This article is authored by a PhD Candidate and her supervisory team at University of Queensland, and reflects the interests of the student’s doctoral project in undertaking the nation’s first qualitative study into experiences of Melanotan use among the general population. Dubbed ‘Project Melanotan’, the investigation aims to directly engage with ‘melanotanners’ in a non-judgemental environment, in an effort to both critically evaluate as well as understand lived experiences of melanotaning as they relate to conceptually relevant notions of risk, technology and the body.
Established immortalized human PDLCs  that maintain the characteristics of primary PDLCs by transfecting human telomerase reverse transcriptase (hTERT) were used. These cell line were kindly provided by Professor Takashi Takata (Hiroshima University, Japan). Cells were cultured in α-MEM supplemented with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin in a humidified atmosphere of 5% CO2 at 37°C. For the experiments, the cells were seeded into culture dishes and then cultured in α-MEM containing 10% FBS for 2 days until 70% confluent, and, then, the media was replaced by serum-free medium in order to minimize any serum-induced effects on PDLCs. Subsequently, the cells were exposed to H2O2 and human Tβ4 peptide (RegeneRx Biopharmaceuticals Inc., Rockville, MD). All treatments were performed in triplicate and approved by the local ethics committee.
Thymosin beta(4), a small ubiquitous protein containing 43 aa, has structure/function activity via its actin-binding domain and numerous biological affects on cells. Since it is the major actin-sequestering molecule in eukaryotic cells and is found essentially in all cells and body fluids, thymosin beta(4) has the potential for significant roles in tissue development, maintenance, repair, and pathology. Several active sites with unique functions have been identified, including the amino-terminal site containing 4 aa (Ac-SDKP) that generally blocks inflammation and reduces fibrosis. Another active site at the amino terminus contains 15 aa, including Ac-SDKP, and promotes cell survival and blocks apoptosis, while a short sequence containing LKKTETQ, the central actin-binding domain (aa 17-23) plus 1 additional amino acid (Q), promotes angiogenesis, wound healing, and cell migration. Several additional biological activities have been identified but not yet localized in the molecule, including its antimicrobial activity, the induction of various genes (including laminin-5, MMPs, TGF beta, zyxin, terminal deoxynucleotidyl transferase, and angiogenesis-related proteins), and the ability to activate ILK/PINCH/Akt, and other signaling molecules important in both apoptosis and inflammatory pathways. This review details these important physiologically and pathologically active sites and their potential therapeutic uses.
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“People got quite excited,” recalls clinical neuroscientist Evdokia Anagnostou, who co-directs the Autism Research Centre at Holland Bloorview Kids Rehabilitation Hospital in Toronto, Canada. But Anagnostou says that some preliminary steps were skipped over as researchers rushed to test oxytocin as a psychiatric drug. “To be honest, if we had done it properly, we wouldn't have done it the way we did. It went a little bit too fast,” she says. Because oxytocin had cleared the early, standard steps of drug development decades earlier, some researchers did not systematically test a range of doses to see whether they had differing psychological effects.
With the TB-500 it seems that pain was reduced even more in my shoulder and it appears that I recovered much faster from my workouts. I took the TB-500 on rest days. I have two more 1mg doses of TB-500 and I am going to site inject intramuscularly to the shoulder to see what happens. Then I will stop taking both for a month to see how things work out. Hopefully I won’t need them again.
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 it appears it may sensitize the body by an increase in neurovegetative panic symptoms and increased anxiety which suggests that serotonin is protective against panic attacks, at least acutely. 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. This has been replicated with cholecystokinin-4 induced panic attack with 200mg 5-HTP in otherwise healthy persons.
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.
The idea that oxytocin is central to social cognition made it an attractive candidate for treating psychiatric disorders, especially autism spectrum disorder. People with this condition, who often have problems with social interaction and communication, may not process social stimuli appropriately — and scientists theorized that oxytocin might reverse some of the symptoms. Beginning in 2010, results emerged that seemed to support this theory: researchers found that single puffs of oxytocin could temporarily improve measures of empathy and social cooperation in people with autism spectrum disorder.
Again, the three groups of mice were exposed to the stressful experience of social defeat in the cages of other more aggressive mice. This time, six hours after the social stress, the mice were put in a box in which they received a brief electric shock, which startles them but is not painful. Then 24 hours later, the mice were returned to the same box but did not receive a shock.
The vascular system in the normal adult brain is stable, but is activated in response to certain pathological conditions including injuries.68 Von Willebrand factor (vWF) staining has been used to identify vascular structure in the brain after TBI.69 TBI alone significantly increased vascular density in the injured cortex, CA3, and DG of the ipsilateral hemisphere when examined at day 35 after TBI compared to sham controls.18,34,64,65 Tβ4 treatment significantly increased the vascular density in these regions compared to saline treatment.34 This is in agreement with in vitro and in vivo pro-angiogenic effect of Tβ4.70,71
Recent reports have stated that inhibitors of Wnt signaling have emerged as promising strategies for bone disease and inflammatory diseases [26, 55]. Wnt5a, one of the most common Wnt molecules that activate the non-canoical pathway, binds to Fzd and its co-receptor, Ror2 . In synoviocytes from rheumatoid arthritis patients, the expressions of Wnt5a and Frizzled5 (Fzd5) were significantly enhanced  and their blockades inhibited synoviocyte activation . Recently, Wnt5a was highly expressed in synovial tissues in a mouse model of rheumatoid arthritis where inhibition of Wnt5a-Ror2 signaling suppressed bone loss . Our data demonstrated that ROS up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2, as well as mRNA and protein expressions in time- and dose-dependent manners in PDLCs.
5-HTP is decarboxylated to serotonin (5-hydroxytryptamine or 5-HT) by the enzyme aromatic-L-amino-acid decarboxylase with the help of vitamin B6. This reaction occurs both in nervous tissue and in the liver. 5-HTP crosses the blood–brain barrier, while 5-HT does not. Excess 5-HTP, especially when administered with vitamin B6, is thought to be metabolized and excreted.