History
Calcifications in the rotator cuff tendon were first described by Ernest Codman in his 1934 book The Shoulder. In 1952, in his study on x-ray therapy for people with such calcifications, Henry Plenk coined the term "calcifying tendinitis". References
External links
eMedicine on Calcific Tendonitis
Extracorporeal shock wave therapy (subscription required)
The loss of a functional ABCC11 gene is caused by a 538G>A single-nucleotide polymorphism, resulting in a loss of body odor in people who are specifically homozygous for it. Firstly, it affects apocrine sweat glands by reducing secretion of odorous molecules and its precursors. The lack of ABCC11 function results in a decrease of the odorant compounds 3M2H, HMHA, and 3M3SH via a strongly reduced secretion of the precursor amino-acid conjugates 3M2H–Gln, HMHA–Gln, and Cys–Gly–(S) 3M3SH; and a decrease of the odoriferous steroids androstenone and androstenol, possibly due to the reduced levels and secretion of DHEAS and DHEA (possibly bacterial substrates for odoriferous steroids). Secondly, it is also associated with a strongly reduced/atrophic size of apocrine sweat glands and a decreased protein (such as ASOB2) concentration in axillary sweat.The non-functional ABCC11 allele is predominant among East Asians (80–95%), but very low in other ancestral groups (0–3%). Most of the worlds population has the gene that codes for the wet-type earwax and average body odor; however, East Asians are more likely to inherit the allele associated with the dry-type earwax and a reduction in body odor. The hypothesized reduction in body odor may be due to adaptation to colder climates by their ancient Northeast Asian ancestors.However, research has observed that this allele is not solely responsible for ethnic differences in scent. A 2016 study analyzed differences across ethnicities in volatile organic compounds (VOCs), across racial groups and found that while they largely did not differ significantly qualitatively, they did differ quantitatively.