It's a nice time to repost this, just to see if someone comes up with some idea...
Wound healing phases
Awesome!
unk:
so Weekly stabbing= Extra blood flow and vasodilation for days..then thicker hair and growth? My head is pink- ish for at least 3 days during after stabbing but my hair looks thicker during that timeframe..
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This compound has already been found, it's called fgf9, it's a growth factor. One problem with do it yourself dermaroller is that the fgf9 has to be timed perfectly or else it won't have the same effect. Now the fgf9 we are able to purchase, even though it is insanely expensive. Like I said before, we need someone that knows the process well and tell us scientifically how are scientists able to determine what the wound is doing at any given time. We need the right sensors and then use our best judgement to apply it when we believe it would be best because the patents don't give an exact time. This is no surprise as it should be different for each individual since everyone heals differently. That would be our best bet I believe.
I was reading about that FGF9 yesterday. Apparently highly active during the progression of cancer...:freaked2:
If the old BBQ dude can grow hair on his bald head without any topicals involved, so why the **** Follica is saying that hair don't regrow only wounded? I had a car accident when I was younger and ended up head first in the windshield.. I had wounds everywhere.. my hair got back on my head.
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You guys should also take in consideration that we all have different blood viscosity and vascular density. Everybody bleeds differently.
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male pattern baldness is a real C-U-N-T! haha what a pain in the arse puzzle!
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Hypoxia-inducible factors as essential regulators of inflammation.
Imtiyaz HZ,
Simon MC.
Source
Abramson Family Cancer Research Institute, University of Pennsylvania, 438 BRB II/III, 421 Curie Boulevard, Philadelphia, PA 19104-6160, USA.
Abstract
Myeloid cells provide important functions in low oxygen (O(2)) environments created by pathophysiological conditions, including sites of infection, inflammation, tissue injury, and solid tumors. Hypoxia-inducible factors (HIFs) are principle regulators of hypoxic adaptation, regulating gene expression involved in glycolysis, erythropoiesis, angiogenesis, proliferation, and stem cell function under low O(2). Interestingly, increasing evidence accumulated over recent years suggests an additional important regulatory role for HIFs in inflammation. In macrophages, HIFs not only regulate glycolytic energy generation, but also optimize innate immunity, control pro-inflammatory gene expression, mediate bacterial killing and influence cell migration. In neutrophils, HIF-1α promotes survival under O(2)-deprived conditions and mediates blood vessel extravasation by modulating β (2) integrin expression. Additionally, HIFs contribute to inflammatory functions in various other components of innate immunity, such as dendritic cells, mast cells, and epithelial cells. This review will dissect the role of each HIF isoform in myeloid cell function and discuss their impact on acute and chronic inflammatory disorders. Currently, intensive studies are being conducted to illustrate the connection between inflammation and tumorigenesis. Detailed investigation revealing interaction between microenvironmental factors such as hypoxia and immune cells is needed. We will also discuss how hypoxia and HIFs control properties of tumor-associated macrophages and their relationship to tumor formation and progression.
http://www.ncbi.nlm.nih.gov/pubmed/20517715
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Regulation of hypoxia-inducible factors during inflammation.
Frede S,
Berchner-Pfannschmidt U,
Fandrey J.
Source
Institut für Physiologie, Universität Duisburg-Essen, Essen, Germany.
Abstract
The microenvironment of inflamed and injured tissue is characterized by low levels of oxygen and glucose and high levels of inflammatory cytokines, reactive oxygen, and nitrogen species and metabolites. The transcription factor complex hypoxia-inducible factor (HIF)-1 is regulated by hypoxia as well as by a broad variety of inflammatory mediators. In cells of the innate and adaptive immune system, HIF-1 is upregulated by bacterial and viral compounds, even under normoxic conditions. This upregulation prepares these cells to migrate to and to function in hypoxic and inflamed tissues. Once extravasated from the vasculature, the activity of cells is further enhanced by stimulation of HIF-1 by proinflammatory cytokines like interleukin (IL)-1beta (beta) and tumor necrosis factor (TNF) alpha (alpha), and locally expressed tissue factors. Crosstalk between hypoxic induction of HIF-1 and other signaling pathways activated by inflammation ensures a cell type-specific and stimulus-adequate cellular response. Prolonged activation of HIF-1 under conditions of inflammation, however, may contribute to the survival of damaged tissue and cells, thus promoting the development of tumors.
http://www.ncbi.nlm.nih.gov/pubmed/17998066
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Androgen Alopecia is nothing but a
local Chronic Inflammation induced by
Dihydrotestosterone
Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. Consequently, chronic inflammation is almost always accompanied by tissue destruction.
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Relationship between inflammation and tissue hypoxia in a mouse model of chronic colitis.
Harris NR,
Carter PR,
Yadav AS,
Watts MN,
Zhang S,
Kosloski-Davidson M,
Grisham MB.
Source
Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, USA.
nharr6@lsuhsc.edu
Abstract
BACKGROUND:
Hypoxia has been reported to be associated with the colonic inflammation observed in a chemically induced mouse model of self-limiting colitis, suggesting that low tissue oxygen tension may play a role in the pathophysiology of inflammatory tissue injury. However, no studies have been reported evaluating whether tissue hypoxia is associated with chronic gut inflammation. Therefore, the objective of the present study was to determine whether hypoxia is produced within the colon during the development of chronic gut inflammation.
METHODS:
Adoptive transfer of CD4(+) T cells obtained from interleukin-10-deficient (IL-10(-/-)) mice into lymphopenic recombinase-activating gene-1-deficient (RAG(-/-)) mice induces chronic colonic inflammation, with the inflammation ranging from mild to severe as determined by blinded histological analyses. Colonic blood flow, hematocrit, and vascular density were determined using standard protocols, whereas tissue hypoxia was determined using the oxygen-dependent probe pimonidazole.
RESULTS:
Adoptive transfer of IL-10(-/-) CD4(+) T cells into RAG(-/-) recipients induced chronic colonic inflammation that ranged from mild to severe at 8 weeks following T-cell transfer. The colitis was characterized by bowel wall thickening, goblet cell dropout, and inflammatory infiltrate. Surprisingly, we found that animals exhibiting mild colonic inflammation had increased hypoxia and decreased systemic hematocrit, whereas mice with severe colitis exhibited levels of hypoxia and hematocrit similar to healthy controls. In addition, we observed that the extent of hypoxia correlated inversely with hematocrit and vascular density.
CONCLUSIONS:
Changes in hematocrit, vascular density, and inflammatory state appear to influence the extent of tissue oxygenation in the T-cell-mediated model of chronic gut inflammation.
Copyright © 2010 Crohn's & Colitis Foundation of America, Inc.
http://www.ncbi.nlm.nih.gov/pubmed/20878754
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Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice.
Ye J,
Gao Z,
Yin J,
He Q.
Source
Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, USA.
yej@pbrc.edu
Abstract
Chronic inflammation and reduced adiponectin are widely observed in the white adipose tissue in obesity. However, the cause of the changes remains to be identified. In this study, we provide experimental evidence that hypoxia occurs in adipose tissue in obese mice and that adipose hypoxia may contribute to the endocrine alterations. The adipose hypoxia was demonstrated by a reduction in the interstitial partial oxygen pressure (Po(2)), an increase in the hypoxia probe signal, and an elevation in expression of the hypoxia response genes in ob/ob mice. The adipose hypoxia was confirmed in dietary obese mice by expression of hypoxia response genes. In the adipose tissue, hypoxia was associated with an increased expression of inflammatory genes and decreased expression of adiponectin. In dietary obese mice, reduction in body weight by calorie restriction was associated with an improvement of oxygenation and a reduction in inflammation. In cell culture, inflammatory cytokines were induced by hypoxia in primary adipocytes and primary macrophages of lean mice. The transcription factor NF-kappaB and the TNF-alpha gene promoter were activated by hypoxia in 3T3-L1 adipocytes and NIH3T3 fibroblasts. In addition, adiponectin expression was reduced by hypoxia, and the reduction was observed in the gene promoter in adipocytes.
These data suggest a potential role of hypoxia in the induction of chronic inflammation and inhibition of adiponectin in the adipose tissue in obesity.
http://www.ncbi.nlm.nih.gov/pubmed/17666485
Cell hypoxia is a known additional fuel for chronic inflammation. 
