One of the misconception about cytokines is that not only that they are supposed to act like Hormones or even Vitamins to specific receptors but that they need sufficient detectable concentrations to induce incremental changes in the body physiology. In cancers, TGB does need to be very noticeable to have a autocrine function for a particular neoplastic cell, helping its growth. In laboratory however acting directly against its receptors may have tangible effect. It may control metastatic spread of disease.
Another interesting aspect is at various levels of the cytokines, the physiologic effect could be contrary to the original effect, that is a Cytokine could be excitatory at low dose, and inhibitory at high level.
Cytokine can affect metabolism so that only a certain direction is imposed to the metabolism such what happens in dementia (ie: effect on Phosphatases). Whether the G proteins have a dramatic role is clearly suggested! And may prone one to open dementia. It is quite clear that the Cytokine found in elderly are different then in the young as if there is a switch from Hormone preponderence to a Cytokine phase. Also a greater Mitochondrial abnormal physiology seems to characterize senility leading to susceptibilty to deadly tone of common infections.
At higher doses, cytokines enleash further actions as if affecting non conventional effects. (ie high dose interferon and high dose IL-2) It is as if at these doses new set of receptors (death receptors, PD-1) become better reachable directly or indirectly. And of course the muscles and vascular receptors are by now overwhelmed and appears the most affected. And here comes depression and memory deficiency the hallmark of these diseases. Increasingly it is now thought that in patients with high blood pressure and diabetic patient, it is the increasing disturbance in Cytokine that lead to stroke and Heart attacks...the dreadful transition from hormone preponderance to the Cytokine kingdom is followed by unhealthy consequences and deterioration of protective effect of hormone is as a result!
The effect on Mitochondrial activities overall push forward immunomodulation and anti-inflammatory role promoting the role of NSAID. But this role is muddled by the various impacts of various agents on JUNK and c-FOS....
to be continued...
CRBCM always continuing its progress! And the circle will be soon closed!
see previous blog
What weakens the blood vessel for stroke to occur
is it an acute process
is it a long standing transformation due to or inducing cytokine release (can we capture the moment?)
what about the the role of the HIF gene? the MTOR, CRE and the Adenyl Cyclase
what is the exact role of VEGF (or the various VEGF)
what is the role of the endothelial genes/integrins/what A4Beta.
what is the level of metalloproteases before and at rupture
stress on the Cateins
can the FGF-1 tell us a thing
what is the PDGFR reaction
secretion of platelet during clotting at blood vessel
what is happening in the endothelial cells, what can preclude the secondary incident that happens within a year
is the therapeutic response adequate
does Aspirin good as an universal response (based on impact on the c-jun--c-fos taken indiviual or by ratio)
what is the c-fos and c-jun behavior ?
Role of Avastin if any
what cytokines are involved?
level of coagulation factors
what factor V has to to
what about the homocystein?
does vitamin D level affected or induces it?
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