Bald scalp in men with androgenetic alopecia retains hair fo

squeegee

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Guys we almost there!


Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.

http://www.jci.org/articles/view/44478#SEC3
 

Nene

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I really hope something comes of this but I'm skeptical. Every few years they make some discovery and nothing ever happens.
 

squeegee

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Nene said:
I really hope something comes of this but I'm skeptical. Every few years they make some discovery and nothing ever happens.


Nene , this study is a solid proof that Oxidation/Inflammation does the damage when it comes to male pattern baldness.. The progenitor cells just need to be activated and we have enough remaining stem cells to make the problem reversible.. This is the best study ever.. :punk:
 

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Association between circulating endothelial progenitor cells and hs-CRP in patients with diabetes

1. Megumi Koshikawa
1.
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan, Division of Blood Transfusion, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan

1. Atsushi Izawa
1.
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan

1. Takeshi Tomita
1.
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan

1. Setsuo Kumazaki
1.
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan

1. Jun Koyama
1.
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan

1. Shigetaka Shimodaira
1.
Division of Blood Transfusion, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan

1. Uichi Ikeda
1.
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan, uikeda@shinshu-u.ac.jp

Abstract

Aim

Endothelial progenitor cells (EPCs) play a critical role in maintaining endothelial function and might affect the progression of vascular disease. This study investigated the relationship between circulating EPCs and high-sensitivity C-reactive protein (hs-CRP) in patients with diabetes.

Methods

Our study population comprised 190 consecutive patients, with and without diabetes. To obtain EPC numbers, CD34+ and CD133+ cells in peripheral blood were counted by flow cytometry.

Results

Significantly higher hs-CRP levels were observed in patients with diabetes than in those without diabetes. However, the number of EPCs was significantly lower in diabetic patients and in patients with high hs-CRP levels. Patients with diabetes and high hs-CRP levels showed a marked decrease in the number of EPCs compared with non-diabetic patients with low hs-CRP levels.

Conclusion

These results suggest that inflammation leads to decreased circulating EPCs in patients with diabetes, which might be related to the pathogenesis of diabetic vascular disease.
 

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COLUMBUS, Ohio – Ohio State University medical researchers have demonstrated that reactive oxygen species at appropriate levels can support the healing of wounds, and specifically that wounds can generate their own low concentration of hydrogen peroxide, which has a role in healing.
A recent Ohio State study showed that at the site of injury, cells of wound tissue convert oxygen to reactive oxygen species, triggering oxidation-reduction, or redox driven mechanisms. Excess levels of reactive oxygen species, such as during chronic inflammation, may impair healing, but low levels offer healing benefits.

The observation that the redox state of the wound tissue may influence healing outcomes could lead to consideration of a novel redox-based principle for wound therapy, said Chandan Sen, lead author of a paper detailing the findings and professor and vice chair of the department of surgery at Ohio State.

The research paper is available in the online version of Molecular Therapy, the journal of the American Society of Gene Therapy.

A key characteristic of problem wounds is that they are hypoxic, or suffer from poor oxygenation, meaning too little oxygen is available to initiate the reactive oxygen-dependent healing processes.

“Proper oxygenation of a wound is a fundamental pre-requisite,†said Sen, also deputy director of the Davis Heart and Lung Research Institute at Ohio State and chief editor of the international journal Antioxidants and Redox Signaling.

Under conditions of sufficient oxygenation, wound-related cells generate small amounts of reactive oxygen products, including hydrogen peroxide, which, at correct levels, acts as a chemical messenger to support healing. The hydrogen peroxide in question is not the typical household strength 3 percent solution, but a lower concentration of the compound that at a molecular level sends a message needed to trigger angiogenesis, or the formation of new blood vessels, the scientists found.

Their study provides the first direct evidence that low levels of hydrogen peroxide are enzymatically generated by the body as a wound heals in healthy tissue.

Problem wounds, however, may suffer from conditions that limit hydrogen peroxide production at the wound site. These conditions cause improper oxygenation and compromised immune function, or stem from genetic defects or chronic conditions such as diabetes that compromise the enzyme NADPH oxidase, a cellular mechanism behind the ability to kill bacteria. In these and similar cases in which the body can’t be counted on to heal itself, appropriate delivery of reactive oxygen species could provide a new basis for therapeutic exploration, the scientists said.

“We’re saying that the body makes hydrogen peroxide at very minute dosages that act as a signal for repair,†Sen said. “An excess of hydrogen peroxide can be damaging, but if we can find an innovative approach to deliver low levels of hydrogen peroxide into wounds that are difficult to heal, that could be helpful.

“Basic science studies have identified hydrogen peroxide as a trigger that drives redox signaling. Redox-based strategies to heal problem wounds may be applicable to a large number of people suffering from chronic wounds, such as diabetics, the immune-challenged and those suffering from chronic granulomatous disease,†he added.

To mirror those conditions, Sen and colleagues designed a study to compare wounds in mice with compromised health – specifically, mice deficient in MCP-1, a protein known for its involvement in recruitment of immune cells to wounds and in the formation of blood vessels, and others deficient in p47phox, a member of NADPH oxidase family – to wounds in mice with normal health to monitor molecular activity under varying conditions. In mice with built-in deficiencies whose wounds were not healing, the topical application of low-dose hydrogen peroxide identical to the concentration that occurred naturally in healthy mice corrected abnormal wound closures, the study reports.

Scientists determined that one key role of hydrogen peroxide in wound healing is to induce vascular endothelial growth factor in wound-related cells, a gene believed to be the most efficient signal to stimulate blood vessel formation in wounds.

Using a viral gene delivery approach involving catalase, an enzyme that rapidly decomposes hydrogen peroxide, scientists also showed that forced decomposition of hydrogen peroxide generated by the wound tissue results in impaired healing. Sen said these observations underscore the significance of hydrogen peroxide, generated by wound cells, in deciding healing outcomes.

Sen said the study sets a new paradigm supporting the role of reactive oxygen species – generated from oxygen – as a signal for repair in the healing process. He added that these new findings also underscore the critical need to ensure that wounds are appropriately oxygenated.

A strong solution of hydrogen peroxide has been historically used clinically to disinfect wounds. While such an approach may be effective in disinfecting, hydrogen peroxide at that strength may hurt newborn regenerating tissue. The study showed that too much hydrogen peroxide can be damaging to a wound.

“Our observation that dermal wound healing is subject to redox control represents an important step toward redox-based therapies in the clinic,†Sen said. “The solution to problem wounds lies in an interdisciplinary multifactorial approach. To enable that solution, all facets of a problem wound need to be mechanistically understood. The redox control aspect represents a new facet.â€

A grant from the National Institute of General Medical Sciences of the National Institutes of Health supported this work.
 

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Scientists have discovered recently that a healthy crop of circulating endothelial progenitor cells -- the stem, or precursor cells to those that line the insides of blood vessels -- is essential to a person's overall cardiovascular health and unimpeded blood circulation. Endothelial cells enable communication between the vessels themselves and circulating blood cells, allowing the blood to flow smoothly.

http://www.sciencedaily.com/releases/20 ... 173213.htm
 

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Folic acid supplementation normalizes the endothelial progenitor cell transcriptome of patients with type 1 diabetes: a case-control pilot study.

van Oostrom O, de Kleijn DP, Fledderus JO, Pescatori M, Stubbs A, Tuinenburg A, Lim SK, Verhaar MC.

Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, the Netherlands. o.vanoostrom@umcutrecht.nl
Abstract

BACKGROUND: Endothelial progenitor cells play an important role in vascular wall repair. Patients with type 1 diabetes have reduced levels of endothelial progenitor cells of which their functional capacity is impaired. Reduced nitric oxide bioavailability and increased oxidative stress play a role in endothelial progenitor cell dysfunction in these patients. Folic acid, a B-vitamin with anti-oxidant properties, may be able to improve endothelial progenitor cell function. In this study, we investigated the gene expression profiles of endothelial progenitor cells from patients with type 1 diabetes compared to endothelial progenitor cells from healthy subjects. Furthermore, we studied the effect of folic acid on gene expression profiles of endothelial progenitor cells from patients with type 1 diabetes.

METHODS: We used microarray analysis to investigate the gene expression profiles of endothelial progenitor cells from type 1 diabetes patients before (n = 11) and after a four week period of folic acid supplementation (n = 10) compared to the gene expression profiles of endothelial progenitor cells from healthy subjects (n = 11). The probability of genes being differentially expressed among the classes was computed using a random-variance t-test. A multivariate permutation test was used to identify genes that were differentially expressed among the two classes. Functional classification of differentially expressed genes was performed using the biological process ontology in the Gene Ontology database.

RESULTS: Type 1 diabetes significantly modulated the expression of 1591 genes compared to healthy controls. These genes were found to be involved in processes regulating development, cell communication, cell adhesion and localization. After folic acid treatment, endothelial progenitor cell gene expression profiles from diabetic patients were similar to those from healthy controls. Genes that were normalized by folic acid played a prominent role in development, such as the transcription factors ID1 and MAFF. Few oxidative-stress related genes were affected by folic acid.

CONCLUSION: Folic acid normalizes endothelial progenitor cell gene expression profiles of patients with type 1 diabetes. Signaling pathways modulated by folic acid may be potential therapeutic targets to improve endothelial progenitor cell function.
 

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High cholesterol causes increased oxidative stress, impairing the function of EPCs. In addition to being implicated in cardiovascular diseases, oxidative stress is also a factor in diabetes.

"Further studies of how oxidative stress impairs the function of EPCs are critical. Eventually you should be able to get a simple blood test measuring your EPCs to see if you are at risk for disease. With this knowledge, in the not too distant future, we should be able to apply antioxidant therapies to prevent that disease," said Dr. Haneline.

In the meantime studies that examine the impact of oxidative stress on specific functions of the EPCs are needed to fully understand the progression of vascular disease.
 

Letac

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I\m not sure if I understand this right... When do they think that they will have something out of this? And what does it really do? Give the smaller bloodvains more "power" and then starts to regrow hair?
 

Jacob

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squeegee said:
This research suggests that Stem-Kine, a commercially-available supplement, can increase the blood circulation of hematopoietic stem cells, which can give rise to all blood cells, and endothelial progenitor cells, which repair damage to blood vessels.

http://www.stem-kine.com/science3.asp

Some Growth Factor Therapy for Hairloss:

http://www.hairlosshelp.com/forums/mess ... adid=91970

There's a thread on Stem Kine etc at HLF...I'd post the link but I think it'd get ****"d out. Not sure why HLH gets a pass :dunno:

http://www.hairlossfight.com/forums/viewtopic.php?t=1853

I knew it :) Just put hair loss fight in place of the *'s

One of the many links/products posted there: http://www.ppginco.com/eng/therapies/beauty.html
 

Jacob

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And colostrum/PRP's:
"The richest of all zoonutrients is the “first mealâ€￾ of all mammals, called colostrum. Colostrum provides a macro and micro nutrient dense “super foodâ€￾. This “first mealâ€￾ for all mammals is also rich in antibodies (Ig), cell signaling messengers (cytokines) that modulate the immune system, and growth factors stimulating stem cell activity

Growth factors in colostrum help activate stem cells.

http://www.biopharmasci.com/downloads/PRPwoundheal.pdf

http://biopharmasci.com/downloads/NanoProAnti-AgingTherapeutics.pdf
 

Jacob

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Topical hGH:

All these diverse efficacies of NL-hGH
seem to indicate that somehow the skin
stem cells of the bulge or transiently amplifying
progenitor cells derived from
the bulge stem cells in the hair follicle
(Fig. 11), are influenced by the presence
of exogenous hGH and involved in the
pharmaceutical and cosmetic outcomes
of the topical NL-hGH application. Based
on this rationale, we further examined
whether hair (follicle) number or the hair
growth cycle of the mouse is affected by
the application of NL-hGH, using minoxidil
as a positive control. Mice were treated
for 2 weeks with NL-hGH after depilation
and before peritoneal BrdU injection
and subsequently sacrificed 3 hrs
after the injection. The results clearly
showed that NL-hGH application on the
back of the mouse increased not only the
hair number but potentially the hair
length and thickness. As, in a given hair
bulb, a more number of actively proliferating hair matrix cells is correlated
with longer duration of anagen phase,
thus with longer and thicker hair (17).
Minoxidil influenced on the hair number
as well, but not the hair length or thickness.
These results are summarized in
Fig. 12. Therefore NL-hGH was superior
to minoxidil in increasing both the hair
number and possibly the hair length and
thickness in the mouse experiments.
 

squeegee

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Thanks a lot Jacob!!! :punk:
 

squeegee

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Jacob said:
squeegee said:
This research suggests that Stem-Kine, a commercially-available supplement, can increase the blood circulation of hematopoietic stem cells, which can give rise to all blood cells, and endothelial progenitor cells, which repair damage to blood vessels.

http://www.stem-kine.com/science3.asp

Some Growth Factor Therapy for Hairloss:

http://www.hairlosshelp.com/forums/mess ... adid=91970

There's a thread on Stem Kine etc at HLF...I'd post the link but I think it'd get ****"d out. Not sure why HLH gets a pass :dunno:

http://www.**********.com/forums/viewtopic.php?t=1853

I knew it :) Just put hair loss fight in place of the *'s

One of the many links/products posted there: http://www.ppginco.com/eng/therapies/beauty.html

That PPG stuff How Much is it??

Probably gonna go on colostrum and Stem-Kine...
 

Jacob

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Not sure about the PPG stuff...at least not the one I referred to. Elsewhere on their site they talk about Dammarane Sapogenins..which are available:

http://www.netriceuticals.com/listing.asp?id=1053

http://www.panagin.com/order/order_page.php

Scientists of Pegasus Canada have successfully extracted Dammarane Sapogenins from ginseng by using Selective Metabolites Compound Drug, and the active compound in the product has reached above 80%. This is an amazing achievement in the field of medicine. Dammarane Sapogenins has been proved through clinical trials that it remarkably improves the multiplication of stem cells such as hematopoietic stem cells, and more importantly, it is safer and more effective when compared with other pharmaceutical drugs.

Dammarane sapogenins, a herbal stem cell stimulating growth factor, is considered to be a milestone in the field of stem cell research of natural herbal medicines. Relationship between the soil and the seed could be used as a metaphor for the relationship between dammarane sapogenins and stem cells, which must be nourished much as seeds are by the soil in which they grow. As dammarane sapogenins acting like an organic fertilizer continuously supplies nutrition to stem cells, living a long life and possessing eternal youth will never be just a dream.



Feel free to send me a few :shock:
 

squeegee

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Jacob said:
Not sure about the PPG stuff...at least not the one I referred to. Elsewhere on their site they talk about Dammarane Sapogenins..which are available:

http://www.netriceuticals.com/listing.asp?id=1053

http://www.panagin.com/order/order_page.php

Scientists of Pegasus Canada have successfully extracted Dammarane Sapogenins from ginseng by using Selective Metabolites Compound Drug, and the active compound in the product has reached above 80%. This is an amazing achievement in the field of medicine. Dammarane Sapogenins has been proved through clinical trials that it remarkably improves the multiplication of stem cells such as hematopoietic stem cells, and more importantly, it is safer and more effective when compared with other pharmaceutical drugs.

Dammarane sapogenins, a herbal stem cell stimulating growth factor, is considered to be a milestone in the field of stem cell research of natural herbal medicines. Relationship between the soil and the seed could be used as a metaphor for the relationship between dammarane sapogenins and stem cells, which must be nourished much as seeds are by the soil in which they grow. As dammarane sapogenins acting like an organic fertilizer continuously supplies nutrition to stem cells, living a long life and possessing eternal youth will never be just a dream.



Feel free to send me a few :shock:


LOL! Holy sh*t not cheap at all! I hope that stuff is effective!


Note: Special quantity discounts apply. Purchase 4 bottles or more and the price becomes $295.00 per bottle. The discount will appear on the invoice.
 

Jacob

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So you're going to send me 4 bottles? Cool! :woot:

BTW.. PQQ has really PQ'd my interest:

http://www.lef.org/magazine/mag2010/ss2010_Rejuvenate-Your-Cells-Growing-New-Mitochondria_01.htm

PQQ’s potential to stimulate mitochondrial biogenesis was foreshadowed by early findings indicating its central role in growth and development across multiple forms of life.
PQQ Is an Essential Micronutrient

PQQ has been shown to be a potent growth factor in plants, bacteria, and higher organisms.21,24,25 Pre-clinical studies reveal that when deprived of dietary PQQ, animals exhibit stunted growth, compromised immunity, impaired reproductive capability, and most importantly, fewer mitochondria in their tissue. Rates of conception, the number of offspring, and survival rates in juvenile animals are also significantly reduced in the absence of PQQ.26-28

When PQQ is introduced back into the diet, it reverses these effects, restoring systemic function while simultaneously increasing mitochondrial number and energy efficiency.

These compelling data prompted a team of researchers at the University of California-Davis to specifically analyze PQQ’s influence on cell signaling pathways involved in the formation of new mitochondria.14

Their work, published last year, led to several extraordinary discoveries. They found that PQQ’s critical biological roles stem from its ability to activate genes directly involved in cellular energy metabolism, development, and function.14

Mitochondrial biogenesis can be defined as the growth and division of pre-existing mitochondria. This phenomenon is not only accompanied by increased mitochondria numbers, but also their size and mass.

Mitochondrial biogenesis requires the coordinated synthesis and import of 1,000-1,500 proteins where they facilitate the production of healthy new mitochondria.

Mitochondrial biogenesis occurs through the combined effects of genes activated by PQQ via the following three mechanisms:

* PQQ increases expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha or PGC-1?. PGC-1? is a “master regulatorâ€￾ gene that mobilizes your cells’ response to various external triggers. It directly activates genes that boost mitochondrial and cellular respiration, growth, and reproduction. Its capacity to modulate cellular metabolism at the genetic level favorably affects blood pressure, cholesterol and triglyceride breakdown, and the onset of obesity.29
* PQQ activates a signaling protein known as cAMP-response element-binding protein or CREB. The CREB gene plays a pivotal role in embryonic development and growth. It also beneficially interacts with histones, molecular compounds shown to protect and repair cellular DNA. CREB also stimulates the growth of new mitochondria.30
* PQQ regulates a recently discovered gene called DJ-1. As with PGC-1? and CREB, DJ-1 is intrinsically involved in cell function and survival. It has been shown to prevent cell death by combating intensive antioxidant stress and is of particular importance to brain health and function. DJ-1 damage and mutation have been conclusively linked to the onset of Parkinson’s disease and other neurological disorders.31-34
 
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