Adhesion is kind of like fibrosis. It says that DHT causes an increase in adhesion of the vascular system. Theoretically the high DHT in the scalp increases adhesion of the scalp's vascular system.
Bingo!
[h=1]Increased monocyte adhesion by endothelial expression of VCAM-1 missense variation in vitro.[/h]
Schmitz B,
Vischer P,
Brand E,
Schmidt-Petersen K,
Korb-Pap A,
Guske K,
Nedele J,
Schelleckes M,
Hillen J,
Rötrige A,
Simmet T,
Paul M,
Cambien F,
Brand SM.
[h=3]
Author information [/h]
- University Hospital Münster, Institute of Sports Medicine, Molecular Genetics of Cardiovascular Disease, Horstmarer Landweg 39, D-48149 Münster, Germany; University Hospital Münster, Internal Medicine D, Nephrology, Hypertension and Rheumatology, Münster, Germany.
[h=3]Abstract[/h][h=4]OBJECTIVE:[/h]In whole genome and single gene analyses, genetic variation at the vascular cell adhesion molecule-1 (VCAM-1) locus has been associated with inflammatory disease and stroke in sickle cell anaemia. In the current work, we investigated the functional impact of VCAM-1 missense variants and their effect on cell-cell adhesion.
[h=4]METHODS AND RESULTS:[/h]To determine the functional in vitro relevance of five missense VCAM-1 variants (S318F; T384A; G413A; L555V; I716L), we generated wild type and single variant VCAM-1 forms [318F, 384A, 413A, 555V, 716L] in EA.hy926 endothelial cells. Real-time PCR, western blot and ELISA analyses revealed significant differences in mRNA and protein levels for VCAM-1 variants. Monocytic cell lines THP-1 and U937 showed significantly increased adhesion to endothelial cells overexpressing VCAM-1 forms 318F, 555V and 716L compared to those overexpressing wild type VCAM-1 (p < 0.05).
[h=4]CONCLUSIONS:[/h]VCAM-1-dependent cell adhesion to endothelial cells in vitro is significantly increased when expressing VCAM-1 missense mutations 318F, 555V and 716L. The underlying mechanism involves altered VCAM-1 protein levels and function.
This observation may be of particular relevance for chronic inflammatory pathophysiologic conditions involving cell-cell adhesion such as atherosclerosis and other proinflammatory conditions.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
Microvascular insufficiency and local tissue hypoxia (male pattern baldness)1: Med Hypotheses 2002 Apr;58(4):261-3
Hormone-induced aberrations in electromagnetic adhesion signaling as a developmental factor of androgenetic alopecia.
Matilainen VA, Keinanen-Kiukaanniemi SM.
Department of Public Health Science and General Practice, University of Oulu, Finland.
In androgenetic alopecia, overactivation of the androgen hormone cascade in genetically predisposed persons leads to miniaturization of the dermal papilla of the hair follicle and to reduction in the number of papilla cells in the scalp, but the mechanisms explaining this miniaturization have remained unclear. According to our hypothesis, the increase of dihydrotestosterone (DHT) production in the overactive androgen state inhibits cell mitosis in the dermal papilla and contributes to the induction of programmed cell death (apoptosis). Normally, DNA molecules have a negative charge, which doubles in every cell mitosis. In the catagen and telogen phases, the sulphur-rich hair moves upwards, dehydrates and develops an increasing positive charge. In a normal hair-growth cycle, the epithelial column shortens and the secondary germ is formed and it invaginates the dermal papilla by electromagnetic attraction. In the mitotic inhibition state induced by DHT, the negative charge decreases, leading to a weakening of the electromagnetic adhesion forces and weaker electrical attraction between the undifferentiated germ cells and the dermal papilla. Insulin resistance has an additional pathogenic role in the excessive miniaturization of the hair follicle. The vasoactive substances associated with endothelial dysfunction in insulin resistance induce microcirculatory disturbance, perifollicular vasoconstriction and stimulation of smooth muscle cell proliferation in the vascular wall. This leads to microvascular insufficiency and local tissue hypoxia and progressive miniaturization of hair follicles.
1: Plast Reconstr Surg 1996 May;97(6)1109-16; discussion 1117
Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.
Goldman BE, Fisher DM, Ringler SL.
Department of Plastic Surgery, Butterworth Hospital, Grand Rapids, Mich., USA.
Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
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squegee btw did you try those growth factors? (those litle bottles someone once posted here and you said that you bought some) any expirience? and gief pics!!!
Dunno man! I just mixed them with minoxidil LOL.. Stick to the derma roller!!
