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Thread: tocopherol

  1. #11
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    Eldar....soooo are you saying this is good or bad for hair?

  2. #12
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    what does that mean in Layman's terms ?

  3. #13
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    Regrows them follicles bra

  4. #14
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    Quote Originally Posted by eldarlmario View Post
    plastochromanol 8 results in decreased expression of BIRC5 mRNA <=== downregulates Survivin

    https://en.wikipedia.org/wiki/Survivin

    Survivin is a member of the inhibitor of apoptosis (IAP) family. The survivin protein functions to inhibit caspase activation, thereby leading to negative regulation of apoptosis or programmed cell death. This has been shown by disruption of survivin induction pathways leading to increase in apoptosis and decrease in tumour growth. The survivin protein is expressed highly in most human tumours and fetal tissue, but is completely absent in terminally differentiated cells.[3] These data suggest survivin might provide a new target for cancer therapy that would discriminate between transformed and normal cells. Survivin expression is also highly regulated by the cell cycle and is only expressed in the G2-M phase. It is known that survivin localizes to the mitotic spindle by interaction with tubulin during mitosis and may play a contributing role in regulating mitosis. The molecular mechanisms of survivin regulation are still not well understood, but regulation of survivin seems to be linked to the p53 protein. It also is a direct target gene of the Wnt pathway and is upregulated by beta-catenin.[4]


    plastochromanol 8 results in decreased expression of HIF1A protein <===anti-hypoxia

    Hypoxia-inducible factor 1-alpha, also known as HIF-1-alpha, is a subunit of a heterodimeric transcription factor hypoxia-inducible factor 1 (HIF-1) that is encoded by the HIF1A gene.[1][2][3] It is a basic helix-loop-helix PAS domain containing protein, and is considered as the master transcriptional regulator of cellular and developmental response to hypoxia.[4][5] The dysregulation and overexpression of HIF1A by either hypoxia or genetic alternations have been heavily implicated in cancer biology, as well as a number of other pathophysiologies, specifically in areas of vascularization and angiogenesis, energy metabolism, cell survival, and tumor invasion.[3][6] Two other alternative transcripts encoding different isoforms have been identified.[3]

    plastochromanol 8 results in decreased expression of MIR22 mRNA <=== http://journals.plos.org/plosgenetic...l.pgen.1005253

    Abstract

    Hair follicles (HF) undergo precisely regulated recurrent cycles of growth, cessation, and rest. The transitions from anagen (growth), to catagen (regression), to telogen (rest) involve a physiological involution of the HF. This process is likely coordinated by a variety of mechanisms including apoptosis and loss of growth factor signaling. However, the precise molecular mechanisms underlying follicle involution after hair keratinocyte differentiation and hair shaft assembly remain poorly understood. Here we demonstrate that a highly conserved microRNA, miR-22 is markedly upregulated during catagen and peaks in telogen. Using gain- and loss-of-function approaches in vivo, we find that miR-22 overexpression leads to hair loss by promoting anagen-to-catagen transition of the HF, and that deletion of miR-22 delays entry to catagen and accelerates the transition from telogen to anagen. Ectopic activation of miR-22 results in hair loss due to the repression a hair keratinocyte differentiation program and keratinocyte progenitor expansion, as well as promotion of apoptosis. At the molecular level, we demonstrate that miR-22 directly represses numerous transcription factors upstream of phenotypic keratin genes, including Dlx3, Foxn1, and Hoxc13. We conclude that miR-22 is a critical post-transcriptional regulator of the hair cycle and may represent a novel target for therapeutic modulation of hair growth.[/I]

    Numerous reports have documented the functions of specific microRNAs on hair development [24,27–29]. Among them, miR-24 and miR-125b have expression patterns similar to that of miR-22 during hair cycling [24]: sharp upregulation at catagen and maximal expression at telogen phase. Consistent with miR-22, ectopic expression of miR-24 in the ORS of hair follicles resulted in hair loss with severe defects in hair follicle morphogenesis. miR-24 repressed hair keratinocyte differentiation by negatively regulating TCF3, an important upstream regulator of hair differentiation [14,27]. miR-125b is another well-characterized microRNA in hair development. Similarly to miR-22, miR-125b overexpression leads to hair loss by repressing hair differentiation. miR-125b directly represses the vitamin D receptor, which plays an important role in hair differentiation [28]. Thus, miR-22, miR-24 and miR-125b might synergistically function to promote hair regression by repressing a keratinocyte differentiation regulatory program in the transition into catagen and telogen. This phenomenon may in fact be more broad. In addition to miR-24, miR-125b, numerous microRNAs including miR-29a, miR-27a, miR-27b, miR-30a, miR-152 and miR-143 also exhibit the same expression pattern as miR-22 [24]. Thus, future studies are warranted to determine the combinatorial effects of this suite of microRNAs in hair cycle transitions.

    plastochromanol 8 results in decreased expression of MIR27B mRNA
    Jesus. I literally have a masters degree in molecular bio and this put me to sleep. c'mon now!

  5. #15
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    eldarlmario can you please sum up what you meant to say there in your reply. Would be curious to know.

  6. #16
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    Quote Originally Posted by ShookOnes View Post
    http://botanicalcraft.com/

    This is the only thing I've tried besides fin that grew back some
    Did you stop taking this?

  7. #17
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    Why don't you add a anti DHT shampoo twice a week, leave on for 10 min. ie, Zinc 2%, Ketoconazole 2%. Not sure about Selinium 2.5% but I use them all along with good vitamins and still have some hair after 30 years. Supplemental treatment or hereditary I will never know.

  8. #18
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    shookones, are you still on the tocopherols?

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