The logic behind this trend is that creating tanned skin (by increasing melanin) with minimal to no sun exposure could protect individuals from skin damage, and even potentially lower melanoma risk. More melanin means more protection from UV radiation, and therefore a healthier (and conveniently, deeper) complexion. In this sense, there is perhaps a kernel of truth to the idea of the “healthy glow”.
In addition to angiogenesis and neurogenesis, cell- and pharmacologically based therapies substantially remodel white matter in the ischemic brain. Treatment of experimental stroke with MCSs, rhEPO, or sildenafil significantly increases axonal density encapsulating the ischemic lesion. Dynamic changes of white matter structure along the ischemic boundary have been imaged in living animals by diffusion tensor imaging (DTI) and fractional anisotropy (FA) measurements. Data from these MRI indices demonstrate that administration of rhEPO or sildenafil augments axonal remodeling and angiogenesis and that both of them are spatially and temporally correlated. Administration of MSCs, rhEPO, and thymosin beta 4 (Tβ4) dramatically increases the number of oligodendrocyte progenitor cells in the corpus callosum, the striatum, and the V/SVZ of the ischemic hemisphere and mature oligodendrocytes in the ischemic boundary adjacent to myelinated axons. These findings suggest that cell- and pharmacologically based therapies promote generation of oligodendrocyte progenitor cells in the ischemic brain that migrate to target axons, where they extend their processes myelinating the axons.
Trust is increased by oxytocin.[95][96][97] Disclosure of emotional events is a sign of trust in humans. When recounting a negative event, humans who receive intranasal oxytocin share more emotional details and stories with more emotional significance.[96] Humans also find faces more trustworthy after receiving intranasal oxytocin. In a study, participants who received intranasal oxytocin viewed photographs of human faces with neutral expressions and found them to be more trustworthy than those who did not receive oxytocin.[95] This may be because oxytocin reduces the fear of social betrayal in humans.[98] Even after experiencing social alienation by being excluded from a conversation, humans who received oxytocin scored higher in trust on the Revised NEO Personality Inventory.[97] Moreover, in a risky investment game, experimental subjects given nasally administered oxytocin displayed "the highest level of trust" twice as often as the control group. Subjects who were told they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk aversion.[99] When there is a reason to be distrustful, such as experiencing betrayal, differing reactions are associated with oxytocin receptor gene (OXTR) differences. Those with the CT haplotype experience a stronger reaction, in the form of anger, to betrayal.[100]
Cells on the surface of the skin are constantly being replaced by regeneration from below. The repair of a wound is a scaling up of this normal process, with additional complex interactions among cells, formation of new blood vessels, collagen, more extensive cell division and cell migration, as well as strict control of inflammatory cells and the cytokines they release to resolve the inflammation.
While the structure of oxytocin is highly conserved in placental mammals, a novel structure of oxytocin was recently reported in marmosets, tamarins, and other new world primates. Genomic sequencing of the gene for oxytocin revealed a single in-frame mutation (thymine for cytosine) which results in a single amino acid substitution at the 8-position (proline for leucine).[117] Since this original Lee et al. paper, two other laboratories have confirmed Pro8-OT and documented additional oxytocin structural variants in this primate taxon. Vargas-Pinilla et al. sequenced the coding regions of the OXT gene in other genera in new world primates and identified the following variants in addition to Leu8- and Pro8-OT: Ala8-OT, Thr8-OT, and Val3/Pro8-OT.[118] Ren et al. identified a variant further, Phe2-OT in howler monkeys.[119]
The pamphlet, titled "Melanotan-2: Safe enhanced tanning" says although the drug is not approved by the Therapeutic Goods Administration (Australia's drug watchdog) and that studies into its effects are under way, it "is safe" and and its use "well documented". It says people can be referred to a "suitable doctor who is trained to prescribe MT2" so the pharmacy can dispense it to them.
"Just that it is completely false that these particular substances and the program wasn't discussed through the highest levels of the club. We have been very firm in terms of our belief in what ASADA, the AFL and Essendon know and for them to remotely suggest that no one knew, to be really blunt, is completely wrong and in some ways offending the process we set up at Essendon Football Club. We were very strict in the protocols we set up."
But what about the three-month warning? Dr Rush, while an advocate for the supplement, sees it as a short-term solution, and not something to rely on long-term, for good reason. "Technically taking 5-HTP alone can deplete important brain chemicals such as dopamine and adrenaline. While 5-HTP is aimed at increasing the amount of serotonin in the body, dopamine and adrenaline are also important for positive mental health states. In order to prevent the depletion of important brain chemicals, taking 5-HTP would need to be balanced with amino acids that support the production of dopamine and adrenaline." That's L-Tyrosine, which you eat in soy, chicken and beef, and can also be found in health food shops as a supplement.
TBI patients frequently suffer from long-term deficits in cognitive and motor performance. No single animal model can adequately mimic all aspects of human TBI owing to the heterogeneity of clinical TBI.11 Some features of cognitive and motor function in humans have been successfully demonstrated in experimental brain trauma models.28-30 The controlled cortical impact (CCI) model is one of the most widely used TBI models. The CCI-TBI model has many clinically relevant features in that CCI causes not only cortical damage but also selective neuronal death in the hippocampus in rodents, leading to sensorimotor dysfunction and spatial learning and memory deficits, respectively.18,31-33
Nature has been very clever in a way. Without oxytocin, you know, babies are what they really are - I probably shouldn't say this on TV - but noisy, smelly animals that don't actually do anything useful. And, um, that's what oxytocin does. It gives them a special salience, a special beauty and allows us to bond with these defenceless little animals.
Oxytocin is known to be metabolized by the oxytocinase, leucyl/cystinyl aminopeptidase.[25][26] Other oxytocinases are also known to exist.[25][27] Amastatin, bestatin (ubenimex), leupeptin, and puromycin have been found to inhibit the enzymatic degradation of oxytocin, though they also inhibit the degradation of various other peptides, such as vasopressin, met-enkephalin, and dynorphin A.[27][28][29][30]
These studies demonstrate that in the animal model of TBI, early (6 hours post injury) treatment with Tβ4 i.p. at doses of 6 and 30 mg/kg reduces cortical lesion volume and hippocampal cell loss and improves functional recovery, suggesting its potential as a neuroprotective therapy for TBI. More importantly, delayed (24 hours post injury) treatment with Tβ4 administered i.p. at a dose of 6 mg/kg does not reduce lesion volume but significantly improves functional outcome in rats.34 Tβ4-induced angiogenesis, neurogenesis and oligodendrogenesis may contribute to functional recovery.34 Therefore, our data suggest that promoting endogenous neurorestorative processes using Tβ4 provides a novel therapeutic option for TBI. It should be noted that systemic administration of Tβ4 is safe and well-tolerated by animals and humans.26 Further investigation of the molecular mechanisms underlying Tβ4-mediated neuroprotection and neurorestoration is warranted.
A: 5-HTP or 5-hydroxytryptophan is sold as a dietary supplement for "anxiety, depression, insomnia, headaches and other conditions." Because dietary supplements (e.g., 5-HTP) have not been thoroughly studied in the clinical setting, possible side effects and interactions with other drugs are not well known. However, 5-HTP does interact with prescription antidepressants, taking them together can lead to serotonin syndrome which is a rare but potentially fatal condition. Also, because herbs and supplements are not strictly regulated by the U.S. Food and Drug Administration, these products are not required to be tested for effectiveness, purity, or safety. 5-HTP has not been proven safe or effective for the treatment of depression or bipolar disorder. There are many prescription medications that have been proven safe and effective for these conditions. In general, dietary supplements should only be taken under the supervision of your health care provider. Laura Cable, Pharm.D., BCPS

Differences among groups were analyzed using a one-way analysis of variance combined with the Bonferroni test. The relative intensities of mRNA and protein bands were assayed using Quantity-One software (Bio-Rad Co., Hercules, CA, USA); results were normalized to the mRNA and protein levels of beta-actin. All values were expressed as mean ± standard deviation. Differences were considered significant at p < 0.05.
Oxidative stress is characterized by an accumulation of ROS and plays a key role in the progression of periodontal diseases [24]. Damage of tissues in inflammatory periodontal disease can be mediated by ROS resulting from the physiological activity of PMN during the phagocytosis of periodontopathic bacteria [27]. In addition, LPS from Porphyromonas gingivalis as well as hypoxia induces a NOX4-dependent increase in H2O2 release in PDLCs [28]. Furthermore, ROS such as H2O2 are small, diffusible, and ubiquitous molecules, can affect human PDLCs and gingival fibroblasts cell injury indirectly by enhancing pro-inflammatory factors such as cytokines, NO, PGE2, and ROS [29–31]. This ROS is known to stimulate osteoclast differentiation and participate in early signaling events associated with osteoclast activation for bone resorption [32]. Since LPS from P. gingivalis increases oxidative stress in PDLCs and contributes to periodontitis [28], human PDLCs treated with H2O2 may serve as an in vitro model relevant to periodontitis.
I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. I would say yes though. Just because you dont “know” or “feel” any injury, you might be one functional movement away from a weakened tendon or muscle – snap, crackle and POP! These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever.
An interesting concept that has emerged from initial findings is that regeneration and fibrosis are competing events in the vertebrate heart. That is, if there is a capacity for injury-stimulated cardiomyocyte hyperplasia beyond a certain threshold, regenerative mechanisms will overcome scarring. Results consistent with this idea came from experiments with zebrafish possessing a ts mutation in the cell-cycle checkpoint kinase Mps1 (Poss et al., 2002b). As mentioned earlier, mps1 mutants were initially identified based on their defects in caudal fin regeneration. Serendipitously, mps1 mutants also showed defects in cardiac regeneration at a temperature restrictive for the mutation (Poss et al., 2002b). Instead of regenerating muscle in response to ventricular resection injury, mps1 mutants repaired wounds by forming large, collagen-rich scars. Inhibition of Fgf signaling also stunts cardiac regeneration and causes scarring (Lepilina et al., 2006). These results indicate that even vertebrates with high cardiac regenerative capacity have a default scarring mechanism; normally, regeneration somehow restricts this pathway (Fig. 8). The implication is exciting; perhaps by stimulating regeneration in a poorly-regenerative system like the mammalian heart, scarring events characteristic of myocardial infarction would be restricted by new muscle formation. Similarly, deterring cardiac scarring mechanisms would perhaps favor regeneration in mammals.
In 1999 researchers in Glasgow University found that an oxidised derivative of thymosin β4 (the sulfoxide, in which an oxygen atom is added to the methionine near the N-terminus) exerted several potentially anti-inflammatory effects on neutrophil leucocytes. It promoted their dispersion from a focus, inhibited their response to a small peptide (F-Met-Leu-Phe) which attracts them to sites of bacterial infection and lowered their adhesion to endothelial cells. (Adhesion to endothelial cells of blood vessel walls is pre-requisite for these cells to leave the bloodstream and invade infected tissue). A possible anti-inflammatory role for the β4 sulfoxide was supported by the group's finding that it counteracted artificially-induced inflammation in mice.
A later experiment by another group took it a step further. This time the volunteers were told how they did, and in half of the cases, they learned that the trustee had burned them and kept the money. The volunteers who were burned were asked whether they wanted to try again. What would you do? This would be like getting that spam from the Nigerian Prince a second time and sending him $5,000 again, right?
 Don't be surprised.  A lot of people haven't heard of Melanotan.  Melanotan is a tanning peptide that stimulates the production of melanin in the body to foster a deep, natural tan.  This is the body's way of protecting itself from too much sun exposure by increasing the level of melanin in the body.  Melanin is your body's natural response to UV damage.  The end result is a darkening of the skin.

In all groups, [intravenous tryptophan] impaired memory and psychomotor performance significantly. In conclusion, cognitive deficits in [bipolar patients] following [intravenous tryptophan] may reflect a central 5-HT vulnerability in frontal brain areas. Independent of [intravenous tryptophan], cognitive deficits in [bipolar patients] provide evidence for a trait marker for [bipolar disorders].

Increasing trust and reducing fear. In a risky investment game, experimental subjects given nasally administered oxytocin displayed “the highest level of trust” twice as often as the control group. Subjects who were told that they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk-aversion.11 Nasally administered oxytocin has also been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).12 There is no conclusive evidence for access of oxytocin to the brain through intranasal administration, however.

5-HTP has been linked in very rare instances to a condition known as EMS, or eosinophilia-myalgia syndrome, which combines extreme muscle tenderness with abnormalities in the blood. A contaminant that was found in some tryptophan supplements in the late 1980s, and was linked to a small number of EMS cases, was also found in some 5-HTP supplements.  It’s important to talk with your doctor before you begin taking 5-HTP or any other supplement, and to make sure you’re getting your supplements from a reliable provider.  
Due to its molecular structure and low molecular weight, TB-500 is very versatile, mobile and possesses the ability to travel long distances through tissues. This means that when targeting injured areas (chronic or acute), TB-500 has the ability to circulate through the body and “find” those areas of injury in order to enhance the healing or growth process. Many users have also noted the added benefits of improved flexibility, reduced inflammation in tendons, re-growth of lost hair, and darkening of grayed hair.
Second, 5-HTP can cause serious drug interactions with many medications, especially those used to treat depression. Because antidepressants generally work by increasing serotonin in the brain, 5-HTP could combine with these medications to cause high concentrations of serotonin. Having too much serotonin can lead to serotonin syndrome, a serious condition characterized by dangerously high heart rate, blood pressure, and temperature. 5-HTP can interact with other classes of drugs, like migraine and pain medications, that also affect serotonin concentrations.
Oxytocin (Oxt; /ˌɒksɪˈtoʊsɪn/) is a peptide hormone and neuropeptide. Oxytocin is normally produced by the paraventricular nucleus of the hypothalamus and released by the posterior pituitary.[3] It plays a role in social bonding, sexual reproduction, and during and after childbirth.[4] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding.[5] This helps with birth, bonding with the baby, and milk production.[5][6] Oxytocin was discovered by Henry Dale in 1906.[7] Its molecular structure was determined in 1952.[8] Oxytocin is also used as a medication to facilitate childbirth.[9][10][11]
Melanotan II first captured the public's imagination when the mainstream media briefly touted it as a Viagra-like panacea for middle-aged men. Norman Levine, a dermatologist who led the team that developed the drug, had first conducted experiments in which he darkened the pigments of frogs by injecting them with a hormone called Alpha MSH. After Melanotan II was modified for human use and put through clinical trials, Levine reported that "one very astute observer who took this drug told us that he was developing spontaneous erections."
I’m curious to know where you got your reconstitution calculation from; you recommend putting approx 3 cc’s in a 5 mg TB-500 which ‘almost fills’ the vial. I have been doing a ton of research on TB-500 and finding contradictory recommendations on how to reconstitute. Because the dosing for TB-500 is higher than what I’m used to with GHRH & GHRP – I felt a lower reconstitution mixture would reduce the amount I needed to take (but now I’m wondering if I’ve been over dosing based on your formula). Would really appreciate knowing how you arrived at filling an insulin syringe ‘three times’ equal to 3 cc’s – just want to make sure i’m dosing correctly

5-HTP is sometimes taken by people coming down from MDMA to relieve post-MDMA dysphoria.[8] As 5-HTP is a necessary precursor for the brain to produce more serotonin, and MDMA use depletes a person's natural serotonin levels, it is believed that taking 5-HTP after consuming MDMA will speed up serotonin production. DanceSafe claims that the anecdotal evidence is widespread and that the theory is physiologically reasonable.[9] Backing up this approach is research conducted by Wang, et al.  in 2007, which observed that MDMA-induced depletions of 5-HT (serotonin) were restored in rats after administration 5-HTP, and suggested that this approach might be clinically useful in abstinent MDMA users.[8]
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