ABSTRACT
Traumatic brain injury (TBI), a growing public health problem, is a leading cause of death and disability worldwide, although its prevention measures and clinical cares are substantially improved. Increasing evidence shows that TBI may increase the risk of mood disorders and neurodegenerative diseases, including Alzheimer's disease (AD). However, the complex relationship between TBI and AD remains elusive. Metabolic dysfunction has been the common pathology in both TBI and AD. On the one hand, TBI perturbs the glucose metabolism of the brain, and causes energy crisis and subsequent hyperglycolysis. On the other hand, glucose deprivation promotes amyloidogenesis via β-site APP cleaving enzyme-1 dependent mechanism, and triggers tau pathology and synaptic function. Recent findings suggest that TBI might facilitate Alzheimer's pathogenesis by altering metabolism, which provides clues to metabolic link between TBI and AD. In this review, we will explore how TBI-induced metabolic changes contribute to the development of AD.
ABSTRACT
Objective To investigate the in vitro and in vivo relative recovery rates of levofloxacin from microdialysis probes. Methods High-performance liquid chromatography (HPLC) was established for determination of levofloxacin concentrations. Column was Kromasil C18 (150 mm×4.6 mm, 5 μm), the mobile phase consisted of acetonitrile and 10 mmol/L of potassium dihydrogen phosphate solution (15:85), with column temperature being 30 °C, detection wavelength being 294 nm, and injection volume being 10 μL. The relative recovery rates of vascular microdialysis probes in vitro were measured by dialysis and reverse dialysis. The effects of drug concentration and flow rate on probe deliveries were investigated. The in vivo recovery rates of the probe in the jugular vein and prostate were measured by reverse dialysis, and the stability of 12 h recovery rate in vivo was investigated. Results When the concentration of levofloxacin was 0.1-50.0 μg/mL, the linear relationship was good in the HPLC analysis (r = 0.998 7), and its specificity was good. The precision and accuracy of high-, medium-, low-concentration quality control samples, and lower limit of quantitation all met the analysis requirements. In the in vitro relative recovery experiments, there was no statistical difference between the recovery rate and reverse recovery rate of the vascular microdialysis probes (P>0.05). Drug concentrations did not affect in vitro recovery rate. The recovery rate decreased with the increase of flow rate. In vivo, the relative recovery rate of the probe was (48.46±1.94)% in the jugular vein and (13.23±1.44)% in the prostate. The relative recovery rates were stable during 12 h. Conclusion The established HPLC can be used for the determination of levofloxacin microdialysis probe. Reverse dialysis can be used to detect the relative recovery rate of levofloxacin microdialysis probe in vivo.