The RANKL and OPG have been identified as a key regulatory component of alveolar bone loss associated with inflammatory periodontal disease . Moreover, PDLCs were shown to express several osteoclastogenic cytokines, including both OPG and RANKL [30, 31]. Our data demonstrated that Tβ4 peptide abolished H2O2-induced RANKL expression and restored OPG expression. Osteoclasts, bone-resorptive multinucleated cells derived from hematopoietic stem cells, are associated with osteolytic diseases. Furthermore, NFATc1, a master modulator of osteoclastogenesis, regulates target genes, such as cathepsin K and calcitonin receptor or Calcr . In our in vitro study using BMMs, Tβ4 peptide directly and indirectly inhibited RANKL-induced osteoclast differentiation and expression of osteoclast markers, such as cathepsin-K, calcitonin receptor or Calcr, NFATc1, and RANK in BMM cells. These results indicated that Tβ4 was a key therapeutic target in controlling inflammation-induced bone loss.
5-HTP has been investigated for its role in hot flashes as Selective Serotonin Reuptake Inhibitors (SSRIs) have been noted to reduce the occurrence of hot flashes and menopausal symptoms. In a study in menopausal females given 150mg 5-HTP daily (50mg taken thrice a day) for a period of one week failed to quantitivatively reduce the occurrance of hot flashes as assessed by a Flashmark Pro recording device.
Oxytocin is relatively safe when used at recommended doses. Potential side effects include: Central nervous system: Subarachnoid hemorrhage, seizures; Cardiovascular: Increased heart rate, blood pressure, systemic venous return, cardiac output, and arrhythmias;Genitourinary: Impaired uterine blood flow, pelvic hematoma, tetanic uterine contractions, uterine rupture, postpartum hemorrhage.
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.
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.
Thymosin beta-4 is a very large molecule. In fact, it is so large that it cannot fit entirely into the receptor. Different sections of the molecule have different activities. TB-500 is the part of thymosin beta-4 hormone which promotes the most useful effects (overall healing, repair, new blood and muscle cells). For medical applications it is more practical to use the TB-500 instead of the entire Thymosin Beta-4 protein.
Angiogenesis is an essential step in the repair process that occurs after injury. In this study, we investigated whether the angiogenic thymic peptide thymosin beta4 (Tbeta4) enhanced wound healing in a rat full thickness wound model. Addition of Tbeta4 topically or intraperitoneally increased reepithelialization by 42% over saline controls at 4 d and by as much as 61% at 7 d post-wounding. Treated wounds also contracted at least 11% more than controls by day 7. Increased collagen deposition and angiogenesis were observed in the treated wounds. We also found that Tbeta4 stimulated keratinocyte migration in the Boyden chamber assay. After 4-5 h, migration was stimulated 2-3-fold over migration with medium alone when as little as 10 pg of Tbeta4 was added to the assay. These results suggest that Tbeta4 is a potent wound healing factor with multiple activities that may be useful in the clinic.
In addition to its intracellular role as the major actin-sequestering molecule in cells of many multicellular animals, thymosin β4 shows a remarkably diverse range of effects when present in the fluid surrounding animal tissue cells. Taken together, these effects suggest that thymosin has a general role in tissue regeneration. This has suggested a variety of possible therapeutic applications, and several have now been extended to animal models and human clinical trials.
Like I said, it’s amazing stuff. And it shouldn’t come as a surprise that it affects that amazing part of your brain so intimately involved in keeping you safe…the amygdala. Remember, trust has a lot to do with survival among social animals who depend on each other for safety and protection. Show someone an untrustworthy face, and the amygdala is one of two areas that become more active than anywhere else in the brain.7 It is apparently programmed for reading trust just as it is for snakes or spiders.
Kim found that when Americans who carry a particular version of the OXTR gene are more likely to turn to their friends for support when they are distressed. But Koreans react to social stress in a different way – for them, it’s less socially acceptable to turn to friends for support during tough times. And distressed Koreans who carry the same version of OXTR are less likely to seek support from their friends.
I have Dupretren’s in my hand. The chords are tightening which is common to this disease pulling the fingers towards the palm. I cannot play guitar any longer. I can still hold a flat palm to the floor when I exercise, but it gets more difficult as the disease takes hold (no pun intended). I’ve read a lot from others inflicted with this. Didn’t like what I read. Hand surgery with modest effects, often adverse effects and too infrequent a fix to the problem. I tried deep tissue massage and scraping too.
Bone loss associated with inflammatory diseases, such as rheumatoid arthritis, periodontal disease, and osteoporosis, and elevated osteoclast activity leads to bone destruction . The most common osteolytic disease, periodontitis, is a multi-factorial irreversible and cumulative condition, initiated and propagated by bacteria and host factors . Destruction of peridontal tissue is mediated via the expression of various tissue-destructive enzymes or inflammatory mediators such as interleukins-1 (IL-1), IL-6 and IL-8, tumor necrosis factor- α (TNF- α), nitric oxide (NO), and prostaglandin E2 (PGE2) . Receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) and osteoprotegerin (OPG) are critical for homeostatic control of osteoclast activity, suggesting that they have vital roles in the progression of bone loss in periodontitis [3, 4]. Therefore, resolution of inflammation and blocking osteoclast differentiation might be a potential therapeutic approach for the prevention and treatment of osteolytic inflammatory disease, such as periodontitis .
If you want to obtain anything other than trivial amounts of milk from animals like dairy cattle, you have to stimulate oxytocin release because something like 80% of the milk is available only after ejection, and milk ejection requires oxytocin. Watch someone milk a cow, even with a machine, and what you'll see is that prior to milking, the teats and lower udder are washed gently - this tactile stimulation leads to oxytocin release and milk ejection.
I found this to be an excellent supplement for myself, which overcomes the rate limiting step when the body converts tryptophan to 5-HTP. I am sleeping much better and handling life's normal stresses better. If you haven't already, become familiar with how/why the body converts L-Tryptophan > 5-HTP > Serotonin > Melatonin. Very interesting! Thank you Bulk Nutrients for making this available.
Research substantiates Wiebe's anecdotal claims. Melanotan.org, a forum dedicated to the peptide that shut down in 2011, had thousands of regular posters, many of whom have since migrated to other discussion boards. In 2009, a BBC report tracking just six needle exchanges found that hundreds of individuals had visited these exchanges in order to receive syringes for Melanotan II use. A year later, the Norwegian Pharmacy Association disclosed that, in Norway alone, several thousand syringes had been distributed to individuals seeking to inject the peptide. Linn Connie Danielsen, a model and blogger, told the Norwegian newspaper Verdens Gangthat Melanotan II helps ease the stressful impact of extended winter sun deprivation. "A nice tan in the winter is good to see," she said.
Jump up ^ Rondanelli M, Opizzi A, Faliva M, Bucci M, Perna S (March 2012). "Relationship between the absorption of 5-hydroxytryptophan from an integrated diet, by means of Griffonia simplicifolia extract, and the effect on satiety in overweight females after oral spray administration". Eating and Weight Disorders. 17 (1): e22–8. doi:10.3275/8165. PMID 22142813.