Thiourea modified low molecular polyamide as a novel room temperature curing agent for epoxy resin.

A thiourea modified low molecular weight polyamide (TLMPA) as a room temperature curing agent was synthesized by a two-step method. Firstly, a low molecular weight polyamide curing agent (LMPA) with low viscosity and high amine value was synthesized by amidation of sebacic acid with tetraethylenepentamine, then the synthesized curing agent was modified with thiourea to increase its reactivity at room temperature. The optimal reaction conditions were studied by L9(33) orthogonal experiments. The structure of the prepared curing agent was analyzed by Fourier transform infrared spectroscopy (FT-IR). The kinetics of TLMPA curing of E-51 epoxy resin was analyzed using the Kissinger method with non-isothermal differential scanning calorimetry (DSC). The activation energy of TLMPA/E-51 calculated by the Kissinger method and FWO method was 38.79 kJ mol-1 and 42.73 kJ mol-1. The nano-SiO2 filler was compounded with E-51 epoxy resin, TLMPA, allyl glycidyl ether diluent, and KH-560 coupling agent to prepare the room temperature curing epoxy resin (EP) system. L9(34) orthogonal experiments were carried out to study the effect of various factors on the mechanical properties of the cured resin systems. The best formulation of the system is that the content of nano-SiO2, curing agent, diluent, and coupling agent is 3, 35, 15, 1 wt%, respectively. With the optimal formulation, the tensile and shear strength, tensile strength, impact strength, and bending strength of the cured EP system was 13.19 MPa, 53.8 MPa, 52.16 kJ m-2, and 94.95 MPa, respectively.

Reactive Molecular Dynamics Calculation and Ignition Delay Test of the Mixture of an Additive and 2-Azido-N,N-dimethylethanamine with Dinitrogen Tetroxide.

In order to shorten the ignition delay of 2-azido-N,N-dimethylethanamine (DMAZ) and dinitrogen tetroxide (NTO), four amines [tert-butylamine, pyrrole, N,N,N',N'-tetramethyl ethylenediamine (TMEDA), and diethylenetriamine (DABH)] with a mass fraction of 5% were added to DMAZ, and the potential energy change and the product change during the reaction of the mixture of an additive and DMAZ with NTO were analyzed by Reactive molecular dynamics (ReaxFF MD) calculation. Then, the ignition delay of the mixture of the additive and DMAZ as well as pure DMAZ with NTO was measured by a drop experiment with a photoelectric sensor and high-speed camera. The results show that the addition of pyrrole greatly reduced the time to reach the maximum system energy and greatly increased the rate of HNO2 formation. The dripping of the fuel was approximately a uniform linear motion, and the expression was y = 43.13 + 7.16x. The ignition delay time recorded by the camera was in good agreement with that of the optical signal. The measured ignition delay time for DMAZ with NTO was 261.5 ms. The mixture of pyrrole and DMAZ with NTO had the shortest ignition delay time of 100 ms, and the proportion of shortening the ignition delay time was the largest. The results of the droplet experiment were consistent with those of ReaxFF MD simulation, indicating that HNO2 plays an important role in the ignition delay, that is, the formation rate of HNO2 is positively correlated with the ignition delay.

Enhanced autophagic retrograde axonal transport by dynein intermediate chain upregulation improves Aß clearance and cognitive function in APP/PS1 double transgenic mice.

Autophagosome accumulation is observed in the distal axons of Alzheimer disease (AD) patients and AD animal models, suggesting that deficient retrograde transport and impaired autophagic clearance of beta-amyloid (A ß) contribute to AD pathogenesis. Expression of the retrograde axonal transport-related protein dynein intermediate chain (DIC) is also reduced in AD patients, but the contributions of DIC to AD pathology remain elusive. This study investigated the effects of DIC expression levels on cognitive function, autophagosome axonal transport, and A ß clearance in the APP/PS1 double transgenic mouse model of AD. Autophagic activity was enhanced in the hippocampus of young (3-month-old) AD mice, as evidenced by greater expression of autophagosome markers, lysosome markers, axonal transport motors (including DIC), and dynein regulatory proteins. The expression levels of autophagosome markers remained elevated, whereas those of autophagic and axonal transport proteins decreased progressively with age, accompanied by spatial learning and memory deficits, axonal autophagosome accumulation, and A ß deposition. Knockdown of DIC exacerbated while overexpression improved axonal transport, autophagosome maturation, Aß clearance, and spatial learning and memory in aged AD mice. Our study provides evidence that age-dependent failure of axonal autophagic flux contributes to AD-associated neuropathology and cognitive deficits, suggesting DIC as a potential therapeutic target for AD.

Enhancing the retrograde axonal transport by curcumin promotes autophagic flux in N2a/APP695swe cells.

The accumulation of autophagosomes and dysfunction at the axonal terminal of neurons play crucial roles in the genesis and development of Alzheimer's disease (AD). Abnormalities in neuron axonal transport-related proteins prevent autophagosome maturation in AD. Curcumin, a polyphenol plant compound, has been shown to exert neuroprotective effects by increasing autophagy in AD, but the underlying mechanism of its effect on autophagy axon transport remains elusive. This study investigated the effects of curcumin on autophagosome formation and axonal transport in N2a/APP695swe cells (AD cell model) as well as the mechanism underlying those effects. Curcumin treatment significantly increased the expression of Beclin1, Atg5, and Atg16L1, induced the formation of autophagosomes, and promoted autophagosome-lysosome fusion in N2a/APP695swe cells. At the same time, curcumin promoted the expression of dynein, dynactin, and BICD2 as well as their binding to form the retrograde axonal transport molecular motor complex. Moreover, curcumin also increased the expression of the scaffolding proteins Rab7- interacting lysosomal protein (RILP) and huntingtin in N2a/APP695swe cells. Taken together, our findings indicate that curcumin increases autophagic flux by promoting interactions among autophagic axonal transport-related proteins and inducing lysosome-autophagosome fusion. This study provides evidence suggesting the potential use of curcumin as a novel treatment for AD.

Expression analysis and clinical significance of eIF4E, VEGF-C, E-cadherin and MMP-2 in colorectal adenocarcinoma.

The underlying mechanisms of colorectal carcinoma (CRC) metastasis remain to be elucidated. The aim of this study is to investigate clinical significance and the expression of eIF4E, VEGF-C, MMP-2, and E-cadherin in the CRC metastasis. We investigated their expressions in 108 patients, analyzed the relationships between their expressions in CRC and evaluated the relationships between their expressions and clinical pathogenic parameters. Furthermore, their roles in patient survival and in CRC metastasis were also investigated. We found that eIF4E, VEGF-C and MMP-2 were up-regulated in CRC, and their expression frequencies (EFs) were higher in cancerous tissues than in adjacent normal tissues. The EF of E-cadherin is lower in cancerous tissues than in adjacent normal tissues. Totally, their EFs were not associated with sex and age of patient, however, their EFs were associated with tumor differentiation, the depth of invasion, lymph node metastasis and tumor stages. Furthermore, eIF4E, VEGF-C, and MMP-2 shortened and E-cadherin prolonged survival in patient-derived CRC xenografts. Similarly, eIF4E, VEGF-C, and MMP-2 promoted and E-cadherin suppressed the lung metastasis of CRC cells. In addition, knockdown of eIF4E inhibited migration of CRC cells, downregulated VEGF-C, MMP-2 and upregulated E-cadherin. In conclusion, eIF4E promoted CRC metastasis via up-regulating the expression of VEGF-C, MMP-2 and suppressing E-cadherin.