Research of Water Absorption and Release Mechanism of Superabsorbent Polymer in Cement Paste.

The water absorption and release properties of superabsorbent polymers' (SAP) internal curing agent are affected by many factors, such as solution properties, the ambient temperature and humidity and the particle size of SAP, which determine the curing effect and the durability of cement concrete structures directly. In this paper, the variation rule of the water absorbing capacity of SAP in simulated cement paste under different solutions and environmental conditions was studied. Based on microscopic image technology, the dynamic swelling behavior of the SAP particles was explored. The water release performance of SAP in cement paste was analyzed by both the tracer method and the negative pressure method. The results show that the water absorption of SAP in cement paste varied from 27 to 33 times. The ionic valence had a significant effect on the water absorption capacity of SAP, which suggests that the larger the ionic radius, the lower the absorption of SAP. The higher the temperature of the solution, the greater the water absorption rate of SAP. While the SAP particle size was less than 40-80 mesh, a slight 'agglomeration effect' was prone to occur, but the absorption state of SAP was more stable. Based on the swelling kinetic equation of SAP and the time-dependent swelling morphology of SAP in cement paste, a swelling kinetic model was established. The water release performance of SAP was less affected by the capillary negative pressures, and it would not release the water prematurely during the plastic stage, which was conducive to the continuous internal curing process of hardened paste in the later stage.

Research on Performance Deterioration of Internally Cured Pavement Concrete under the Coupling Effect of Salt Freeze-Thaw.

This paper aims at solving the material durability problem caused by spraying deicing salt on pavement concrete in the northern winter. Super absorbent polymer (SAP) was adopted as an internal curing agent to enhance the durability of pavement concrete. Curing parameters including particle size and dosage of SAP and curing condition were optimized based on mortar tests by means of the grey target decision method. The deterioration rule of durability and mechanical properties of pavement concrete internally cured by different SAP dosages after salt freeze-thaw cycles were explored through rapid freeze-thaw test. Combined with the characteristics of pore structure, hydration and microstructure, the influence mechanism of SAP on the salt freeze-thaw resistance of pavement concrete was revealed. The experimental results showed that: (i) The reduction in mass loss rate and relative dynamic modulus was significantly improved by SAP internal curing with moderate dosage; (ii) The more freeze-thaw cycles the specimen underwent, the greater the increase in strength; (iii) After 75 cycles, the chloride ion erosion depth could be decreased by approximately 23.18%. Moreover, the addition of SAP could refine the pore size, inhibit the generation of shrinkage microcracks, and promote the degree of cement hydration in the late stage, which improved the internal density of the cement concrete structure. Therefore, the deterioration of pavement under the coupling effect of salt freeze-thaw was reduced.

Limb Ischemic Conditioning Improved Cognitive Deficits via eNOS-Dependent Augmentation of Angiogenesis after Chronic Cerebral Hypoperfusion in Rats.

Intracranial and extracranial arterial stenosis, the primary cause of chronic cerebral hypoperfusion (CCH), is a critical reason for the pathogenesis of vascular dementia and Alzheimer's disease characterized by cognitive impairments. Our previous study demonstrated that limb remote ischemic conditioning (LRIC) improved cerebral perfusion in intracranial arterial stenosis patients. The current study aimed to test whether LRIC promotes angiogenesis and increases phosphorylated endothelial nitric oxide synthase (p-eNOS) activity in CCH rat model. Adult male Sprague-Dawley rats were randomly assigned to three different groups: sham group, bilateral carotid artery occlusion (2VO) group and 2VO+LRIC group. Cerebral Blood Flow (CBF) was measured with laser speckle contrast imager at 4 weeks. Cognitive testing was performed at four and six weeks after 2VO surgery. We demonstrated that LRIC treatment increased cerebral perfusion and improved the CCH induced spatial learning and memory impairment. Immunohistochemistry confirmed that LRIC prevented cell death in the CA1 region, and increased the number of vessels and angiogenesis in the hippocampus after 2VO. Western blot analysis shows that LRIC therapy significantly increased p-eNOS expression in the hippocampus when compared with 2VO rats. Moreover, eNOS inhibitor reduced the effect of LRIC on angiogenesis in the hippocampus and spatial learning and memory function. Our data suggested that LRIC promoted angiogenesis, which is mediated, in part, by eNOS/NO.

Hypoxia, hibernation and Neuroprotection: An Experimental Study in Mice.

Hibernation is a unique physiological state that evolved to survive periods of food shortages. It is characterized by profound decreases in metabolic rate, body temperature and physiological functions. Studies have shown that animals in hibernation can resist neurological damage. Here, we aimed to study whether hypoxia can induce a hibernation-like state in a traditionally non-hibernating animal and whether it is neuroprotective. All procedures were conducted according to international guidelines on laboratory animal safety. Mice C57BL/6 (19-21g) were placed into a 125 mL jar with fresh air and the jar was sealed with a rubber plug. For each run, the tolerance limit was judged by the animals' appearance for "air hunger". The animal was removed from the jar as soon as its first gasping breath appeared and was moved to another fresh-air-containing jar of similar volume. This procedure was performed in four runs. The hypoxia exposure significantly decreased oxygen (O2) consumption, carbon dioxide (CO2) production, respiratory rate and heart rate. Meanwhile, rectal temperature reached a minimum of 12.7±2.56°C, which is lower than a wide range of ambient temperatures. The mimicked hibernation decreased the infarct size in a focal cerebral ischemia mouse model. Our findings suggest the possibility of inducing suspended animation-like hibernation states for medical applications post injury.

Cerebral ischemia induces angiogenesis in the peri-infarct regions via Notch1 signaling activation.

The Notch1 signaling pathway is considered as one of important regulators of angiogenesis during development, but its role in cerebral ischemia-induced angiogenesis is less well understood. Here, we used human and rodent brains to explore whether Notch1 signaling was involved in the angiogenesis after focal cerebral ischemia. Using immunohistochemistry on surgically resected ischemic stroke brain tissue, we found that the area, volume, and length of the blood vessels in the peri-infarct regions were significantly increased after ischemic stroke in humans, compared with non-ischemic stroke specimens. In addition, the expression of the activated form of Notch1 (Notch intracellular domain; NICD) was increased in endothelial cells of the peri-infarct region. The Notch1 ligand, Jagged1, also increased in abundance in the peri-infarct regions in human. We further confirmed that Notch1 signaling was activated in the peri-infarct regions in a mouse distal middle cerebral artery occlusion (dMCAO) model. Lentivirus-mediated Notch1 knockdown reduced ischemia-induced angiogenesis in the peri-infarct regions of the brain. Our findings suggest that ischemic stroke in human can also induce angiogenesis in the peri-infarct regions as does in animal models of focal ischemia and that Notch1 signaling plays a critical role in mediating this process, which may provide fundamental knowledge regarding the potential mechanisms underlying angiogenesis after ischemic stroke.

Limb Remote Ischemic Conditioning Promotes Myelination by Upregulating PTEN/Akt/mTOR Signaling Activities after Chronic Cerebral Hypoperfusion.

Limb Remote ischemic conditioning (LRIC) has been proved to be a promising neuroprotective method in white matter lesions after ischemia; however, its mechanism underlying protection after chronic cerebral hypoperfusion remains largely unknown. Here, we investigated whether LRIC promoted myelin growth by activating PI3K/Akt/mTOR signal pathway in a rat chronic hypoperfusion model. Thirty adult male Sprague Dawley underwent permanent double carotid artery (2VO), and limb remote ischemic conditioning was applied for 3 days after the 2VO surgery. Cognitive function, oligodendrocyte counts, myelin density, apoptosis and proliferation activity, as well as PTEN/Akt/mTOR signaling activity were determined 4 weeks after treatment. We found that LRIC significantly inhibited oligodendrocytes apoptosis (p<0.05), promoted myelination (p<0.01) in the corpus callosum and improved spatial learning impairment (p<0.05) at 4 weeks after chronic cerebral hypoperfusion. Oligodendrocytes proliferation, along with demyelination, in corpus callosum were not obviously affected by LRIC (p>0.05). Western blot analysis indicated that LRIC upregulated PTEN/Akt/mTOR signaling activities in corpus callosum (p<0.05). Our results suggest that LRIC exerts neuroprotective effect on white matter injuries through activating PTEN/Akt/mTOR signaling pathway after chronic cerebral hypoperfusion.

Enhanced oxidative stress response and neuroprotection of combined limb remote ischemic conditioning and atorvastatin after transient ischemic stroke in rats.

BACKGROUND: Limb remote ischemic conditioning (LRIC) and atorvastatin (AtS) both provide neuroprotection in stroke. We evaluated the enhanced neuroprotective effect of combining these two treatments in preventing ischemia/reperfusion (I/R)-induced cerebral injury in a rat model and investigated the corresponding molecular mechanisms. MATERIALS AND METHODS: Transient cerebral ischemia was induced in Sprague-Dawley male rats by middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion (I/R). Rats were divided into 5 groups, sham, I/R, I/R + AtS, I/R + LRIC and I/R + AtS + LRIC. Pretreatment with LRIC and/or AtS for 14 days before MCAO surgery. Infarct volume, neurological score, Western blot, immuno-histochemical analyses were performed. RESULTS: The combination of LRIC plus AtS pretreatment decreased infarct volume and inhibited neuronal apoptosis. Combination treatment achieved stronger neuroprotection than monotherapy with LRIC or AtS. These therapies reduced reactive oxygen species production in the peri-ischemia region, associated with significantly increased expression and activation of superoxide dismutase 1, hemeoxygenase 1 and nuclear factor erythroid 2-related factor 2. CONCLUSIONS: Both LRIC and AtS + LRIC treatments conferred neuroprotection in ischemic stroke by reducing brain oxidative stress. AtS plus LRIC is an attractive translational research option due to its ease of use, tolerability, economical, and tremendous neuroprotective potential in stroke.