Objective To observe the corneal nerve fibres damage in different stage of diabetic retinopathy (DR) with type 2 diabetes. Methods A cross-sectional study. One hundred and twenty eyes of 120 patients with type 2 diabetes served as diabetes group. According to International Clinical Diabetic Retinopathy Disease Severity Scales (2002), diabetes patients were classified into 4 subgroups: patients without diabetic retinopathy (NDR), patients with mild or moderate non-proliferative diabetic retinopathy (mNPDR), patients with severe non-proliferative diabetic retinopathy (sNPDR) and patients with proliferative diabetic retinopathy (PDR), each subgroup has 30 eyes of 30 patients. Another 30 eyes of 30 healthy participants served as control group. All eyes were scanned with HRT3 in vivo corneal confocal microscopy. Images of sub-basal nerve plexus were quantified including nerve fiber length (NFL), nerve fiber density (NFD), nerve fiber branch density (NFB), and nerve tortuosity (NT). The correlations of corneal nerve fiber with age, duration of diabetes and glycated hemoglobin (HbA1c) were analyzed using Spearman correlation analysis. Results NFL, NFD and NFB were found to be significantly lower in diabetic patients (F=147.315, 142.586, 65.898;P=0.000, 0.000, 0.000), NT was significantly greater in diabetic patients (F=39.431,P=0.000), when compared to control group. In diabetic patients, NFL, NFD and NFB were gradually reduced with DR severity, NT was gradually increased with DR severity. While the difference of NFL, NFD, NFB, NT was not statistically significant between sNPDR and PDR subgroups (P＞0.05), but was statistically significant between other subgroups (P＜0.05). Spearman correlation analysis results showed that age (r=－0.071, －0.080, 0.001, 0.100;P=0.391, 0.328, 0.991, 0.224) and HbA1c (r=－0.109, －0.115, －0.126, 0.025;P=0.238, 0.211, 0.169, 0.781) had no correlation with NFL, NFD, NFB, NT. Duration of diabetes was negatively correlated with the NFL, NFD (r=－0.212, －0.264;P= 0.020, 0.004), positive correlated with NT (r=0.261,P=0.004), and had no correlation with NFB (r=－0.119,P=0.194). Conclusions Corneal nerve fiber loss and nerve tortuosity increased were found in patients with type 2 diabetes, and even without diabetic retinopathy. The progress of corneal neuropathy was correlated with the severity of DR, but it was not change significantly between sNPDR and PDR.
The objective of this study is to combine troponin and indicators of cardiac acoustics for synthetically evaluating cardiac fatigue of rabbits, analyzing exercise-induced cardiac fatigue (EICF) and exercise-induced cardiac damage (EICD). New Zealand white rabbits were used to conduct a multi-step swimming experiments with load, reaching an exhaustive state for evaluating if the amplitude ratio of the first to second heart sound (S1/S2) and heart rate (HR) during the exhaustive exercise would decrease or not and if they would be recovered 24-48 h after exhaustive exercise. The experimental end point was to complete 3 times of exhaustions or death from exhaustion. Circulating troponin I (cTnI) were detected from all of the experimental rabbits at rest [(0.02±0.01) ng/mL], which, in general, indicated that there existed a physiological release of troponin. After the first exhaustive swim, cTnI of the rabbits increased. However, with 24-hour rest, S1/S2, HR, and cTnI of the tested rabbits all returned toward baseline levels, which meant that the experimental rabbits experienced a cardiac fatigue process. After repeated exhaustion, overloading phenomena were observed, which led to death in 3 out of 11 rabbits, indicating their cardiac damage; the troponin elevation under this condition could be interpreted by pathological release. Evaluation of myocardial damage can not be based on the troponin levels alone, but can only be based on a comprehensive analysis.