Mercury is one of the common heavy-metal toxins,which can cause damage throughout the body in a variety of ways. Cases of renal toxicity of mercury poisoning are increasing clinically. However,little is known about nephrotoxicity mechanisms,and treatment remains unsatisfactory. The mechanism of mercury toxic nephropathy is reviewed in this paper,including the direct toxic effect on the kidney,the injury to the biomembrane system,generation of Hg-metallothionein,imbalance of intra?cellular calciumion,oxidative damage,induced apoptosis,and immune injury. Besides,the mechanism and limitation of common therapies,potential developments of the field are discussed. This review will facilitate further investigations therapies about both the mechanism and treatment of mercury toxic nephropathy.

ObjectiveTo determine thallium in whole blood by atomic absorption detection method, and to investigate the eliminating effect of hemoperfusion (HP) for thallium in blood.Methods The blood of Beagle dogs which had not exposed to thallium before were obtained for preparation of thallium nitrate (TlNO3)-containing solution in three concentrations according to the conversion formula based on animal weight and volume of blood. HP was performed in the simulated in vivo environment. The content of TlNO3 in blood of the next group was determined on the amount of TlNO3 for the last HP of the former dose group. Thallium quantity in different samples was measured with atomic absorption spectrometer blood samples before and after HP. Finally, the thallium concentration in blood was analyzed statistically.Results Thallium concentrations showed a good linear relationship in the range of 0-200μg/L (r = 0.998 4). The intra-day precision (RSD) was lower than 4.913%, the intra-day recovery rate was 96.2%-111.9%; the inter-day precision (RSD) was lower than 7.502%, the inter-day recovery rate was 89.6%-105.2%. The concentration of thallium in blood was significantly reduced after HP per time in high, middle, and low dose groups [(453.43±27.80) mg/L to (56.09±14.44) mg/L in high dose group,F = 8.820,P = 0.003;(64.51±13.60) mg/L to (3.19±0.23) mg/L in middle dose group,F = 36.312,P = 0.000; (5.40±0.98) mg/L to (0.38±0.25) mg/L in low dose group,F = 46.240,P = 0.000]. The adsorption rate of four times of HP in high, middle and low dose group were (87.63±2.48)%, (95.06±1.54)% and (92.76±4.87)%, respectively, without significant difference (F = 4.231,P = 0.070 ).Conclusions The method for measuring thallium was established, and it shows a very stable, simple, sensitive for determination of thallium. HP can effectively remove thallium from blood. Thallium concentration can be reduced by 90% after four times of HP. HP is also effective even when thallium concentration is not high.

Fibroblast growth factors (FGF) are a group of structurally related polypeptides which constitute an elaborate signaling system with their receptors. Evidence accumulated in the years suggests that the FGF family plays a key role in the repair of central nervous system injury. The main protective mechanisms include activating the expression of PI3K-Akt, peroxisome proliferator-activated receptor (PPARγ) and other signals; inhibiting NF-κB-mediated inflammatory response, oxidative stress and apoptosis; regulating neuronal differentiation and neuronal excitability as well as participating in protection of neurovascular units and nerve function repair. This paper comprehensively summarizes the latest research progress in FGF signaling related to diseases of the central nervous system such as cerebral infarction, cerebral hemorrhage, traumatic brain injury, Alzheimer's disease, Parkinson's disease, epilepsy and depression, aiming to provide scientific basis and reference for the development of innovative FGF drugs for the prevention and treatment of neurological diseases.
Humans ; Fibroblast Growth Factors ; Phosphatidylinositol 3-Kinases/metabolism* ; Central Nervous System/metabolism* ; Signal Transduction/physiology* ; Alzheimer Disease