Actual injection can be done Subq or IM that is - subcutaneous or intramuscular. Injection site does not matter, there is no one site better than others so use one which is more comfortabe to reach, after injection product is absorbed into bloodstream and spread through the body evenly. Subq injection takes place by pinching the skin loose from the muscle and raising it so the needle can be inserted in the fat layer of skin.
Wow I wonder if it will help those of us with Ehlers Danlos Syndrome – a collagen disorder that causes ligament laxity and makes those with it prone to easy subluxations and early onset arthritis. I have so many injuries from my daily life due to this disorder. I know this won’t fix my faulty collagen since that is encoded in my genes but perhaps it would help with the symptoms – a bunch of torn ligaments and worn out joints. Thanks for sharing!
Oxidative stress is characterized by an accumulation of ROS and plays a key role in the progression of periodontal diseases . Damage of tissues in inflammatory periodontal disease can be mediated by ROS resulting from the physiological activity of PMN during the phagocytosis of periodontopathic bacteria . In addition, LPS from Porphyromonas gingivalis as well as hypoxia induces a NOX4-dependent increase in H2O2 release in PDLCs . Furthermore, ROS such as H2O2 are small, diffusible, and ubiquitous molecules, can affect human PDLCs and gingival fibroblasts cell injury indirectly by enhancing pro-inflammatory factors such as cytokines, NO, PGE2, and ROS [29–31]. This ROS is known to stimulate osteoclast differentiation and participate in early signaling events associated with osteoclast activation for bone resorption . Since LPS from P. gingivalis increases oxidative stress in PDLCs and contributes to periodontitis , human PDLCs treated with H2O2 may serve as an in vitro model relevant to periodontitis.
The neurotransmitter serotonin is synthesized from the amino acid tryptophan through 5-HTP. In which tryptophan gets converted into 5-HTP via the enzyme tryptophan hydroxylase and 5-HTP gets converted into serotonin via the enzyme L-amino acid decarboxylase. Serotonin is later degraded into 5-hydroxyindoleacetic acid (5-HIAA) by monoamine oxidase.
Oxytocin production does not exist separately from the evolved neurophysiological mechanisms that regulate gonadotropin releasing hormone (GnRH) pulsatility. There are mammalian pheromones that are known to directly influence the GnRH pulse, for example androstenol. Oxytocin is not considered to be a pheromone by anyone I know who is involved in olfactory research. Sniffing it is simply a delivery method that we now can see might have negative consequences.
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.
There have been encouraging results for the use of Tβ4 as a topical gel to treat venous stasis ulcers, a type of wound that develops on the lower leg of patients with chronic vascular disease. Two other reports indicated that Tβ4, formulated in eye-drops, may enhance corneal wound healing in diabetic patients, and improve ocular discomfort. These are the most advanced trials to date. As of yet, despite promising animal models, there has been no significant study exploring the efficacy of intravenous Tβ4 injections in treating ischemic heart injury.
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.