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Foods and ht healing

topccat29

topccat29

29 year HT veteran
Bullitnut most of those foods listed I would agree with being very beneficial to one €™s health even the beer which drastically raises uric acid levels can be beneficial depending on the source. If one looks at old world ways of making slow healthy food then one can understand why. Most beer in Germany for instance is not pasteurized. It is sold the way it was meant to be consumed as a true fermented beverage no different than eating sauerkraut. Replenishing gut bacteria which greatly increases health and reduces disease. Pasteurization when it comes to food has more to do with shelf life and profit one only needs to understand the system.

I just made some fermented vegetables which takes about 1 week and it has 10 strains of bacteria in the recipe. My wife made some fermented apple juice. Both easy to make and essential for peak health avoiding cancers of the stomach, colon, etc.

Where does the food come from is probably more important and what was the process used in bringing it to market. It would take too long to go over every little detail. I can tell you this for certain. Money is mostly made in the food industry branding and trade marking and growing commodities also plays a huge part. When food becomes a commodity it can be exchanged just like cash and it can go up and down in value. This is why crops like soybeans are so prevalent in the system. They are extremely easy to grow, you can do anything with them and they can be stored like putting money in a bank account. We are only talking about one commodity here of which there are many. Fresh meats, vegetables, raw milk etc have zero shelf life. No money to be made as they can only be sold locally in small quantities. So the system has done a good job of brain washing the masses.

The chickens I am now raising eat a natural diet and that is evident in the eggs they produce. There are no estrogens in the yolks, nor are they top heavy in free radical producing poly unsaturated fatty acids, etc. They are in fact a healthy food. These eggs specifically and not the eggs you buy in the store and there is a big difference. Guaranteed the store eggs regardless of if they organic or not are fed soy €¦ €¦ €¦ €¦ €¦ €¦ €¦.guaranteed. It €™s cheap, chickens will eat it and they will produce more eggs.

It is also guaranteed that the whey protein comes from a cow fed soy, antibiotics, estrogen, etc. Because those are the economics of mass food production. But with enough promotion anybody can be convinced that a estrogen laden, oxidized powder which has been sitting on a shelf in a giant plastic container has some type of miracle healing properties. IDK €¦ €¦ €¦..maybe just put some picture of a guy with big muscles on the label.

The Mail had an article the other day which I thought was unusual as most newspaper and magazine are filled with inaccurate information and PR type pieces. I pasted it below and below that I took a picture of some of my eggs recently produced.

Female sex hormone is 'fuelling male obesity epidemic and causing sperm counts to drop' as men become 'feminised'
  • Female sex hormone oestrogen is known to cause weight gainThis is because it inhibits the thyroid which slows down metabolismScientists said Western men exposed to oestrogen are becoming 'feminised' Could also explain the drop in sperm count in men in affluent countries Oestrogen is present in plastics, PVC and soy products
By Madlen Davies for MailOnline


Published: 05:55 EST, 10 October 2014 | Updated: 11:31 EST, 10 October 2014

The obesity epidemic in men could be fuelled by the female sex hormone oestrogen, scientists claim.

Experts believe the hormone could also be causing the well-documented drop in sperm count among Western men.

They said men in affluent countries are becoming 'feminised', as they come into contact with products contain the female sex hormone.

Compounds found in some plastic items, including drainpipes, and soy food products can mimic the effects of oestrogen, scientists said.

Secreted by the ovaries in pre-menstrual women, oestrogen is known to cause weight gain, inhibiting the thyroid gland and affecting other areas of the brain.

Scroll down for video


Obesity rates in the West could be caused by the female sex hormone obesity, scientists claim

The authors noticed that in Western societies men have closer rates of obesity to women than in the developing world, where rates of obesity in women are significantly higher than rates of male obesity.

Study author James Grantham, from the University of Adelaide's School of Medical Sciences, compared obesity rates among men and women from around the world with measures such as Gross Domestic Product to determine the impact of affluence on obesity.

He found that while it was normal for women in the developing world to have significantly greater levels of obesity than men, the developed world offers a different picture.

He said: 'Hormonally driven weight gain occurs more significantly in females than in males, and this is very clear when we look at the rates of obesity in the developing world.
'However, in the Western world, such as in the United States, Europe and Australia, the rates of obesity between men and women are much closer.

'In some Western nations, male obesity is greater than female obesity.

'While poor diet is no doubt to blame, we believe there is more to it than simply a high calorie intake.'

Co-author Professor Maciej Henneberg added that exposure to oestrogen is known to cause weight gain, through inhibiting the thyroid.

The thyroid is a gland which releases hormones, and if it is inhibited it causes the body's metabolism to slow down, leading to weight gain.

Prof Hennenberg added that soy products contain 'xenestrogens', a compound which imitates the effects of the oestrogen.

She said: 'We are concerned that in societies with a high dietary saturation of soy, such as the United States, this could be working to 'feminise' the males.







Notice the color of the egg near the bottom when compared to the rest and notice that gelatin ring that keeps the egg tight. Is your egg the same?


I can tell you this with absolute certainty. There is a market for honest information and as the public is slowly becoming aware that is where they will be heading. Frankly they are sick of being lied to and being harmed in the process.












 
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topccat29

topccat29

29 year HT veteran
I can tell you this for certain. Slowly more and more people are becoming aware of food and health. It has been a very slow process but with so many bloggers out there generating content the pace has quickened. If you look at some of them like Mercola for example. He is a multi millionaire but he still stays true to himself and his passion. Money in fact is not a driving force for him but it has always been the truth.

Some have a hard time dealing with too much success and money and simply goes to their head and they lose their way. I remember going to Whole Foods and Wild Oats 30 years ago when there were less than a handful of stores on the west coast. It was different and not what it is today. I joined the Life Extension Foundation about 34 years ago and it too is not what it was back then. It €™s seems like the money has gotten to them the same can be seen in the HT industry.

When the citizens in California wanted to have GMO products labeled who actively worked and donated their own money to help pass it, people like Mercola. It €˜s not what a person says it is what they do, it €™s their actions. Mercola never needed sponsors all he needed was truthful content and associating with honest people the rest just comes naturally.

Truthful content is what most are in search of and eventually we will all be able to find it. That is where the market is, in the truth. Business sometimes rises and falls on the truth and sometimes fortunes are lost and sometimes people even go to prison.

I just fed these chickens a half a jar of worms the other day which they ate in about 30 seconds. Because that is what they eat. Bugs, worms, grass etc and not concentrated sources of grain.

 
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topccat29

topccat29

29 year HT veteran
Some of the foods that I eat in fact most of the foods I eat directly modulate MTOR the mammalian target of Rampmycin. The short explanation is that driving MTOR is critical in promoting protein synthesis (putting on muscle and burning bodyfat) the number one driver of MTOR is the branched chain amino acid Leucine and the number one food with the highest level of usable leucine is raw eggs. Other drivers of MTOR include cocoa, curcumin, caffeine, and fasting in such a way that one can load protein. Nothing surpasses the usability of the raw egg €¦ €¦ €¦ €¦ €¦..whey protein that sits on a shelf in a plastic container does not even come close.

During my post surgery I consumed at least a dozen raw eggs mixed with cocoa a day and usually more. I enjoy it blended and sweetened with stevia. I €™m not suggesting you do this as you should do what you think is right this is just me relaying my experience. What €™s interesting about this is that one can find research on MTOR and accelerated wound healing. I see so many articles presented in which pharmaceuticals are used when in my opinion food works so much better but of course it €™s not going to be promoted much as there is no monetary incentive but many should research this area and it does require research because it simply will not be promoted.

I cannot tell you to eat raw eggs in fact if you buy store bought eggs there is a good chance they could be contaminated. I purchase farm eggs from the farm and know the source and I have been eggs loads of eggs including raw for at least 15 years or more.

Below is an article on MTOR and accelerated wound healing and that is the very long version. I don €™t expect most would want to read it as it does become somewhat long and boring but it does also explain why something as simple as an egg can make a difference even though it does not mention the egg specifically applies.

The pictures are not going to show up but I will add 2 and you can see the difference when the MTOR pathway is activated.

Abstract
Background
The management of slow or non-healing ulcerations constitutes an increasing clinical challenge in the developed world because of the ageing of the population and the pandemic rise in type II diabetes. Recent studies suggest that molecular circuitries deployed by tumor cells to promote cancerous growth may also contribute to tissue regeneration. Here, we exploited this emerging information to search for novel molecular targets to accelerate wound healing.
Methodology/Principal Findings
We found that the activation of the PI3K-Akt-mTOR pathway, whose aberrant function is a frequent event in human neoplasia, represents an integral component of the normal wound healing process. By the use of genetically defined approaches, including the epithelial-specific ablation of Pten and Tsc1, we show that mTOR activation can dramatically increase epithelial cell proliferation, migration, and cutaneous wound healing, while pharmacological inhibition of mTOR with rapamycin delays wound closure.
Conclusions/Significance













12
Citation: Squarize CH, Castilho RM, Bugge TH, Gutkind JS (2010) Accelerated Wound Healing by mTOR Activation in Genetically Defined Mouse Models. PLoS ONE 5(5): e10643. doi:10.1371/journal.pone.0010643
Editor: Maria G. Castro, UCLA and Cedars-Sinai Medical Center, United States of America
Received: February 17, 2010; Accepted: April 8, 2010; Published: May 13, 2010
This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
Funding: This research was supported by the Intramural Research Program of NIH, National Institute of Dental and Craniofacial Research. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
[1], [2], [3].
[4], [5], [6]. In this regard, the phosphatidylinositol 3 kinase (PI3K)-Akt pathway is one of the most frequently aberrantly activated intracellular signaling routes in cancer [7], [8], [9], [10]. The persistent activation of growth factor receptors by mutations or autocrine and paracrine mechanisms, gene amplification resulting in overexpression of PI3K and/or mutations in its coding sequence rendering this lipid kinase constitutively active, as well as decreased activity of the lipid phosphatase PTEN by multiple genetic or epigenetic events, all converge to promote the aberrant accumulation phosphatidylinositol-3,4,5-triphosphate (PIP[sub]3[/sub]) in cancer cells, thereby causing the activation of the serine-theronine kinase Akt and its downstream targets, including the mammalian target of rapamycin (mTOR) [7], [8], [11]. These observations prompted us to explore whether the PI3K-Akt pathway participates in wound repair, as well as whether the targeted activation of this signaling pathway represents a suitable approach to accelerate wound healing. We show here that PI3K-Akt activation promotes cutaneous wound repair via mTor. More importantly, we demonstrate that elevating mTor activity dramatically accelerates the healing process, suggesting a novel strategy for the clinical management of slow or non-healing ulcerations.
Figure 1, normal) is organized into the basal layer that progressively differentiates into the spinous layer, granular layer and finally the stratum corneum. These four layers express distinct cytokeratins. For example, cytokeratin (K) 14 is expressed on the basal layer while and K10 is expressed in the suprabasal layers. During wound healing, migrating keratinocytes form a thin wedge-shape epithelial tongue of a few cell layers which establish the leading wound edge (figure 1- Epithelial tongue). There is also an increase in the thickness of the spinous layer adjacent to the wound and a rapid proliferation of epithelial cells immediately next to the migrating epithelial tongue (figure 1- Transitional)[1]. During the healing process, proliferation and migration are intimately related, with hyperproliferative cells in the transitional tissue feeding the migrating epithelial sheaths that form the epithelial tongue, as part of an interdependent process [1], [12].


Figure 1. The Akt-mTOR pathway is upregulated during wound healing.
[13], [14], accumulate in the granular layer, consistent with our recent findings in postnatal skin development [15]. During wound healing, however, there is an expansion of the cell layers exhibiting pAkt[sup]473[/sup] and pS6 in the spinous layer of the transitional epithelium, and a remarkable phosphorylation of these molecules in all layers in the migrating epithelial tongue. The most striking was the presence of pAkt[sup]473[/sup] and pS6 in the basal layer of the epithelial tongue, which was always absent from the normal epithelium (Figure 1).
Pten excision accelerates wound closure
[11]. We specifically removed Pten from the epithelial compartment of the skin by crossing mice harboring a floxed Pten allele (Pten[sup]F/F[/sup]) with mice expressing the Cre recombinase under the control of the K14 promoter (K14Cre). Incisional skin wounds were performed in control and Pten epithelial-specific conditional knockout mice (K14Cre Pten[sup]F/F[/sup]). A clearly faster rate of healing upon Pten excision from the skin mice was apparent as early as 4 days after wounding (Figure 2A), which was confirmed by quantification of the wound area (p = 0.0071, Figure 2B). Analysis of wound closure also indicated that the Pten epithelial-specific conditional knockout mice display a significant increase in the rate of wound healing, with half of the K14Cre Pten[sup]F/F[/sup] mice healing by day 7, compared to the control mice that displayed a median wound closure of 11 days (p<0.0001, Figure 2C).


Figure 2. Accelerated wound closure upon epidermal Pten deletion: Enhanced mTor activation and re-epithelization.
Figure 2D-transition) as compared to non-wounded epithelium (Figure 2D, normal). Pten excision enhanced epidermal proliferation as reflected by the number of BrDU-positive keratinocytes in the transitional compartment adjacent to the wound edge (Figure 2E, p = 0.0331). In addition, the wounds of K14Cre Pten[sup]F/F[/sup] mice were characterized by the presence of an elongated migrating epithelial tongue that displayed high levels of expression of pAkt[sup]473[/sup] and pS6 (Figure 2D). In line with this observation, the Pten epithelial-specific conditional knockout mice showed accelerated re-epithelization as judged by the direct quantification of the length of the epithelial migrating tongue (p = 0.0268, Figure 2F). This increased migratory behavior could be recapitulated in primary keratinocyte cultures from control and K14Cre Pten[sup]F/F[/sup] mice (Figure 3A €“3B). As expected, Pten was almost absent in keratinocytes isolated from K14Cre Pten[sup]F/F[/sup] mice (Figure 4A, top panel). Using a scratch wound assay, we observed that excision of Pten accelerated keratinocyte migration into the denuded area (p = 0.0002, Figure 3A €“3B). These results are aligned with in vitro studies linking Pten with cell polarization and directional migration [16], [17]. In addition, the lack of Pten expression led to an enhanced proliferation of the primary keratinocytes (p<0.001, Figure 3C). The addition of EGF, a growth and pro-migratory factor that stimulates the PI3K-Akt pathway, served as an internal control. While EGF promoted the proliferation of control keratinocytes to nearly the same levels than Pten deficient cells, this growth factor failed to increase the proliferation of keratinocytes lacking Pten, likely because they may have already achieved a maximal proliferative capacity due to the persistent activation of Akt in the absence of Pten. Indeed, elevated levels of pAkt[sup]308[/sup], pAkt[sup]473[/sup], and pS6 were also observed in primary cultures of keratinocytes isolated from K14Cre Pten[sup]F/F[/sup] mice (Figure 4A), albeit primary keratinocyte cultures from control mice often have demonstrable basal levels of pS6. Rapamycin treatment, which inhibits mTOR [14], [18], led to a complete ablation of pS6 phosphorylation, although it had only a limited impact on pAkt[sup]Ser473[/sup] levels (Figure 4A), aligned with a direct effect of rapamycin on the mTORC1 complex after short time treatment [19], [20]. Rapamycin caused a decreased proliferation of control and Pten knock out keratinocytes (Figure 4B), supporting a role for mTOR in epithelial cell growth in wild type cells as well as downstream from Pten.


Figure 3. Keratinocyte migration in vitro is enhanced upon Pten excision.


Figure 4. Rapamycin regulates the Akt-mTOR network in Pten-deficient keratinocytes and delays wound healing.
methods for details) and wound closure was used as endpoint; n = 8 for each genotype and time point; p values are indicated.
doi:10.1371/journal.pone.0010643.g004
Rapamycin delays healing in vivo
[21], [22]. This was reflected in a significant delay in wound closure upon rapamycin treatment of control mice when compared to mice treated with vehicle (p = 0.0154, Figure 4C). We also analyzed the consequences of chronic and long term use of rapamycin by performing incisional wounds on mice treated for more than 6 months with rapamycin, which delayed wound closure to an extent similar to that caused by rapamycin administration during the acute wound healing studies (data not shown). Using this pharmacological approach, we next investigated whether mTor contributes to the acceleration of wound healing caused by Pten deletion. K14Cre Pten[sup]F/F[/sup] mice treated with rapamycin presented a delayed wound closure when compared to vehicle injected K14Cre Pten[sup]F/F[/sup] mice (p<0.0001, Figure 4D). These results showed that inhibition of mTOR in vivo abrogates the accelerated wound healing caused by Pten deletion in the epithelial compartment, thus suggesting an important role for mTor in the wound healing process downstream from PI3K and Pten.
Activation of mTor in the epithelial compartment accelerates wound closure
[23]. TSC2 associates with a second tumor-suppressor protein, tuberous sclerosis complex protein 1 (TSC1), acting together as a GTPase activating protein (GAP) for the small GTPase Rheb1. The inactivation of TSC2/TSC1 complex by Akt leads to the accumulation of the GTP-bound (active) form of Rheb1, which in turn promotes the direct activation of mTOR (reviewed in [23]. Thus, as a genetically defined approach to further examine the role of epithelial mTOR in accelerated wound healing, we conditionally excised Tsc1 from keratinocytes thereby activating mTOR by perturbing a negative regulatory step acting immediately downstream from PI3K and Akt. After wounding, the area of the wounds was measured daily (Figures 5A and 5B) and the time to wound closure was determined. Epithelial specific excision of Tsc1 accelerates wound healing in vivo (figure 5A, B, & C), which is evident throughout the healing process as early as day 1 (p<0.0001, Figure 5B). Indeed, the median wound closure time in K14Cre Tsc1[sup]F/F[/sup] mice is 9 days, as compared to day 11 in littermate control mice (p = 0.0150, Figure 5C). Histological analysis of the wounds confirmed the upregulation of mTOR signaling on the K14Cre Tsc1[sup]F/F[/sup] mice, which displayed an overexpression of pS6 in the normal, transitional and the elongated migrating epithelial tongue of the skin epithelium when compared to the control mice (Figure 6A). Moreover, ablation of Tsc1 in the skin compartment resulted in the increased re-epithelization in the K14Cre Tsc1[sup]F/F[/sup] mice as judged by the length of the epithelial tongue (p = 0.0381, Figure 6B). Quantification of the wound size confirmed that K14Cre Tsc1[sup]F/F[/sup] mice displayed accelerated wound closure (p = 0.0048, Figure 6C).


Figure 5. Accelerated wound closure in upon epithelial Tsc1 excision.


Figure 6. Acceleration of wound healing upon ablation of Tsc1 in the skin.
[24], we can now begin to take advantage of the emerging information on growth promoting pathways in cancer cells to accelerate the healing of injured tissues. We observed here that the activation of the PI3K-Akt-mTOR pathway, whose aberrant function is one of the most frequent events in human neoplasia, represents an integral component of the normal cutaneous healing process. Most importantly, we demonstrate that the targeted activation of this signaling pathway can dramatically accelerate wound healing rates. Indeed, by the use of pharmacological and genetically-defined approaches we found that the activation of the PI3K-Akt pathway enhances the rate of wound closure dependent on the activation of mTOR, and that the activation of mTOR in epithelial cells by genetic ablation of either of two of its upstream regulators, Pten and Tsc1, suffices to accelerate cutaneous wound healing.
[15], [25], [26], together suggesting that the basal keratinocytes may not strictly depend on mTOR activity to proliferate. However, during wound healing, mTOR activation is observed in the basal, subrabasal, and spinous layers of the stratified epithelium adjacent to the wound wedge and in the migrating epithelial tongue, suggesting that both the proliferative capacity and migratory activity of these cells may be controlled by mTOR. In addition, the formation of the epithelial tongue and wound closure involves of the interaction between the proliferating and migrating keratinocytes and the stromal cells. Thus, it is possible that mTOR activity in the epithelial cells may also regulate the expression of cytokines such as TGFβ, TGFα, FGF, and VEGF, which are known to contribute to the epithelial/stromal interactions during wound healing (reviewed in [27], [28], [29]). In this context, it is possible that mTOR activity in the epithelial cell compartment may facilitate wound closure by regulating epithelial cell proliferation and migration, together with its ability to regulate paracrine mechanisms involved in cellular communication processes that contribute to the wound microenvironment.
[26], [30]. The need to activate mTOR as part of the normal cutaneous healing process may now explain why mTOR inhibitors can cause a delay in wound closure as recently reported [21], [26]. This potential undesirable side effect could be controlled with countermeasure therapies or by the interruption of the treatment with mTOR inhibitors during the healing process [31].
[32], [33]. In this regard, small molecules interfering with PTEN function can enhance wound closure and rapidly restore lung epithelial monolayer integrity following injury in relevant models in vitro [34], [35]. Although their current off-target toxicities may prevent their clinical application, future studies may provide opportunities for the development of therapeutically relevant agents inhibiting PTEN and other molecules on its signaling pathway as a molecular-targeted approach to accelerate wound healing upon local delivery.
[36], [37], the deletion of Tsc1 did not have a demonstrable impact on normal biology of the skin, nor did we observe spontaneous tumor formation in mice with conditional Tsc1 deletion in the skin after more than one year of observation (not shown). These findings may provide a rationale for the future development of small molecule inhibitors of TSC1/TSC2 and/or other molecules suppressing the mTOR pathway for local delivery to accelerate wound healing. Whereas the cancer risk of this approach should be carefully examined, we have recently observed that epithelial stem cells are endowed with protective mechanisms triggering stem cell differentiation or senescence upon aberrant activation of mTOR [15]. Thus, pharmacological or genetic strategies aimed at the local activation of mTOR in the epidermis may accelerate the ability to epithelial cells to migrate and repopulate damaged skin areas hence accelerating wound closure without resulting in the aberrant growth of basal keratinocytes and their stem cells.
[38] and Tsc1 alleles [39] with mice expressing Cre recombinase under the control of cytokeratin 14 promoter (K14-Cre) [40] as previously described [25]. Mice were anesthetized and dorsal surfaces were shaved and cleaned with 10% povidone-iodine topical solution. Fifteen millimeters full-thickness incisional skin wounds were made in the mid-dorsal area. The wound field was excised and fixed in aqueous buffered zinc formalin for 24 h, transferred to 70% ethanol, paraffin embedded and sectioned. The wound sites were monitored and measured daily utilizing wound closure as endpoint as previously described [41].
Rapamycin administration and Bromodeoxyuridine (BrDU) incorporation in vivo
[25].
Culture of primary keratinocytes, in vitro wound closure (scratch) assay, BrDU incorporation, and Western blotting
[42]. Briefly, the mouse skin was peeled off, stretched out with the dermis faced down in a 60 mm culture dish, and floated on the surface of 0.25% trypsin at 4 °C for 18 h. The epidermis was then separated from the dermis, minced in keratinocyte growth medium (KGM, Gibco, Carlsbad, CA) supplemented with high Ca[sup]2+[/sup]. The undigested cornified fragments were removed by filtering the cell suspension through a sterile nylon cell strainer. The cells were collected by centrifugation, resuspended in fresh KGM Ca[sup]2+[/sup] supplemented with 10% FBS, and plated. After 24 h, attached keratinocytes were rinsed with PBS and incubated with fresh KGM in low Ca[sup]2+[/sup]. Primary keratinocytes were assay with BrDU incorporation. After 24 hours starvation, cells were left untreated or treated for 24 h with 10 ng/ml EGF and 50 nM Rapamycin where indicated; and 10 µM BrDU was added for the last 2 h. Cells were fixed with Carnoy's fixative and then treated with 2 N HCl. BrDU was detected by immunofluorescence with anti-BrDU antibody (Axyll-Accurate Chemical & Scientific Corporation, Westbury, NY). Images were taken using Zeiss Axio Imager Z1 microscope equipped with an Apotome device (Carl Zeiss, Thornwood, NY). Quantitative analyses were performed by counting the total number of cells and cells expressing nuclear BrDU stain. Scratch assays were performed with keratinocytes grown to confluence on fibronectin coated wells and starved overnight. Scratches were made with a plastic pipette tip across the diameter of each well. Quantitative analysis of the scratch area of closure was performed using the Axiovision Rel. 4.7 (Carl Zeiss, Thornwood, NY). Cells were also lysed and 30 µg of cellular proteins were separated on 10% SDS-PAGE, transferred to nitrocellulose membranes, and analyzed by Western blot using primary antibodies against Akt, phospho-specific Akt (pAkt[sup]Ser473[/sup] and pAkt[sup]Thr308[/sup]) and S6 (pS6) (Cell Signaling Technology, MA), PTEN (Cascade Bioscience, MA), and GAPDH (Santa Cruz Biotechnology, CA). Results are representative of three independent experiments performed in triplicate.
Histology and Immunofluorescence
[15]. For nuclear staining, propidium iodide or mounting media with DAPI (Vector Laboratories, Burlingame, CA) was used. Images were taken using Zeiss Axio Imager Z1 microscope equipped with an Apotome device (Carl Zeiss, Thornwood, NY) and ScanScope (Aperio, CA). Quantitative analysis of the migrating epithelial tongue and wound size were done with ImageScope (Aperio, CA) and Axiovision Rel. 4.6 (Carl Zeiss, Thornwood, NY). H&E stain and immunofluorescence were performed in all the samples from every control and transgenic mice.
Statistical analysis
Statistical analyses were performed by ANOVA analysis of variance test, followed by the Bonferroni's multiple comparison. The Kaplan-Meier analysis followed by log rank test was performed to analyze time to wound closure. T-test was used for comparisons of histological wounded size and area, migration of the epithelial tongue, and BrDU incorporation using GraphPad Prism 4.03 (GraphPad Software, San Diego, CA). Asterisks denote statistic significance (NS, P>0.05; * P<0.05; ** P<0.01; and *** P<0.001).
Author Contributions
Conceived and designed the experiments: CHS RMC TB JSG. Performed the experiments: CHS RMC. Analyzed the data: CHS RMC TB JSG. Contributed reagents/materials/analysis tools: CHS RMC. Wrote the paper: CHS RMC TB JSG.
 
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topccat29

topccat29

29 year HT veteran
I like to add foods here and there which help heal the body. It is something I have done for years and probably the easiest way to adopt a healthy lifestyle as it just happens over time.

Recently I added fermented blueberries which are absolutely fantastic. Something blueberries are known for are lowering blood pressure and increasing blood flow. I can attest to this fact since I have incorporated blueberries into my diet for many years. It they were patentable they would be a multi billion dollar product.

Anyone that has fluid build up around the eyes give it a try as it €™s a natural diuretic and fluid build up is often a matter of too much sodium and carbs €¦ €¦ €¦.blueberries will definitely help.

With the fermentation it lowers the sugar levels which are low to begin with even further. I use some of my sauerkraut juice about half a cup to get it started. Then the good bacteria starts to feed off of the sugar and multiplies. This is exactly the good bacteria that replenishes in your gut raising serotonin levels and keeping bad bacteria in check also preventing many other diseases.

The white bubbles you see are carbon dioxide as the liquid becomes a refreshing beverage. Many are unaware that sodas, beers, etc were healthy foods at one time until profit came into the picture. Give it a try it €™s delicious.

The old world ways when it comes to food have been tested for centuries through observation.


 
topccat29

topccat29

29 year HT veteran
I separate the liquid from the rest of the skins eating the skins separately. The liquid ferments further and becomes blueberry soda much more tartness and with an extremely reduced fructose level. It is filled will beneficial bacteria along with being delicious. Very, very high in resveratrol.


This is a superior food for increasing blood flow and lowering blood pressure. For those into bodybuilding a trick the old timers back in the 50 €™s would use to increase vascularity would be to drink red wine vinegar or simply red wine. This in my opinion is not only healthier but infinitely better.


 
topccat29

topccat29

29 year HT veteran
One of the best foods for healing in my opinion are eggs and even though I have my own flock of 24 birds my wife likes to give eggs to family and friends and I don €™t want to take away that joy so I also purchase eggs from some Amish farmers.

What €™s great about the egg is that it is a very dense form of nutrition very high in the fat soluble vitamins A, D, E, and K along with plenty of other critical components to help in the healing process. Personally I eat about a dozen a day and on some days a couple dozen depending on if I substitute that second protein serving with something else like pastured beef liver for example and I have been doing this well over 15 years now. The cholesterol issue of course is going to be a stumbling block for most which I completely understand. What that comes down to is taking in more information which is not based on marketing and that is a long/slow process requiring extensive reading.

The point of the post is that I recently found another provider of eggs which I visited about 4 weeks ago. They are also pastured and soy free and these are better because the farmer follows a protocol that was designed by Joel Saltin who is also a farmer/author. One of my favorite reads is €œFolks This Ain €™t Normal € and that would actually be a good title for a book on some of what goes on in the hair transplant industry. If you look at the picture below you can see the difference in the color of the egg yolks. Also the structure pictured below is a giant sled that moves from pasture to pasture after the cows have grazed it. Now the chickens have access to the shorter grass blades along with all the bugs and worms attracted by the cow manure and the result is an extremely nutrient dense food. The farm is about a 45 minute drive and well worth the effort and time and as long as the eggs are not washed one can buy enough for 2 months and they don €™t require refrigeration. This is due to the film that the egg is coated with when the chicken lays it.

What's nice about looking at a picture of an egg is that you can actually see the proof. With something like a piece of meat it all looks the same but it in fact is not.


BTW I wanted to spend some time in the summer on the Saltin farm a few years back which is in Virgina. They were offering I believe it was 4 week internship. But then I started thinking about having to bring concealer and all those issues and decided not to which is a good example of how a ht can affect your life in way you never even thought of, so understand what you are getting into and make sure you have a good long term plan. Opt for less hair is you have to but make sure you don €™t have other issues to deal with or at least try to reduce them.

I also just took a picture about 5 minutes ago of a hawk that came around the backyard and it's posted at the bottom. It €™s a nice bird but it can be destructive as it is a bird of prey and one can see the after effects in my next door neighbors backyard as that is what is left of a pigeon. I put some netting up over my own coop a few days ago, my wife thought it was overkill but for me it was worth the extra work. I like to be able to leave the house without having to worry about an animal that can €™t defend itself. I believe the hawk flew into the yard for a reason and it €™s a metaphor for the ht industry. Everything happens for a reason.






















 
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