pubhealth:

Growing Number of Chemicals Linked to Brain Disorders in Children
A new study finds that toxic chemicals may be triggering the recent increases in neurodevelopmental disabilities among children, including autism, attention-deficit hyperactivity disorder, and dyslexia.
Researchers at Harvard School of Public Health (HSPH) and Icahn School of Medicine at Mount Sinai say a new way to control the use of these substances is urgently needed.
“The greatest concern is the large numbers of children who are affected by toxic damage to brain development in the absence of a formal diagnosis,” said Philippe Grandjean, adjunct professor of environmental health at HSPH. “They suffer reduced attention span, delayed development, and poor school performance. Industrial chemicals are now emerging as likely causes.”
The new report follows up on a similar study conducted by the researchers in 2006 that identified five industrial chemicals as “developmental neurotoxicants,” or chemicals that can cause brain deficits.
The new study offers updated findings about those chemicals and adds information on six newly recognized ones, including manganese; fluoride; chlorpyrifos and DDT (pesticides); tetrachloroethylene (a solvent); and polybrominated diphenyl ethers (flame retardants).
The study outlines possible links between these newly recognized neurotoxicants and negative health effects on children.
For instance, manganese is associated with diminished intellectual function and impaired motor skills. Solvents are linked to hyperactivity and aggressive behavior, while certain types of pesticides may cause cognitive delays.
Grandjean and co-author Philip Landrigan, Dean for Global Health at Mount Sinai, postulate that many other chemicals contribute to a “silent pandemic” of neurobehavioral deficits that erodes intelligence and disrupts behaviors.
But controlling this pandemic is difficult because of a lack of data to guide prevention and the huge amount of proof needed for government regulation, according to the researchers.
“Very few chemicals have been regulated as a result of developmental neurotoxicity,” they write in the study, which was published in Lancet Neurology.
The researchers say it’s crucial to control the use of these chemicals to protect children’s brain development worldwide. They propose mandatory testing of industrial chemicals and the formation of a new international clearinghouse to evaluate industrial chemicals for potential developmental neurotoxicity.
“The problem is international in scope, and the solution must therefore also be international,” said Grandjean. “We have the methods in place to test industrial chemicals for harmful effects on children’s brain development — now is the time to make that testing mandatory.”
(From PsychCentral.com via Harvard School of Public Health)

pubhealth:

Growing Number of Chemicals Linked to Brain Disorders in Children

A new study finds that toxic chemicals may be triggering the recent increases in neurodevelopmental disabilities among children, including autism, attention-deficit hyperactivity disorder, and dyslexia.

Researchers at Harvard School of Public Health (HSPH) and Icahn School of Medicine at Mount Sinai say a new way to control the use of these substances is urgently needed.

“The greatest concern is the large numbers of children who are affected by toxic damage to brain development in the absence of a formal diagnosis,” said Philippe Grandjean, adjunct professor of environmental health at HSPH. “They suffer reduced attention span, delayed development, and poor school performance. Industrial chemicals are now emerging as likely causes.”

The new report follows up on a similar study conducted by the researchers in 2006 that identified five industrial chemicals as “developmental neurotoxicants,” or chemicals that can cause brain deficits.

The new study offers updated findings about those chemicals and adds information on six newly recognized ones, including manganese; fluoride; chlorpyrifos and DDT (pesticides); tetrachloroethylene (a solvent); and polybrominated diphenyl ethers (flame retardants).

The study outlines possible links between these newly recognized neurotoxicants and negative health effects on children.

For instance, manganese is associated with diminished intellectual function and impaired motor skills. Solvents are linked to hyperactivity and aggressive behavior, while certain types of pesticides may cause cognitive delays.

Grandjean and co-author Philip Landrigan, Dean for Global Health at Mount Sinai, postulate that many other chemicals contribute to a “silent pandemic” of neurobehavioral deficits that erodes intelligence and disrupts behaviors.

But controlling this pandemic is difficult because of a lack of data to guide prevention and the huge amount of proof needed for government regulation, according to the researchers.

“Very few chemicals have been regulated as a result of developmental neurotoxicity,” they write in the study, which was published in Lancet Neurology.

The researchers say it’s crucial to control the use of these chemicals to protect children’s brain development worldwide. They propose mandatory testing of industrial chemicals and the formation of a new international clearinghouse to evaluate industrial chemicals for potential developmental neurotoxicity.

“The problem is international in scope, and the solution must therefore also be international,” said Grandjean. “We have the methods in place to test industrial chemicals for harmful effects on children’s brain development — now is the time to make that testing mandatory.”

(From PsychCentral.com via Harvard School of Public Health)

(via kammartinez)

stufftoblowyourmind:

Cluttered Desks, Cluttered Minds and Toddler Hands: Toddlers might not seem like scientists when they mash up a banana or throws noodles at the wall, but research reveals that messy hands often indicate a hungry mind.

mymodernmet:

Coloring my kids art by Tatsputin

A dad lovingly colors in his kids’ drawings while on out-of-state business trips.

Toddler Science: Babbling Away - Epic Science

Our human larva love to babble on about nothing, but what’s actually going on inside their un-languaged minds? Find out in this Epic Science episode of Stuff to Blow Your Mind.

"Many adults are put off when youngsters pose scientific questions. Children ask why the sun is yellow, or what a dream is, or how deep you can dig a hole, or when is the world’s birthday, or why we have toes. Too many teachers and parents answer with irritation or ridicule, or quickly move on to something else. Why adults should pretend to omniscience before a five-year-old, I can’t for the life of me understand. What’s wrong with admitting that you don’t know? Children soon recognize that somehow this kind of question annoys many adults. A few more experiences like this, and another child has been lost to science. There are many better responses. If we have an idea of the answer, we could try to explain. If we don’t, we could go to the encyclopedia or the library. Or we might say to the child: “I don’t know the answer. Maybe no one knows. Maybe when you grow up, you’ll be the first to find out."

— Carl Sagan (via kenobi-wan-obi)

(via scinerds)

mothernaturenetwork:

Fasting as a family for Ramadan?Ramadan began this week, and Muslims around the world are observing the month-long holiday by fasting during the daylight hours. According to tradition, young Muslims are not required to fast until they reach the age of puberty, but that doesn’t stop many Muslim kids and tweens from wanting to join the fast with family and friends.  It’s a family decision about when kids will start to fast. Here are some great tips for those who want to help young children ease into the tradition.

mothernaturenetwork:

Fasting as a family for Ramadan?
Ramadan began this week, and Muslims around the world are observing the month-long holiday by fasting during the daylight hours. According to tradition, young Muslims are not required to fast until they reach the age of puberty, but that doesn’t stop many Muslim kids and tweens from wanting to join the fast with family and friends.
 
It’s a family decision about when kids will start to fast. Here are some great tips for those who want to help young children ease into the tradition.

howstuffworks:

Do you know a mad scientist in training? A tiny Einstein? A miniature Mendel? A chibi Marie Curie?

Kids in grades K-8 can win $10,000 towards lab equipment for their school by entering our Science Challenge. Deadline extended to May 26th! Find the details on Stuff to Blow Your Mind.

Shamelessly reblogging own post ‘cause the deadline approacheth and this weekend would be a lovely time for your kids to talk about science.

(via women-in-science)

stuffmomnevertoldyou:

stufftoblowyourmind:

torteen:

picadorbookroom:

In honor of Children’s Book Week, here’s a photo of an awesome kid.

Every kid should have this picture taken of them.

-
Go out of your way to read banned books. As if you could resist…

a) this is awesome.
b) Cristen wrote “How does banning a book work?” for HowStuffWorks in case you want to give your lit brain a present.

stuffmomnevertoldyou:

stufftoblowyourmind:

torteen:

picadorbookroom:

In honor of Children’s Book Week, here’s a photo of an awesome kid.

Every kid should have this picture taken of them.

-

Go out of your way to read banned books. As if you could resist…

a) this is awesome.

b) Cristen wrote “How does banning a book work?” for HowStuffWorks in case you want to give your lit brain a present.

(Source: unapproachableblackchicks)

ikenbot:

Dances from Around the World: Children learn to program using KIWI robots

A robotics curricular unit integrating themes of dance, music, and culture with engineering, building, and programming. A research project directed Professor Marina Umaschi Bers at the DevTech Research Group at Tufts University.

The KIWI robotics construction set is designed to work with CHERP software (Creative Hybrid Environment for Robotic Programming). CHERP is a hybrid tangible/graphical computer language designed to provide an engaging introduction to computer programming for children in both formal and informal educational settings. CHERP was designed at Tufts University by the DevTech Research Group (NSF Grant No. DRL-0735657).

(Ready For Robotics)

(Source: kenobi-wan-obi)

Do you know a mad scientist in training? A tiny Einstein? A miniature Mendel? A chibi Marie Curie?

Kids in grades K-8 can win $10,000 towards lab equipment for their school by entering our Science Challenge. Deadline extended to May 26th! Find the details on Stuff to Blow Your Mind.

neuromorphogenesis:

Rare, Lethal Childhood Disease Tracked to Specific Protein
For the first time, a defective protein that plays a specific role in degrading intermediate filaments (IF), one of three classes of filaments that form the structure of nerve cells, has been discovered by an international team of researchers. 
Presented by postdoctoral fellow Saleemulla Mahammad, PhD, at the American Society for Cell Biology Annual Meeting, the research discusses how the defective protein, gigaxonin, was first identified in children with a rare and untreatable genetic disease known as giant axonal neuropathy (GAN). 
The knowledge of gigaxonin’s specific role explains why a failure in protein degradation would lead to massive aggregations of IF in the neuronal cells of GAN children, said Mahammad, who works in the laboratory of Robert Goldman, PhD,chair of cell and molecular biology. 
Mahammad and other members of the Goldman Laboratory collaborated with Puneet Opal, MD, PhD, associate Professor in the Ken and Ruth Davee Department of Neurology and cell and molecular biology, along with researchers in the laboratory of Pascale Bomont at the INSERM neurological institute in Montpelier, France, and the laboratory of Jean-Pierre Julien at the Université Laval in Quebec, Canada. 
The GAN gene was first identified in 2000 by the Bomont Laboratory, reporting that it encoded for the protein gigaxonin. Based on sequence homology, gigaxonin is involved in the normal turnover of proteins by the well-studied ubiquitin-proteasome system. But it wasn’t clear why a failure in protein degradation would lead to massive aggregations of IF in a patient’s neuronal cells. 
Because it is not possible to study nerve cells experimentally from patients, Mahammad and collaborators instead used fibroblasts from skin biopsies of children with GAN because previous studies have revealed that other classes of IF are also altered in GAN patients. In particular, the IF vimentin expressed in fibroblasts of children with GAN also forms abnormally large aggregates. These cells can readily be obtained from skin biopsies and grown in lab cultures. 
When the researchers introduced the gigaxonin gene into both control and patient fibroblasts, the results were dramatic. In the fibroblasts cultured from GAN patients, the complex network of vimentin filaments and abnormal aggregates disappeared. The vimentin filaments in the control cells also disappeared following the overexpression of the gigaxonin protein. Boosting gigaxonin to higher levels in normal cultured nerve cells also led to a degradation of neuronal forms of IF. However, the cytoskeleton’s two other major systems, microtubules and actin filaments, were not affected by this treatment. 
These findings point to a central role for gigaxonin in regulating the normal turnover of IF proteins. When gigaxonin is defective, neurofilaments, the specific type of IF located in nerve cells, pile up to form aggregates that eventually disrupts the normal functioning of neurons in GAN. 
Gigaxonin is the first factor to be identified that plays a specific role in the degradation of several types of IF proteins, including neurofilaments, according to Mahammad. This discovery may have implications for more common types of neurodegenerative diseases that are also characterized by large accumulations of IF proteins, including Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, Charcot-Marie-Tooth disease, neuronal intermediate filament inclusion disease, and diabetic neuropathy. 
GAN is an extremely rare genetic disorder that strikes both the central and peripheral nervous systems of children. The leading GAN disease foundation, Hannah’s Hope Fund, currently knows of 31 cases worldwide, 19 in the United States alone. But its rarity doesn’t dull its severity in children. Although, there are no symptoms at birth, by age three the first signs of muscle weakness usually appear and progress slowly but steadily. With increasing difficulty in walking and coordinating hand movements, children with GAN are often wheelchair-bound by age 10. Over time, they become dependent on feeding and breathing tubes; only a few will survive into young adulthood. The pathological markers for GAN are swollen (thus “giant”) axons, filled with abnormal aggregates rich in neurofilaments. 
Image: In the fibroblasts derived from the skin biopsies of giant axonal neuropathy (GAN) patients, the vimentin intermediate filaments (green) form large abnormal aggregates (indicated by arrow). In some cases these abnormal aggregates are larger than the nucleus (blue). Presented by postdoctoral fellow Saleemulla Mahammad, PhD, at the American Society for Cell Biology Annual Meeting, new research discusses how the defective protein, gigaxonin, was first identified in children with the rare and untreatable genetic disease known as GAN.

neuromorphogenesis:

Rare, Lethal Childhood Disease Tracked to Specific Protein

For the first time, a defective protein that plays a specific role in degrading intermediate filaments (IF), one of three classes of filaments that form the structure of nerve cells, has been discovered by an international team of researchers. 

Presented by postdoctoral fellow Saleemulla Mahammad, PhD, at the American Society for Cell Biology Annual Meeting, the research discusses how the defective protein, gigaxonin, was first identified in children with a rare and untreatable genetic disease known as giant axonal neuropathy (GAN). 

The knowledge of gigaxonin’s specific role explains why a failure in protein degradation would lead to massive aggregations of IF in the neuronal cells of GAN children, said Mahammad, who works in the laboratory of Robert Goldman, PhD,chair of cell and molecular biology

Mahammad and other members of the Goldman Laboratory collaborated with Puneet Opal, MD, PhD, associate Professor in the Ken and Ruth Davee Department of Neurology and cell and molecular biology, along with researchers in the laboratory of Pascale Bomont at the INSERM neurological institute in Montpelier, France, and the laboratory of Jean-Pierre Julien at the Université Laval in Quebec, Canada. 

The GAN gene was first identified in 2000 by the Bomont Laboratory, reporting that it encoded for the protein gigaxonin. Based on sequence homology, gigaxonin is involved in the normal turnover of proteins by the well-studied ubiquitin-proteasome system. But it wasn’t clear why a failure in protein degradation would lead to massive aggregations of IF in a patient’s neuronal cells. 

Because it is not possible to study nerve cells experimentally from patients, Mahammad and collaborators instead used fibroblasts from skin biopsies of children with GAN because previous studies have revealed that other classes of IF are also altered in GAN patients. In particular, the IF vimentin expressed in fibroblasts of children with GAN also forms abnormally large aggregates. These cells can readily be obtained from skin biopsies and grown in lab cultures. 

When the researchers introduced the gigaxonin gene into both control and patient fibroblasts, the results were dramatic. In the fibroblasts cultured from GAN patients, the complex network of vimentin filaments and abnormal aggregates disappeared. The vimentin filaments in the control cells also disappeared following the overexpression of the gigaxonin protein. Boosting gigaxonin to higher levels in normal cultured nerve cells also led to a degradation of neuronal forms of IF. However, the cytoskeleton’s two other major systems, microtubules and actin filaments, were not affected by this treatment. 

These findings point to a central role for gigaxonin in regulating the normal turnover of IF proteins. When gigaxonin is defective, neurofilaments, the specific type of IF located in nerve cells, pile up to form aggregates that eventually disrupts the normal functioning of neurons in GAN. 

Gigaxonin is the first factor to be identified that plays a specific role in the degradation of several types of IF proteins, including neurofilaments, according to Mahammad. This discovery may have implications for more common types of neurodegenerative diseases that are also characterized by large accumulations of IF proteins, including Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, Charcot-Marie-Tooth disease, neuronal intermediate filament inclusion disease, and diabetic neuropathy. 

GAN is an extremely rare genetic disorder that strikes both the central and peripheral nervous systems of children. The leading GAN disease foundation, Hannah’s Hope Fund, currently knows of 31 cases worldwide, 19 in the United States alone. But its rarity doesn’t dull its severity in children. Although, there are no symptoms at birth, by age three the first signs of muscle weakness usually appear and progress slowly but steadily. With increasing difficulty in walking and coordinating hand movements, children with GAN are often wheelchair-bound by age 10. Over time, they become dependent on feeding and breathing tubes; only a few will survive into young adulthood. The pathological markers for GAN are swollen (thus “giant”) axons, filled with abnormal aggregates rich in neurofilaments. 

Image: In the fibroblasts derived from the skin biopsies of giant axonal neuropathy (GAN) patients, the vimentin intermediate filaments (green) form large abnormal aggregates (indicated by arrow). In some cases these abnormal aggregates are larger than the nucleus (blue). Presented by postdoctoral fellow Saleemulla Mahammad, PhD, at the American Society for Cell Biology Annual Meeting, new research discusses how the defective protein, gigaxonin, was first identified in children with the rare and untreatable genetic disease known as GAN.