1           The most common pattern was global anhidrosis.

2 blepharoptosis, pupillary miosis, and facial anhidrosis.

3 tic cholinergic neurons in the skin, causing anhidrosis.

4 ht on other Orai1 channelopathies, including anhidrosis (an inability to sweat).

5 ore, Best2-deficient mice display comparable anhidrosis and glycoprotein accumulation.

6 ith these CRAC channel mutations suffer from anhidrosis and hyperthermia at high ambient temperatures

7 result in X-linked ectodermal dysplasia with anhidrosis and immunodeficiency, also referred to as NEM

8 ase in addition to ectodermal dysplasia with anhidrosis and immunodeficiency.

9 d immunologic analysis of patients with CID, anhidrosis, and ectodermal dysplasia of unknown etiology

10 CID, autoimmunity, ectodermal dysplasia with anhidrosis, and muscular dysplasia.

11 anguineous family with generalized, isolated anhidrosis, but morphologically normal eccrine sweat gla

12        Congenital insensitivity to pain with anhidrosis (CIPA) is a rare autosomal recessive disorder

13        Congenital insensitivity to pain with anhidrosis (CIPA) is caused by mutations in the NKTR1 ge

14 nsP3R2-mediated Ca2+ release causes isolated anhidrosis in humans and suggest that specific InsP3R in

15 ient patients have dental enamel defects and anhidrosis, representing a new form of anhidrotic ectode

16 in humans; therefore, an inability to sweat (anhidrosis) results in heat intolerance that may cause i