Some differences in cardiac anatomy exist between mammals and teleosts. The zebrafish ventricle has a thin wall of compact muscle surrounding a much larger compartment of myofibers organized into elaborate trabeculae. It is intriguing that this structure is very similar to that of the embryonic mammalian ventricle prior to its septation and fusion of trabeculer myofibers into a thick, vascularized wall (Sedmera et al., 2000). That the mammalian heart has a more differentiated, contractile anatomy is apparent not only in gross cardiac structure, but also in cellular features. Teleost cardiomyocytes are 2–10 times smaller, mononucleated, have a greatly-reduced sarcoplasmic reticulum and lack the T-tubule system found in skeletal muscle and mammalian cardiac muscle (Farrell, 1992). One might speculate that the teleost heart is better designed for growth and regeneration, while the mammalian heart is better designed for sheer contractile force. Nevertheless, none of the mentioned differences between lower and higher vertebrate hearts preclude the idea that the mammalian heart could be stimulated to regenerate, especially if that regeneration is due to mobilization of a progenitor cell population.
A number of factors can inhibit oxytocin release, among them acute stress. For example, oxytocin neurons are repressed by catecholamines, which are released from the adrenal gland in response to many types of stress, including fright. As a practical endocrine tip - don't wear a gorilla costume into a milking parlor full of cows or set off firecrackers around a mother nursing her baby.

As reactive oxygen species (ROS) have been implicated in the pathogenesis of periodontitis [24], we examined whether H2O2 could down-regulate or up-regulate Tβ4 expression in PDLCs. As shown in Fig 1A and 1B, Tβ4 mRNA and protein expressions were down-regulated by H2O2 in a time- and concentration-dependent manner. Because maximal Tβ4 mRNA and protein expressions were achieved with 200 μM H2O2 within 48 hours in PDLCs, this concentration was used in subsequent experiments.
Both the production of oxytocin and response to oxytocin are modulated by circulating levels of sex steroids. The burst of oxytocin released at birth seems to be triggered in part by cervical and vaginal stimulation by the fetus, but also because of abruptly declining concentrations of progesterone. Another well-studied effect of steroid hormones is the marked increase in synthesis of uterine (myometrial) oxytocin receptors late in gestation, resulting from increasing concentrations of circulating estrogen.

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.

Wonderful column. My expertise is the psychology of risk perception, and I have done some reading on oxytocin and trust (not the kind you want to boost in a bar with Liquid Trust – you can the stuff with pheromones – to boost THAT kind of trust). It turns out there is a high concentration of oxytocin receptors on the amygdala, the area of the brain where fear starts. As oxytocin levels go up, the ability of the amygdala to be warry and more mistrustful goes down. I describe this in Ch. 3 of How Risky Is It, Really? Why Our Fears Don’t Always Match the Facts. A few graphs of which are below. I wonder whether the influence of oxytocin on the amygdala might be connected with the finding of the study you write about.
The pamphlet, titled "Melanotan-2: Safe enhanced tanning" says although the drug is not approved by the Therapeutic Goods Administration (Australia's drug watchdog) and that studies into its effects are under way, it "is safe" and and its use "well documented". It says people can be referred to a "suitable doctor who is trained to prescribe MT2" so the pharmacy can dispense it to them.
Oxytocin is known as the hormone that promotes feelings of love, bonding and well-being. It's even being tested as an anti-anxiety drug. But new research shows oxytocin also can cause emotional pain. Oxytocin appears to be the reason stressful social situations, perhaps being bullied at school or tormented by a boss, reverberate long past the event and can trigger fear and anxiety in the future. That's because the hormone actually strengthens social memory in the brain.
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.
A Risk Quiz; Let’s say you are one of the volunteers to whom researchers gave $100, and this option: you can either keep the money, or give it to an anonymous trustee who will either invest it and double it to $200 and return half of the extra hundred bucks to you–$50–or keep all the money for herself. So you can either increase your money by 50%, or lose it all. What would you do? Would you trust that anonymous trustee? (Remember Loss Aversion from Chapter Two, where in a similar experiment most people decided to avoid the gamble and take the sure cash.)
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]