Join Now
danettejett 
11:43pm, December 2, 2008
"A Reflection of Me"
I look into the mirror, and what do I see.
I am not quite sure, but I dont feel like me.
My spirit yearns to dance, laugh, and be free,
Yet my exhausted body and mind have control over me.
My being is consumed with no free will,
I cant choose what I want, for I am too ill.
The passion and drive that I once possessed,
Has been sweep away and replaced with bedrest.
Was it not enough to loose my strength and health,
I must loose it all, my security, friends, and wealth.
Our lifes become shattered, which way do we turn,
Our days are unpredictable, that is what we learn.
We wake up and relize we are in a battle everyday,
We are forced to fight, we cant escape or run away.
The enemy invades and poisons our body and minds,
We are peirced with its painful arrows from behind.
As I drag my lifeless, tired body out of the bed,
I look in the mirror but I dont know whats ahead.
I put on my courageous armour to face the day,
I ask God to help me endure the suffering along the way.
This deliberating illness has control over my life,
It can not steal my peace and joy, even with the strife.
For I will not grow weary in doing good,
I will fight a good fight of faith like I should.
No chronic illness will bring me completely down.
When I look in the mirror, I will not frown.
I may not be the same person I used to be.
With this new life I do struggle with my identity.
Have I forgotten what its like to live and be symptom free?
To have a life of abundance and good will following me.
To feel normal and healthy is something of the past.
My recollection of it is like a good dream that didnt last.
When I look in the mirror, what do I see.
Someone who is trying to be the best they can be.
For the old me died a long time ago when my body failed,
The new me has awakened and by faith we all can prevail.
Written by: Danette Jett
November 24, 2008
Dedicated to my dear friends who suffer with CFIDS/ME, and Fibromyagia.
Comments
Hey you all I am just doing some research on why we seem to have such brain fog and or why our symptoms seem to have effects on our brain functioning - especially the hypothalamus. Our brains ofcourse are the center of our nervous system and we need them to signal all areas of our bodies (organs, hormones) to function right. What happens with CFS that causes our systems to malfunction? Could it be that our brains are being poisoned?
What is the blood brain barrier (BBB)? The BBB is there to protect high density cells restricting passages of foreign substances from the bloodvessels to the brain.
I was reading that viruses can bypass through the blood-brain barrier by attaching themselves to circulatory immune cells. (I have the EBV) Therefore it can reach our brains and do damage to certain areas.
The hypothalamus specifically the Subfornical Organ is outside of the blood-brain barrier so nuerons in this region can respond to factors that are present in the systemic circulation. The Subfornical Organ regulates fluid and electrolyte balance, thrist, soduim excretion, blood volume regulation, vasopression, osmotic pressure of blood. CFS patients have these symptoms.
Again, The Blood Brain Barrier is there to protect high density cells restricting passage of substances from the blood stream to the brain. The blood-brain barrier is composed of high density cells restricting passage of substances from the bloodstream much more than endothelial cells in capillaries elsewhere in the body. Astrocyte cell projections called astrocytic feet (also known as "glia limitans") surround the endothelial cells of the BBB, providing biochemical support to those cells. The BBB is distinct from the similar blood-cerebrospinal fluid barrier, a function of the choroidal cells of the choroid plexus, and from the Blood-retinal barrier, which can be considered a part of the whole[1]
What do you all think? Help me out here....
Posted on 11/13/08, 06:11 pm
What is the blood brain barrier (BBB)? The BBB is there to protect high density cells restricting passages of foreign substances from the bloodvessels to the brain.
I was reading that viruses can bypass through the blood-brain barrier by attaching themselves to circulatory immune cells. (I have the EBV) Therefore it can reach our brains and do damage to certain areas.
The hypothalamus specifically the Subfornical Organ is outside of the blood-brain barrier so nuerons in this region can respond to factors that are present in the systemic circulation. The Subfornical Organ regulates fluid and electrolyte balance, thrist, soduim excretion, blood volume regulation, vasopression, osmotic pressure of blood. CFS patients have these symptoms.
Again, The Blood Brain Barrier is there to protect high density cells restricting passage of substances from the blood stream to the brain. The blood-brain barrier is composed of high density cells restricting passage of substances from the bloodstream much more than endothelial cells in capillaries elsewhere in the body. Astrocyte cell projections called astrocytic feet (also known as "glia limitans") surround the endothelial cells of the BBB, providing biochemical support to those cells. The BBB is distinct from the similar blood-cerebrospinal fluid barrier, a function of the choroidal cells of the choroid plexus, and from the Blood-retinal barrier, which can be considered a part of the whole[1]
What do you all think? Help me out here....
Posted on 11/13/08, 06:11 pm
Comments
-
Articles I have read about over the past couple of years seem to support the view that ME is caused by a neurophilic virus that lives deep in the brain stem and damages critical systems that control the regulatory functions of the body through the HPA axis, etc. It would not show up in blood work if it does not normally maintain high levels in the circulatory system, residing instead primarily in neural tissues. After all, the virus that causes shingles, Varicella zoster, does not show up as a viral infection when blood work is done, even though everyone who has ever had chicken pox carries it in their bodies. It just lives in neural tissue as a permanent resident of the body, causing problems only when the immune system is compromised or the person is extremely stressed.
I have often thought to myself that ME may be originally a childhood disease like chicken pox, nothing distinctive about it, and transmitted among children. Then later on, when we are stressed by something it becomes ME, just like Varicella zoster becomes shingles.
-
A friend of mine who also has chronic fatigue (she didn't have EBV though she became ill after a blood transfusion 4 years ago) She also lives in London Uk like me and she was part of a study where quite a few CFS patients had brain scans but she still doesn't know what the study showed. I hope she finds out as I would be very interested to know aswell as many others.
I think we can definately say that CFS is caused by a virus, your, mine and a majority was caused by the EBV.
I do think though that somehow this virus attacks the nervous system and this is why I have now been started on weekly vitamin B12 injections which helps the nervous system and aids healthy red blood cells.
It definatley affects the brain somehow though and I really think there should be a lot more research into this and hopefully one day they will come up with a cure to correct what has gone wrong in our bodies. I am forever hopeful though and truly believe that we will all get better again sometime.
Glucocorticoids promote the proliferation and antagonize the retinoic acid-mediated growth suppression of Epstein-Barr virus-immortalized B lymphocytes.
Quaia M, Zancai P, Cariati R, Rizzo S, Boiocchi M, Dolcetti R.
Division of Experimental Oncology 1, Centro di Riferimento Oncologico, Aviano, Italy.
Glucocorticoids are able to release Epstein-Barr virus-immortalized (EBV-immortalized) lymphoblastoid B cell lines (LCLs) from the persistent growth arrest induced in these cells by retinoic acid (RA).
Moreover, physiologic concentrations of glucocorticoids efficiently antagonized LCL growth inhibition induced by 13-cis-RA; 9-cis-RA; all-trans-RA; and Ro 40-6055, an RA alpha receptor (RAR alpha) selective agonist. RAR alpha expression levels, however, were not affected by glucocorticoids. Glucocorticoids, but not other steroid hormones, directly promote LCL proliferation, a phenomenon that was mainly mediated by down-regulation of the cyclin-dependent kinase (CDK) inhibitor p27(Kip-1).
Moreover, glucocorticoids contrasted the up-regulation of p27(Kip-1), which was underlying the RA-induced LCL growth arrest, thereby indicating that glucocorticoids and RA signalings probably converge on p27(Kip-1). Both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486, indicating that all of these effects were mediated by GR. Of note, RU486 also proved to be effective in vivo and, in mice, was able to significantly inhibit the growth of untreated LCLs as well as LCLs growth-arrested by RA in vitro.
These findings provide a rational background to further evaluate the possible role of glucocorticoids in the pathogenesis of EBV-related lymphoproliferations of immunosuppressed patients. Moreover, GR antagonists deserve further consideration for their possible efficacy in the management of these disorders, and the use of schedules, including both RA and a GR antagonist, may allow a more thorough evaluation of the therapeutic potential of RA in this setting.
Related website information:
http://bloodjournal.hematologylibr...
Quaia M, Zancai P, Cariati R, Rizzo S, Boiocchi M, Dolcetti R.
Division of Experimental Oncology 1, Centro di Riferimento Oncologico, Aviano, Italy.
Glucocorticoids are able to release Epstein-Barr virus-immortalized (EBV-immortalized) lymphoblastoid B cell lines (LCLs) from the persistent growth arrest induced in these cells by retinoic acid (RA).
Moreover, physiologic concentrations of glucocorticoids efficiently antagonized LCL growth inhibition induced by 13-cis-RA; 9-cis-RA; all-trans-RA; and Ro 40-6055, an RA alpha receptor (RAR alpha) selective agonist. RAR alpha expression levels, however, were not affected by glucocorticoids. Glucocorticoids, but not other steroid hormones, directly promote LCL proliferation, a phenomenon that was mainly mediated by down-regulation of the cyclin-dependent kinase (CDK) inhibitor p27(Kip-1).
Moreover, glucocorticoids contrasted the up-regulation of p27(Kip-1), which was underlying the RA-induced LCL growth arrest, thereby indicating that glucocorticoids and RA signalings probably converge on p27(Kip-1). Both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486, indicating that all of these effects were mediated by GR. Of note, RU486 also proved to be effective in vivo and, in mice, was able to significantly inhibit the growth of untreated LCLs as well as LCLs growth-arrested by RA in vitro.
These findings provide a rational background to further evaluate the possible role of glucocorticoids in the pathogenesis of EBV-related lymphoproliferations of immunosuppressed patients. Moreover, GR antagonists deserve further consideration for their possible efficacy in the management of these disorders, and the use of schedules, including both RA and a GR antagonist, may allow a more thorough evaluation of the therapeutic potential of RA in this setting.
Related website information:
http://bloodjournal.hematologylibr...
Past Entries
Hey!!! u- know me!! tickey HEE!!HEE!! What about dedicateing to us m.s. suffers??? (just messing with you!) really its like a good dream that did'nt last !! very moving and God bless you so much! Hugs Tickey
tickey
The was beautifully written and says it all! So sad, but true.
JerryJsMom
You should try to get it published. Hope you had a good thanksgiving.
-Merry Christmas/Happy Hanukkah or whatever else you may be celebrating this Dec.
EP
EPagain