Adipose-derived mesenchymal stem cell transplantation promotes adult neurogenesis in the brains of Alzheimer's disease mice

In the present study, we transplanted adipose-derived mesenchymal stem cells into the hippo-campi of APP/PS1 transgenic Alzheimer＇s disease model mice. Immunofluorescence staining revealed that the number of newly generated （BrdU＋） cells in the subgranular zone of the dentate gyrus in the hippocampus was signiifcantly higher in Alzheimer＇s disease mice after adipose-de-rived mesenchymal stem cell transplantation, and there was also a significant increase in the number of BrdU＋/DCX＋neuroblasts in these animals. Adipose-derived mesenchymal stem cell transplantation enhanced neurogenic activity in the subventricular zone as well. Furthermore, adipose-derived mesenchymal stem cell transplantation reduced oxidative stress and alleviated cognitive impairment in the mice. Based on these ifndings, we propose that adipose-derived mes-enchymal stem cell transplantation enhances endogenous neurogenesis in both the subgranular and subventricular zones in APP/PS1 transgenic Alzheimer＇s disease mice, thereby facilitating functional recovery.

Amyloid beta-peptide worsens cognitive impairment following cerebral ischemia-reperfusion injury

Amyloid 13-peptide, a major component of senile plaques in Alzheimer＇s disease, has been implicated in neuronal cell death and cognitive impairment. Recently, studies have shown that the pathogenesis of cerebral ischemia is closely linked with Alzheimer＇s disease. In this study, a rat model of global cerebral ischemia-reperfusion injury was established via occlusion of four arteries; meanwhile, fibrillar amyloid [3-peptide was injected into the rat lateral ventricle. The Morris water maze test and histological staining revealed that administration of amyloid 13-peptide could further aggravate impairments to learning and memory and neuronal cell death in the hippocampus of rats subjected to cerebral ischemia-reperfusion injury. Western blot showed that phosphorylation of tau protein and the activity of glycogen synthase kinase 313 were significantly stronger in cerebral ischemia-reperfusion injury rats subjected to amyloid [3-peptide administration than those undergo- ing cerebral ischemia-repetfusion or amyloid 13-peptide administration alone. Conversely, the activ- ity of protein phosphatase 2A was remarkably reduced in rats with cerebral ischemia-reperfusion injury following amyloid 13-peptide administration. These findings suggest that amyloid 13-peptide can potentiate tau phosphorylation induced by cerebral ischemia-reperfusion and thereby aggravate cognitive impairment.

Phosphorylation of tau protein over time in rats subjected to transient brain ischemia

Transient brain ischemia has been shown to induce hyperphosphorylation of the micro- tubule-associated protein tau. To further determine the mechanisms underlying these processes, we investigated the interaction between tau, glycogen synthase kinase （GSK）-313 and protein phos- phatase 2A. The results confirmed that tau protein was dephosphorylated during brain ischemia; in addition, the activity of GSK-3β was increased and the activity of protein phosphatase 2A was de- creased. After reperfusion, tau protein was hyperphosphorylated, the activity of GSK-3β was de- creased and the activity of protein phosphatase 2A remained low. Importantly, the interaction of tau with GSK-3β and protein phosphatase 2A was altered during ischemia and reperfusion. Lithium chloride could affect tau phosphorylation by regulating the interaction of tau with GSK-3β and pro- tein phosphatase 2A, and improve learning and memory ability of rats after transient brain ischemia. The present study demonstrated that it was the interaction of tau with GSK-3β and protein phos- phatase 2A, rather than their individual activities, that dominates the phosphorylation of tau in tran- sient brain ischemia. Hyperphosphorylated tau protein may play an important role in the evolution of brain injury in ischemic stroke. The neuroprotective effects of lithium chloride partly depend on the inhibition of tau phosphorylation during transient brain ischemia.

tructure and Composition of Crystalline Carbon Nitride Films Synthesized by Microwave Plasma Chemical Vapor Deposition

Crystalline carbon nitride thin films were prepared on Si (100) substrates by a microwave plasma chemical vapor deposition method, using CH4/N2 as precursor gases. The surface morphologies of the carbon nitride films deposited on Si substrate at 830℃ are consisted of hexagonal crystalline rods. The effect of substrate temperature on the formation of carbon nitrides was investigated. X-ray photoelectron spectroscopy analysis indicated that the maximum value of N/C in atomic ratio in the films deposited at a substrate temperature of 830℃ is 1 .20, which is close to the stoichiometric value of C3N4. The X-ray diffraction pattern of the films deposited at 830℃ indicates no amorphous phase in the films, which are composed of β- and α-C3N4 phase containing an unidentified C-N phase. Fourier transform infrared spectroscopy supports the existence of C-N covalent bond.

Profiling biotoxicities of hexafluoropropylene oxide trimer acid with human embryonic stem cell-based assays

Hexafluoropropylene oxide trimer acid(HFPO-TA), an emerging replacement of perfluorooctanoic acid(PFOA), has recently been reported to be a potential environmental contaminant.Due to the similar structure to PFOA, HFPO-TA may cause comparable adverse effects on human health. Therefore, evaluating the toxic profiles of HFPO-TA has become an urgent task.In this study, we investigated the cytotoxicity and hepatoxicity of HFPO-TA using human embryonic stem cell(h ESC)-based assays. Results showed that HFPO-TA reduced h ESCs’ viability in a dose dependent manner, and the calculated IC50 for 24, 48 and 72 hr were 222.8,167.4, and 80.6 μmol/L, respectively. Significant intracellular ROS accumulation and mitochondrion membrane potential reduction were detected with HFPO-TA exposure, and increased apoptotic/necrotic cells were also observed in high dose of HFPO-TA treated group.Moreover, HFPO-TA at noncytotoxic concentrations also significantly impaired the functions of induced hepatocytes by diminishing cell glycogen storage ability and deregulating specific functional genes. Transcriptome sequencing analysis identified a set of hepatic associated biological processes responding to HFPO-TA exposure. PPAR was the most significantly enriched pathway. Genes including FGA, FGB, FGG, AHSG, HRG, ITIH2, ALB were characterized as hub genes by cyto Hubba plug-in. These data indicated that HFPO-TA is a potential hepatotoxicant, and may not be a safe replacement for PFOA.

Correlation between tension softening relation and crack extension resistance in concrete

Changes of the material fracture toughness with crack propagation can be described by a crack extension resistance curve,one of the fundamental fracture criteria in crack mechanics.Recently,experimental observation of the fracture behavior in concrete was used to develop a new fracture criterion,the crack extension GR resistance curve,to analyze crack propagation during the entire concrete fracture process.The variation of the crack extension resistance is mainly associated with the energy consumption in the fracture process zone ahead of the stress-free crack tip.The crack extension resistance is then a function of the softening curve,which is a basic mechanical property in the fracture process zone.The relationship between the softening curve and the crack extension GR resistance curve is then analyzed based on results of three-point bending beams tests.The results indicate that the characteristic points of the crack extension resistance GR curve is closely related to the characteristic point on used tension softening curve.