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When genetic mutations in RP lead to loss of rods, oxygen consumption in the retina decreases, leading to excess unconsumed oxygen in the retina, resulting in hyperoxia [7]

We postulate that the resulting bacterial toxins and pro-inflammatory cytokines contribute directly to the inflammatory microenvironment of adjacent OLP lesions, perpetuating the disease state

It is also understood to enhance the production of our T cells which are the bodys first line of defence against infection and viruses

While these effects are typically milder than exogenous growth hormone, they still represent systemic hormonal changes

Cognitive and Neuroprotective Models BPC-157 has emerging neuroprotective data , primarily from the Zagreb group and including Vukojevi et al