Sunday, October 23, 2005

NYT: When health insurance is not a safeguard

The NYT's series on health care continues with a piece about the increasing gap in the protection afforded by health insurance:
After decades in which private and government insurance covered a progressively larger share of medical expenses, insurance companies are now shifting more costs to consumers, in the form of much higher deductibles, co-payments or premiums. At the same time, Americans are saving less and carrying higher levels of household debt, and even insured families are exposed to medical expenses that did not exist a decade ago. Many, like the Dorsetts, do not realize how vulnerable they are until the bills arrive. Lawyers and accountants say that for the more than 1.5 million American families who filed for bankruptcy protection last year, the most common causes were job loss and medical expenses.

Link (free reg req'd).


Beth said...

This is off-topic- but I think it would interest you. I saw a talk by Jeffry Rothstein last week. He studies the loss of glutamate transporters in motorneurons in ALS, but there is also a loss of glutamate transporters in oligodendrocytes in MS. Taking antibiotics increased the expression of glutamate transporters in mice and people- with Ceftriaxione (an antibiotic that gets across the blood brain barrier).

I know you keep up with stuff on pub med- here is the address for one of Rothstein's studies published in Nature.

Doug Lee-Knowles said...

Interesting. "These studies provide a class of potential neurotherapeutics that act to modulate the expression of glutamate neurotransmitter transporters ,via gene activation."

How does "gene activation" work?

Beth said...

Gene activation is when machinery of the cell is told to start making mRNA, which is then translated into protein. There is DNA sequence (called the promoter) upstream of the portion of the DNA that encodes for a protein (called the gene). Lots of things can activate the promoter- things that are in our body like steroids bind the steroid receptor and the complex then activates transcription (or making of RNA) of the gene. Protein hormones usually activate a receptor (a lock and key idea) on the cell membrane and then it sets of a cascade of protein activation that ultimately activating the promoter, which starts transcription (making RNA) and translation (protein).

So in the case of the glutmate transporter EAAT2- normal people's DNA may be constantly transcribed in mRNA and translated into protein. In those with MS, there isn't enough EEAT2 protein in oligodendrocytes, but for some reason beta lactam antibiotics happen to stimulate the EEAT2 gene promoter, thus making more mRNA, which is then translated into making more EEAT2 protein.

The caveat is that in those with MS- the oligodendrocytes that are problematic are in the CNS- so any beta lactam has to get across the blood brain barrier. Ceftriaxone dose cross the BBB, and they started a clinical trial with ALS patients, but had to stop it b/c 6% developed a weird type of meningitis. They are currently screening other chemicals to see if there are more that activate EEAT2.

All the clinical trials so far have been done on ALS, not MS- but I think they should definately try it in those with MS.