This site is dedicated to providing teachers and homeschoolers with fun, educational games for free. If you'd like to learn more about how to use file folder games in your classroom, please check out our tutorials section. We are a Christian Homeschooling family, and file folder games have been an amazing help to our small budget for teaching supplies, so we started this website to help families.
We are a Christian Homeschooling Family living in Oregon!
We have a 7 year old daughter "Sissy", and a 5 year old son "Bubba", a 1 year old little "Monkey", and another little boy coming Christmas 2010! (He's already in the picture above!)Our homeschool is very "Art" orientated, as we believe that creativity fosters learning. Education wise, I have a Bachelors of Science in Psychology, and my husband has a Masters in Education......Which is all fine and dandy, and sounds real fancy..... But daily life with our children has been the most challenging, and rewarding "education" we've yet to receive. We're blessed to be able to spend the extra time with them, helping to steer them towards the path that God has provided for them. We're taking our homeschool one day at a time, and we haven't made any long term commitments quite yet....but we're enjoying the journey along the way! You can read more about our daily homeschool life on our personal blog here:
Clemyjontri Park features a uniqueplayground where children of all abilities can play side-by-side. It is a playground where every child is welcome.
This park is a place where children who use wheelchairs, walkers or braces, or who have sensory or developmental disabilities, can have a parallel playground experience of fun and exploration.
At Clemyjontri...
Ramps connect structures
Swings have high backs, arm rests and special safety features
Rubber ground surfaces are not-slip and allow wheelchairs to roll easily
Lowered monkey bars provide easy access
Equipment is designed to be sensory rich so all children can participate with peers
Wider openings allows easy access to play structures
Tent sails provide areas of shade in the playground and benches are located throughout the play area
The two-acre playground consists of 4 Outdoor "Rooms" surrounding a centerpiece carousel, as well as a large covered picnic area and restrooms.
The Rainbow Room:
With rainbow archway, surface with colors of the rainbow and a variety of swings
Accommodates all physical levels
Integrates sign, Braille, pictures and language
Teaches colors of the rainbow
The Schoolhouse & Maze:
With learning panels forming a maze that may be reconfigured
Focuses on educational learning games
Teaches where am I reading, maps and a globe
Teaches what time it is using time zones and clocks
Movin & Groovin Transportation Area:
Designed with transportation themed equipment such as a race track, motorcycles, planes, and trains
Stimulates imagination
Teaches balance and special skills
Mimics true roadway situations
Fitness & Fun:
Includes the largest piece of play equipment along with various jungle gym components
A wise woman knows the importance of speaking life into her man. If you love him: believe in him, encourage him & be his peace -Denzel Washington
State of grace: Oneness with God. Being open to receive his message. A state of mind. Recognizing the power of the sacraments. Letting God do his works through you.
How do we reach a state of grace? By opening our hearts. Starting with opening our hearts to God and then opening our hearts to others in our lives. "Peace be with you" really means "I wish you a state of grace".
It's not something that can be rushed or forced on someone. But it is something that someone can see in you and for you to project that sense of inner peace. It truly gives you the feeling that no matter what happens, above all, you have God. And that is enough. Even death for ourselves and for our loved ones. While it may cause some pain and suffering, God knows the plan for each of us. We have to trust in that plan.
Health concerns, financial strife, work and home stresses, the struggles we all face today...are all not a big deal if we do as God commands us to do. Pray to him. Ask for his grace.
It doesn't automatically make anything go away but with a different mindset, it changes your way of thinking and therefore you place less emphasis on it. Change has to occur step by step. We have to change our way of thinking and make the correct choices in order to have control over the situation.
Yesterday at mass, Fr Escalante said if you want to grow closer to God, start with 1 Kings. Look closely at how he did his works. Trust fully that he is doing the same in your life. What do you have to lose? Do as he asks and pray to him about what is weighing you down. Pray about the big things and pray about the little things. He wants you to come to him in prayer. Don't expect the changes to happen over night. But trust that things will start to fall into place. Open your heart. Believe in him. Trust in him. Go to him. He's there and waiting.
Ms. Usrey-Roos with her son, Parker. The experimental drug he took for years, she said, “opened the lid and let Parker out.”
It was the first time she had ever heard her son say he loved her — or say much of anything for that matter. Parker, now 14, has fragile X syndrome, which causes intellectual disability and autistic behavior.
Ms. Usrey-Roos is certain that Parker’s new verbal ability resulted from an experimental drug he was taking in a clinical trial, and has continued to take for three years since then. She said she no longer had to wear sweaters to cover up the bruises on her arms she used to get from Parker hitting or biting her.
Now, however, the drug is being taken away. It has not met the goals set for it in clinical trials testing it as a treatment for either autism or fragile X syndrome. And Seaside Therapeutics, the company developing it, is running out of money and says it can no longer afford to supply the drug to former participants in its trials.
The setback is a blow in the effort to treat autism since the drug, arbaclofen, was one of the furthest along in clinical trials. And the company’s decision has caused both heartbreak and outrage among some parents.
“I waited 10 and a half years for him to tell me he loved me,” said Ms. Usrey-Roos, who lives in Canton, Ill. “With fragile X, you’re like living in a box and someone is holding the lid down. The medication opened the lid and let Parker out.”
“I don’t want to go back to the way life was,” she added.
The situation raises questions about what, if anything, drug companies owe to patients participating in their clinical trials. It also points out the difficulties in developing drugs to treat autism and fragile X syndrome. If the drug worked so well in some patients, why has it not succeeded so far in clinical trials?
One reason is that the symptoms and behaviors associated with autism and fragile X vary widely among individuals, making it hard to capture the effects of a drug by looking at any one measure, like irritability or social withdrawal. Seaside and doctors who participated in the trials said that there were improvements in some aspects of behavior in some studies, just not those considered critical to a trial’s overall success.
But could it also be that the parents are deluding themselves into seeing changes that are not there? Could improvements be the result of the children simply growing older?
“It’s kind of hard to make the argument that the company should keep providing it if it’s not working,” said Dr. Michael R. Tranfaglia, medical director of the Fraxa Research Foundation, of Newburyport, Mass., which provides money for research on fragile X syndrome.
Dr. Tranfaglia, whose son has fragile X but was not in a Seaside trial, said arbaclofen appeared to significantly help about a third of patients. It also made some patients worse. Without being able to tell in advance which patients would benefit, it would be hard for the drug to succeed in a clinical trial and win approval, he said.
Similar situations have risen occasionally in the past. In 2004, patients with Parkinson’s disease protested when Amgen stopped providing an experimental drug that some patients said had restored their lives. Amgen said the drug had failed in a clinical trial and might even be dangerous.
Two patients even sued, but a court ruled the company had no obligation to continue to supply the drug to participants in its trials.
In the case of arbaclofen, parents are appealing to Congress and have started an online petition hoping to find financing for the drug’s development. They are also organizing through social media.
Seaside executives declined to be interviewed.
Until recently, Seaside, one of the few companies pursuing autism drugs, was considered a shining light by family members of those with the condition.
The company, in Cambridge, Mass., grew out of the research of Mark F. Bear, a neuroscience professor at the M.I.T. Its co-founder and chief executive, Dr. Randall L. Carpenter, has a sister with an intellectual disability.
As of a year ago, privately held Seaside had raised about $90 million. Most of it had come from the Barony Trust, run by the family of Peter Whipp, a wealthy Briton. But it apparently never was the plan for Mr. Whipp to carry the company indefinitely.
Last year, Seaside entered a partnership with Roche, the Swiss pharmaceutical giant, which provided an undisclosed amount of money in exchange for intellectual property rights covering a different class of autism drug and an option to license arbaclofen.
But given the failures in the clinical trials, Roche says it has decided not to license arbaclofen, apparently ending financial support for studies of the drug.
“We concluded that arbaclofen wasn’t going to provide that real difference for patients,” Luca Santarelli, head of neuroscience research at Roche, said in an interview.
Dr. Bear of M.I.T. said he was hopeful new financing could be found. He said the company was started to help families, “not a play to make money.”
He added, “I think the signs are sufficiently encouraging. It would be really tragic if we abandon this now.”
On May 1, Seaside announced that arbaclofen, which is also known as STX209, had not met the main goal of reducing social withdrawal in a 150-patient midstage study of children and young adults with autism. But the drug did succeed on a different measure — the clinicians’ assessment of the patients.
The drug had previously failed in a Phase 2 trial for fragile X, which is caused by a mutation in a gene on the X chromosome and affects about 100,000 Americans.
In that trial, the main goal was to reduce irritability. While it did not do that, it appeared to ease social withdrawal. So Seaside began two Phase 3 trials for fragile X, one for young children and one for adolescents and adults. This time, social withdrawal was the main measure.
But the company said recently in a letter to parents that the trial in adolescents and adults had not succeeded. Results from the trial of children should be known this summer.
In the middle of May, Seaside told doctors and patients that because of “resource limitations” it could no longer supply the drug. “We know that this termination will be disruptive and disappointing for many families,” executives said in a letter to parents.
That is putting it mildly. Christina Murphy of Holton, Kan., wrote on the Web site stx209stories set up by families wanting the drug back, that her 11-year-old son Rhett, who has fragile X, made friends for the first time ever once he started taking the drug and sang in the school talent show, overcoming his usual fear of crowds and getting a standing ovation.
“I had never in my life witnessed something like that,” she wrote. “There was hardly a dry eye among the adults in the room. I have never seen him so happy in his entire life as when he finished that song and looked out at the crowd.”
Only a few hours later, she learned that the drug would be taken away. “I am sad, I am hurt and my heart is breaking,” she wrote.
Parents and patient advocates say there could be 300 patients or more taking the drugs. Some say they were promised the drug would be available until it reached the market or was totally abandoned as ineffective.
“When I found out, I went upstairs to my husband. I was crying so hard he thought someone had died,” said Cortney AbouElSeoud of Holt, Mich.
Ms. AbouElSeoud said her 5-year-old son Ayden, who has fragile X, spoke only a few words before entering the trial last October. Now he is up to 50 words. “He talks to us and answers us,” she said. “It’s crazy and awesome to see him emerging into a little person.”
Some parents say that they feel betrayed by Seaside and that the company has not communicated enough.
“I believe I, along with many others, are entitled to a better explanation of why our lives are being turned upside down,” Lori Armer of Newport News, Va., wrote on a Facebook page for families weaning their children off arbaclofen. She and other parents wrote on the site that behavioral problems were returning as the drug dosage was reduced.
There are some options. Arbaclofen is a derivative of baclofen, a generic muscle relaxer that is already on the market as a treatment for spasticity. While there is some evidence that arbaclofen is more potent, some parents are turning to baclofen.
Others hope to enroll their children into trials of other drugs for fragile X and autism being run by Roche and Novartis.
Ms. Usrey-Roos, who works for the National Fragile X Foundation, based in Walnut Creek, Calif., said she was hopeful that if one drug worked, another might, too.
While sad that the study ended, she said, “I’m still thankful for this experience. It has given me such hope.”
The genetic malady known as Fragile X syndrome is the most common cause of inherited autism and intellectual disability. Brain scientists know the gene defect that causes the syndrome and understand the damage it does in misshaping the brain's synapses — the connections between neurons. But how this abnormal shaping of synapses translates into abnormal behavior is unclear.
Now, researchers at UCLA believe they know. Using a mouse model of Fragile X syndrome (FXS), they recorded the activity of networks of neurons in a living mouse brain while the animal was awake and asleep. They found that during both sleep and quiet wakefulness, these neuronal networks showed too much activity, firing too often and in sync, much more than a normal brain.
This neuronal excitability, the researchers said, may be the basis for symptoms in children with FXS, which can include disrupted sleep, seizures or learning disabilities. The findings may lead to treatments that could quiet the excessive activity and allow for more normal behavior.
The study results are published in the June 2 online edition of the journal Nature Neuroscience.
According to the National Fragile X Foundation, approximately one in every 3,600 to 4,000 males has the disorder, as does one in 4,000 to 6,000 females. FXS is caused by a mutation in the gene FMR1, which encodes the fragile X mental retardation protein, or FMRP. That protein is believed to be important for the formation and regulation of synapses. Mice that lack the FMR1 gene — and therefore lack the FMRP protein — show some of the same symptoms of human FXS, including seizures, impaired sleep, abnormal social relationships and learning defects.
"We wanted to find the link between the abnormal structure of synapses in the FXS mouse and the behavioral abnormalities at the level of brain circuits. That had not been previously established," said senior author Dr. Carlos Portera-Cailliau, an associate professor in the departments of neurology and neurobiology at UCLA. " So we tested the signaling between different neurons in Fragile X mice and indeed found there was abnormally high firing of action potentials — the signals between neurons — and also abnormally high synchrony — that is, too many neurons fired together. That's a feature that is common in early brain development, but not in the adult."
"In essence, this points to a relative immaturity of brain circuits in FXS," added Tiago Gonçalves, a former postdoctoral researcher in Portera-Cailliau's laboratory and the first author of the study.
The researchers used two-photon calcium imaging and patch-clamp electrophysiology — two sophisticated technologies that allowed them to record the signals from individual brain cells. Abnormally high firing and network synchrony, said Portera-Cailliau, is evidence of the fact that neuronal circuits are overexcitable in FXS.
"That likely leads to aberrant brain function or impairments in the normal computations of the brain," he said. "For example, high synchrony could lead to seizures; more neurons firing together could cause entire portions of the brain to fire synchronously, which is the basis of seizures."
And epilepsy, Portera-Cailliau said, is seen in up to 20 percent of children with FXS. High firing rates could also impair the ability of the brain to decode sensory stimuli by causing an overwhelming response to even simple sensory stimuli; this could lead to autism and the withdrawal from social interactions, he noted.
"Interestingly, we found that the high firing and synchrony were especially apparent at times when the animals were asleep," said Portera-Cailliau. "This is curious because a prominent symptom of FXS is disrupted sleep and frequent awakenings."
And, he noted, since sleep is important for encoding memories and consolidating learning, this hyperexcitability of brain networks in FXS may interfere with the process of laying down new memories, and perhaps explain the learning disability in children with FXS.
"Because brain scientists know a lot about the factors that regulate neuronal excitability, including inhibitory neurons, they can now try to use a variety of strategies to dampen neuronal excitation," he said. "Hopefully, this may be helpful to treat symptoms of FXS."
The next step, said Portera-Cailliau, is to explore whether Fragile X mice indeed exhibit exaggerated responses to sensory stimuli.
"An overwhelming reaction to a slight sound or caress, or hyperarousal to sensory stimuli, could be common to different types of autism and not just FXS," he said. "If hyperexcitability is the brain-network basis for these symptoms, then reducing neuronal excitability with certain drugs that modulate inhibition could be of therapeutic value in these devastating neurodevelopmental disorders."
Other authors on the study included Peyman Golshani of UCLA and James E. Anstey of the Oregon Health and Science University School of Medicine. The research was funded by grants from the National Institutes of Health (NICHD R01HD054453 and NINDS RC1NS068093), the FRAXA Research Foundation, and the Dana Foundation.
The UCLA Department of Neurology, with over 100 faculty members, encompasses more than 20 disease-related research programs, along with large clinical and teaching programs. These programs cover brain mapping and neuroimaging, movement disorders, Alzheimer's disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranks in the top two among its peers nationwide in National Institutes of Health funding.
For the first time in his life, Arbaclofen gave him the ability to hug us and tell us he loved us.
His coping skills were better in regard to transitioning. He was less shy. He was less emotional. He was less aggitated. He had stopped running away from me. He hadn't bit me or pulled my hair. He was far less concerned about having to go to the doctor. He wanted to socialize with people in public. He wanted to go to school. He didn't tell me no. He followed commands better. He seemed to learn easier. Potty training went better. He could cope better with being told no. He smiled more.
His last dose was 3 days ago. It feels like we are missing something really important by not giving him the tiny little pill to chew that helped him so much!
We will find another trial. We will move on. Just sucks to have to start all over again. But we were blessed to be a part of stx 209.
Researchers discover new therapy for fragile X chromosome syndrome April 10, 2013 in Medical research Researchers at the University of the Basque Country (UPV/EHU) and the Achucarro neurosciences centre have discovered a new therapy for the fragile X chromosome syndrome. This new therapy proposes the modulation of the cerebral endocannabinoid system in order to ameliorate the symptoms of the disease. "Clearly, a cure as such is not going to be achieved, as it involves a disease of genetic origin, but the fact that, by manipulating in a certain way at a cerebral level in order to obtain an improvement in the symptoms of the disease is something highly positive", stated Ms Susana Mato, researcher at the Department of Neurosciences at the UPV/EHU and at the Achucarro centre. This scientific finding has just been published in Nature Medicine.
Enhancing the Quality of Human Life The Future of Stem Cell Therapy
Fragile X chromosome syndrome (FXS) is the most frequent known cause of inherited mental retardation and disorders in the autistic range. It involves a genetic disease, with an incidence in Spain estimated at 1 in every 4,000 individuals. The syndrome arises from a deficit in the expression of the FMRP protein (fragile X mental retardation protein), which plays a fundamental role in the regulation of the neuronal function. Patients with FXS present mental retardation, attention deficit, anxiety, self-harming and autistic behaviour, hyposensitivity to pain and a high rate of epileptic crises. All these anomalous neuronal expressions are regulated by the endocannabinoid system. The research, using genetically modified mice that lacked FMRP protein and that partially reproduced the symptomatology of fragile X chromosome syndrome in humans, have shown that blocking CB1 cannabinoid receptors with the Rimonabant pharmaceutical drug normalizes cognitive alterations, sensitivity to pain and epileptic crises.
This finding suggests that the administration of pharmaceutical drugs that block the function of the cerebral endocannabinoid system may well be a chnew strategy for treating patients with fragile X chromosome syndrome. Rimonabant pharmaceutical drug has been on the market for some time "for the treatment of obesity", explained Ms Mato. "Then, however, it was used in much higher doses and these high dosages gave rise to certain psychiatric problems, and this is why it was taken off the market". Nonetheless, it involves a drug which "has been used a lot in preclinical research into the endocannabinoid system, and its action mechanism is very well established". The next step, Ms Mato pointed out, should be "to better characterise the action mechanism of this treatment, and test the various dosages to see what would be the optimum one to normalize the deficit.
And the following stage would be the clinical trials. In fact, we believe this would be relatively feasible, because as it has already been marketed, all that preclinical stage regarding toxicity of the drug for humans has been undertaken, and it is a relatively safe pharmaceutical drug". Although Ms Mato considers it to be a great advance that it has been shown in animal models that "the cognitive deficit caused by the disease has been normalised to a certain extent", she is aware that it could be that "the clinical trials do not produce such good results, as it is common for this to happen when developing therapies for psychiatric disorders". More information: Busquets-Garcia, A. et al. Targeting the endocannabinoid system in the treatment of fragile X syndrome. Nature Medicine doi:10.1038/nm.3127
They loved it!!!!!!! 
