The CCI model we used causes cortical tissue loss. Traditionally, the target for neuroprotective treatment of TBI is to reduce the lesion volume.39,40 A major limitation of neuroprotection strategies is the short time window between injury and treatment. In the vast majority of preclinical TBI studies, the treatment compounds provide neuroprotection only when administered early (usually several hours after brain injury).11 The administration of a compound early in the clinical setting is not practical.41 The neuroprotective effects demonstrated in rodents may diminish if the treatment compounds are given in the clinical setting beyond the short neuroprotective window. We are able to stimulate recovery of neurological function without altering the lesion volume, which has also been demonstrated in our experimental studies of stroke,19,42,43 and is in essence, enhancement of neurorecovery.19 The extended 24-hour window for treatment which improves neurological recovery, without altering CCI cortical volume, is a major benefit of the neurorestorative therapy. Recently, we evaluated the efficacy of delayed Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by CCI.34 Briefly, TBI rats received Tβ4 at a dose of 6 mg/kg or a vehicle (saline) administered i.p. starting at 24 hours after injury and then every third day for 2 weeks. The dose of Tβ4 was selected based on our previous studies in animal models of stroke and EAE.25,27 Tβ4 did not alter lesion volume (14.2 ± 3.9% for saline treatment vs. 15.7 ± 3.6% for Tβ4 treatment). TBI caused neuronal cell loss in the ipsilateral CA3 and DG examined 35 days after injury compared to sham controls. Tβ4 treatment initiated 24 hours post injury significantly reduced cell loss in these two regions compared to saline controls. Tβ4-treated TBI rats showed significant improvement in spatial learning (MWM test) and sensorimotor (mNSS test) functional recovery compared to the saline-treated TBI rats.34
Serotonin syndrome (Serotonin toxicity) is caused by an excess of serotonin in the brain. It is most often caused by taking more than one Serotonin-enhancing substance at the same time, such as 5-HTP and an antidepressant medication. Symptoms range in severity according to the level of intoxication and may include increased heart rate, tremor, sweating, mental agitation, seizures, shock, organ failure and death (9).
In this study, Tβ4 mRNA down-regulation was detected in in vitro in PDLCs stimulated with the ROS. This down-regulation of Tβ4 was also observed in GCF of periodontitis patient [19] and endotoxin-induced septic shock of rats [39]. ROS were generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and involved in tissue destruction associated with periodontal diseases [40]. Thus, we chose to use ROS-stimulated PDLCs in this study since ROS, such as superoxide and H2O2, have been proposed as key players in bone resorption [41] and implicated in the pathogenesis of rheumatoid arthritis and periodontitis [29].
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
First, dietary supplements are not regulated as drugs in the US, and the careful testing and quality control that are required of prescription drugs do not apply to supplements like 5-HTP. This is why serious adverse effects and major outbreaks, like the one associated with tryptophan, can occur. You can minimize this risk by using only USP-Verified supplements.
Delayed Tβ4 treatment increases vascular density in the injured cortex, ipsilateral dentate gyrus, and CA3 region 35 days after TBI. Arrows show vWF-stained vascular structure. TBI alone (B) significantly increases the vascular density in the injured cortex compared to sham controls (A, P < 0.05). Tβ4 treatment (C) further enhances angiogenesis after TBI compared to the saline-treated groups (P < 0.05). The density of vWF-stained vasculature in different regions is shown in (D). Scale bar = 25 μm (C). Data represent mean + SD. *P < 0.05 vs Sham group. #P < 0.05 vs Saline group. N (rats/group) = 6 (Sham); 9 (Saline); and 10 (Tβ4).
Uterine contractions. These are important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.16
Jump up ^ Carlier MF, Hertzog M, Didry D, Renault L, Cantrelle FX, van Heijenoort C, Knossow M, Guittet E (September 2007). "Structure, function, and evolution of the beta-thymosin/WH2 (WASP-Homology2) actin-binding module". Annals of the New York Academy of Sciences. 1112: 67–75. Bibcode:2007NYASA1112...67C. doi:10.1196/annals.1415.037. PMID 17947587.
Although obtaining Melanotan II and Bremelanotide is relatively easy to do, both substances come in powder form and then must be reconstituted using sterile water prior to subcutaneous injection—a method of administration that can cause lead to skin bruising, cross-contamination, or infection, if the person performing the injection is inexperienced and the syringe isn't clean.
The group had first identified the thymosin sulfoxide as an active factor in culture fluid of cells responding to treatment with a steroid hormone, suggesting that its formation might form part of the mechanism by which steroids exert anti-inflammatory effects. Extracellular thymosin β4 would be readily oxidised to the sulfoxide in vivo at sites of inflammation, by the respiratory burst.[21]
At least one study using an extract of Griffonia simplicifolia (10.24mg giving 2.56mg 5-HTP; confounded with Centella asiatica and Taraxacum officinale at 11.7mg and 4.55mg Paulina cupana and 9.75mg Artichoke extract) taken in three hits, five times a day (40mg 5-HTP total), by 20 overweight or obese females (non-depressive and without eating disorders) for 4 weeks has noted an increase in satiety and reduced binge eating tendencies; the increase in satiety was said to account for the improved weight loss results seen in the experimental group when both were given weight loss advice and diets.[3] This spray has been noted elsewhere to increase satiety (and vicariously through that, body weight) over 2 months in a similar demographic of women.[2]
Oxytocin secreted from the pituitary gland cannot re-enter the brain because of the blood-brain barrier. Instead, the behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland. Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala, ventromedial hypothalamus, septum and brainstem.
To explore whether Tβ4 peptide-induced anti-inflammatory and anti-osteoclastogenesis were dependent on the up-regulation of Wnt5a, the effects of recombinant human (rh) Wnt5a (500 ng/mL) and Wnt5a-specific siRNA were assessed. Pretreatment of Wnt5a siRNA reversed the inhibitory effects of Tβ4 peptide on H2O2-induced iNOS and COX-2 expressions, NO and PGE2 productions, osteoclastogenic cytokines, and RANKL expression (Fig 10A–10E). In contrast, pretreatment with rhWnt5a enhanced the anti-inflammatory effects of Tβ4 peptide whereas control siRNA showed no effect on PDLCs. In accordance with anti-inflammatory results, Tβ4 peptide-suppressed osteoclast number and TRAP activity in BMM cells were reversed by exogenous treatment with Wnt5a siRNA but enhanced by rh-Wnt5a (Fig 11A–11C).
Bulletproof™ supplements are backed by the most cutting-edge research, science, and technology to kick performance into overdrive. Sourced from the best, most bioavailable ingredients possible — all Bulletproof supplements are 100% non-GMO, soy, and gluten-free, with no artificial colours, added preservatives, or any other junk. They undergo strict lab testing to ensure they meet the rigorous quality standards of the Bulletproof Process™ — ensuring purity and potency. So you can focus on being more awesome, in every way.

Research in the early 1960s showed that in rats, administration of α-MSH caused sexual arousal, and work on this continued in many labs up through the 1980s, when scientists at University of Arizona began attempting to develop α-MSH and analogs as potential sunless tanning agents, and synthesized and tested several analogs, including melanotan-I and melanotan II.[6][9]

The biologically active form of oxytocin, commonly measured by RIA and/or HPLC techniques, is also known as the octapeptide "oxytocin disulfide" (oxidized form), but oxytocin also exists as a reduced straight-chain (non-cyclic) dithiol nonapeptide called oxytoceine.[120] It has been theorized that oxytoceine may act as a free radical scavenger, as donating an electron to a free radical allows oxytoceine to be re-oxidized to oxytocin via the dehydroascorbate / ascorbate redox couple.[121]
For now, Bartz isn’t sure why oxytocin can have such different effects. Her most educated guess is that the hormone triggers a biased trip down memory lane. Under its influence, people are more likely to remember information about their mother that fits with their current attitudes to relationships. If they are anxious, they’re more likely to remember the negative side of their early life. It’s a reasonable enough idea, and one that Bartz intends to test in the future. It will also be good to repeat the study in a larger group – 31 men make for a relatively small study.
A: While it is possible there is an interaction, it most likely is not severe or life-threatening. Keep in mind that the "T" in HTP stands for tryptophane, which is an essential amino acid that your body processes routinely. The most common interaction involved with 5-HTP is with antidepressants or other medications that are intended to affect brain chemistry, as 5-HTP is converted into serotonin, an important brain chemical that helps regulate mood.

Oxytocin production is controlled by a positive feedback mechanism. This mechanism allows the release of the oxytocin hormone when a trigger occurs. The hormone then causes an action in the body, such as the letdown of milk or the start of labor contractions, which signals more production of oxytocin. The feedback cycle continues until the action, such as childbirth or feeding the baby, is complete.
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Jump up ^ Wei D, Lee D, Cox CD, Karsten CA, Peñagarikano O, Geschwind DH, Gall CM, Piomelli D (November 2015). "Endocannabinoid signaling mediates oxytocin-driven social reward". Proceedings of the National Academy of Sciences of the United States of America. 112 (45): 14084–9. Bibcode:2015PNAS..11214084W. doi:10.1073/pnas.1509795112. PMC 4653148. PMID 26504214.

I’m always interested in learning about better supplements for my health. I’ve heard a lot of good things about peptides, but this was the first time I’ve read about TB-500 in particular. It sounds like it can have a major impact on helping you recover from injuries, which is a huge deal in today’s world. I may need to look into it some more before actually buying it, but thank you so much for taking the time to explain it!
During the 2000s, the Melanotan II peptide and the metabolite derived from it, the erectile dysfunction-focused Bremelanotide (also known as PT-141), were patented and then licensed to biotechnology companies hoping to develop them into profitable prescription drugs. However, these companies also offer the peptides for direct sale to researchers. These transactions occupy a legal gray area, since the peptides are banned for human use outside clinical trials. While they can be purchased from various websites specializing in research chemicals, the purchaser usually has to affirm prior to final sale that the peptide "will not be used for human consumption" and is being acquired for "research purposes only."
Many early studies of oxytocin for autism were limited because they assessed only a single dose and had relatively few participants, and later experiments with more doses failed to show the same promise. In 2010, clinical psychologist Adam Guastella at the University of Sydney in Australia studied 16 male adolescents with autism spectrum disorder, and found that one dose of oxytocin could improve their ability to gauge the emotions of others by looking at their eyes13. But when he tried giving twice-daily doses of the hormone for two months, he found no significant improvements in social interaction or social cognition14. “Studies to this point have really shown limited benefit of oxytocin in improving psychiatric illnesses over time,” he says. Guastella says that getting to the bottom of oxytocin's complex neurological effects will take time. “If we want a simple answer, we're not going to get it.”
In December 2010, the delegate made a delegate only decision to include afamelanotide (also known as melanotan I) with a cross-reference to melanocyte stimulating hormone (MSH) for inclusion into the current Poisons Standard. It was noted that afamelanotide should not be confused with a similar substance commonly known as Melanotan-II, which is a cyclic lactam synthetic analogue of α-MSH. It was noted that melanotan-II was under investigation for treating sexual dysfunction, although this has been abandoned due to side effects associated with the immune and cardiovascular systems. Its metabolite, bremelanotide, is under investigation for treating haemorrhagic shock.
Expanding upon the possible anti-panic effects of 5-HTP, one study using 2mg/kg 5-HTP to children (3.2-10.6 years of age) at bedtime for 20 days noted that 5-HTP was asssociated with beneficial response (more than 50% reduction in night terror frequency) of 93.5% of children relative to 28.6% in placebo.[42] Oddly, 6 months after the initial supplementation period the 5-HTP group still reported less sleep terrors (83.9% reporting improvement).[42]
Silencing of the Tβ4 or Wnt5a gene was achieved by transfecting cells with small interfering RNA (siRNA). Cells were transfected with Tβ4 or Wnt5a siRNAs (30 nM) for 24 hours using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's instructions. Cells were transfected with Silencer negative control siRNA using the same protocol.
Oxytocin has been of keen interest to neuroscientists since the 1970s, when studies started to show that it could drive maternal behaviour and social attachment in various species. Its involvement in a range of social behaviours2, including monogamy in voles, mother–infant bonding in sheep, and even trust between humans, has earned it a reputation as the 'hug hormone'. “People just concluded it was a bonding molecule, a cuddling hormone, and that's the pervasive view in the popular press,” says Larry Young, a neuroscientist at Emory University in Atlanta, Georgia, who has been studying the molecule since the 1990s.
Serotonin appears to be associated with panic attacks. Although studies that have used tryptophan depletion techniques in humans do not necessarily induce a panic attack[34][35][36] it appears it may sensitize the body by an increase in neurovegetative panic symptoms and increased anxiety[37] which suggests that serotonin is protective against panic attacks, at least acutely.[38][39] A study in 24 unmedicated panic disorder patients and normal participants given 200mg 5-HTP prior to a 35% CO2 test (used to induce a panic attack-like response) noted that the test was able to induce panic attack in both panic disorder patients and normal persons and that 200mg 5-HTP was protective in both conditions but to a greater degree in persons suffering from panic disorders.[40] This has been replicated with cholecystokinin-4 induced panic attack with 200mg 5-HTP in otherwise healthy persons.[41]
Feeding: a 2012 paper suggested that oxytocin neurons in the para-ventricular hypothalamus in the brain may play a key role in suppressing appetite under normal conditions and that other hypothalamic neurons may trigger eating via inhibition of these oxytocin neurons. This population of oxytocin neurons are absent in Prader-Willi syndrome, a genetic disorder that leads to uncontrollable feeding and obesity, and may play a key role in its pathophysiology.[54]
It turns out oxytocin is responsible for a lot more than just love. New science has found that this amazing molecule also influences how sociable each of us is, allowing us to 'tune in' to the social information around us, perceiving it in much higher resolution. Scientists are now applying this new knowledge in the lab, and as reporter Dr Graham Phillips finds out, they're discovering oxytocin's great potential to treat social disorders, like drug addiction and alcoholism.
Maintenance doses are taken once the desired pigmentation has been reached and requires much less frequent dosing. Unfortunately, this is where too many variables come into play to give exact instructions. Skin type, bodyweight, metabolism regulating speed of skin fading, uv ray exposure, preferred tan level – all that makes impossible to give correct advice on maintenance dose. Everyone will find their own perfect dose and dosing frequency through some trial and error. To not leave you completely disinformed on this subject here is example of loading and maintenance which can be used as starting point where to adjust from:

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]
The diverse activities related to tissue repair may depend on interactions with receptors quite distinct from actin and possessing extracellular ligand-binding domains. Such multi-tasking by, or "partner promiscuity" of, proteins has been referred to as protein moonlighting.[14] Proteins such as thymosins which lack stable folded structure in aqueous solution, are known as intrinsically unstructured proteins (IUPs). Because IUPs acquire specific folded structures only on binding to their partner proteins, they offer special possibilities for interaction with multiple partners.[15] A candidate extracellular receptor of high affinity for thymosin β4 is the β subunit of cell surface-located ATP synthase, which would allow extracellular thymosin to signal via a purinergic receptor.[16]
It has been shown that oxytocin differentially affects males and females. Females who are administered oxytocin are overall faster in responding to socially relevant stimuli than males who received oxytocin.[75][86] Additionally, after the administration of oxytocin, females show increased amygdala activity in response to threatening scenes; however, males do not show increased amygdala activation. This phenomenon can be explained by looking at the role of gonadal hormones, specifically estrogen, which modulate the enhanced threat processing seen in females. Estrogen has been shown to stimulate the release of oxytocin from the hypothalamus and promote receptor binding in the amygdala.[86]
Johansson, A., Westberg, L., Sandnabba, K., Jern, P., Salo, B., & Santtila, P. (2012). Associations between oxytocin receptor gene (OXTR) polymorphisms and self-reported aggressive behavior and anger: Interactions with alcohol consumption [Abstract]. Psychoneuroendocrinology 37(9), 1546-56. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22421562
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Interestingly, there are numerous differences in the biology of teleosts and mammals, as well as specific differences in cardiomyocyte cellular structure and anatomy, all of which might contribute to regenerative variability. Unlike mammals, zebrafish can grow throughout most of adulthood, a phenomenon called “indeterminate growth” (Jordan, 1905). In fact, their growth can be affected markedly by changes in nutrition and population density (Goldsmith et al., 2006). It is thus possible that the capacity to replace cardiac tissue rapidly in teleosts has been retained in evolution as a function of the need for robust animal and cardiac growth. Indeed, a recent study has found that experimentally-induced adult cardiac growth in zebrafish is hyperplastic, and appears to rely on the same signals present or required during cardiac regeneration (Wills et al., 2008).

I went to a neurologist, He said it was just in my head because I have depression–the exact reason why I took 5HTP. Not satisfied with that doctor, I went to an immunologist. He said I got myositis. Eosinophilic Myositis. From my blood test, I got positive ANA IF, very high number of IgE, elevated Creatine Kinase, and very low Vitamin D 25(OH)D. But my ANA Profile test showed negative.
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