LAWRENCE PUBLIC SCHOOLS
and HEWLETT-WOODMERE SEPTA
are hosting a workshop on…
“Bringing the Birds and the Bees Down to Earth: Sexuality Education for Children and Adults with Autism Spectrum and Related Disabilities”
Presenter : Lisa Mitchell. LCSW, CODY CENTER
This workshop is for parents, caregivers and professionals. Lisa Mitchell will focus on puberty, relationships, abuse prevention, promotion of appropriate behavior and teaching communication about sexuality.
Date: Wednesday, March 4, 2009
Time: 7:30 – 9:00 PM
Location: Lawrence Middle School
**To RSVP by phone, please contact Rosanne Bogard (516) 812-7505 or
Michelle Kinhackl (516) 374-4662
Please mail RSVP form to: Rosanne Bogard – Lawrence Middle School
Pupil Personnel Services
195 Broadway
Lawrence, NY 11559
Parent’s name: ______________________________________________________________
Student’s name:_____________________________________________________________
School: ___________________________________________________________________
Home Address: _____________________________________________________________
Phone: _____________________ Email:__________________________________________
Tuesday, February 24, 2009
Thursday, February 12, 2009
FW: Multiple Genes Implicated In Autism; Discovery Could Lead To Drugs Targeting Gene Interactions
http://www.sciencedaily.com/releases/2009/02/090209205049.htm
Multiple Genes Implicated In Autism; Discovery Could Lead To Drugs Targeting Gene Interactions
ScienceDaily (Feb. 10, 2009) — By pinpointing two genes that cause autism-like symptoms in mice, researchers at MIT's Picower Institute for Learning and Memory have shown for the first time that multiple, interacting genet ic risk factors may influence the severity of autistic symptoms.
The study, reported in the Feb. 9 advance online edition of the Proceedings of the National Academy of Sciences (PNAS), lends support to researchers' long-suspected belief that in individuals whose autism is genetic in origin, more than one gene is implicated.
The work could lead to drugs targeting signaling mechanisms between the two interacting genes responsible for some autism spectrum disorders (ASDs) symptoms. The molecular intersection of the two genes' pathways in the brain may also serve as a diagnostic target or biomarker for a subset of individuals with ASDs.
"We found that two genetic risk factors for ASDs act cooperatively in mice to influence brain size and social behavior, both of which are altered in ASDs," said Damon T. Page, a Picower Institute postdoctoral fellow and lead investigator of the study.
Approximately 24 percent of humans with autism have macrocephaly — head circumference above the 98th percentile — and increased brain size. Studies in ASDs patients have shown that brain size is correlated with the severity of behavioral problems.
Individuals with ASDs show deficits in social interaction, impaired communication and repetitive behaviors. According to the Centers for Disease Control, ASDs are the second most common serious developmental disability after mental retardation.
"Our results provide evidence that the severity of autistic symptoms may be the product of variations in DNA in multiple locations in the genome," Page added.
"An important implication is that because the majority of instances of autism appear to involve multiple genes, specific gene combinations may worsen effects. New therapeutics may one day be developed that influence particular signaling mechanisms in the disorder," said Mriganka Sur, the Newton Professor of Neuroscience and head of the MIT Department of Brain and Cognitive Sciences.
Page and colleagues found that mice carrying mutations in two different candidate autism susceptibility genes have more severe symptoms than those with only a single mutation.
The researchers studied the effects on mouse brain development and behavior of mutations in the PTEN gene, which encodes the phosphatase and tensin homolog protein, and the serotonin transporter gene.
Double whammy of symptoms
The researchers found that mice with a mutation in PTEN alone or in the serotonin transporter gene alone had brains that were larger than normal, while mice with simultaneous mutations in PTEN and serotonin transporter genes had even larger brains.
In female mice, a mutation in PTEN impaired sociability, while those that also had a mutation in serotonin transporter had worse symptoms.
The authors concluded that interaction between the two genes influences brain growth and sociability in mice, noting that mutations in serotonin transporter may be one of multiple risk factors that could modify the severity of autistic symptoms in individuals who previously developed mutations in PTEN. Future work will be aimed at characterizing how genetic, environmental and pharmacological manipulations impact these animals' autism-related traits.
This work was supported by the Nancy Lurie Marks Family Foundation, the Simons Foundation and the Autism Consortium.
________________________________________
Adapted from materials provided by Massachusetts Institute of Technology. Original article written=2 0by Deborah Halber.
Email or share this story:
Need to cite this story in your essay, paper, or report? Use one of the following formats:
APA
MLA
Massachusetts Institute of Technology (2009, February 10). Multiple Genes Implicated In Autism; Discovery Could Lead To Drugs
Multiple Genes Implicated In Autism; Discovery Could Lead To Drugs Targeting Gene Interactions
ScienceDaily (Feb. 10, 2009) — By pinpointing two genes that cause autism-like symptoms in mice, researchers at MIT's Picower Institute for Learning and Memory have shown for the first time that multiple, interacting genet ic risk factors may influence the severity of autistic symptoms.
The study, reported in the Feb. 9 advance online edition of the Proceedings of the National Academy of Sciences (PNAS), lends support to researchers' long-suspected belief that in individuals whose autism is genetic in origin, more than one gene is implicated.
The work could lead to drugs targeting signaling mechanisms between the two interacting genes responsible for some autism spectrum disorders (ASDs) symptoms. The molecular intersection of the two genes' pathways in the brain may also serve as a diagnostic target or biomarker for a subset of individuals with ASDs.
"We found that two genetic risk factors for ASDs act cooperatively in mice to influence brain size and social behavior, both of which are altered in ASDs," said Damon T. Page, a Picower Institute postdoctoral fellow and lead investigator of the study.
Approximately 24 percent of humans with autism have macrocephaly — head circumference above the 98th percentile — and increased brain size. Studies in ASDs patients have shown that brain size is correlated with the severity of behavioral problems.
Individuals with ASDs show deficits in social interaction, impaired communication and repetitive behaviors. According to the Centers for Disease Control, ASDs are the second most common serious developmental disability after mental retardation.
"Our results provide evidence that the severity of autistic symptoms may be the product of variations in DNA in multiple locations in the genome," Page added.
"An important implication is that because the majority of instances of autism appear to involve multiple genes, specific gene combinations may worsen effects. New therapeutics may one day be developed that influence particular signaling mechanisms in the disorder," said Mriganka Sur, the Newton Professor of Neuroscience and head of the MIT Department of Brain and Cognitive Sciences.
Page and colleagues found that mice carrying mutations in two different candidate autism susceptibility genes have more severe symptoms than those with only a single mutation.
The researchers studied the effects on mouse brain development and behavior of mutations in the PTEN gene, which encodes the phosphatase and tensin homolog protein, and the serotonin transporter gene.
Double whammy of symptoms
The researchers found that mice with a mutation in PTEN alone or in the serotonin transporter gene alone had brains that were larger than normal, while mice with simultaneous mutations in PTEN and serotonin transporter genes had even larger brains.
In female mice, a mutation in PTEN impaired sociability, while those that also had a mutation in serotonin transporter had worse symptoms.
The authors concluded that interaction between the two genes influences brain growth and sociability in mice, noting that mutations in serotonin transporter may be one of multiple risk factors that could modify the severity of autistic symptoms in individuals who previously developed mutations in PTEN. Future work will be aimed at characterizing how genetic, environmental and pharmacological manipulations impact these animals' autism-related traits.
This work was supported by the Nancy Lurie Marks Family Foundation, the Simons Foundation and the Autism Consortium.
________________________________________
Adapted from materials provided by Massachusetts Institute of Technology. Original article written=2 0by Deborah Halber.
Email or share this story:
Need to cite this story in your essay, paper, or report? Use one of the following formats:
APA
MLA
Massachusetts Institute of Technology (2009, February 10). Multiple Genes Implicated In Autism; Discovery Could Lead To Drugs
Dine at Off the Grill and Support Kulanu
Off the Grill in collaboration with Kulanu,
is excited to announce an opportunity for a truly
rewarding and satisfying meal.
Come in and dine from February 23-28 and 10% of
your bill will go to Kulanu
Enjoy a meal with your family knowing that you’re
helping others in need
600 Central Ave
Cedarhurst, NY 11516
(516) 569-4140
is excited to announce an opportunity for a truly
rewarding and satisfying meal.
Come in and dine from February 23-28 and 10% of
your bill will go to Kulanu
Enjoy a meal with your family knowing that you’re
helping others in need
600 Central Ave
Cedarhurst, NY 11516
(516) 569-4140
P.A.R.C. , Keren Eliana Parent Advocacy & Resource Center presents -- 2e The Paradox of the Gifted and Learning Disabled Student
On Tuesday, February 24th at 7:30 pm Kulanu’s PARC Coordinator, Melissa Sornik, LMSW will present a workshop on reaching and teaching the “twice exceptional” (2e) student.
The guidelines of No Child Left Behind leave little room for the divergent learning styles of some of our most gifted students. Among those are 2e students; those who possess superior strengths and abilities combined with areas of deficit. They can be among the most challenging students, both academically and behaviorally. As a result, these high potential students remain largely unidentified and underserved, and are at risk of failure.
This workshop is designed for parents, educators and related service providers. It will present a view of the Twice Exceptional (2e) student through a positive lens, promoting a shift in focus from disability to ability.
Key strategies and accommodations will be presented to help uniquely gifted learners reach their potential.
Melissa Sornik is the co-founder and past president of TECA, Long Island Twice Exceptional Children’s Advocacy.
This workshop is free and will be held at Temple Beth El -- 46 Locust Avenue, Cedarhurst
Space is limited. RSVP by Thursday, February 19th by phone at (516) 569-3083, or by e-mail to melissa@kulanukids.org.
The guidelines of No Child Left Behind leave little room for the divergent learning styles of some of our most gifted students. Among those are 2e students; those who possess superior strengths and abilities combined with areas of deficit. They can be among the most challenging students, both academically and behaviorally. As a result, these high potential students remain largely unidentified and underserved, and are at risk of failure.
This workshop is designed for parents, educators and related service providers. It will present a view of the Twice Exceptional (2e) student through a positive lens, promoting a shift in focus from disability to ability.
Key strategies and accommodations will be presented to help uniquely gifted learners reach their potential.
Melissa Sornik is the co-founder and past president of TECA, Long Island Twice Exceptional Children’s Advocacy.
This workshop is free and will be held at Temple Beth El -- 46 Locust Avenue, Cedarhurst
Space is limited. RSVP by Thursday, February 19th by phone at (516) 569-3083, or by e-mail to melissa@kulanukids.org.
Thursday, February 5, 2009
NIDA STUDY SHOWS THAT METHYLPHENIDATE (RITALIN) CAUSES NEURONAL CHANGES IN BRAIN REWARD AREAS
-----Original Message-----
From: NIH news releases and news items [mailto:NIHPRESS@LIST.NIH.GOV] On Behalf Of NIH OLIB (NIH/OD)
Sent: Tuesday, February 03, 2009 9:21 AM
To: NIHPRESS@LIST.NIH.GOV
Subject: NIDA STUDY SHOWS THAT METHYLPHENIDATE (RITALIN) CAUSES NEURONAL CHANGES IN BRAIN REWARD AREAS
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute on Drug Abuse (NIDA)
Embargoed for Release: Monday, February 2, 2009, 5:00 p.m. EST
CONTACT: Stephanie Older, 301-443-6245,
NIDA STUDY SHOWS THAT METHYLPHENIDATE (RITALIN) CAUSES NEURONAL CHANGES IN BRAIN REWARD AREAS
Similarities and Differences Compared to Cocaine were Found
Investigators funded by the National Institute on Drug Abuse have shown that the medication methylphenidate (Ritalin), which is commonly prescribed to treat attention-deficit hyperactivity disorder (ADHD), can cause physical changes in neurons in reward regions of mouse brains-in some cases, these effects overlapped with those of cocaine. Both methylphenidate and cocaine are in the class of drugs known as psychostimulants. While methylphenidate is widely prescribed, this study highlights the need for more research into its long-term effects on the brain. These research findings will be published Feb. 3 in Proceedings of the National Academy of Sciences.
"Studies to date suggest that prescribed use of methylphenidate in patients with ADHD does not increase their risk for subsequent addiction. However non-medical use of methylphenidate and other stimulant medications, can lead to addiction as well as a variety of other health consequences," said NIDA Director Dr. Nora Volkow. "This study highlights the fact that we know very little about how methylphenidate affects the structure of and communication between brain cells."
The researchers exposed mice to two weeks of daily injections of cocaine or methylphenidate, after which reward areas of the brain were examined for changes in dendritic spine formation -- related to the formation of synapses and the communication between nerve cells; and the expression of a protein (delta Fos B) which has been implicated in the long term actions of addictive drugs. Both drugs increased dendritic spine formation, and the expression of delta Fos B; however the precise pattern of their effects was distinct. It differed in the types of spines affected, the cells that were affected, and the brain regions. In some cases there was overlap between the two drugs, and in some cases, methylphenidate produced greater effects than cocaine -- for example, on protein expression in certain regions.
"Methylphenidate, which is thought to be a fairly innocuous compound, can have structural and biochemical effects in some regions of the brain that can be even greater than those of cocaine," stated Dr.Yong Kim, lead author of the study. "Further studies are needed to determine the behavioral implications of these changes and to understand the mechanisms by which these drugs affect synapse formation" he added.
Previous studies, including two reported by NIDA on April 1, 2008 (NIH Research Suggests Stimulant Treatment for ADHD Does Not Contribute to Substance Abuse Later in Life) have shown that children treated with stimulants for ADHD early in life have no greater risk of drug addiction as adults.
The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports most of the world's research on the health aspects of drug abuse and addiction. The Institute carries out a large variety of programs to inform policy and improve practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA home page at. To order publications in English or Spanish, call NIDA's new DrugPubs research dissemination center at 1-877-NIDA-NIH or 240-645-0228 (TDD) or fax or email requests to 240-645-0227 or .
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit;.
From: NIH news releases and news items [mailto:NIHPRESS@LIST.NIH.GOV] On Behalf Of NIH OLIB (NIH/OD)
Sent: Tuesday, February 03, 2009 9:21 AM
To: NIHPRESS@LIST.NIH.GOV
Subject: NIDA STUDY SHOWS THAT METHYLPHENIDATE (RITALIN) CAUSES NEURONAL CHANGES IN BRAIN REWARD AREAS
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute on Drug Abuse (NIDA)
Embargoed for Release: Monday, February 2, 2009, 5:00 p.m. EST
CONTACT: Stephanie Older, 301-443-6245,
NIDA STUDY SHOWS THAT METHYLPHENIDATE (RITALIN) CAUSES NEURONAL CHANGES IN BRAIN REWARD AREAS
Similarities and Differences Compared to Cocaine were Found
Investigators funded by the National Institute on Drug Abuse have shown that the medication methylphenidate (Ritalin), which is commonly prescribed to treat attention-deficit hyperactivity disorder (ADHD), can cause physical changes in neurons in reward regions of mouse brains-in some cases, these effects overlapped with those of cocaine. Both methylphenidate and cocaine are in the class of drugs known as psychostimulants. While methylphenidate is widely prescribed, this study highlights the need for more research into its long-term effects on the brain. These research findings will be published Feb. 3 in Proceedings of the National Academy of Sciences.
"Studies to date suggest that prescribed use of methylphenidate in patients with ADHD does not increase their risk for subsequent addiction. However non-medical use of methylphenidate and other stimulant medications, can lead to addiction as well as a variety of other health consequences," said NIDA Director Dr. Nora Volkow. "This study highlights the fact that we know very little about how methylphenidate affects the structure of and communication between brain cells."
The researchers exposed mice to two weeks of daily injections of cocaine or methylphenidate, after which reward areas of the brain were examined for changes in dendritic spine formation -- related to the formation of synapses and the communication between nerve cells; and the expression of a protein (delta Fos B) which has been implicated in the long term actions of addictive drugs. Both drugs increased dendritic spine formation, and the expression of delta Fos B; however the precise pattern of their effects was distinct. It differed in the types of spines affected, the cells that were affected, and the brain regions. In some cases there was overlap between the two drugs, and in some cases, methylphenidate produced greater effects than cocaine -- for example, on protein expression in certain regions.
"Methylphenidate, which is thought to be a fairly innocuous compound, can have structural and biochemical effects in some regions of the brain that can be even greater than those of cocaine," stated Dr.Yong Kim, lead author of the study. "Further studies are needed to determine the behavioral implications of these changes and to understand the mechanisms by which these drugs affect synapse formation" he added.
Previous studies, including two reported by NIDA on April 1, 2008 (NIH Research Suggests Stimulant Treatment for ADHD Does Not Contribute to Substance Abuse Later in Life) have shown that children treated with stimulants for ADHD early in life have no greater risk of drug addiction as adults.
The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports most of the world's research on the health aspects of drug abuse and addiction. The Institute carries out a large variety of programs to inform policy and improve practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA home page at
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
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