Autoimmune sensorineural hearing loss/Meniere's disease possibly triggered by neurocysticercosis: a case report.

Background: Meniere's disease arises when an abnormal fluid accumulation results in heightened pressure within the inner ear or labyrinth. Its symptoms encompass vertigo, tinnitus, hearing loss, and a sensation of fullness in the ear. Various triggers for Meniere's disease are known, from smoking and alcohol consumption to recent viral illnesses, allergies, and anxiety.

Interference with transforming growth factor-beta/ Smad3 signaling results in accelerated healing of wounds in previously irradiated skin.

Transforming growth factor (TGF)-beta regulates many aspects of wound repair including inflammation, chemotaxis, and deposition of extracellular matrix. We previously showed that epithelialization of incisional wounds is accelerated in mice null for Smad3, a key cytoplasmic mediator of TGF-beta signaling. Here, we investigated the effects of loss of Smad3 on healing of wounds in skin previously exposed to ionizing radiation, in which scarring fibrosis complicates healing.

Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation.

Transforming growth factor-beta (TGF-beta) plays a central role in the pathogenesis of inflammatory and fibrotic diseases, including radiation-induced fibrosis. We previously reported that mice null for Smad3, a key downstream mediator of TGF-beta, show accelerated healing of cutaneous incisional wounds with reduced inflammation and accumulation of matrix. To determine if loss of Smad3 decreases radiation-induced injury, skin of Smad3+/+ [wild-type (WT)] and -/- [knockout (KO)] mice was exposed to a single dose of 30 to 50 Gy of gamma-irradiation.