Structural impairment patterns in peripapillary retinal fiber layer and retinal ganglion cell layer in mitochondrial optic neuropathies.

Aim: To evaluate the structural injure patterns in peripapillary retinal fiber layer (pRNFL), retinal ganglion cell layer (RGCL) and their correlations to visual function in various mitochondrial optic neuropathies (MON) to offer help to their differential diagnosis.

Methods: Totally 32 MON patients (60 eyes) were recruited within 6mo after clinical onsets, including 20 Leber hereditary optic neuropathy (LHON) patients (37 eyes), 12 ethambutol-induced optic neuropathy (EON) patients (23 eyes), and 41 age-gender matched healthy controls (HC, 82 eyes). All subjects had pRNFL and RGCL examinations with optic coherence tomography (OCT) and visual function tests.

Retinal segmented layers with strong aquaporin-4 expression suffered more injuries in neuromyelitis optica spectrum disorders compared with optic neuritis with aquaporin-4 antibody seronegativity detected by optical coherence tomography.

Purpose: To evaluate retinal segmented layer alterations in optic neuritis (ON) in an AQP4-Ab seropositive (AQP4-Ab+/ON) cohort and in neuromyelitis optica (NMO) with ON eyes (NMO-ON) compared with an AQP4-Ab seronegative ON (AQP4-Ab-/ON) cohort using optical coherence tomography (OCT).

Methods: We recruited 109 patients with ON (161 eyes) and 47 healthy controls. All patients with ON were subdivided into three subcohorts: 37 patients (54 eyes) with AQP4-Ab+/ON, 45 patients (65 eyes) with AQP4-Ab-/ON and 27 patients (42 eyes) with NMO-ON.

Macular thickness as a predictor of loss of visual sensitivity in ethambutol-induced optic neuropathy.

Ethambutol is a common cause of drug-related optic neuropathy. Prediction of the onset of ethambutol-induced optic neuropathy and consequent drug withdrawal may be an effective method to stop visual loss. Previous studies have shown that structural injury to the optic nerve occurred earlier than the damage to visual function.

[Current opinions about using of medication intervention as neuroprotective therapy for degenerative ocular fundus diseases].

Recently, many studies indicated that certain medications can delay the apoptosis of retinal nerve cells at different points during the process of apoptosis and have neuroprotective effect on preventing degenerative ocular fundus diseases. N-methyl-D-aspartate receptor (NMDAR) antagonists, NMDAR-associated calcium channel blockers and acetylcholine receptor agonists have been shown to have neuroprotective effects for retinal damages by inhibiting NMDA-induced excitotoxicity. The inhibitors of nitric oxide synthase (NOS) can prevent the cell apoptosis and reduce the retinal cell loss by suppressing the activity of NOS as well as the production of the nitric oxide.

Effect of brain-derived neurotrophic factor on c-jun expression in the rd mouse retina.

Aim: To determine the location of c-jun protein, dynamic changes in c-jun mRNA and protein expression, and ultrastructure characteristics in the rd mouse retina, following a single dose of brain-derived neurotrophic factor (BDNF) in a short period of time.

Methods: A single intravitreal injection of BDNF at two dosages (25µg/L or 50µg/L) was given to the right eye of the rd mouse at age 2 and 3 weeks respectively. Two weeks after injection, the location of c-jun protein in the retina was observed by immunofluorescence detection, c-jun mRNA and protein expression in retinas were detected by quantitative real time polymerase chain reaction (RT-PCR) and western immunoblotting analysis, ultrastructure characteristics of retinas were detected by transmission electron microscope (TEM) observation.

[Studies of the physiological function of carbonic anhydrase].

Carbonic anhydrases (CA) is a zinc-enzyme family. They are involved in multiple aspects of systemic and cellular acid-base balance. This review is a general introduction to the disposition, molecular constitution,biological function and physiological function of CA.