Objective To quantitatively analyze the palpebral fissure changes in the neostigrnine tests with videonystagmography.Methods Thirty-five patients with myasthenia gravis ( MG),21 non-MG patients and 23 healthy volunteers were intramuscular injected with neostigmine methylsulfate(0.02 mg/kg) and atropine(0.5 mg).The width of palpebral fissure was measured before and after the injection for one hour( once every 10 minutes).The differences of palpebral fissure width of each time point within each group and between groups were analyzed quantitatively with repetitive measure ANOVA.Results There was a significant difference of palpebral fissures (mm) width at different time points within the MG group( before the test:4.67 ± 1.87,after the test:10 min:0.88 ±0.96,20 min:1.49 ± 1.38,30 min:1.71 ± 1.53,40 min:1.77 ± 1.82,50 min:1.79 ± 1.52,60 min:1.62 ± 1.68 ; F =11.202,P =0.002).There were also significant changes of palpebral fissures width in the MG group compared to the non-MG group and the normal control group (F =15.569,P ＜ 0.01; F =15.104,P ＜ 0.01 ).There was alsostatistical significance in the rate of change between these groups.Receiver operating characteristic analytical procedure indicated that 1.17 mm or 17.5％ was of better diagnostic capability in the neostigmine test.Conclusions Measuring palpebral fissure width with videonystagmography could be seen as an objective and accurate method.A patient with palpebral fissure width higher than 1.17 mm or 17.5％ should be highly suspected as MG.

OBJECTIVE: To investigate the persistent damage of learning and memory ability after the cessation of sub-chronic manganese(Mn)-exposure in rats. METHODS: Specific pathogen free weaning male SD rats were randomly divided into control group and low-, medium-and high-dose groups based on body weight, with 6 rats in each group. Rats were intraperitoneally injected with Mn chloride(MnCl_2·4 H_2O) at the concentrations of 0, 5, 10, or 20 mg/kg body weight, 5 days per week for 6 weeks and continued to be observed for 12 weeks after the cessation of Mn-exposure. During the experiment, the body mass of the rats was weighed. Learning and memory ability was evaluated by a Morris water-maze task at the 6 th weeks of Mn-exposure(cessation of Mn-exposure of week 0), the 6 th and 12 th week of the cessation of Mn-exposure. The organ coefficients of heart, liver, spleen, kidney and testicles were evaluated after the cessation of Mn-exposure on week 12. RESULTS: The body mass of the high-dose group was lower than that of the other 3 groups(P<0.05) at the 4 th and 6 th week of Mn-exposure and the 2 nd week of the cessation of Mn-exposure. There was no significant difference in body mass between the groups(P>0.05) on the 12 th week of the cessation of Mn-exposure. The escape latency of high-dose group was higher than that of the control group(P<0.05), and the number of platform crossings in the low-, medium-and high-dose groups were fewer than that in the control group(P<0.05) after the cessation of Mn-exposure. The escape latency was shorter and the numbers of platform crossings were higher on the 6 th and 12 th week of the cessation of Mn-exposure(P<0.05) when compared with that of the 6 th week of Mn-exposure rats. There was no statistical significance in the organ coefficients of heart, liver, spleen, kidney and testicles among the 4 groups at the 12 th week of the cessation of Mn-exposure in rats(P>0.05).CONCLUSION: Sub-chronic Mn exposure can impair learning and memory ability of rats, and the damage persists after the cessation of Mn-exposure.

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl₄). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl₄ solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl₄-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.
Animals ; Dogs ; Antioxidants/metabolism* ; Carbon Tetrachloride ; Chemical and Drug Induced Liver Injury/drug therapy* ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Liver ; Metabolic Networks and Pathways ; Mitochondria/metabolism* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Polysaccharides/pharmacology* ; Lycium/chemistry*