She recruited 31 men* and asked them to sniff either an oxytocin nasal spray or another spray with the same ingredients minus oxytocin – a placebo. A few weeks later, the sprays were swapped so that the men who took oxytocin now took the placebo, and vice versa. At the time, neither the scientists nor the volunteers knew which was which – that was only revealed after the experiment was over.

In the hypothalamus, oxytocin is made in magnocellular neurosecretory cells of the supraoptic and paraventricular nuclei, and is stored in Herring bodies at the axon terminals in the posterior pituitary. It is then released into the blood from the posterior lobe (neurohypophysis) of the pituitary gland. These axons (likely, but dendrites have not been ruled out) have collaterals that innervate neurons in the nucleus accumbens, a brain structure where oxytocin receptors are expressed.[31] The endocrine effects of hormonal oxytocin and the cognitive or behavioral effects of oxytocin neuropeptides are thought to be coordinated through its common release through these collaterals.[31] Oxytocin is also produced by some neurons in the paraventricular nucleus that project to other parts of the brain and to the spinal cord.[32] Depending on the species, oxytocin receptor-expressing cells are located in other areas, including the amygdala and bed nucleus of the stria terminalis.
TB-500 is a synthetic version of the naturally occurring peptide present in virtually all human and animal cells, Thymosin Beta-4. This potent peptide is a member of a ubiquitous family of 16 related molecules with a high conservation of sequence and localization in most tissues and circulating cells in the body. TB-500 not only binds to actin, but also blocks actin polymerization and is the actin-sequestering molecule in eukaryotic cells.
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].

In the male mammal, the small peptide hormone oxytocin is produced in similar quantities within the hypothalamo-pituitary magnocellular system as in the female, yet for the male little is known about the physiology associated with this hormone. The present review summarizes what is known about the function of oxytocin in the male mammal and tries to take account of both central and systemic effects, and those linked with a local production of oxytocin within the male reproductive organs. In several species a pulse of systemic oxytocin, presumably of hypothalamic origin, appears to be associated with ejaculation. The systemic hormone could act peripherally stimulating smooth muscle cells of the male reproductive tract, but could also reflect central effects in the brain modulating sexual behaviour. In addition to systemic oxytocin, the peptide is also made locally within the testis, and possibly also the epididymis and prostate. In the former tissue it appears to have an autocrine/paracrine role modulating steroid metabolism, but may in addition be involved in contractility of the seminiferous tubules. However, the latter function may involve the mediacy of Sertoli cells which under some circumstances can also exhibit the components of a local oxytocin system. In the prostate of the rat and the dog oxytocin is linked again to steroid metabolism and may also act as a growth regulator. Finally, oxytocin in seminal fluid is discussed and its possible role in respect to the fate of the semen following ejaculation.
Three groups of mice were individually placed in cages with aggressive mice and experienced social defeat, a stressful experience for them. One group was missing its oxytocin receptors, essentially the plug by which the hormone accesses brain cells. The lack of receptors means oxytocin couldn't enter the mice's brain cells. The second group had an increased number of receptors so their brain cells were flooded with the hormone. The third control group had a normal number of receptors.
Addiction vulnerability: Concentrations of endogenous oxytocin can impact the effects of various drugs and one's susceptibility to substance use disorders. Additionally, bilateral interactions with numerous systems, including the dopamine system, Hypothalamic–pituitary–adrenal axis and immune system, can impact development of dependence. The status of the endogenous oxytocin system might enhance or reduce susceptibility to addiction through its interaction with these systems. Individual differences in the endogenous oxytocin system based on genetic predisposition, gender and environmental influences, may therefore affect addiction vulnerability.[72] Oxytocin may be related to the place conditioning behaviors observed in habitual drug abusers.
These proteins, which typically contain 2-4 repeats of the β-thymosin sequence, are found in all phyla of the animal kingdom, with the probable exception of sponges[21] The sole mammalian example, a dimer in mice, is synthesised by transcriptional read-through between two copies of the mouse β15 gene, each of which is also transcribed separately.[22] A uniquely multiple example is the protein thypedin of Hydra which has 27 repeats of a β-thymosin sequence.[23]
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).
I broke my neck this year at C6-C7 facets. Started taking TB-500 immediately following the accident. I don’t sit still well and was back in the gym almost immediately, simply to not go stir crazy and pump the blood anyway I could. 8 weeks later I was hitting bodyweight overhead squats for reps with the jerk, 0 pain and completely stable spine. I’m in my late 30s. I eat well, sleep well, and drink a lot of water. I doubt I would have been as well off, had I not taken the TB.
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To pursue the sexual dysfunction agent, melanotan-II was licensed by Competitive Technologies to Palatin Technologies.[9] Palatin ceased development of melanotan-II in 2000 and synthesized, patented, and began to develop bremelanotide, a likely metabolite of melanotan-II that differs from melanotan-II in that it has a hydroxyl group where melanotan-II has an amide.[6][13] Competitive Technologies sued Palatin for breach of contract and to try to claim ownership of bremelanotide;[13] the parties settled in 2008 with Palatin retaining rights to bremelanotide, returning rights to melanotan-II to Competitive Technologies, and paying $800,000.[14]
Another interesting agent reported to significantly accelerate chronic wound repair is infrared (700–1200 nm wavelength) and near infrared (600–700 nm) light delivered through lasers or light-emitting diodes (LEDs) (Mester et al., 1968; Rochkind et al., 1989; Conlan, 1996; Schindl et al., 2000; Enwemeka, 2004). Spectroscopic measurements indicate that photons at wavelengths of 630–800 nm penetrate through the skin and muscles of the forearm and lower leg (Chance et al., 1988; Beauvoit et al., 1994, 1995). The effect of the light may be to stimulate cytochrome c oxidase in the mitochondria, resulting in increased oxygen consumption and production of ATP (Karu, 1999).
The product can be of unknown quality and subject to contamination and stability concerns with use of multi-dose vials. There is no experience with the product other than through unregulated channels. There are health risks from the substance itself and its route of administration – documented in medical literature, case reports as well as reports from NSW PIC.
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.
But Carter and other scientists are concerned by reports from the physicians and parents of children with autism spectrum disorder who say that they are already using oxytocin off-label — before it has been thoroughly tested. “We do not understand how the hormone works yet, or have enough information about what happens when it's given repeatedly,” Carter says. “This is not a molecule that people should be self-administering or playing with.”
Oxytocin is a peptide of nine amino acids (a nonapeptide). The sequence is cysteine - tyrosine - isoleucine - glutamine - asparagine - cysteine - proline - leucine - glycine (CYIQNCPLG). The cysteine residues form a sulfur bridge. Oxytocin has a molecular mass of 1007 daltons. One international unit (IU) of oxytocin is the equivalent of about 2 micrograms of pure peptide.
Why have zebrafish retained the ability to regenerate? It is thought that the capacity for organ regeneration is an ancestral condition that has occasionally been diminished in the course of vertebrate evolution (Scadding, 1977; Goss, 1992; Wagner and Misof, 1992). Thus, most biologists suspect that the molecular machinery to optimize regeneration is present but poorly-utilized in mammals. By this line of reasoning, zebrafish heart regeneration may represent an optimal utilization of universal cardiac machinery.
To investigate whether the newborn neurons generated in the DG are capable of projecting their axons into the CA3 region of the hippocampus after TBI, we stereotactically injected a fluorescent tracer, 1,1″-dioleyl-3,3,3″,3″-tetramethylindocarbocyanine methanesulfonate (Dil, Delta 9-DiI; AnaSpec, San Jose, CA) into the ipsilateral CA3 region (stereotaxic coordinates AP, -3.6 mm bregma, ML, 3.6 mm, DV, 3.0 mm, Paxinos and Watson, 1994) at day 28 after TBI. BrdU (100mg/kg, ip) was injected i.p. daily starting at day 1 after TBI for 10 days to label newly generated cells. One week after DiI injection (i.e., 35 days after TBI), the animals were anesthetized and sacrificed. Their brains were fixed in 4% paraformaldehyde. The brain was cut into seven equally spaced 2-mm coronal blocks using a rat brain matrix. The brain blocks containing the hippocampus were processed for vibratome sections (100 μm) followed by BrdU staining. BrdU and DiI labeling in the hippocampus on brain sections was analyzed with a Bio-Rad MRC 1024 (argon and krypton) laser-scanning confocal imaging system mounted onto a Zeiss microscope (Bio-Rad, Cambridge, MA). Co-localization of BrdU-positive nuclei within retrogradely DiI-labeled granule cells was found, indicating that newborn granule neurons extend axons into the CA3 region that are capable of retrogradely transporting DiI from the CA3 to their cell bodies within the DG after TBI (Fig.2). This finding suggests that newborn granule neurons may be incorporated into functional hippocampal circuitry after TBI.

But long before that, say researchers, oxytocin could use a rebranding. “It doesn't induce love; it doesn't induce massive amounts of trust,” Guastella says. “The problem we've got ourselves into is that we're trying to look for a simple answer: either oxytocin does or does not work in a patient population, or it does or does not enhance a certain social process.”

^ Jump up to: a b Hurlemann R, Patin A, Onur OA, Cohen MX, Baumgartner T, Metzler S, Dziobek I, Gallinat J, Wagner M, Maier W, Kendrick KM (April 2010). "Oxytocin enhances amygdala-dependent, socially reinforced learning and emotional empathy in humans". The Journal of Neuroscience. 30 (14): 4999–5007. doi:10.1523/JNEUROSCI.5538-09.2010. PMID 20371820.
The mRNA and protein expressions were determined by PCR analysis (A) and Western blot analysis (B), respectively. The bar graph shows the fold increase in protein or mRNA expression compared with control cells * Statistically significant differences compared with the control, p<0.05. The data presented were representative of three independent experiments.

The oxytocin peptide is synthesized as an inactive precursor protein from the OXT gene.[18][19][20] This precursor protein also includes the oxytocin carrier protein neurophysin I.[21] The inactive precursor protein is progressively hydrolyzed into smaller fragments (one of which is neurophysin I) via a series of enzymes. The last hydrolysis that releases the active oxytocin nonapeptide is catalyzed by peptidylglycine alpha-amidating monooxygenase (PAM).[22]

Moreover, Tβ4 concentration revealed wide variability, and it decreased in the gingival crevicular fluid (GCF) as periodontal disease progressed [19]. In contrast, Tβ4 mRNA expression was 3.76 fold higher in periodontitis-affected gingival tissue, compared with healthy individuals’ tissue obtained from public microarray data (GEO assession: GSE 23586) [20]. However, the Tβ4 mRNA level did not change in the periodontal-diseased gingival tissue (arbitrary units; 6.249) when compared with healthy tissue (arbitrary units; 6.242) (GEO assession: GSE 10334) [21]. Although Tβ4 exerts anti-inflammatory effects in vivo and in vitro, the precise role of Tβ4 in the inflammatory response remains unclear.
Doctors have noticed cancer patients have a higher amount of Thymosin in the affected tissues than other people. So in the early stages of research, doctors assumed that this meant Thymosin may cause cancer. After more research was conducted, it was discovered that the main action of Thymosin Beta 4 was to produce new white blood cells – so its presence in the body in the areas affected by cancer was likely not a cause of the cancer, but instead, a matter of “showing up” in the body where cancer lived to help the body mount an immune system response.
Skin is the largest organ of the body, which makes up 16% of total body weight. It is also the largest organ that provides immune protection and plays a role in inflammation. Composed of specialized epithelial and connective tissue cells, skin is our major interface with the environment, a shield from the outside world and a means of interacting with it. As such, the skin is subjected to insults and injuries: burns from the sun’s ultraviolet radiation that elicit inflammatory reactions, damage from environmental pollutants and wear and tear that comes with aging.

Thymosin beta-4 (Tβ4) is a water-soluble, 43-amino acid, and 4.9 kDa protein that was originally isolated from bovine thymus [6]. Since Tβ4 is the major actin-sequestering molecule in eukaryotic cells and is found in all cells [7], Tβ4 has multiple diverse cellular functions, including tissue development, migration, angiogenesis, and wound healing [7]. We previously reported that Tβ4-overexpressing transgenic mice, using a construct on the skin-specific keratin-5 promoter, have abnormal tooth development and enhanced stimulation of hair growth [8]. Moreover, exogenous Tβ4 has anti-inflammatory effects in the bleomycin-induced mouse model of lung fibrosis [9], tooth extraction sockets in rats [10], rat model of myocardial ischemia [11], corneal wound healing [12], wound healing of rat palatal mucosa [13], in vitro model of cultured human gingival fibroblasts [14], and cardiac fibroblasts [15]. However, the effects of Tβ4 over expression or inhibition on differentiation are controversial. Exogenous β4 peptide inhibited osteogenic differentiation but facilitated adipogenic differentiation in human bone marrow-derived-mesenchymal stem cells (MSCs) [16]. In contrast, Tβ4 inhibition by Tβ4 siRNA attenuated odontoblastic differentiation in the odontoblast-like cells, MDPC-23 [17]. Moreover, we recently demonstrated that odontoblastic differentiation was enhanced by activation of Tβ4 by Tβ4 peptide but was decreased by Tβ4 siRNA in human dental pulp cells (HDPCs) [18]. However, the effects of Tβ4 on osteoclastic differentiation have not been reported.
One way to clarify that question is to give individuals oxytocin rather than just measure naturally occurring levels. In experiments by couple therapist and researcher Beate Ditzen at the University of Zurich, couples each sprayed a liquid containing oxytocin up their noses (which ensures that the hormone reaches the brain). Ditzen then got them to talk with each other about an issue that both partners said often lead to disagreement or fighting, such as who did the housework or how they spent their free time. She observed how they communicated with each other during the discussion compared with couples who didn’t get the hormone.
A user knowing their skin type in relation to the Fitzpatrick scale is important because it will dictate dosing needs. It should be noted that those who will benefit the most from this product are those in the upper spectrum of the Fitzpatrick scale (Types 1, 2 and 3 especially). Skin type 1 and 2 users will typically take longer to see any results from this product, however once beautiful tan is obtained maintenance is easy.
The promise of repairing sun parched aging skin is alluring, especially if damage control may be attained by applying a substance that is abundant in our body. Thymosin beta 4 (Tb4), a molecule that accelerates wound healing in animals and cultured cells, "may be valuable in repairing skin damage caused by sun or even by the wear and tear of aging?" This hopeful message of Tb4's potential to restore damaged human skin was voiced at the 5th International Symposium on Aging Skin, in California (May 2001), by Dr. Allan Goldstein, Chairman of the Biochemistry Department at George Washington University and founder of RegeneRX Biopharmaceuticals. RegeneRX is carrying out preclinical research on Tb4 as a wound healer, in collaboration with scientists at the National Institutes of Health.

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.
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.

Injected oxytocin analogues are used to induce labour and support labour in case of non-progression of parturition. It has largely replaced ergotamine as the principal agent to increase uterine tone in acute postpartum haemorrhage. Oxytocin is also used in veterinary medicine to facilitate birth and to increase milk production. The tocolytic agent atosiban (Tractocile®) acts as an antagonist of oxytocin receptors; this drug is registered in many countries to suppress premature labour between 24 and 33 weeks of gestation. It has fewer side-effects than drugs previously used for this purpose (ritodrine, salbutamol and terbutaline).

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.
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.
The soluble form of Ac-SDKP peptide, derived from thymosin beta-4, has been described as a natural inhibitor of pluripotent hematopoietic stem cell proliferation and as a stimulator of angiogenesis, both in vitro and in vivo (Koutrafouri et al., 2001; Wang et al., 2004). This peptide has been selectively bound to acrylated hyaluronic acid hydrogels via thiol groups from cysteine residues (Song et al., 2014). Unfortunately, the immobilization process was poorly characterized and the effect of hydrogels on EC function was not tested in vitro. In a mouse model of chronic myocardial infarction, hydrogels with immobilized Ac-SDKP did not show improved regeneration potential. Yet, Ac-SDKP-HA hydrogels with entrapped stem cell homing factor SDF-1 showed a significant increase of myocardial regeneration and recovery of heart function, as compared to groups with only one or none of these factors, suggesting a potentially interesting synergistic effect.
Stimulation of uterine smooth muscle contraction at birth: At the end of gestation, the uterus must contract vigorously and for a prolonged period of time in order to deliver the fetus. During the later stages of gestation, there is an increase in abundance of oxytocin receptors on uterine smooth muscle cells, which is associated with increased "irritability" of the uterus (and sometimes the mother as well). Oxytocin is released during labor when the fetus stimulates the cervix and vagina, and it enhances contraction of uterine smooth muscle to facilitate parturition or birth. 

Outside the brain, oxytocin-containing cells have been identified in several diverse tissues, including in females in the corpus luteum[34][35] and the placenta;[36] in males in the testicles' interstitial cells of Leydig;[37] and in both sexes in the retina,[38] the adrenal medulla,[39] the thymus[40] and the pancreas.[41] The finding of significant amounts of this classically "neurohypophysial" hormone outside the central nervous system raises many questions regarding its possible importance in these different tissues.
Adam Guastella, a clinical psychologist at University of Sydney’s Brain and Mind Research Institute, and a pioneer in studies of how oxytocin can help people with autism, thinks the hormone can also help people in couple therapy by facilitating empathic communication. His research has shown that people who get oxytocin are more focused on positive emotion: they remember happy faces better than angry and neutral ones. Research by others has shown that oxytocin increases trust, generosity and our ability to identify emotion in facial expressions. It is perhaps by these mechanisms that the hormone improves communication.
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.

Tβ4 is not a thymus-specific peptide but also present in most tissue and all cells except red blood cells [35]. High amounts of Tβ4 were detected in human white blood cells, especially in neutrophils and in macrophages [34], expressed in developing mandible (embryonic day 12) [36] and hair follicles (HF) of mice [37]. In addition, the peptide is also detected outside cells, in blood plasma and in wound and blister fluids [34]. Although the mechanism(s) of action of exogenous Tβ4 on anti-inflammatory effects remains unclear, the high levels of Tβ4 present in human wound fluid (13 μg/mL) suggest its importance in wound healing or anti-inflammation [38]. However, the level of Tβ4 is variable (unchanged, decreased, and increased) in GCF or biopsied gingival tissue of periodontal patients [20, 21]. Based on the observations that Tβ4 has anti-inflammatory effects [11–14], the hypothesis is that Tβ4 regulates inflammatory mediators and osteoclastogenesis in osteolytic bone disease, such as periodontitis.
Jump up ^ Gauquelin G, Geelen G, Louis F, Allevard AM, Meunier C, Cuisinaud G, Benjanet S, Seidah NG, Chretien M, Legros JJ (1983). "Presence of vasopressin, oxytocin and neurophysin in the retina of mammals, effect of light and darkness, comparison with the neuropeptide content of the neurohypophysis and the pineal gland". Peptides. 4 (4): 509–15. doi:10.1016/0196-9781(83)90056-6. PMID 6647119.
^ Jump up to: a b Marazziti D, Dell'Osso B, Baroni S, Mungai F, Catena M, Rucci P, Albanese F, Giannaccini G, Betti L, Fabbrini L, Italiani P, Del Debbio A, Lucacchini A, Dell'Osso L (October 2006). "A relationship between oxytocin and anxiety of romantic attachment". Clinical Practice and Epidemiology in Mental Health. 2 (1): 28. doi:10.1186/1745-0179-2-28. PMC 1621060. PMID 17034623.
Injected oxytocin analogues are used to induce labour and support labour in case of non-progression of parturition. It has largely replaced ergotamine as the principal agent to increase uterine tone in acute postpartum haemorrhage. Oxytocin is also used in veterinary medicine to facilitate birth and to increase milk production. The tocolytic agent atosiban (Tractocile®) acts as an antagonist of oxytocin receptors; this drug is registered in many countries to suppress premature labour between 24 and 33 weeks of gestation. It has fewer side-effects than drugs previously used for this purpose (ritodrine, salbutamol and terbutaline).
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).
"There was no substance labelled unfit for human use so anyone that tries to bandy that comment around apart from the fact the comment is totally false, we are now starting to accrue our legal case against people that have suggested as such. Under no circumstances was anything ever injected or given to a player which was unfit for human consumption," Dank told ABC News Radio on Sunday.
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.
This current literature is notable for its apparent irrelevancy to an AFL footballer. It begs the question; did Tβ4 make a difference to the Essendon players? The only honest answer is that we don’t know. Most of our understanding exists on a molecular and cellular level, without any significant appreciation of how Tβ4 influences applicable outcomes such as exercise performance, endurance, muscle strength, and time to recovery. Furthermore, as the majority of research has been performed on mice, rat and pig models, any results are not directly translatable to a human, let alone an elite athlete. This is a stark contrast to a supplement such as EPO, which has been investigated thoroughly.
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.
The tb-500 has a systematic effect regardless of where it is injected. Some believe that thymosin beta-4 should be injected as close to the injury as possible however there is no evidence to show this would be superior. It can be injected subcutaneously (stomach fat) or intramuscularly (shoulders, thighs, buttocks). Injections should be given in different sites (rotated) each time. Depending on the spot, you can either feel nothing or you can feel slight pain - you will learn your favorite spots in time.
Our research mainly focusses on this early social experiences that people have that can be positive or negative, and that can really shape our developing brain. There have been some very interesting studies, for example, with children that grew up in Romanian orphanages. And we know that that early start, where it's really deprived from social contact and physical contact, had a massive impact. So we see that oxytocin levels, for example, are much lower than we would expect in other kids.
Bromodeoxyuridine (BrdU), a thymidine analogue, can be incorporated into the DNA of dividing cells and is widely used to label new cells.61-63 To label proliferating cells, BrdU (100 mg/kg) was injected i.p. daily starting at day 1 post TBI for 10 days. The number of BrdU-positive cells found in the ipsilateral cortex, DG, and CA3 areas was significantly increased 35 days after TBI compared with sham controls.18,34,64,65 Tβ4 treatment further increased the number of BrdU-positive cells compared to saline controls.34 The increased number of BrdU-positive cells may result from effects of Tβ4 on either increasing cell proliferation or reducing cell death of newborn cells. Our recent data show Tβ4 increases oligodendrocyte precursor cell proliferation and differentiation in animal models of stroke25 and experimental autoimmune encephalomyelitis.27 Tβ4 may not directly affect cell proliferation but inhibit cell death, for example, in corneal and conjunctival epithelial cells treated with benzalkonium chloride in vitro66 and endothelial precursor cells under serum deprivation.67 Our data further show that neurogenesis increases in TBI rats treated with Tβ4, suggesting that Tβ4 promotes newborn cells to differentiate into neurons. This is consistent with the effect of Tβ4 on promoting epicardium-derived progenitor cell differentiation into endothelial and smooth muscle cells to form the coronary vasculature.22 Whether the increased number of BrdU-positive cells in the brain of TBI rats treated with Tβ4 is tissue specific remains unknown. Tβ4 may not directly affect cell proliferation. Increased cell proliferation and neurogenesis are also possibly secondary to that Tβ4-mediated angiogenesis, as described later.
Combined treatments of 5-HTP and SSRI seem to have strong synergistic effects on serotonin levels in rats and humans so that some clinicians recommend the use of slow-released 5-HTP in combination with SSRIs (R, R2, R3). However, additional clinical trials are required to demonstrate the safety and effectiveness of this approach, and combinations of 5-HTP and medications should only be used under medical supervision.
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