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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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The World Health Organization (WHO) has created a new Web site to help researchers, doctors and
patients obtain reliable information on high-quality clinical trials. Now you can go to one website and search all registers to identify clinical trial research underway around the world!





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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 Feb 9, 2015

Overeating can be the result and cause of stress in pregnancy.
But the fetus will suffer malnutrition.

 







 

 

Stress in pregnancy can affect babys' weight

Stress hormones in a mom can affect baby. Research has found that increased levels of glucocorticoid stress hormones in pregnant mice cause the moms to eat more but reduces baby weight.

According to a study published in The Journal of Physiology high stress levels in pregnant mice have an impact on their offspring. Pregnant mice received the natural glucocorticoid corticosterone (1) at different times during pregnancy, either days 11 to 16 (in 20 females), days 14 to 19 (in 31 females), or not at all (in 74 control females).


"Together with previous work, we show maternal glucocorticoids regulate fetal nutrition. Higher glucocorticoid hormone levels in the mother (under stressful conditions), can reduce glucose transport across the placenta and decrease fetal weight.

"Glucocorticoid levels in pregnant women may determine the specific combination of nutrients received by the fetus and influence the long-term metabolic health of that child as a result. This could have implications for women stressed during pregnancy or treated clinically with glucocorticoids, if these mechanisms are similar in humans.

"Our research revealed that under stress, certain genes in the placenta were modified. One of the genes altered by stress hormones was Redd1. This gene is believed to signal the availability of substances such as oxygen, and interact with intracellular pathways regulating growth and nutrient uptake in the placenta. Future studies may prove this molecule is important for linking environmental cues to fetal nutrition."

Dr Owen Vaughan, Department of Physiology, Development and Neuroscience, Cambridge, UK, lead author of the study.


Researchers believe that glucocorticoid levels in pregnant women may therefore determine the specific combination of nutrients received by the fetus and influence the long term metabolic health of their children.

(1) Corticosterone is a steroid hormone produced in the cortex of the adrenal glands in rodents and other non-human animals. However, in humans, corticosterone is produced primarily in the adrenal cortex. It is the precursor molecule to the mineralocorticoid aldosterone, one of the major homeostatic modulators of sodium and potassium levels in vivo. Source: Wikipedia

Abstract
Glucocorticoids affect glucose metabolism in adults and fetuses, although their effects on materno-fetal glucose partitioning remain unknown. The present study measured maternal hepatic glucose handling and placental glucose transport together with insulin signalling in these tissues in mice drinking corticosterone either from day (D) 11 to D16 or D14 to D19 of pregnancy (term = D21). On the final day of administration, corticosterone-treated mice were hyperinsulinaemic (P < 0.05) but normoglycaemic compared to untreated controls. In maternal liver, there was no change in glycogen content or glucose 6-phosphatase activity but increased Slc2a2 glucose transporter expression in corticosterone-treated mice, on D16 only (P < 0.05). On D19, but not D16, transplacental 3H-methyl-d-glucose clearance was reduced by 33% in corticosterone-treated dams (P < 0.05). However, when corticosterone-treated animals were pair-fed to control intake, aiming to prevent the corticosterone-induced increase in food consumption, 3H-methyl-d-glucose clearance was similar to the controls. Depending upon gestational age, corticosterone treatment increased phosphorylation of the insulin-signalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3β, in maternal liver (P < 0.05) but not placenta (P > 0.05). Insulin receptor and insulin-like growth factor type I receptor abundance did not differ with treatment in either tissue. Corticosterone upregulated the stress-inducible mechanistic target of rapamycin (mTOR) suppressor, Redd1, in liver (D16 and D19) and placenta (D19), in ad libitum fed animals (P < 0.05). Concomitantly, hepatic protein content and placental weight were reduced on D19 (P < 0.05), in association with altered abundance and/or phosphorylation of signalling proteins downstream of mTOR. Taken together, the data indicate that maternal glucocorticoid excess reduces fetal growth partially by altering placental glucose transport and mTOR signalling.

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