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Hi! I am a Bachelor of NSC research post grad University of Texas at Dallas seeking data to aid in the development of a model and subsequently treatment for male pattern balding; efficacy of treatment aimed to surpass that of all prior anti-androgen treatments via targeting the source.
My original investigation led to suspecting a gene mutation effectively knocking out the glutamate cysteine ligase modifier (GCLM) subunit; this being the only valid model as other knockout result in unsuccessful or terminal fetuses. Therein explaining discrepancies in data on inguinal hernia by claiming 2 models of action - the more novel mode being through oxidative damage. This pointing to a potential treatment upon following the model through being oral Vitamin E supplementation. Unfortunately, surely this alone is not effective though does impact testi size in roosters so we know we are on the right track. Suggesting likely rather than the entire model being incorrect, more likely so the model is incomplete.
I, whom also suffers from hair loss, have been unable yet to resolve the other (at least one) remaining portion of mechanism by which male pattern balding occurs. In other words, there exist a trait, likely subtle, that we all have in common.
I strongly suspect this trait to be poison oak/ivy immunity; note that immuno-compromised persons will likley experience a lack of immunity here. What is known supports the possibility of a type of T-cell antigen mode of inflammation warranting further investigation - possibly.
What I need to know is this:
1) Have you ever been diagnosed with inguinal hernia?
2) Do you possess immunity to poison oak/ivy/sumac?
Having only one of the conditions will not produce hair loss given the validity of hypotheses & not all that possess GCLM subunit deficiency will develop full blown inguinal hernias.
Thank you for your participation.
#ProjectAmori
My original investigation led to suspecting a gene mutation effectively knocking out the glutamate cysteine ligase modifier (GCLM) subunit; this being the only valid model as other knockout result in unsuccessful or terminal fetuses. Therein explaining discrepancies in data on inguinal hernia by claiming 2 models of action - the more novel mode being through oxidative damage. This pointing to a potential treatment upon following the model through being oral Vitamin E supplementation. Unfortunately, surely this alone is not effective though does impact testi size in roosters so we know we are on the right track. Suggesting likely rather than the entire model being incorrect, more likely so the model is incomplete.
I, whom also suffers from hair loss, have been unable yet to resolve the other (at least one) remaining portion of mechanism by which male pattern balding occurs. In other words, there exist a trait, likely subtle, that we all have in common.
I strongly suspect this trait to be poison oak/ivy immunity; note that immuno-compromised persons will likley experience a lack of immunity here. What is known supports the possibility of a type of T-cell antigen mode of inflammation warranting further investigation - possibly.
What I need to know is this:
1) Have you ever been diagnosed with inguinal hernia?
2) Do you possess immunity to poison oak/ivy/sumac?
Having only one of the conditions will not produce hair loss given the validity of hypotheses & not all that possess GCLM subunit deficiency will develop full blown inguinal hernias.
Thank you for your participation.
#ProjectAmori