Mad Angry

I’m so angry that if I saw my health insurance agent on the side of the road I would run him over.

I lost medicaid for Matthew and Rachel this past year. I lost Rachel’s in May and Matthew’s in September. I contacted my agent in April telling him about the change. He said that he would get on it.

In June, I still hadn’t heard anything or received any forms. I contacted him again. He sent me the forms and I turned them in to personnel. Personnel faxed them to him.

In August, Rachel had to have that thing removed from her ear and it cost $300. This post talks all about it.

Well, October rolls around and I get a bill from the pediatrician. Insurance didn’t cover it. I called my agent and he said he would resend it to BCBS. I also informed him that Matthew had just been dropped from SSI, and, in turn, lost his medicaid. He said he would add him as well. I filled out those forms and went through that whole process again. This month rolls around and I get another bill from the pediatrician. This one is saying that if I don’t pay, it will get sent to collections! I faxed the bill to my agent and then we had the following email conversation that ended on December 12, 2007.

Me: Hi Terry, I just wanted to check in and see if you received the fax that I had sent you on Tuesday, December 4, 2007. If you had not, then I will resend it.Thanks for your time.

Agent: I have a meeting with BCBS today. I will make her process today. Thanks

Me: Good afternoon Terry J Were they able to get this taken care of?

Agent: Yes, The claim is being processed..I will call ** Pediatrics and give them the information.

Earlier this week I get a notice from a collections agency requesting their $300 for their client!!

I’m a thinker, so I decided to think it over and decide the best way to handle this situation. Yesterday, I called the pediatrician’s office and left a message in billing to see if they ever heard from him on the claim. They never returned my call.

So, this morning I called the main BCBS office in our state and talked to a representative. You are not going to believe this but my agent never even put my kids on my insurance!!

At this point in the game, it is too late to add Rachel, so that bill cannot be covered. If this $@#^ would have done his job like he should have, it could have been, but it’s been over three months since she lost her medicaid. I could add Matt and go retroactive, but miracalously he doesn’t have any old medical bills.

I have to now add my kids on at the beginning of the year. So all those papers I had filled out, I got to fill out again this morning.

I am so stinking, hopping angry.

I got to think now on how I get this guy to pay, financially or with his lying, lazy arse!

The most frustrating thing is that I got more accomplished in a 30 minute call to a far off town than with a local man in 7 months!! 

As Matthew says, “Mom is mad angry!”

Closer to a Cure

I am still a bit anxious about the thought of finding a cure for fragile x syndrome.  I hit on some of my issues in my Trepidation post back in July.  I also go between thinking that God gave me Matthew and Rachel like they are for a reason, and that God created the science to find this cure for a reason.  Irregardless of my issues with it, here is a news release from Katie Clapp with Fraxa on how researchers are closer to a cure for FXS.

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Researchers Reverse Key Symptoms of Fragile X in Mice In the December 20thissue of Neuron, MIT researchers Mark Bear, Gul Dolen, and others, along with Sumantra Chattarji of India’s National Center for Biological Sciences, show that they can correct major symptoms of Fragile X by reducing expression of a single receptor in the brain. This receptor, a protein called mGluR5, is a prime target for drugs to treat Fragile X – and possibly autism – in humans.The findings support the theory that key Fragile X symptoms – learning disabilities, autistic behavior, and seizures – stem from too much activation of one of the brain’s chief network managers – the metabotropic glutamate receptor mGluR5. People with Fragile X lack a protein called FMRP(Fragile X Mental Retardation Protein). This study found that FMRP and mGluR5 are at opposite ends of a kind of molecular seesaw. They keep each other in check, and without FMRP, mGluR5 signals run rampant. To test this theory, the researchers knocked out one of the two copies of the mGluR5 gene in mice already lacking FMRP. The mice lacking FMRP showed many of the symptoms observed in humans who have Fragile X. By knocking out one copy of mGluR5, the researchers created mice that produced only half the normal amount of mGluR5 protein, hoping to compensate for the lack of FMRP and eliminate symptoms of Fragile X.”We decided to reduce the mGluR5 levels by 50 percent to reflect what might be a therapeutically relevant condition that would be achievable with carefully titrated drug treatment,” said Bear. “Total knockout of mGluR5 has deleterious effects, whereas reducing it by half is innocuous.”The researchers found that reducing mGluR5 eliminated many symptoms of the disorder. Like humans with Fragile X, mice without FMRP experience seizures, impaired memory, and accelerated body growth. When mGluR5 was diminished, these problems were corrected.Reducing mGluR5 also compensated for changes in the brain associated with increased protein synthesis. With less mGluR5, the brain of each mouse no longer formed an excessive number of neuronalconnections. The mice did not have the high density of dendritic spines that is characteristic of Fragile X syndrome. Furthermore, the total rate of protein synthesis was reduced to normal levels in the brains of Fragile X mice with reduced mGluR5.The researchers used genetic engineering to reduce mGluR5, but the same thing could be accomplished by a drug. Pharmaceutical companies have already developed experimental drugs that block mGluR5. Clinical trials are underway, but none of the drugs has yet been approved for humans.These findings may lead to further targets for drug discovery, since scientists can now study other drugs which affect other elements of the brain’s mGluR pathway. It should be possible to identify biomarkers, substances which can be measured in the blood, which can identify changes in the function of the mGluR pathway in people with developmental disorders. Through biomarkers, other people with autism and developmental disorders who do not have Fragile X, but do have abnormalities in this pathway, can be identified. It is likely that these individuals would respond to many of the treatments currently being developed for Fragile X.FRAXA has provided funding for the work of Mark Bear and colleagues every year since 2000 and also funds Sumantra Chattarji . FRAXA is now working with several companies to help speed development of mGluR5 blockers to treat Fragile X. Stay tuned for future announcements!