Webster's New World Medical Dictionary

taste bud
One of the tiny, barrel-shaped endings
of the gustatory nerve located around the base of the
papillae (small bumps) on the tongue.
tattoo
The permanent insertion of ink below the
skin, using a sharp instrument. Humans have done
tattooing for cosmetic and ritual purposes since at
least the Neolithic era. Today the practice is made
relatively safe by the use of nonreactive pigments;
sterile, disposable needles; and sterile work condi-
tions. Without these refinements, inks may cause
inflammation, and infection is an ever-present dan-
ger. Persons who are prone to keloids should be
aware that tattoos can trigger these heaped-up dis-
figuring scars. Ink lines may also spread or change
color over the years, a fact of special concern for
those interested in so-called “permanent cosmet-
ics” (tattooed lip color, eyebrows, eyeliner, and the
like). 
tattoo removal
Removal of a tattoo, as with the
use of lasers to destroy the ink itself. Multiple treat-
ments may be necessary, depending on the size of
the piece and the inks used. Some tattoos cannot be
completely removed with lasers, and lasers may
scar some types of skin.
Tay-Sachs disease
A genetic metabolic disorder
caused by deficiency of the enzyme hexosaminidase
A (hex-A) that results in failure to process GM2 gan-
glioside, a lipid (fat) that then accumulates in the
brain and other tissues. Abbreviated TSD. The clas-
sic form of TSD begins in infancy. The child usually
develops normally for the first few months, but head
control is lost by 6 to 8 months of age; the infant
cannot roll over or sit up, spasticity and rigidity
develop, and excessive drooling and convulsions
become evident. Blindness and head enlargement
occur by the second year. The disease worsens as
the central nervous system progressively deterio-
rates. Death generally occurs by age 5, due usually
to cachexia (wasting away) or aspiration pneumo-
nia. There are several forms of TSD. With juvenile
TSD and adult TSD, the person has somewhat more
hex-A and hence a later onset of clinical disease
than with infantile TSD. All forms of TSD are inher-
ited in an autosomal recessive manner and are due
to mutation of the gene for the alpha subunit of hex-
A that is on chromosome 15. The frequency of TSD
is relatively high in Ashkenazi Jews (particularly
those whose ancestors came from Lithuania and
Poland). Knowledge of the biochemical basis of TSD
now permits screening for carrier status and prena-
tal diagnosis. Also known as amaurotic familial
idiocy, type 1 GM2-gangliosidosis, B variant GM2-
gangliosidosis, hexosaminidase A deficiency, and
hex-A deficiency. See also 
Sandhoff disease.