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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 Aug 23, 2013

 

Mitochondria (9) contain their own DNA which recombine more frequently than nuclear DNA.
This accumulation of recombinant changes reduces the energy level of mitochondria.
We each inherit our mother's mitochondrial DNA—which  also contains damage.

Image credit: Wikipedia.org
Components of a typical animal cell:
(1) Nucleolus
(2) Nucleus
(3) Ribosome (little dots)
(4) Vesicle
(5) Rough endoplasmic reticulum
(6) Golgi apparatus (or "Golgi body")
(7) Cytoskeleton
(8) Smooth endoplasmic reticulum
(9) Mitochondrion
(10) Vacuole
(11) Cytosol (fluid that contains organelles)
(12) Lysosome
(13) Centrosome
(14) Cell membrane





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Study finds mother's genes can impact aging process

As we age, our cells change and become damaged. Now, researchers at Karolinska Institutet and the Max Planck Institute for Biology of Aging have shown that aging is determined not only by the accumulation of changes during our lifetime but also by the genes we acquire from our mothers.

The results of the study are published in the journal Nature.

There are many causes of aging that are determined by an accumulation of various kinds of changes that impair the function of bodily organs. Of particular importance in aging, however, seems to be the changes that occur in the cell's power plant – the mitochondrion. This structure is located in the cell and generates most of the cell's supply of ATP which is used as a source of chemical energy.

"The mitochondria contains their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the aging process," said Nils-Göran Larsson, Ph.D., professor at the Karolinska Institutet and principal investigator at the Max Planck Institute for Biology of Aging, and leader of the current study alongside Lars Olson, Ph.D., professor in the Department of Neuroscience at the Karolinska Institutet. "Many mutations in the mitochondria gradually disable the cell's energy production," said Larsson.

For the first time, the researchers have shown that the aging process is influenced not only by the accumulation of mitochondrial DNA damage during a person's lifetime, but also by the inherited DNA from their mothers.


"Surprisingly, we also show that our mother's mitochondrial DNA seems to influence our own aging. If we inherit mDNA with mutations from our mother, we age more quickly."

Nils-Göran Larsson, Ph.D., professor at the Karolinska Institutet, principal investigator at the Max Planck Institute for Biology of Aging, and co-leader of the current study


Normal and damaged DNA is passed down between generations. However, the question of whether it is possible to affect the degree of mDNA damage through lifestyle intervention is yet to be investigated. All that the researchers know now is that mild DNA damage transferred from the mother contributes to the aging process.

"The study also shows that low levels of mutated mDNA can have developmental effects and cause deformities of the brain," said lead author Jaime Ross, Ph.D., at the Karolinska Institutet.

"Our findings can shed more light on the aging process and prove that the mitochondria play a key part in aging; they also show that it's important to reduce the number of mutations," said Larsson.

"These findings also suggest that therapeutic interventions that target mitochondrial function may influence the time course of aging," said Barry Hoffer, M.D., Ph.D.


"There are various dietary manipulations and drugs that can up-regulate mitochondrial function and/or reduce mitochondrial toxicity. An example would be antioxidants. This mouse model would be a 'platform' to test these drugs/diets."

Dr. Barry Hoffer, co-author of the study from the Department of Neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine. He is also a visiting professor at the Karolinska Institutet.


The data published in the paper come from experiments on mice. The researchers now intend to continue their work on mice, and on fruit flies, to investigate whether reducing the number of mutations can extend their lifespan.

Abstract
Ageing is due to an accumulation of various types of damage1, 2, and mitochondrial dysfunction has long been considered to be important in this process3, 4, 5, 6, 7, 8. There is substantial sequence variation in mammalian mitochondrial DNA (mtDNA)9, and the high mutation rate is counteracted by different mechanisms that decrease maternal transmission of mutated mtDNA10, 11, 12, 13. Despite these protective mechanisms14, it is becoming increasingly clear that low-level mtDNA heteroplasmy is quite common and often inherited in humans15, 16. We designed a series of mouse mutants to investigate the extent to which inherited mtDNA mutations can contribute to ageing. Here we report that maternally transmitted mtDNA mutations can induce mild ageing phenotypes in mice with a wild-type nuclear genome. Furthermore, maternally transmitted mtDNA mutations lead to anticipation of reduced fertility in mice that are heterozygous for the mtDNA mutator allele (PolgAwt/mut) and aggravate premature ageing phenotypes in mtDNA mutator mice (PolgAmut/mut). Unexpectedly, a combination of maternally transmitted and somatic mtDNA mutations also leads to stochastic brain malformations. Our findings show that a pre-existing mutation load will not only allow somatic mutagenesis to create a critically high total mtDNA mutation load sooner but will also increase clonal expansion of mtDNA mutations17 to enhance the normally occurring mosaic respiratory chain deficiency in ageing tissues18, 19. Our findings suggest that maternally transmitted mtDNA mutations may have a similar role in aggravating aspects of normal human ageing.

Original press release:http://www.eurekalert.org/pub_releases/2013-08/uhcm-sfm082013.php