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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
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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 Jan 29, 2014

 

This is a schematic of  calcium channels in open , inactive, normal, and closed states.

Image from the following article:
"Calcium-dependent inactivation of neuronal calcium channels,"
by Thomas Budde, Sven Meuth & Hans-Christian Pape
Nature Reviews Neuroscience 3, 873-883 (November 2002)






WHO Child Growth Charts

 

 

 

How our body uses free calcium

Scientists at Johns Hopkins report they have figured out a key step in how “free” calcium — the kind not contained in bones — is managed in the body, a finding that could aid in developing new treatments for a variety of neurological disorders such as Parkinson’s.

Appearing online this week in Nature Chemical Biology, the researchers describe how tiny “lights” and chemical “leashes” unveil how calcium is controlled.


Electrical signals carried by free-floating calcium ions are “wildly important to keeping the second-by-second functions of the body going,” says David Yue, M.D., Ph.D., professor of biomedical engineering and neuroscience at The Johns Hopkins University.


A calcium channel is made up of membrane proteins that attach to cell walls. Yue, who led the research team of graduate students Philemon Yang and Manu Ben Johny, explains that protein calcium channels are the gatekeepers that determine when calcium enters a cell. Embedded in cell membranes, these gatekeepers open and shut channels to regulate calcium flow. When calcium enters a cell, it sets off a cascade of vital activity, but just the right amount of calcium must enter - or problems arise.

To this end, two chemical regulators bind to calcium channels acting as a brake and accelerator precisely regulating calcium entry. Calmodulin, stops calcium from flowing into a cell, while calcium-binding proteins accelerate calcium entry.  In their research, Yue and team examined calcium channels embedded in the membranes of brain nerve cells to find out exactly how calmodulin and a particular calcium-binding protein, CaBP4, latch onto calcium channels.

They made certain calmodulin bound to calcium by genetically engineering short, flexible strands of amino acids to tether the two together. But to their surprise, calcium-binding proteins stuck to the calcium channels all at the same time. This suggests that each regulator protein had its own parking space in the calcium channel, whereas previous theories suggested the calcium channel was only a single space up for grabs to all calcium-proteins that entered.


To further examine relationships between calcium regulators, scientists marked calmodulin and CaBP4 each with their own glowing color.

When two molecules locked together, another color emerged. By measuring color changes, researchers could then tell which molecules bound to each other.


“Our experiments established that calmodulin and calcium-binding proteins work by binding to distinct parts of a calcium channel,” Yue says. “More generally, we have been able to investigate how large molecules such as these function within living cells.”

The “live light show” permitted by the use of light markers should help scientists develop new drugs to target calcium channels, Yue adds. Some such drugs already exist, including calcium channel blockers that lower blood pressure by targeting a particular kind of calcium channel found in blood vessels.


Blocking calcium channels might help with other diseases as well. Researchers have found that an overload of calcium in certain parts of the brain drive some neurodegenerative diseases, such as Parkinson's. Blocking calcium channels found in those trouble spots — the kind found in Yue's study — could be a new way to fight debilitating brain diseases.


Abstract
Distinguishing between allostery and competition among modulating ligands is challenging for large target molecules. Out of practical necessity, inferences are often drawn from in vitro assays on target fragments, but such inferences may belie actual mechanisms. One key example of such ambiguity concerns calcium-binding proteins (CaBPs) that tune signaling molecules regulated by calmodulin (CaM). As CaBPs resemble CaM, CaBPs are believed to competitively replace CaM on targets. Yet, brain CaM expression far surpasses that of CaBPs, raising questions as to whether CaBPs can exert appreciable biological actions. Here, we devise a live-cell, holomolecule approach that reveals an allosteric mechanism for calcium channels whose CaM-mediated inactivation is eliminated by CaBP4. Our strategy is to covalently link CaM and/or CaBP to holochannels, enabling live-cell fluorescence resonance energy transfer assays to resolve a cyclical allosteric binding scheme for CaM and CaBP4 to channels, thus explaining how trace CaBPs prevail. This approach may apply generally for discerning allostery in live cells.

This work was supported by grants from the National Heart, Lung and Blood Institute (MERIT Award), the National Institute on Deafness and Other Communication Disorders and the National Institute of Mental Health.