are in an advanced stage of decay (d). Platelet depletion of the mother with anti-GP1bα antibody treatment (e and f) results in normal-appearing ThbdProPro embryos. Pictures were taken at different magnifications. Bars, 1 mm.

Rashmi Sood, et al. J Exp Med. 2007 May 14;204(5):1049-1056.
3.
Figure 4.

Figure 4. From: Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

Placental thrombosis in FvL mice. The number of placental thrombi was similar in placentas of wild-type and ThbdProPro embryos (see Results). Thrombi were identified on serial sections by hematoxylin and eosin staining (a, c, and e), and immunostaining with antifibrinogen antibodies (b) and anti–p-selectin antibodies (d and f). e and f are enlarged views of the boxed areas in c and d. Arrows indicate clots. Bars, 0.1 mm.

Rashmi Sood, et al. J Exp Med. 2007 May 14;204(5):1049-1056.
4.
Figure 5.

Figure 5. From: Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

Assessment of decidual and placental vascular patency by FITC-dextran infusion. Whole-mount (a and b) and sections (c–f) of decidual-placental units corresponding to a wild-type embryo in a wild-type mother (a, c, and e) and a FvQ+ThbdProPro embryo in a FvQQThbdPro+ mother (b, d, and f) are shown. From the fetal aspect of the placenta, a characteristic ring of maternal placental vasculature, marked by FITC-dextran, is observed in wild-type pregnancies but not in placenta of a FvQ+ThbdProPro embryo in a FvQQThbdPro+ mother (a and b). Decidual and placental regions in both types of pregnancies are perfused with FITC-dextran (c and d). Hematoxylin and eosin–stained sections adjacent to c and d are shown in e and f. Arrows show maternal blood spaces in the placenta. Bars, 1 mm.

Rashmi Sood, et al. J Exp Med. 2007 May 14;204(5):1049-1056.
5.
Figure 3.

Figure 3. From: Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

Placental phenotype of ThbdProPro embryos and littermate controls in FvQQThbdPro+ mothers. Histological sections through placentas of ThbdPro+ (a, c, and e) and a phenotypically normal ThbdProPro (b, d, and f) embryo at E9.5. a and b show cytokeratin-expressing trophoblast cells (brown staining). The placenta of ThbdProPro embryos (stained area) is smaller than that of ThbdPro+ embryos. c and d are higher magnification images of hematoxylin and eosin–stained sections adjacent to a and b, respectively. e and f correspond to boxes in c and d, respectively. Dashed lines in c and d mark the border of the placenta and decidua, as determined by cytokeratin staining. ThbdPro+ placentas (c and e) have formed a labyrinth characterized by maternal (bright red enucleated maternal red blood cells; dashed arrows) and fetal (purple hematoxylin-stained nucleated fetal red blood cells; continuous arrow) blood spaces. The labyrinth is distinctly absent in the placentas of littermate ThbdProPro embryos (d and f). Bars, 0.1 mm.

Rashmi Sood, et al. J Exp Med. 2007 May 14;204(5):1049-1056.

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