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Goose bumps, goosebumps or goose pimples [1] (also called chill bumps [citation needed]) are the bumps on a person's skin at the base of body hairs which may involuntarily develop when a person is tickled, cold or experiencing strong emotions such as fear, euphoria or sexual arousal.
Cutis, often termed the "true skin", is composed of the epidermis and the dermis. [1] The dermis contains blood vessels, sweat glands, sebaceous glands, and hair follicles. [2] The epidermis and the dermis contain sensory nerve endings to detect changes in the environment. [2] The cutis is the layer located above the subcutis. [2
Skin appendages (or adnexa of skin) are anatomical skin-associated structures that serve a particular function including sensation, contractility, lubrication and heat loss in animals.
The word skin originally only referred to dressed and tanned animal hide and the usual word for human skin was hide. Skin is a borrowing from Old Norse skinn "animal hide, fur", ultimately from the Proto-Indo-European root *sek-, meaning "to cut" (probably a reference to the fact that in those times animal hide was commonly cut off to be used as garment).
Pileipellis type is an important character in the identification of fungi. Pileipellis types include the cutis, trichoderm, epithelium, and hymeniderm types. Types
This disorder was recognized as a distinct syndrome in 1997 and named macrocephaly-cutis marmorata telangiectasia congenita or M-CMTC. [12] [13] A new name, macrocephaly-capillary malformation, abbreviated M-CM, was recommended in 2007. [14] This new name was chosen to more accurately describe the skin markings associated with this disorder.
Aplasia cutis congenita is a rare disorder characterized by congenital absence of skin. Ilona J. Frieden classified ACC in 1986 into 9 groups on the basis of location of the lesions and associated congenital anomalies. [2] The scalp is the most commonly involved area with lesser involvement of trunk and extremities.
Cutis laxa may be caused by mutations in the genes: ELN, [8] ATP6V0A2, [9] ATP7A, [10] FBLN4, [11] FBLN5, [12] and PYCR1. [13] A related neurocutaneous syndrome may be caused by mutations in the gene ALDH18A1 (P5CS). [14] Cutis laxa may also be seen in association with inherited connective tissue disorders such as Ehlers–Danlos syndromes.