Characteristics of visual fatigue under the effect of 3D animation.

Visual fatigue is commonly encountered in modern life. Clinical visual fatigue characteristics caused by 2-D and 3-D animations may be different, but have not been characterized in detail. This study tried to distinguish the differential effects on visual fatigue caused by 2-D and 3-D animations. A total of 23 volunteers were subjected to accommodation and vergence assessments, followed by a 40-min video game program designed to aggravate their asthenopic symptoms. The volunteers were then assessed for accommodation and vergence parameters again and directed to watch a 5-min 3-D video program, and then assessed again for the parameters. The results support that the 3-D animations caused similar characteristics in vision fatigue parameters in some specific aspects as compared to that caused by 2-D animations. Furthermore, 3-D animations may lead to more exhaustion in both ciliary and extra-ocular muscles, and such differential effects were more evident in the high demand of near vision work. The current results indicated that an arbitrary set of indexes may be promoted in the design of 3-D display or equipments.

Recovery of the pulmonary chemoreflex and functional role of bronchopulmonary C-fibers following chronic cervical spinal cord injury.

Persistent impairment of pulmonary defense reflexes is a critical factor contributing to pulmonary complications in patients with spinal cord injuries. The pulmonary chemoreflex evoked by activation of bronchopulmonary C-fibers has been reported to be abolished in animals with acute cervical hemisection (C2Hx). The present study examined whether the pulmonary chemoreflex can recover during the chronic injury phase and investigated the role of bronchopulmonary C-fibers on the altered breathing pattern after C2Hx. In the first protocol, bronchopulmonary C-fibers were excited by intrajugular capsaicin administration in uninjured and complete C2Hx animals 8 wk postsurgery. Capsaicin evoked pulmonary chemoreflexes in both groups, but the reflex intensity was significantly weaker in C2Hx animals. To examine whether spared spinal white matter tissue contributes to pulmonary chemoreflex recovery, the reflex was evaluated in animals with different extents of lateral injury. Linear regression analyses revealed that tidal volume significantly correlated with the extent of spared tissue; however, capsaicin-induced apnea was not related to injury severity when the ipsilateral-to-contralateral white matter ratio was <50%. In the second protocol, the influence of background bronchopulmonary C-fiber activity on respiration was investigated by blocking C-fiber conduction via perivagal capsaicin treatment. The rapid shallow breathing of C2Hx animals persisted after perivagal capsaicin treatment despite attenuation of pulmonary chemoreflexes. These results indicate that the pulmonary chemoreflex can recover to some extent following spinal injury, but remains attenuated even when there is moderate spinal tissue sparing, and that altered breathing pattern of C2Hx animals cannot be attributed to endogenous activation of bronchopulmonary C-fibers.

Neuroactive steroids inhibit spinal reflex potentiation by selectively enhancing specific spinal GABA(A) receptor subtypes.

Recently, we demonstrated a spinal GABA(A) receptor (GABA(A)R)-dependent inhibition on the induction of repetitive stimulation-induced spinal reflex potentiation. However, it remains unclear whether steroid hormones modulate such an inhibition. Here, we show that progesterone is capable of producing GABA(A)Rs-dependent inhibition of the induction of spinal reflex potentiation by actions through neurosteroid metabolites. Progesterone (5mg/kg, twice daily for 4 days) up-regulates the expression of GABA(A)R alpha2, alpha3, alpha4 and delta subunits, and is associated with attenuated repetitive stimulation-induced spinal reflex activity in ovariectomized rats. These changes were blocked by finasteride (50mg/kg, twice daily), an antagonist of neurosteroid synthesis from progesterone, but not by the progesterone receptor antagonist, RU486 (100mg/kg, twice daily). The induction of spinal reflex potentiation was attenuated after a short (30 min) intrathecal treatment with the neurosteroids, allopregnanolone (ALLOP, 10 microM, 10 microL) and 3 alpha,5 alpha-tetrahydrodeoxycorticosterone (THDOC, 10 microM, 10 microL). Acute intrathecal administration of the GABA(A)R antagonist, bicuculline (10 microM, 10 microL) reversed the inhibition produced by progesterone, THDOC and allopregnanolone. These results imply that progesterone-mediated effects on GABA(A)R expression and neural inhibition are regulated by neurosteroids synthesis rather than progesterone receptor activation.