The process of development involves mechanisms at the molecular, cellular and tissue levels to arrive at the complex anatomical and physiological structure of an organism. The study of development can shed light into the processes of many diseases and disorders that afflict people worldwide.
Reblogged from biovisual  435 notes

biovisual:

Baby Squid Photography by Jeannot Kuenzel - Malta
All rights reserved by Jeannot Kuenzel
sharing enabled / downloading enabled
Posted on Flickr March 29 and 31, 2014

top image
EGGS of Loligo vulgaris: the European squid, a large squid belonging to the family Loliginidae.

bottom image

Two stages of the development of a [European squid] are visible in the picture. These eggs are about 3mm in diameter; when the little squid inside has used up all the nutrients (all the yolk that is attached to it), it plops its suckers to the inside of the diaphragm and releases enzymes that will aid opening the shell, pushing through the opening - and a tiny new ALIEN of the DEEP is born :]

Notice the CHROMATOPHORES already embedded in its skin and the tiny little SIPHON… BTW, the SQUID on the left is actually laying on its back…





2013 Cool Science Image Contest Winners
Beta Catenin in Prostate Cancer
Beta catenin (CTNNB1) plays an important role during prostate cancer in humans and mice. In transgenic mice, where CTNNB1 is induced in the prostate, a cluster of cells expressing high levels of beta catenin protein (red) are observed. These cells have the unique capability to alter the adjacent microenvironment by attracting other cellular layers towards it, as stained by the basal layer protein- laminin (green) and nuclei (blue). Mouse models such as this are increasingly being used to understand how CTNNB1 plays a role during normal prostate development and at the same time help to understand how these cells communicate and interact with their surrounding environment.Vatsal Mehta, staff, Comparative Biosciences Department

Wisconsin: The University of Wisconsin–Madison

2013 Cool Science Image Contest Winners

Beta Catenin in Prostate Cancer

Beta catenin (CTNNB1) plays an important role during prostate cancer in humans and mice. In transgenic mice, where CTNNB1 is induced in the prostate, a cluster of cells expressing high levels of beta catenin protein (red) are observed. These cells have the unique capability to alter the adjacent microenvironment by attracting other cellular layers towards it, as stained by the basal layer protein- laminin (green) and nuclei (blue). Mouse models such as this are increasingly being used to understand how CTNNB1 plays a role during normal prostate development and at the same time help to understand how these cells communicate and interact with their surrounding environment.

Vatsal Mehta, staff, Comparative Biosciences Department

Self-Healing Engineered Muscle Grown in the Laboratory

Duke, Pratt School of Engineering

Biomedical engineers have grown living skeletal muscle that looks a lot like the real thing. It contracts powerfully and rapidly, integrates into mice quickly, and for the first time, demonstrates the ability to heal itself both inside the laboratory and inside an animal.

The study conducted at Duke University tested the bioengineered muscle by literally watching it through a window on the back of living mouse. The novel technique allowed for real-time monitoring of the muscle’s integration and maturation inside a living, walking animal.

Both the lab-grown muscle and experimental techniques are important steps toward growing viable muscle for studying diseases and treating injuries, said Nenad Bursac, associate professor of biomedical engineering at Duke.

The results appear the week of March 31 in the Proceedings of the National Academy of Sciences Early Edition.

“The muscle we have made represents an important advance for the field,” Bursac said. “It’s the first time engineered muscle has been created that contracts as strongly as native neonatal skeletal muscle.”

Through years of perfecting their techniques, a team led by Bursac and graduate student Mark Juhas discovered that preparing better muscle requires two things—well-developed contractile muscle fibers and a pool of muscle stem cells, known as satellite cells.

Every muscle has satellite cells on reserve, ready to activate upon injury and begin the regeneration process. The key to the team’s success was successfully creating the microenvironments—called niches—where these stem cells await their call to duty.

“Simply implanting satellite cells or less-developed muscle doesn’t work as well,” said Juhas. “The well-developed muscle we made provides niches for satellite cells to live in, and, when needed, to restore the robust musculature and its function.”

To put their muscle to the test, the engineers ran it through a gauntlet of trials in the laboratory. By stimulating it with electric pulses, they measured its contractile strength, showing that it was more than 10 times stronger than any previous engineered muscles. They damaged it with a toxin found in snake venom to prove that the satellite cells could activate, multiply and successfully heal the injured muscle fibers.

Then they moved it out of a dish and into a mouse.

With the help of Greg Palmer, an assistant professor of radiation oncology in the Duke University School of Medicine, the team inserted their lab-grown muscle into a small chamber placed on the backs of live mice. The chamber was then covered by a glass panel. Every two days for two weeks, Juhas imaged the implanted muscles through the window to check on their progress.

By genetically modifying the muscle fibers to produce fluorescent flashes during calcium spikes—which cause muscle to contract— the researchers could watch the flashes become brighter as the muscle grew stronger.

“We could see and measure in real time how blood vessels grew into the implanted muscle fibers, maturing toward equaling the strength of its native counterpart,” said Juhas.

The engineers are now beginning work to see if their biomimetic muscle can be used to repair actual muscle injuries and disease.

“Can it vascularize, innervate and repair the damaged muscle’s function?” asked Bursac. “That is what we will be working on for the next several years.”

Images:

1.Long, colorful strands of engineered muscle fiber have been stained to observe growth after implantation into a mouse.

2. This series of images shows the destruction and subsequent recovery of engineered muscle fibers that had been exposed to a toxin found in snake venom. This marks the first time engineered muscle has been shown to repair itself after implantation into a living animal.

3. This series of images shows the progress of veins slowly growing into implanted engineered muscle fibers.

“Biomimetic engineered muscle with capacity for vascular integration and functional maturation in vivo.” Juhas, M., Engelmayr, Jr., G.C., Fontanella, A.N., Palmer, G.M., Bursac, N. PNAS Early Edition, March, 2014. DOI: 10.1073/pnas.1402723111

A PDF of the article is available for download for free courtesy of DukeSpace.

Very cool image from Desert Labrador Retriever Rescue on Facebook!!!
“Our newest intake Bella gave us quite the surprise – turns out she wasn’t a chunky monkey but pregnant! We are guessing there are about 9 little ones in that tummy and we’ll find out soon too as Bella is almost ready to be a mom! We thought it would be fun for our FB fans to follow these little pups as they begin their new life adventures so we plan to post updates on their birth and milestones so you can all enjoy seeing them grow like we will!”
AND you can become an approved adopter here: www.dlrrphoenix.org/adopt

Very cool image from Desert Labrador Retriever Rescue on Facebook!!!

Our newest intake Bella gave us quite the surprise – turns out she wasn’t a chunky monkey but pregnant! We are guessing there are about 9 little ones in that tummy and we’ll find out soon too as Bella is almost ready to be a mom! We thought it would be fun for our FB fans to follow these little pups as they begin their new life adventures so we plan to post updates on their birth and milestones so you can all enjoy seeing them grow like we will!”

AND you can become an approved adopter here: www.dlrrphoenix.org/adopt

Reblogged from futuristech-info  116 notes
futuristech-info:





Researchers overcome huge challenges as they have converted embryonic stem cells into a fish embryo

By Josh Barney -Scientists at the University of Virginia School of Medicine have overcome one of the greatest challenges in biology and taken a major step toward being able to grow whole organs and tissues from stem cells. By manipulating the appropriate signaling, the U.Va. researchers have turned embryonic stem cells into a fish embryo, essentially controlling embryonic development.READ MORE ON UNIVERSITY OF VIRGINIA
Reblogged from coolsciencegifs  878 notes
coolsciencegifs:

Your body contains ~50 trillion cells, each cell contains 23 pairs of chromosomes, these chromosomes are made of over 3 billion base pairs of DNA, containing 20,000 genes, coding for millions of different proteins. Phew!
If you’d like to find out more about how this genetic information relates to your breakfast, check out this video, 'How To Make A Chicken': http://youtu.be/qnOVByfyFOQ 
(via Ross Exton)

coolsciencegifs:

Your body contains ~50 trillion cells, each cell contains 23 pairs of chromosomes, these chromosomes are made of over 3 billion base pairs of DNA, containing 20,000 genes, coding for millions of different proteins. Phew!

If you’d like to find out more about how this genetic information relates to your breakfast, check out this video, 'How To Make A Chicken': http://youtu.be/qnOVByfyFOQ 

(via Ross Exton)

Erasing a genetic mutation
MIT team reverses a liver disorder in mice by correcting a mutated gene.

Using a new gene-editing system based on bacterial proteins, MIT researchers have cured mice of a rare liver disorder caused by a single genetic mutation.
The findings, described in the March 30 issue of Nature Biotechnology, offer the first evidence that this gene-editing technique, known as CRISPR, can reverse disease symptoms in living animals. CRISPR, which offers an easy way to snip out mutated DNA and replace it with the correct sequence, holds potential for treating many genetic disorders, according to the research team.
“What’s exciting about this approach is that we can actually correct a defective gene in a living adult animal,” says Daniel Anderson, the Samuel A. Goldblith Associate Professor of Chemical Engineering at MIT, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the paper.
Read more from MIT News

Erasing a genetic mutation

MIT team reverses a liver disorder in mice by correcting a mutated gene.

Using a new gene-editing system based on bacterial proteins, MIT researchers have cured mice of a rare liver disorder caused by a single genetic mutation.

The findings, described in the March 30 issue of Nature Biotechnology, offer the first evidence that this gene-editing technique, known as CRISPR, can reverse disease symptoms in living animals. CRISPR, which offers an easy way to snip out mutated DNA and replace it with the correct sequence, holds potential for treating many genetic disorders, according to the research team.

“What’s exciting about this approach is that we can actually correct a defective gene in a living adult animal,” says Daniel Anderson, the Samuel A. Goldblith Associate Professor of Chemical Engineering at MIT, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the paper.

Read more from MIT News

Reblogged from ucsdhealthsciences  463 notes
ucsdhealthsciences:

Gulf War Illness Not in Veterans’ Heads, But in Their Mitochondria
Researchers at the UC San Diego School of Medicine have demonstrated for the first time that veterans of the 1990-91 Persian Gulf War who suffer from “Gulf War illness” have impaired function of mitochondria – the energy powerhouses of cells.
The findings, published in the March 27, 2014 issue of PLOS ONE, could help lead to new treatments benefitting affected individuals – and to new ways of protecting servicepersons (and civilians) from similar problems in the future, said principal investigator Beatrice A. Golomb MD, PhD, professor of medicine.
Golomb, with associate Hayley Koslik and Gavin Hamilton, PhD, a research scientist and magnetic resonance physicist, used the imaging technology to compare Gulf War veterans with diagnosed Gulf War illness to healthy controls. Cases were matched by age, sex and ethnicity.
The technique used – 31-phosphorus magnetic resonance spectroscopy or 31P-MRS – reveals amounts of phosphorus-containing compounds in cells. Such compounds are important for cell energy production, in particular phosphocreatine or PCr, which declines in muscle cells during exercise. PCr recovery takes longer when mitochondrial function is impaired, and delayed recovery is recognized as a robust marker of mitochondrial dysfunction.
Affected Gulf War veterans displayed significantly delayed PCr recovery after an exercise challenge. In fact, said Golomb, there was almost no overlap in the recovery times of Gulf War illness veterans compared to controls: All but one control participant had a recovery time-constant clustered under 31 seconds. In contrast, all but one Gulf Illness veteran had a recovery time-constant exceeding 35 seconds, with times ranging as high as 70 seconds.
There were 14 participants in the study: seven Gulf War illness cases and seven matching controls. Golomb notes that the use of 1:1 matching markedly improves statistical “power,” allowing a smaller sample size. The separation between the two groups was “visibly striking, and the large average difference was statistically significant,” she said.
Golomb noted that impaired mitochondrial function accounts for numerous features of Gulf War illness, including symptoms that have been viewed as perplexing or paradoxical.
“The classic presentation for mitochondrial illness involves multiple symptoms spanning many domains, similar to what we see in Gulf War illness. These classically include fatigue, cognitive and other brain-related challenges, muscle problems and exercise intolerance, with neurological and gastrointestinal problems also common.”
There are other similarities between patients with mitochondrial dysfunction and those suffering from Gulf War illness: Additional symptoms appear in smaller subsets of patients; varying patterns of symptoms and severity among individuals; different latency periods across symptoms, or times when symptoms first appear; routine blood tests that appear normal.
“Some have sought to ascribe Gulf War illness to stress,” said Golomb, “but stress has proven not to be an independent predictor of the condition. On the other hand, Gulf veterans are known to have been widely exposed to acetylcholinesterase inhibitors, a chemical class found in organophosphate and carbamate pesticides, nerve gas and nerve gas pre-treatment pills given to troops.
“These inhibitors have known mitochondrial toxicity and generally show the strongest and most consistent relationship to predicting Gulf War illness. Mitochondrial problems account for which exposures relate to Gulf War illness, which symptoms predominate, how Gulf War illness symptoms manifest themselves, what objective tests have been altered, and why routine blood tests have not been useful.”
Pictured: mitochondria, false colored.

ucsdhealthsciences:

Gulf War Illness Not in Veterans’ Heads, But in Their Mitochondria

Researchers at the UC San Diego School of Medicine have demonstrated for the first time that veterans of the 1990-91 Persian Gulf War who suffer from “Gulf War illness” have impaired function of mitochondria – the energy powerhouses of cells.

The findings, published in the March 27, 2014 issue of PLOS ONE, could help lead to new treatments benefitting affected individuals – and to new ways of protecting servicepersons (and civilians) from similar problems in the future, said principal investigator Beatrice A. Golomb MD, PhD, professor of medicine.

Golomb, with associate Hayley Koslik and Gavin Hamilton, PhD, a research scientist and magnetic resonance physicist, used the imaging technology to compare Gulf War veterans with diagnosed Gulf War illness to healthy controls. Cases were matched by age, sex and ethnicity.

The technique used – 31-phosphorus magnetic resonance spectroscopy or 31P-MRS – reveals amounts of phosphorus-containing compounds in cells. Such compounds are important for cell energy production, in particular phosphocreatine or PCr, which declines in muscle cells during exercise. PCr recovery takes longer when mitochondrial function is impaired, and delayed recovery is recognized as a robust marker of mitochondrial dysfunction.

Affected Gulf War veterans displayed significantly delayed PCr recovery after an exercise challenge. In fact, said Golomb, there was almost no overlap in the recovery times of Gulf War illness veterans compared to controls: All but one control participant had a recovery time-constant clustered under 31 seconds. In contrast, all but one Gulf Illness veteran had a recovery time-constant exceeding 35 seconds, with times ranging as high as 70 seconds.

There were 14 participants in the study: seven Gulf War illness cases and seven matching controls. Golomb notes that the use of 1:1 matching markedly improves statistical “power,” allowing a smaller sample size. The separation between the two groups was “visibly striking, and the large average difference was statistically significant,” she said.

Golomb noted that impaired mitochondrial function accounts for numerous features of Gulf War illness, including symptoms that have been viewed as perplexing or paradoxical.

“The classic presentation for mitochondrial illness involves multiple symptoms spanning many domains, similar to what we see in Gulf War illness. These classically include fatigue, cognitive and other brain-related challenges, muscle problems and exercise intolerance, with neurological and gastrointestinal problems also common.”

There are other similarities between patients with mitochondrial dysfunction and those suffering from Gulf War illness: Additional symptoms appear in smaller subsets of patients; varying patterns of symptoms and severity among individuals; different latency periods across symptoms, or times when symptoms first appear; routine blood tests that appear normal.

“Some have sought to ascribe Gulf War illness to stress,” said Golomb, “but stress has proven not to be an independent predictor of the condition. On the other hand, Gulf veterans are known to have been widely exposed to acetylcholinesterase inhibitors, a chemical class found in organophosphate and carbamate pesticides, nerve gas and nerve gas pre-treatment pills given to troops.

“These inhibitors have known mitochondrial toxicity and generally show the strongest and most consistent relationship to predicting Gulf War illness. Mitochondrial problems account for which exposures relate to Gulf War illness, which symptoms predominate, how Gulf War illness symptoms manifest themselves, what objective tests have been altered, and why routine blood tests have not been useful.”

Pictured: mitochondria, false colored.