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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Dec 26, 2014

Carnegie Stage 4 - Implantation of embryo into uterus begins 5 to 6 days after egg fertilized.

As the blastocyst enters the uterus free from the zona, the outer layer of trophoblast cells secrete an enzyme to erode the epithelial lining of the uterus and allow the blastocyst to implant.

 






 

 

Trophoblasts the first immune cells of pregnancy?

Trophoblasts are the cells surrounding a fertilized egg which in time develop into a major part of the placenta. Research shows how these cells respond to danger triggered by inflammation.

Trophoblast inflammatory responses vary from one woman's pregnancy to another. In this latest study, researchers believe their findings advance our understanding of how inflammation in the placenta contributes to development disorders in the fetus. In preeclampsia, inflammation of the placenta leads to systemic inflammation in the mother manifesting in high blood pressure and spilling protein into the mother's urine.

Results of the study are published in the Journal of Reproductive Immunology, in the December 2014 issue.


"This is the first time researchers have shown the many different inflammatory mechanisms in trophoblasts."

Guro Stødle and Line Tangerås, PhD candidates, first authors, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology


Infection caused by bacteria or viruses and the resulting tissue injury — can set off an inflammatory response in which numerous cell types work together in an effort to eliminate the threat and repair any damage.


"Pregnancy is a delicate balance, the mother and fetus must adapt to each other and coexist. An inflammatory response can disturb this delicate balance causing complications as seen in preeclampsia, a potentially severe placental inflammatory disorder threatening both the mother and fetus."

Guro Stødle PhD candidate


Inflammatory responses are directed by Toll-like receptors (TLRs) a class of proteins that are key to our innate immune system. TLRs got their name from how similar they are to proteins coded by the toll gene, identified as the gene most important in establishing a back from front (or dorsal-ventral) axis in the embryo. Although thirteen TLRs (named simply TLR1 to TLR13) have been identified in humans and mice, equivalent forms of many have been found in other mammalian species — and only one through 10 are functional in humans.

TLRs initiate inflammation — the protective response which removes the stimuli that can injure us — and then initiate healing by recruiting all cell types needed to fix an injury. Although infection is caused by a microorganism, inflammation can occur without infection. Destruction of tissue in the absence of inflammation would compromise our survival. On the other hand, chronic inflammation can lead to a host of diseases, such as preeclampsia. Inflammation is considered a mechanism of our innate immune response, as compared to adaptive immunity which is specific to a pathogen.

Fetal-derived trophoblasts are the main cell type of the placenta and initial reports indicate that these cells may express [turn on and make active] TLRs.


"To investigate a role for trophoblasts in placental inflammation, we studied trophoblasts of early pregnancy and when they expressed the ten TLRs — and then whether these receptors were responsive to danger signals."

Line Tangerås, PhD candidate, first authors, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology

"We discovered that trophoblasts isolated from first trimester placentas showed broad TLR expression [turning ON of the TLR protein]."

Guro Stødle, PhD candidate, added.


Functional responses to danger signals were detected in six of the ten TLRs, and their activation led to production of pro-inflammatory cytokines. The research group at CEMIR will now continue to study the trophoblast-mediated immune activation going on in the placenta to help us understand the underlying harmful inflammation associated with a pre-eclamptic pregnancy.

Abstract
Toll-like receptors (TLRs) are an important part of the body's danger response system and crucial for initiating inflammation in response to cellular stress, tissue damage, and infections. Proper placental development is sensitive to inflammatory activation, and a role for TLRs in trophoblast immune activation has been suggested, but no overall examination has been performed in primary trophoblasts of early pregnancy. This study aimed to broadly examine cell surface and endosomal TLR gene expression and activation in first-trimester trophoblasts. Gene expression of all ten TLRs was examined by quantitative RT-PCR (RT-qPCR) in primary first-trimester trophoblasts (n = 6) and the trophoblast cell line BeWo, and cytokine responses to TLR ligands were detected by quantitative multiplex immunoassay. Primary first-trimester trophoblasts broadly expressed all ten TLR mRNAs; TLR1, TLR2, TLR3, TLR4, and TLR6 mRNA were expressed by all primary trophoblast populations, while TLR5, TLR7, TLR8, TLR9, and TLR10 mRNA expression was more restricted. Functional response to ligand activation of cell surface TLR2/1, TLR4, and TLR5 increased IL-6 and/or IL-8 release (P < 0.01) from primary trophoblasts. For endosomal TLRs, TLR3 and TLR9 ligand exposure increased receptor-specific production of IL-8 (P < 0.01) and IFN-γ-induced protein 10 (IP-10; P < 0.001) or vascular endothelial growth factor A (VEGFA; P < 0.01). In contrast, BeWo cells expressed lower TLR mRNA levels and did not respond to TLR activation. In conclusion, primary first-trimester trophoblasts broadly express functional TLRs, with inter-individual variation, suggesting that trophoblast TLR2, TLR3, TLR4, TLR5, and TLR9 might play a role in early placental inflammation.


The researchers collected first trimester placenta tissue samples at the Department of Gynecology and Obstetrics at St. Olavs Hospital. The laboratory experiments were performed at the Centre of Molecular Inflammation Research (CEMIR) at Norwegian University of Science and Technology.

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