Astrocytes constitute the largest population of cells in the central nervous system, constituting approximately 90% of human parenchymal cells. Astrocytes are highly responsive to injury, undergoing rapid hyperplasia and hypertrophy. Astrocytes act as physical and biochemical barriers to axonal regeneration by forming glial scars along ischemic lesions and producing axonal growth-inhibitory proteoglycans. Administration of MSCs significantly attenuates the glial scar in the ischemic boundary and reduces expression of inhibitory proteins, such as Nogo. Analysis of single-cell astrocytes isolated from the ischemic boundary by laser capture microdissection reveals that administration of MSCs dramatically down regulates neurocan, an axonal growth-inhibitory proteoglycan. Coculture of MSCs with astrocytes also substantially reduces neurocan expression in astrocytes activated by oxygen glucose deprivation. These findings suggest that injected MSCs reduce physical and biochemical barriers of astrocytes, which also contribute to axonal and neurite outgrowth.
I am not a doctor and nothing I say should be taken as medical advice. If you have a read through the article, I would suggest following the recommendations there. If you want to go into detail book a consult at
It would have been interesting if Bartz had asked about *both* parents’ parenting styles. (Spoken by a guy writing a book on fathers.) It would have been easy enough; just add another question. Any differences between perceptions of mothers and fathers might have been illuminating. But, as in so much family research, fathers were once again ignored or excluded. (As if fathers don’t have parenting styles…)
I have bee suffering from severe symptoms of post concussion syndrome for several.months after a car accident. The use of TB500 has been the only trratment ease my symptoms and give me my life back. I ceased use last week after 3 weeks and had reoccuring concussion symptoms. As such? I recommenced injections as of last night. Have you read much about the impact of TB500 on brain injury as I’d love to know if more prolonged use would have a permanent impact/remedy for me? Thanks for your time and interest.
Dr Sohère Roked is a GP in the UK with a specialist interest in integrative medicine. She prescribes 5-HTP to patients with anxiety and depression, alongside vitamins and other natural supplements, and sees no problem with it being used for mild conditions. "With the patients I see, generally I've seen good results with it. Antidepressants do work for some people, so I'm not against them completely, but others don't want to go down that path straight away. This gives them another option."

To determine the direct effect of Tβ4 peptide on osteoclastogenesis, mouse BMMs were directly exposed to Tβ4 peptide. Direct treatment with Tβ4 peptide also reduced the number of multinucleated TRAP-positive cells and TRAP activity in a dose-dependent manner (Fig 7A and 7B). Since Tβ4 downregulated H2O2-induced various cytokines expression, the indirect effect of Tβ4 on osteoclast formation through PDLC cells using co-culture system were investigated. After addition of Tβ4 peptide to the BMMs-PDLCs co-culture, the number of osteoclast and TRAP activity were also significantly decreased (Fig 7C and 7D).


In addition, in the Phase 1 clinical trial in healthy volunteers using a randomised, double-blind, placebo-controlled single- and multiple-dose Phase 1 clinical trial, the safety and pharmacokinetics of the intravenous administration of TB-4 was evaluated. From this, intravenous administration of TB-4 appears to be safe and well-tolerated by all subjects with no dose limiting toxicity or serious adverse events reported.
Supplementation of 5-HTP has been shown to be more effective than tryptophan supplementation alone. This additional benefit of 5-HTP supplementation arises because 5-HTP bypasses the cell's L-tryptophan's own self-regulation on the IDO enzyme, in which it upregulates the activity of IDO (discussed in next section) to maintain body homeostasis of tryptophan[6] and it bypasses the tryptophan hydroxylase enzyme, which is the rate limiting step in serotonin biosynthesis.[7]
Affecting generosity by increasing empathy during perspective taking. In a neuroeconomics experiment, intranasal oxytocin increased generosity in the Ultimatum Game by 80% but has no effect in the Dictator Game that measures altruism. Perspective-taking is not required in the Dictator Game, but the researchers in this experimental explicitly induced perspective-taking in the Ultimatum Game by not identifying to participants which role they would be in.13

Low oxytocin levels have been linked to autism and autistic spectrum disorders (e.g. Asperger syndrome) – a key element of these disorders being poor social functioning. Some scientists believe oxytocin could be used to treat these disorders. In addition, low oxytocin has been linked to depressive symptoms and it has been proposed as a treatment for depressive disorders. However, there is not enough evidence at present to support its use for any of these conditions.
Thymosin beta 4 (Tβ4) is a highly conserved, naturally occurring, water-soluble regenerative peptide that is found in all tissues and in all cell types, except red blood cells (Goldstein, Hannappel, Sosne, & Kleinman, 2012; Goldstein & Kleinman, 2015). It is also found in the blood and in other body fluids, including tears, saliva, cerebrospinal fluid, and wound fluids (Badamchian et al., 2007; Huang, Wang, Barnes, & Elmets, 2006; Mohring, Kellmann, Jurgens, & Schrader, 2005). Both platelets and leukocytes release Tβ4 into the wound fluid such that the final concentration is 13 μg/mL (Fromm, Gunne, Bergman, et al., 1996; Hannappel & van Kampen, 1987).

Dosages for maintenance begin once you have achieved your desired level of tan. It requires considerably less frequent dose than once every day. In spite of the fact that levels are diverse for everybody, all things considered 500mcg each 3 to 4 days or 1mg a week with a little measure of UV exposure will keep your tan maintained. It maintains the colour without further darkening the skin.

Oxytocin production does not exist separately from the evolved neurophysiological mechanisms that regulate gonadotropin releasing hormone (GnRH) pulsatility. There are mammalian pheromones that are known to directly influence the GnRH pulse, for example androstenol. Oxytocin is not considered to be a pheromone by anyone I know who is involved in olfactory research. Sniffing it is simply a delivery method that we now can see might have negative consequences.


Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all Phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta4 (Tβ4) is the major G-actin-sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including anti-apoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.
To investigate the effect of Tβ4 peptide on H2O2-induced signaling cascades, the activation states of three mitogen-activated protein kinases (MAPKs; p38, c-Jun N-terminal kinase [JNK] and extracellular signal-related kinase [ERK]) as well as NF-κB p65 were examined in PDLCs. H2O2 treatment induced the phosphorylation of p38, ERK, and JNK MAPK(s) and the nuclear translocation of NF-κB p65 (Fig 5A). Treatment of cells with Tβ4 peptide blocked H2O2-induced nuclear translocation of NF-κB p65 and phosphorylation of ERK and JNK (Fig 5B).

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.

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.
Despite these many roles, oxytocin is often reduced to a misleading label. While “hormone of love” may be great for catchy headlines and compelling marketing slogans, they are ultimately misleading. Jennifer Bartz from the Mount Sinai School of Medicine has found that oxytocin can have completely opposite effects on the way people behave, depending on how they view their relationships to other people.
Some work has pointed to a potential dark side to oxytocin. Carter's group found that a single low dose of the hormone given to baby prairie voles improved their pair bonding as adults, but that higher doses interfered with that behaviour — possibly because oxytocin started to activate other receptors16. And human studies have suggested that in certain contexts, a puff of oxytocin can cause people to be more aggressive in defending themselves against outsiders or competitors17. In patients with a psychiatric condition known as borderline personality disorder, a single dose of oxytocin has been found to hinder trust and cooperation18.
To investigate the effect of Tβ4 peptide on H2O2-induced signaling cascades, the activation states of three mitogen-activated protein kinases (MAPKs; p38, c-Jun N-terminal kinase [JNK] and extracellular signal-related kinase [ERK]) as well as NF-κB p65 were examined in PDLCs. H2O2 treatment induced the phosphorylation of p38, ERK, and JNK MAPK(s) and the nuclear translocation of NF-κB p65 (Fig 5A). Treatment of cells with Tβ4 peptide blocked H2O2-induced nuclear translocation of NF-κB p65 and phosphorylation of ERK and JNK (Fig 5B).
Oxytocin produces antidepressant-like effects in animal models of depression,[81] and a deficit of it may be involved in the pathophysiology of depression in humans.[82] The antidepressant-like effects of oxytocin are not blocked by a selective antagonist of the oxytocin receptor, suggesting that these effects are not mediated by the oxytocin receptor.[17] In accordance, unlike oxytocin, the selective non-peptide oxytocin receptor agonist WAY-267,464 does not produce antidepressant-like effects, at least in the tail suspension test.[83] In contrast to WAY-267,464, carbetocin, a close analogue of oxytocin and peptide oxytocin receptor agonist, notably does produce antidepressant-like effects in animals.[83] As such, the antidepressant-like effects of oxytocin may be mediated by modulation of a different target, perhaps the vasopressin V1A receptor where oxytocin is known to weakly bind as an agonist.[84][85]
To identify newborn neurons, double immunofluorescent staining for BrdU/NeuN (mature neuronal marker) was performed (Fig.1). TBI alone significantly increased the number of newborn neurons (NeuN/BrdU-colabeled cells) in the DG of injured hemisphere. Tβ4 treatment significantly further increased the number of newborn neurons compared to saline controls. These data suggest that Tβ4 administration initiated 24 hours after TBI promotes neurogenesis in rats.

The reason for the difference is the density of oxytocin receptors in the brain. Life pair bonders, like prairie voles or, indeed, ourselves, have a high density of receptors in the reward centre of the brain. Non-pair bonders, like meadow voles, certainly enjoy sex, but their lower density of receptors means it doesn't matter so much who the partner is. So it's not the oxytocin itself making sex enjoyable. What it's doing is influencing our mating behaviour.

In the experiments, an epithelial wound was made in the corneas of sedated rats. A Tb4 solution was applied at several concentrations to the injured eyes in one group of rats while another group was treated with a solution without Tb4. Following 12, 24 and 36 hours, the eyes were tested by microscopic observation for epithelial growth over the injured site. Investigators found the Tb4 accelerated corneal wound repair at doses of Tb4 similar to those found to repair skin wounds. When tested 24 hours after treatment, the rate of accelerated repair was proportional to the concentration of Tb4, with the highest dose (25 microgram) showing a threefold acceleration of epithelial cell migration, compared to untreated. Treatment with Tb4 showed anti-inflammatory effects, helping resolve the injury. An application to human cells in a model of human corneal cells in culture showed that Tb4 enhanced epithelial cell migration in vitro.
In 20 persons undergoing alcohol withdrawal taking 5-HTP (5mg) alongside Glutamine (150mg) and D-Phenylalanine (300mg) and some minerals such as Calcium and Magnesium, it was noted that after 40 days of nutritional therapy (in a hospital setting) that all withdrawal symptoms assessed via SCL-90-R except for anxiety noted a greater reduction with nutritional support relative to placebo.[1]
About three months after quitting, I did have a major relapse, which was falling back into old habits for about two weeks. And the whole time I knew what was happening, I knew how dangerous it was, but I couldn't stop myself. I felt like I couldn't connect to anyone without drinking. I couldn't talk to my friends, I couldn't be open and honest with anybody in my life without already having had a few drinks. It was a really disconnected, really unpleasant feeling. That's what I couldn't sit with and I couldn't cope with that feeling, so I went back to drinking.

Advice & Tips: 5-HTP is a serotonin precursor. Serotonin is well-known as a hormone that affects one's mood in a positive way, but it is probably less-well known that it increases intestinal motility. It has worked magic for my symptoms. I am completely regular now, and the majority of my days are good days, whereas before I began taking it the majority of my days were bad days that began with symptoms of constipation and intestinal pain or discomfort. For me, at least, this is not a prescription. I began taking 5-HTP after my fiancee'--who had already been taking it to help her mood and, primarily, her difficulty sleeping through the night--learned it can be helpful when taken for gastrointestinal motility, and I began taking it myself shortly after that (and felt its effects almost immediately). Although not entirely unexpected, my slightly enhanced good moods are a nice side benefit of taking the supplement. I do get some very mild undesirable side effects, especially during mid-day when I take twice my morning and evening dose of 100 mg. Sometimes my face feels hot and flushes fairly noticeably--and this may be intensified with eating--but those symptoms subside within probably 30 minutes or less.
Virtually all vertebrates have an oxytocin-like nonapeptide hormone that supports reproductive functions and a vasopressin-like nonapeptide hormone involved in water regulation. The two genes are usually located close to each other (less than 15,000 bases apart) on the same chromosome, and are transcribed in opposite directions (however, in fugu,[44] the homologs are further apart and transcribed in the same direction).
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.
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).
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]