Diagnosis of ischemic optic neuropathy caused by dissection of the internal carotid artery: A case report.

RATIONALE: Ischemic optic neuropathy (ION), due to diseases of the arteries supplying the optic nerve, is an ischemic damage of the optic nerve. This report highlights a case with monocular decreasing visual acuity caused by dissection of the internal carotid artery (ICA), which is a relatively rare cause for ION. PATIENT CONCERNS: A 44-year-old woman presented with a decreasing visual acuity and defected visual field in the right eye for 1 week. The best corrected visual acuity (BCVA) was 20/400 in the right eye, and 20/20 in the left eye. In the right eye, the pupil showed little reaction to light with a relative afferent pupillary defect. The visual field test disclosed a defect in the inferior field connecting to the blind spot. Electroretinogram recording showed no obviously declined retinal function. No recognizable waveforms were presented in pattern visual-evoked potential (PVEP) examination, whereas the flash visual-evoked potential result revealed a delayed peak time and a reduced amplitude of P2-wave. DIAGNOSIS: The patient was diagnosed as ION with the aid of computed tomographic angiography of the brain and neck, which revealed a stenosis in the right ICA and an occlusion in the right cerebral middle artery. The stenosis was verified as dissection of the ICA by digital subtraction angiography. INTERVENTIONS: Based on the clinical findings, stent implantation inside the right ICA was performed. OUTCOMES: The ICA was recanalized soon and the BCVA of the right eye was improved to be 20/25 five months later. A second PVEP examination revealed a recognizable waveform in the right eye, although the peak time and amplitude of the P100-wave was a bit abnormal compared to that of the left eye. LESSONS: ION with the sign of decreasing monocular visual acuity could occur due to dissection of the ICA, with no obvious neurologic symptom at the beginning. The present case emphasizes the importance of suspicion of ICA problems as the underlying cause for ION, which could help to take in-time measure to save the vision and avoid further complications.

Protection of retinal function and morphology in MNU-induced retinitis pigmentosa rats by ALDH2: an in-vivo study.

BACKGROUND: Retinitis pigmentosa (RP) is a kind of inherited retinal degenerative diseases characterized by the progressive loss of photoreceptors. RP has been a conundrum without satisfactory countermeasures in clinic until now. Acetaldehyde dehydrogenase 2 (ALDH2), a major enzyme involved in aldehyde detoxification, has been demonstrated to be beneficial for a growing number of human diseases, such as cardiovascular dysfunction, diabetes mellitus and neurodegeneration. However, its protective effect against RP remains unknown. Our study explored the impact of ALDH2 on retinal function and structure in N-methyl-N-nitrosourea (MNU)-induced RP rats. METHODS: Rats were gavaged with 5 mg/kg Alda-1, an ALDH2 agonist, 5 days before and 3 days after MNU administration. Assessments of retinal function and morphology as well as measurement of specific proteins expression level were conducted. RESULTS: Electroretinogram recordings showed that Alda-1 administration alleviated the decrease in amplitude caused by MNU, rendering protection of retinal function. Mitigation of photoreceptor degeneration in MNU-treated retinas was observed by optical coherence tomography and retinal histological examination. In addition, Western blotting results revealed that ALDH2 protein expression level was upregulatedwith increased expression of SIRT1 protein after the Alda-1 intervention. Besides, endoplasmic reticulum stress (ERS) was reduced according to the significant downregulation of GRP78 protein, while apoptosis was ameliorated as shown by the decreased expression of PARP1 protein. CONCLUSIONS: Together, our data demonstrated that ALDH2 could provide preservation of retinal function and morphology against MNU-induced RP, with the underlying mechanism at least partly related to the modulation of SIRT1, ERS and apoptosis.

Up-regulation of glutathione metabolism and changes in redox status involved in adaptation of reed (Phragmites communis) ecotypes to drought-prone and saline habitats.

The glutathione (GSH) metabolic characteristics and redox balance in three ecotypes of reed (Phragmites communis), swamp reed (SR), dune reed (DR), and heavy salt meadow reed (HSMR), from different habitats in desert regions of northwest China were investigated. The DR possessed the highest rate of GSH biosynthesis and metabolism with the lowest levels of total and reduced GSH and its biosynthetic precursors, gamma-glutamylcysteine (gamma-EC) and cysteine (Cys), of the three reed ecotypes. This suggests that a higher rate of GSH biosynthesis and metabolism, but not GSH accumulation, might be involved in the adaptation of this terrestrial reed ecotype to its dry habitat. The HSMR shared this profile although it exhibited the highest reduced thiol levels of the three ecotypes. Two key enzymes in the Calvin-cycle possessing exposed sulfhydryl groups, NADP(+)-dependent glyceraldehydes-3-phosphate dehydrogenase (G3PD) and fructose-1,6-bisphosphatase (FBPase), and other two key enzymes in the pentose-phosphate pathway (PPP), glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6-PGD), had very similar activities in the three reed ecotypes. Compared to the SR, the DR and HSMR had higher ratios of NADPH/NADP+ and NADH/NAD+, indicating that a more reduced redox status in the plant cells might be involved in the survival and adaptation of the two terrestrial reed ecotypes to long-term drought and salinity, respectively. These results suggest that changes of GSH metabolism and redox balance were important components of the adaptation of reed, a hydrophilic plant, to more extreme dune and saline habitats. The coordinated up-regulations of the rate of GSH biosynthesis and metabolism and reduction state of redox status of plant cells, conferred on the plant high resistance or tolerance to long-term drought and salinity.