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The cornea is the outer thin layer of epithelial cells protecting the eye. After wounding, timely resurfacing of the cornea with new cells is critical, to prevent loss of normal function and loss of vision. Corneal epithelial healing occurs in stages, with cells migrating, dividing and differentiating. Therapies for corneal injury are limited. Therefore, the recent finding that Tb4 promotes corneal wound repair in animal models offers hope for a therapeutic product that will improve the clinical outcome of patients with injured corneas.
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.
Hi Jesse, while I cant make specific sarms recommendations as it would be teetering on giving medical advice, I have a ton of resources on this on BenGreenfieldFitness.com that you can easily search through. There is also a lot of invaluable discussion on sarms going on in the comments sections of these articles. The Kion Community is also a great place to ask a question like this: https://Facebook.com/groups/GetKion
This mother-child bonding is the most glorified myth that is not re-thought as often as it should. Its apparant purpose is just to make a dangerously selfish mother (such frustrated mothers do exist a lot more than we read in the news) to think twice before harming her defenseless child which is oftentimes in her sole custody in our society. Acts of such mothers are branded as mental illness rather than plain cruelty. While most people (men and women alike) tend to protect, and not harm a child, the real bonding can happen beetween two independent, mature adults.
Much of human behavior is influenced by hormones. There’s cortisol, involved in our stress response and energy balance. Testosterone, a male sex hormone, tends to make men more competitive. Oxytocin has various social and physiological functions in the brain and the body, but is sometimes referred to as the “love hormone” due to its role in social bonding. These are all simplifications, but hormones do underlie many aspects of what we do and what we feel.
Mental health is so under-funded in the UK that pills can be used as the quick-fix option. In 2014/15, 57.8million prescriptions for antidepressants or SSRIs are filled out in England alone. You can wait months on a waiting list for cognitive behavioural therapy or to see a psychiatrist, and as you wait, medication is a lifeline. In addition to this mess, pharma giants have stopped looking for the 'next Prozac', cutting funding into new treatments by 70 percent in the last decade. The bottom line is clear: SSRIs, with all their pros and cons, are here to stay.
Exogenous Tβ4 can function like a hormone on cells in terms of its ability to modulate their biological behavior. Since one of the primary roles of Tβ4 in cells is the sequestration of actin monomers, and the protein is not secreted, previously indicated that it was unlikely that Tβ4 could have a hormonal function . However, other studies have shown that the intracellular level of Tβ4 or its mRNA can be significantly and rapidly altered by external stimuli and that change in the level of Tβ4 often are correlated with cell differentiation [18, 43]. In the present study, exogenous Tβ4 peptide activate intracellular Tβ4, which results suggested that exogenous Tβ4 spontaneously enter the cytoplasm through rapid internalization, and acts their functions same as endogenous one [8, 18].
But returning hunters also need to share meat with their families and friends; this is where oxytocin comes into play. It can help overcome the potentially negative social effects of testosterone. Men who were absent for longer seem to need more oxytocin to reconnect with their families; it seems that absence does indeed make the heart grow fonder, via an oxytocin blast.
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.
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.
Uterine contractions. These are important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.16
5-HTP, along with other L-Tryptophan supplements, have been implicated in the flu-like, potentially fatal Eosinophilic Myalgia Syndrome. This syndrome was initially tied to impurities - Amino Acids called "Peak E" and "Peak X" - which were present in these products because of poor manufacturing processes by a single major supplier. Some people reject this idea and believe that the syndrome is caused by an excess of tryptophan itself (10, 11).
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, the homologs are further apart and transcribed in the same direction).
In some studies that record appetite suppression with 5-HTP supplementation, nausea appears to also be reported at higher freqencies than placebo, although some interventions note this as the only relevant side effect. Short term studies tend to note that nausea persists throughout the study period while those expanding beyond three weeks note that reports of nausea tend to decline at this time point.
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.
The relationship between oxytocin and human sexual response is unclear. At least two non-controlled studies have found increases in plasma oxytocin at orgasm – in both men and women.1718 The authors of one of these studies speculated that oxytocin’s effects on muscle contractibility may facilitate sperm and egg transport.19 Murphy et al. (1987), studying men, found that oxytocin levels were raised throughout sexual arousal and there was no acute increase at orgasm.20 A more recent study of men found an increase in plasma oxytocin immediately after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted that these changes “may simply reflect contractile properties on reproductive tissue.”21
Work with cell cultures and experiments with animals have shown that administration of thymosin β4 can promote migration of cells, formation of blood vessels, maturation of stem cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. These multiple properties have provided the impetus for a worldwide series of on-going clinical trials of potential effectiveness of thymosin β4 in promoting repair of wounds in skin, cornea and heart.
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.
Due to its molecular structure and low molecular weight, TB-500 is very versatile, mobile and possesses the ability to travel long distances through tissues. This means that when targeting injured areas (chronic or acute), TB-500 has the ability to circulate through the body and “find” those areas of injury in order to enhance the healing or growth process. Many users have also noted the added benefits of improved flexibility, reduced inflammation in tendons, re-growth of lost hair, and darkening of grayed hair.
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.
Cells that line blood vessels (endothelial cells), taken from human umbilical chord veins, were grown in culture and the layer of cells subjected to a scratch wound. Cultures were then treated with Tb4 or kept in growth medium without Tb4. When examined four hours later, Tb4 treatment attracted cells to migrate into the wound and accelerated their movement, showing it is a chemoattractant. Cell migration was four to six times faster in the presence of Tb4 compared to the migration of untreated cells. Tb4 also hastened wound closure and increased the production of enzymes, called metalloproteases, that could pave the way for angiogenesis by breaking down barrier membranes and facilitating the invasion of new cells to the needy area, to form new vessels. Other experiments showed Tb4 acts in vivo. When endothelial cells were implanted under the skin in a gel supplemented with Tb4, the cells formed vessel-like structures containing red blood cells, indicating the ability to stimulate angiogenesis in the animals.
Even if you did look after yourself adequately and monitor the amount of 5-HTP you were taking, it doesn't appear to be a permanent or lasting solution. A couple of the doctors talked about something that comes up time and time again with long-term SSRI use: a dissipating effect, meaning they can feel less and less effective over time. It seems that people may have the same problem with 5-HTP. "If you push on your biochemistry hard enough, it may downregulate," Dr Paddock explained. "If you're taking SSRIs your body may downregulate the amount of serotonin it puts out so you get waning effects over time. It's similar with 5-HTP. There may be a certain level of serotonin your body is keeping you at and if you raise it or push it, your body then may say, 'Okay, we're above the set point, let's then raise that point again.'"
Autism. A 1998 study found significantly lower levels of oxytocin in blood plasma of autistic children. A 2003 study found a decrease in autism spectrum repetitive behaviors when oxytocin was administered intravenously. A 2007 study reported that oxytocin helped autistic adults retain the ability to evaluate the emotional significance of speech intonation.
The pore-forming subunit of the cardiac sodium channel Nav1.5 encoded by SCN5A is a critical determinant of myocardial excitability and conduction. Loss-of-function mutations in SCN5A can clinically manifest as progressive cardiac conduction disorders or as arrhythmic syndromes, such as Brugada syndrome. In addition to electrophysiological dysfunction, SCN5A mutations are also associated with myocardial fibrosis manifesting as global cardiomyopathy. In a 10-year old child exhibiting Brugada syndrome, the mutation SCN5AE555X was discovered. Therefore, cardiac sodium channelopathy pig models were generated by homologous recombination in the genetic background of outbred Yucatan minipigs via SCNT exhibiting the orthologous porcine heterozygous mutation SCN5AE558X. The heterozygous mutant animals were viable and fertile, and showed no sudden death over a 2-year monitoring period. They showed reduced SCN5A protein expression, which resulted in diminished total sodium conductance. The heterozygous mutant hearts showed slowed conduction and increased susceptibility for ventricular arrhythmias in the absence of structural defects of the myocardium or specialized conduction system. In total, a novel animal model was established for understanding the mechanisms linking sodium channel dysfunction to cardiac pathophysiology (Park et al., 2015b).
Oxytocin's story starts back in the early 1900s, when biochemists discovered that a substance from the posterior pituitary gland could promote labour contractions and lactation. When scientists later discovered the hormone responsible, they named it oxytocin after the Greek phrase meaning 'rapid birth'. Oxytocin is produced mainly by the brain's hypothalamus; in the 1970s, studies revealed that oxytocin-producing neurons send signals throughout the brain, suggesting that the hormone had a role in regulating behaviour.