In years past, oxytocin had the reputation of being an "uncomplicated" hormone, with only a few well-defined activities related to birth and lactation. As has been the case with so many hormones, further research has demonstrated many subtle but profound influences of this little peptide, particularly in regards to its effects in the brain. Oxytocin has been implicated in setting a number of social behaviors in species ranging from mice to humans. For example, secretion or administration of oxytocin in humans appears to enhance trust and cooperation within socially-close groups, while promoting defensive aggression toward unrelated, competing groups.
Disclaimer: Thymosin Beta 4 is a peptide that should only be purchased for use in experimentation and research. It should not be purchased for human use or any other purpose than for research. It is advised that once purchased, the peptide is used within experimental circumstances that are under strict lab regulations. It is recommended that researchers use protective gear in order to prevent contact with the substance. However, if exposure is made with the peptide, it is very important to cleanse the area immediately to prevent harm.
Hypoxic heart disease is a predominant cause of disability and death worldwide. As adult mammals are incapable of cardiac repair after infarction, the discovery of effective methods to achieve myocardial and vascular regeneration is crucial. Efforts to use stem cells to repopulate damaged tissue are currently limited by technical considerations and restricted cell potential. We discovered that the small, secreted peptide thymosin beta4 (Tbeta4) could be sufficiently used to inhibit myocardial cell death, stimulate vessel growth, and activate endogenous cardiac progenitors by reminding the adult heart on its embryonic program in vivo. The initiation of epicardial thickening accompanied by increase of myocardial and epicardial progenitors with or without infarction indicate that the reactivation process is independent of injury. Our results demonstrate Tbeta4 to be the first known molecule able to initiate simultaneous myocardial and vascular regeneration after systemic administration in vivo. Given our findings, the utility of Tbeta4 to heal cardiac injury may hold promise and warrant further investigation.
The first study to show that Tβ4-promoted tissue repair was a dermal study performed in rats (Malinda et al., 1999). It had previously been found to promote angiogenesis and was reported to be high in platelets (Grant et al., 1995; Hannappel & van Kampen, 1987; Malinda, Goldstein, & Kleinman, 1997; Philp, Huff, Gho, Hannappel, & Kleinman, 2003). Since platelets are the first cells to enter a wound, it was clear that Tβ4 should be tested in dermal wounds in an animal model (Malinda et al., 1997, 1999; Philp, Badamchian, et al., 2003). In the first dermal study using 8 mm full-thickness punch wounds in rats, Tβ4 at 5 μg/50 μL of phosphate-buffered saline was found to accelerate wound closure, increase angiogenesis, and accelerate collagen deposition (Malinda et al., 1999). Tβ4 was only applied at the time of injury and at 48 h since after that the crust had formed. Visible macroscopic improvement was seen in the treated group by day 4. The study also found that Tβ4 promoted keratinocyte migration in vitro with activity in the picogram range. The findings were confirmed in various additional animal models (Table 1) and led to the clinical trials for hard to heal wound in patients as detailed in Table 2.
But we have to be just as good at recognizing who we can trust, so the system needs fine-tuned control. That’s apparently where oxytocin comes in. The amygdala, that critical organ for our biological risk response, has a high concentration of receptors for oxytocin. In the second set of those gambling experiments with the volunteers and the trustees, researchers used fMRI to watch the brains of the volunteers as they made their choices. As the levels of oxytocin in the brain went up compared with the placebo group, activity in the amygdala went down! Oxytocin diminishes the amygdala’s ability to send out the message “Warning! Warning! I don’t trust this guy.”
Nolen, W. A., van de Putte, J. J., Dijken, W. A., Kamp, J. S., Blansjaar, B. A., Kramer, H. J., and Haffmans, J. Treatment strategy in depression. II. MAO inhibitors in depression resistant to cyclic antidepressants: two controlled crossover studies with tranylcypromine versus L-5-hydroxytryptophan and nomifensine. Acta Psychiatr.Scand 1988;78:676-683. View abstract.
I don’t recall any literature (research or anecdotal) suggesting that TB 500 showed efficacy with regard to repair of brain tissue. I have however read anecdotal comments regarding N-Acetyl Semax Amidate with regard to increase in BDNF (Brain-derived neurotrophic factor) and the growth of new neurons. I am currently testing N-Acetyl Semax Amidate for its nootropic properties however I have read post in which people suggest that it is “healing” brain damage.
Potential side effects of 5-HTP include heartburn, stomach pain, nausea, vomiting, diarrhea, drowsiness, sexual problems, vivid dreams or nightmares, and muscle problems.[19] Because 5-HTP has not been thoroughly studied in a clinical setting, possible side effects and interactions with other drugs are not well known. According to the US National Institute of Health TOXNET, 5-HTP has not been associated with serotonin syndrome or any serious adverse events in humans.[20] Across multiple studies, 5-HTP also been reported to not cause any noticeable hematological or cardiovascular changes.[21] 5-HTP also has not been associated with eosinophilia.[22]
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