Welcome to The Visible Embryo

 

 

Home-- -History-- -Bibliography- -Pregnancy Timeline- --Prescription Drugs in Pregnancy- -- Pregnancy Calculator- --Female Reproductive System- -Contact
 

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.

WHO International Clinical Trials Registry Platform


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!



Home

History

Bibliography

Pregnancy Timeline

Prescription Drug Effects on Pregnancy

Pregnancy Calculator

Female Reproductive System

Contact The Visible Embryo

News Alerts Archive

Disclaimer: The Visible Embryo web site is provided for your general information only. The information contained on this site should not be treated as a substitute for medical, legal or other professional advice. Neither is The Visible Embryo responsible or liable for the contents of any websites of third parties which are listed on this site.
Content protected under a Creative Commons License.

No dirivative works may be made or used for commercial purposes.

 

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
Google Search artcles published since 2007
 
 

Home | Pregnancy Timeline | News Alerts |News Archive May 12, 2014

 

Classic Model of cell division producing daughter cell.

Related material: The Cell Cycle by North Eastern University & Science Technology

 






WHO Child Growth Charts

 

 

 

Resetting the clock in cell division
 
Melbourne researchers suggest overturning a 40-year-old theory on when and how cells divide.

Research by scientists at the Walter and Eliza Hall Institute shows that both phases of a cell cycle contribute to changing cell division timing — a flexible rather than fixed timing as thought for the past 40 years.

The researchers have developed a new model to predict how a population of cells divides which could impact calculations of drug interaction timing response, and even our expectation of how cancer cells grow and progress.

Their work is published in the journal Proceedings of the National Academy of Sciences.

Institute scientists Professor Phil Hodgkin, Dr Mark Dowling, Dr John Markham, Dr Andrey Kan and colleagues made the discovery while studying how B and T immune cells divide over time. Using time-lapse microscopy, the research group followed individual cells and observed each phase of the cell cycle over time as the cells divided into two new ‘daughter’ cells.


The cell cycle can be broken into two phases. In the first phase, cells grow in size and make proteins to copy their own DNA.

In the second/final stage — mitosis — the DNA is copied and the cell splits in half, creating a "daughter" cell.

Since 1973, scientists have predicted cell division based on the length of both phases of the cell cycle, but not on how long each phase may last.

Dr Markham and colleagues have found the time for each phase of cell division varies from cell to cell.


“The old model of cell cycle times didn’t fit our observations, so we developed a new model. Imagine the cell cycle as an elastic band, representing the time a cell takes to divide. Each phase of the cell cycle is in a fixed place on the elastic band, but the band itself can stretch or shrink, effectively elongating or shortening the time taken for each phase of the cycle.”


Professor Hodgkin believes the new model is not only a better fit for how cells divide, it also gives clues as to why there is so much variability in cell cycle times within the same cell type.

Professor Hodgkin: “The old model assumed the second phase of cell division took a fixed amount of time, with all the variability coming from the first phase. It used a concept called ‘transition probability’ to predict how a population of cells may behave, which couldn’t be applied to individual cells.

“Our study revealed that when a cell divides, its two ‘daughter’ cells share the same division time as each other, but this time is different from their ‘parent’. From this we can conclude that cell division times are programmed by the parent cell when preparing to divide, but that time is not carried across generations. While we don’t yet understand exactly how it is set, this internal timing mechanism has replaced the external ‘transition probability’ used in the old model.”

Although the study provides a better understanding of fundamental science, there are practical applications, for example in investigating how immune cells responded to infection.

Professor Hodgkin: “Our model will allow researchers to take fewer, simpler measurements to complete the picture of how B cells and T cells have divided. However more work is still needed to determine whether these mechanisms are the same in other types of cells in the body, such as cancer cells.”

Significance
Cell division is essential for an effective immune response. Estimates of rates of division are often based on DNA measurements interpreted with an appropriate model for internal cell cycle steps. Here we use time-lapse microscopy and single cell tracking of T and B lymphocytes from reporter mice to measure times spent in cell cycle phases. These data led us to a stretched cell cycle model, a novel and improved mathematical description of cell cycle progression for proliferating lymphocytes. Our model can be used to deduce cell cycle parameters for lymphocytes from DNA and BrdU labeling and will be useful when comparing the effects of different stimuli, or therapeutic treatments on immune responses, or to understand molecular pathways controlling cell division.

Abstract
Stochastic variation in cell cycle time is a consistent feature of otherwise similar cells within a growing population. Classic studies concluded that the bulk of the variation occurs in the G1 phase, and many mathematical models assume a constant time for traversing the S/G2/M phases. By direct observation of transgenic fluorescent fusion proteins that report the onset of S phase, we establish that dividing B and T lymphocytes spend a near-fixed proportion of total division time in S/G2/M phases, and this proportion is correlated between sibling cells. This result is inconsistent with models that assume independent times for consecutive phases. Instead, we propose a stretching model for dividing lymphocytes where all parts of the cell cycle are proportional to total division time. Data fitting based on a stretched cell cycle model can significantly improve estimates of cell cycle parameters drawn from DNA labeling data used to monitor immune cell dynamics.

The research was funded by the Australian National Health and Medical Research Council, Australian Research Council and the Victorian Government.


Return to top of page