Yay division!

AX is pretty much done with multiplication. He knows double-digit multiplication. I wished that I could introduce him to division last December 2009 but so many things got in the way. Nonetheless, I taught him division in the 3rd week of January 2010. He got it fast right after I thought him using sticks to segregate in order to come up with an answer.

He was introduced by his mainstream teacher to Geography. In fact, he will have this 4th time to take the test of eastern states of the US. At the moment, he is done with 15 states and their capitals. He also takes multiplication table test every Friday.

Creeping days

It is the first day of February 2010 and I happen to visit my blog after posting a news story that I did not realize I posted. The year entered a little less on the financial side but also less in spending which is darn good. It was also a year of thinking about what will happen to us tomorrow and the coming days. January was filled with so much wishing and worrying. Yes, we should have not done it but you can not really help it. Papi is getting fed up with his work and that's it. He wants to fly this time around. I am not trying to clip his wings but I always tell him to wait a bit and when that time comes, we will surely fly anywhere with so much determination.

More Evidence That Autism Is a Brain 'Connectivity' Disorder

Source: http://www.sciencedaily.com/releases/2010/01/100110151333.htm

ScienceDaily (Jan. 11, 2010) — Studying a rare disorder known as tuberous sclerosis complex (TSC), researchers at Children's Hospital Boston add to a growing body of evidence suggesting that autism spectrum disorders, which affect 25 to 50 percent of TSC patients, result from a miswiring of connections in the developing brain, leading to improper information flow. The finding may also help explain why many people with TSC have seizures and intellectual disabilities.

Findings were published online in Nature Neuroscience on January 10.

TSC causes benign tumors throughout the body, including the brain. But patients with TSC may have autism, epilepsy or intellectual disabilities even in the absence of these growths. Now, researchers led by Mustafa Sahin, MD, PhD, of Children's Department of Neurology, provide evidence that mutations in one of the TSC's causative genes, known as TSC2, prevent growing nerve fibers (axons) from finding their proper destinations in the developing brain.

Studying a well-characterized axon route -- between the eye's retina and the visual area of the brain -- Sahin and colleagues showed that when mouse neurons were deficient in TSC2, their axons failed to land in the right places. Further investigation showed that the axons' tips, known as "growth cones," did not respond to navigation cues from a group of molecules called ephrins. "Normally ephrins cause growth cones to collapse in neurons, but in tuberous sclerosis the axons don't heed these repulsive cues, so keep growing," says Sahin, the study's senior investigator.

Additional experiments indicated that the loss of responsiveness to ephrin signals resulted from activation of a molecular pathway called mTOR, whose activity increased when neurons were deficient in TSC2. Axon tracing in the mice showed that many axons originating in the retina were not mapping to the expected part of the brain.

Although the study looked only at retinal connections to the brain, the researchers believe their findings may have general relevance for the organization of the developing brain. Scientists speculate that in autism, wiring may be abnormal in the areas of the brain involved in social cognition.

"People have started to look at autism as a developmental disconnection syndrome -- there are either too many connections or too few connections between different parts of the brain," says Sahin. "In the mouse models, we're seeing an exuberance of connections, consistent with the idea that autism may involve a sensory overload, and/or a lack of filtering of information."

Sahin hopes that the brain's miswiring can be corrected by drugs targeting the molecular pathways that cause it. The mTOR pathway is emerging as central to various kinds of axon abnormalities, and drugs inhibiting mTOR has already been approved by the FDA. For example, one mTOR inhibitor, rapamycin, is currently used mainly to prevent organ rejection in transplant patients, and Sahin plans to launch a clinical trial of a rapamycin-like drug in approximately 50 patients with TSC later this year, to see if the drug improves neurocognition, autism and seizures.

In 2008, Sahin and colleagues published related research in Genes & Development showing that when TSC1 and TSC2 are inactivated, brain cells grow more than one axon -- an abnormal configuration that exacerbates abnormal brain connectivity. The mTOR pathway was, again, shown to be involved, and when it was inhibited with rapamycin, neurons grew normally, sprouting just one axon.

Supporting the mouse data, a study by Sahin and his colleague Simon Warfield, PhD, in the Computational Radiology Laboratory at Children's, examined the brains of 10 patients with TSC, 7 of whom also had autism or developmental delay, and 6 unaffected controls. Using an advanced kind of MRI imaging called diffusion tensor imaging, they documented disorganized and structurally abnormal tracts of axons in the TSC group, particularly in the visual and social cognition areas of the brain (see image). The axons also were poorly myelinated -- their fatty coating, which helps axons conduct electrical signals, was compromised. (In other studies, done in collaboration with David Kwiatkowski at Brigham and Women's Hospital, giving rapamycin normalized myelination in mice.)

Sahin has also been studying additional genes previously found to be deleted or duplicated in patients with autism, and finding that deletion of some of them causes neurons to produce multiple axons -- an abnormality that, again, appears to be reversed with rapamycin.

"Many of the genes implicated in autism may possibly converge on a few common pathways controlling the wiring of nerve cells," says Sahin. "Rare genetic disorders like TSC are providing us with vital clues about brain mechanisms leading to autism spectrum disorders. Understanding the neurobiology of these disorders is likely to lead to new treatment options not only for TSC patients, but also for patients with other neurodevelopmental diseases caused by defective myelination and connectivity, such as autism, epilepsy and intellectual disability."

The current study was funded by grants from the National Institutes of Health, the John Merck Scholars Fund, Tuberous Sclerosis Alliance, the Manton Foundation, the Children's Hospital Boston Translational Research Program, and the Children's Hospital Boston Mental Retardation and Developmental Disabilities Research Center.

Duyu Nie was first author on the paper. Coauthors were Duyu Nie, Alessia Di Nardo, Juliette M Han, Hasani Baharanyi, Ioannis Kramvis, and ThanhThao Huynh, all of the F.M. Kirby Neurobiology Center and Department of Neurology, Children's Hospital Boston; Sandra Dabora of Brigham and Women's Hospital; Simone Codeluppi and Elena B Pasquale of the Burnham Institute for Medical Research, and University of California San Diego; and Pier Paolo Pandolfi of Beth Israel Deaconess Cancer Center.

Story Source:

Adapted from materials provided by Children's Hospital Boston, via EurekAlert!, a service of AAAS.

---

Journal Reference:

1. Duyu Nie et al. Tsc2-Rheb signaling regulates EphA-mediated axon guidance. Nature Neuroscience, January 10, 2010

Need to cite this story in your essay, paper, or report? Use one of the following formats:

APA

MLA

Children's Hospital Boston (2010, January 11). More evidence that autism is a brain 'connectivity' disorder. ScienceDaily. Retrieved January 12, 2010, from http://www.sciencedaily.com­ /releases/2010/01/100110151333.htm

Note: If no author is given, the source is cited instead.

Source: http://www.sciencedaily.com/releases/2006/10/061023192716.htm

New Imaging Technique Discovers Differences In Brains Of People With Autism

ScienceDaily (Oct. 24, 2006) — Using a new form of brain imaging known as diffusion tensor imaging (DTI), researchers in the Center for Cognitive Brain Imaging at Carnegie Mellon University have discovered that the so-called white matter in the brains of people with autism has lower structural integrity than in the brains of normal individuals. This provides further evidence that the anatomical differences characterizing the brains of people with autism are related to the way those brains process information.

The results of this latest study were published in the journal NeuroReport. The scientists used DTI — which tracks the movement of water through brain tissue — to measure the structural integrity of the white matter that acts as cables to wire the parts of the brain together. Normally, water molecules move, or diffuse, in a direction parallel to the orientation of the nerve fibers of the white matter. They're aided by the coherent structure of the fibers and a process called myelination, in which a sheath is formed around the fibers that speeds nerve impulses. The movement of water is more dispersed if the structural integrity of the tissue is low — i.e., if the fibers are less dense, less coherently organized, or less myelinated — as it was with the participants with autism in the Carnegie Mellon study. Researchers found this dispersed pattern particularly in areas in and around the corpus callosum, the large band of nerve fibers that connects the two hemispheres of the brain.

"These reductions in white matter integrity may underlie the behavioral pattern observed in autism of narrowly focused thought and weak coherence of different streams of thought," said Marcel Just, director of the Center for Cognitive Brain Imaging and a co-author of the latest study. "The new findings also provide supporting evidence for a new theory of autism that attributes the disorder to underconnectivity among brain regions," Just said.

In 2004, Just and his colleagues proposed the underconnectivity theory based on a groundbreaking study in which they discovered abnormalities in the white matter that suggested a lack of coordination among brain areas in people with autism. This theory helps explain a paradox of autism: Some people with autism have normal or even superior skills in some areas, while many other types of thinking are disordered.

Last summer, Just led a team of researchers that found for the first time that the abnormality in synchronization among brain areas is related to the abnormality in the white matter. They discovered that key portions of the corpus callosum seem to play a role in the limitation on synchronization. In people with autism, anatomical connectivity — based on the size of the white matter — was found to be positively correlated with functional connectivity, which is the synchronization of the active brain regions. They also found that the functional connectivity was lower in those participants in whom the autism was more severe.

These studies, along with the latest paper, are providing a comprehensive picture of the autistic brain, whose components operate with less coordination than is normally the case, and which is less reliant on frontal components and more reliant on posterior components. The latest DTI finding shows that some of the frontal-posterior communication fiber tracts are abnormal, consistent with the lower degree of frontal-posterior coordination.

"The brain components in autism function more like a jam session and less like a symphony," Just said.

The latest study was co-authored by Rajesh K. Kana and Timothy A. Keller of the Center for Cognitive Brain Imaging. This research was supported by the National Institute of Child Health and Human Development.

Story Source:

Adapted from materials provided by Carnegie Mellon University.

---

Need to cite this story in your essay, paper, or report? Use one of the following formats:

APA

MLA

Carnegie Mellon University (2006, October 24). New Imaging Technique Discovers Differences In Brains Of People With Autism. ScienceDaily. Retrieved January 12, 2010, from http://www.sciencedaily.com­ /releases/2006/10/061023192716.htm

Note: If no author is given, the source is cited instead.

Repost from Source: Scientific Link to Autism Identified

The article below seems interesting.

Source: http://www.prnewswire.com/news-releases/scientific-link-to-autism-identified-70354482.html

Scientific Link to Autism Identified

JACKSON, N.J., Nov. 18 /PRNewswire/ -- During its research into the application of neuroscience in business, a New Jersey based think tank, The Center for Modeling Optimal Outcomes®, LLC (The Center) made an inadvertent and amazing discovery.

The Center examined the neuroscientific dynamics of logic and emotion in decision making while researching neuroscience in business. They found unique corollary relationships between various brain chemicals (neurohormones, neurotransmitters, etc.). This apparent pattern led to a new path of research for the team outside of business. By looking at extensive scientific literature they discovered a cascade of hormones that emanate from the brain (hypothalamus). This same pattern of correlations was again apparent throughout the cascade. The group added a research biologist and started to test the pattern on genes (proteins). It remained consistent. The Center then called upon advisors from chemistry and physics to see if the pattern would apply in physical sciences.

To the amazement of the group, it became apparent that this pattern of corollary relationships could be applied to scientific processes for maintaining equilibrium (homeostatic relationships) throughout all of science; from subatomic particles to chemistry as well as between biological substances.

While the entire scientific community knows that homeostasis exists, this tacit knowledge has not been converted into a step-by-step, replicable model. The Center identified precisely such an explicit process.

Challenged by several of The Center's advisors, members of the team decided to test the efficacy of the model to determine if the disruptions that cause autism could be identified.

After careful review of countless scientific studies, meeting with several renowned scientists to discuss their findings, and then applying the modeling process to numerous hypotheses, The Center's Life Sciences group was able to formulate a scientifically verifiable model for the highly probable causal path of autism. Through the application of their model, it became apparent that autism is an outcome of several variables that, when the homeostatic relationship of each one is disrupted, a "perfect storm" scenario results in autism. The application of the model identified several of the variables that account for why boys have a 4 to 1 ratio of instances over girls as well as why not every boy is affected.

While the scientific community will have to validate The Center's findings, the model for assessing homeostatic relationships indicates the "trigger" behind autism is an imbalance between a pair of amino acid neurotransmitters; glutamate and glycine.

According to The Center's founder, William McFaul, a retired business person and not a member of the scientific community, "Because of its universal applicability, our Life Sciences group has already used the model as a tool to identify highly probable causal paths for several illnesses and disease entities. Autism was one of most difficult illnesses The Center had attempted to analyze. If it hadn't been for so many parents insisting that vaccines were responsible for the condition, we might never have found the fact that the stabilizer in MMR and a few other vaccines is hydrolyzed gelatin; a substance that is approximately 21% glycine. It appears that, based on readily verifiable science, the use of that form of glycine triggers an imbalance between the amino acid neurotransmitters responsible for the absorption rate of certain classes of cells throughout the body. It is that wide-spread disruption that apparently results in the systemic problems that encompass the mind and the body characterized in today's 'classic' autism." He also added, "The use of our model indicates each of the disorders within Autism Spectrum Disorder (ASD) is attributable to different disruptions in homeostasis. We look forward to sharing our findings relative to each disorder with the scientific community."

According to Linda Oliver-Perrier, The Center's spokesperson for their Life Sciences group, "The details of the disruptive process are somewhat complex and not conducive for explanation in a press release. We have posted a more detailed explanation on our web site, www.TheCenterNJ.com/lifesciences.html." She added, "Undoubtedly, this finding based on the application of the model for homeostasis will cause immense controversy. Our Life Sciences group is prepared to meet with members of the scientific community to explain the model as well as the variables that create the 'perfect storm' that results in autism."

McFaul added, "The Center is seeking to affiliate with academic centers to provide its model for homeostasis to the scientific community for use as a tool to enable researchers to identify root causes of illnesses and disease entities. The Center is a think tank that creates models. We are not an operating company with the resources to educate individuals or organizations on the application of the models we create.

For more information about The Center go to its web site; www.TheCenterNJ.com or for information regarding its model for homeostasis, contact Linda Oliver-Perrier at loliverperrier@TheCenterNJ.com

SOURCE The Center for Modeling Optimal Outcomes LLC

Could it be the medication used during childbirth?

Source: http://www.prnewswire.com/news-releases/new-treatment-for-autism-holds-promise-69878372.html

New Treatment for Autism 'Holds Promise'

Brain waves normalize after treatment, EEG's reveal

Notice to Los Angeles media: Fred S. Starr, MD and Elaine DeLack holding seminar for physicians, members of the press, November 15, 2009 2:00 - 5:00 PM Members of the press may call (877) 963-3338 for reservations

SEATTLE, Nov. 12 /PRNewswire/ -- A new treatment for autism appears to normalize brain function, according to Nashville physician Fred S. Starr, MD, FAACAP, BCIA-EEG.

In addition to high serotonin levels, autistic children have a characteristically common "u" EEG pattern reflecting impaired brain function, particularly in areas of the brain responsible for social interaction, communication, speech and bonding.

However, Quantitative EEG's conducted by Dr. Starr on autistic children after three weeks on the medication Respen-A showed that the children's brain patterning changed to "normal" patterning. Starr says that behavioral improvement was also "evident". "Speech, interaction and social skills improved markedly in patients using Respen-A, and displays of frustration and anger markedly diminished," Starr said.

The theory behind the use of Respen-A was developed by private researcher Elaine DeLack, Stanwood, WA. Unlike theories that center on negative reaction to vaccinations, DeLack looked at exposure to a commonly used drug used during delivery, and at brain enzymes that affect the brain both at birth, and again as the child enters childhood.

DeLack's hypothesis (which can be viewed in slide show format at www.Neuro-Med.net) connects autism to the use of epidurals during childbirth. Epidurals were introduced into this country in the 1960's. By the mid-80's, 22 percent of women received an epidural during delivery. In the mid-90's, the number grew to 67%. Today, nearly 90% of women receive an epidural during pregnancy.

However, DeLack contends that it may not be the epidural procedure, but the drugs given in conjunction with the procedure, in combination with the drug Pitocin, that has contributed to increasing numbers in autism.

Pitocin crosses the placenta to the infant's system during childbirth. The drug requires adequate production of an enzyme found in the liver (CYP 3A4) in order to rid it from the body. If the infant has a genetic inadequacy of the CYP 3A4 enzyme (found more often to be lacking statistically in boys than girls), the drug's intensity could become elevated in the infant's system, and build with another naturally occurring neurotransmitter that plays a key role in brain development: the hormone Oxytocin.

Oxytocin builds naturally in the brain during the first 7 - 10 days of life, ensuring that nerve patterning develops as it should in the brain. Once Oxytocin levels reach a naturally predetermined level, the development of the brain's nerve system (HNS system) ceases.

DeLack theorizes that the addition of Pitocin into the bloodstream of infants without adequate CYP 3A4 genetic enzymes, causes brain development to "shut off" early, stunting crucial neuro-development.

DeLack hypothesizes that a second enzyme may explain why autism shows up in many children around the age of three. The enzyme MAO-A is essential in regulating serotonin levels in the brain. In the first years of life, MAO-A levels remain high, assisting brain function. The impact of MAO-A may, in fact, cover symptoms of brain impairment in infants and toddlers.

MAO-A levels diminish as the child ages - allowing serotonin levels to rise, impacting the areas of the brain associated with communication, speech, emotion and bonding. Respen-A curbs the level of serotonin in the autistic brain.

"We see promise in all of this," DeLack says. "Further study will determine if simple modification during childbirth could be all that is needed to stem the surging tide of autism," states DeLack. And for those who have autism? "Respen-A could give them a quality of life that they - and their parents - deserve."

Prescriptions for Respen-A require a daily calcium supplement. For further information about Respen-A, go to www.neuro-med.net

REPORTERS ARE WELCOME TO ATTEND SUNDAY'S SEMINAR AT PREECE AND TOFF SALON AT FRED SEGAL, 420 BROADWAY, SANTA MONICA, CALIFORNIA. TO RESERVE SPACE, CALL 877-963-3338.

Dr. Fred S. Starr may be reached at doc@5starrpsych.com

Elaine DeLack may be reached at elaine@edmsllc.com

SOURCE Neuro-Med.net

FOXP2 - Hope we are nearing the answers to speech and language!

Source: http://www.chinadaily.com.cn/world/2009-11/12/content_8953997.htm

WASHINGTON: Chimps, our nearest relatives, don't talk. We do. Now scientists have pinpointed a mutation in a gene that might help explain the difference.

The mutation seems to have helped humans develop speech and language. It's probably not the only gene involved, but researchers found the gene looks and acts differently in chimps and humans, according to a study published online yesterday by the journal Nature.

Lab tests showed that the human version regulated more than 100 other genes differently from the chimp version. This particular gene - called FOXP2 - mutated around the time humans developed the ability to talk.

"It's really playing a major role in chimp-human differences," said the study's author, Daniel Geschwind, a professor of neurology, psychiatry and human genetics at the University of California, Los Angeles. "You mutate this gene in humans and you get a speech and language disorder." This tells you "what may be happening in the brain," he said.

Frances Vargha-Khadem, head of developmental cognitive neuroscience at the University College London, who wasn't part of the research, said the study "is very much in line with what we had always suspected."

Vargha-Khadem has studied people with other inherited mutations in the gene and their speech and language problems. People with a certain mutation have subtle physical differences in the lower part of the jaw, the tongue and roof of the mouth, and she suspects chimps do, too. That physical part is important because "you can't produce the dance unless you have the feet to do the dance," she said.

Eventually, work on this gene and others could potentially lead to genetic treatments for people with certain developmental difficulties, such as autism, Geschwind said.

AP