A Novel Method to Characterize the Damping Capacity of EPDM/CIIR Blends Using Vibrating Rubber Balls.

An experimental device fixed with a laser displacement sensor was assembled to investigate the rebound behaviors and damping mechanism of rubber balls prepared with ethylene-propylene-diene monomer (EPDM)/chlorinated butyl rubber (CIIR) blends. The result showed that a prediction model was proposed to characterize the damping capacity by using the rebound height of the rubber balls. The lower rebound height corresponded to better damping capacity. A modified equation relating to the rebound height has been obtained from the theoretical derivation on the basis of the dynamic mechanical analysis, showing that the rebound height was affected by the deformation frequency, the external excitation, and the nature of rubber blends. Furthermore, the energy dissipation rate (EDR), defined by the ratio of the height loss to the rebound time, was proposed to further characterize the damping capacity. The EDR value was shown to be highest for the pure CIIR and lowest for the pure EPDM, exhibiting a decreasing trend with the increase in EPDM content in the rubber blends. It can be expected that the damping capacity of the EPDM/CIIR blends decreases with the decrease in external excitation, the conclusion of which plays a key role in the formulation design of viscoelastic damping rubber materials.

Multicolor fluorescence switching material induced by force and acid.

A novel D-A-D chromophore TBQM based on triphenylamine, acylhydrazone and dimethylamino was synthesized, and the emission properties of TBQM was studied in solutions as well as in aggregated state. TBQM showed obvious solvatochromism in different solutions. In addition, the reversible multicolor fluorescence switching properties under the stimulation of external forces and acid were also obtained. The fluorescence of TBQM changed from blue to bright blue, and finally to blue-green as the degree of grinding increased, which would recover after being fumigated by CH2Cl2. Meanwhile, TBQM could undergo twice protonation after fumigated by TFA. The fluorescence color changed from blue to bright blue, blue-green, and yellow-green until the fluorescence was quenched with the increasing of TFA fumigation time, which can be restored automatically or by TEA fumigation. Moreover, TBQM could be used as an advanced fluorescent anti-counterfeiting ink.

Force-, heat- and acid-induced fluorescent switching properties of an anthracene-based hydrazide derivative.

A novel anthracene-based hydrazide derivative (3,4-ENS) was designed and synthesized, and 3,4-ENS can form stable organogel in dimethyl sulfoxide (DMSO) solvent. Firstly, 3,4-ENS xerogel from DMSO exhibits mechanofluorochromic property and its maximum emission shifts from 433 nm to 484 nm upon grinding. Secondly, DMSO xerogel exhibits thermofluorochromic behavior and its maximum emission shifts from 433 nm to 481 nm upon heating at 110 °C. Thirdly, DMSO xerogel exhibits acidofluorochromic behavior and its maximum emission shifts from 433 nm to 466 nm upon fuming by TFA vapors. The experimental results confirmed that the different luminescent property of 3,4-ENS attributed to the phase transition from well-ordered crystals to metastable disordered aggregation.

Thioredoxin-interacting protein is a favored target of miR-125b, promoting metastasis and progression of pancreatic cancer via the HIF1α pathway.

MicroRNAs (miRs) are vital in the development of pancreatic cancer (PC) targeting several cellular processes. This study was aimed at evaluating the function of miR-125b and the mechanism involved in PC. Cell migration, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), and Bromodeoxyuridine/5-bromo-2'-deoxyuridine (BrdU) study was done to establish the migration capability, cell viability, and cell proliferation, respectively. Binding sites for miR-125b were recognized by luciferase assay, and the expression of protein by Western blot and immunofluorescence assay. In vivo study was done by BALB/c nude xenograft mice for evaluating the function of miR-125b. The study showed that expression of miR-125b was elevated in PC cells and tissues and was correlated to proliferation and migration of cells. Also, overexpression of miR-125b encouraged migration, metastasis, and proliferation of BxPC-3 cells, and suppression reversed it. We also noticed that thioredoxin-interacting protein (TXNIP) was the potential target of miR-125b. The outcomes also suggested that miR-125b governed the expression of TXNIP inversely via directly attaching to the three prime untranslated region (3'-UTR) activating hypoxia-inducible factor 1α (HIF1α). Looking into the relation between HIF1α and TXNIP, we discovered that TXNIP caused the degradation and export of HIF1α by making a complex with it. The miR-125b-TXNIP-HIF1α pathway may serve as a useful strategy for diagnosing and treating PC.

miR-125b enhances metastasis and progression of cancer via the TXNIP and HIF1α pathway in pancreatic cancer.

BACKGROUND: MicroRNAs (miRNAs) play potential role in the development of various types of cancer conditions including pancreatic cancer (PC) targeting several cellular processes. Present study was aimed to evaluate function of miR-125b and the mechanism involved in PC. METHODS: Cell migration, MTT and BrdU study was done to establish the migration capability, cell viability and cell proliferation respectively. Binding sites for miR-125b were recognized by luciferase assay, expression of protein by western blot and immunofluorescence assay. In vivo study was done by BALB/c nude xenograft mice for evaluating the function of miR-125b. RESULTS: The study showed that expression of miR-125b was elevated in PC cells and tissues, and was correlated to proliferation and migration of cells. Also, over-expression of miR-125b encouraged migration, metastasis and proliferation of BxPC-3 cells, the suppression reversed it. We also noticed that thioredoxin-interacting protein (TXNIP) was the potential target of miR-125b. The outcomes also suggested that miR-125b governed the expression of TXNIP inversely via directly attaching to the 3'-UTR activating hypoxia-inducible factor 1α (HIF1α). Looking into the relation between HIF1α and TXNIP, we discovered that TXNIP caused the degradation and export of HIF1α by making a complex with it. CONCLUSION: The miR-125b-TXNIP-HIF1α pathway may serve useful strategy for diagnosing and treating PC.

Stimuli-responsive behavior of naphthyl acylhydrazone derivative and its application in information security protection.

Acylhydrazone derivatives containing naphthyl group, namely, 3,5-bis-octyloxy-benzoic acid naphthalen-1-ylmethylene-hydrazide (NTH-mB8) and 4-methoxy-benzoic acid naphthalen-1-ylmethylene-hydrazide (NTH-P1) were synthesized. π-π interactions between naphthalene groups and -N-H···O=C- intermolecular hydrogen bondings were observed in NTH-P1 single crystal, in which -C=N- bonds exhibited trans-isomer. NTH-mB8 showed photo-responsive behavior due to photo-induced trans-cis isomerizations of -C=N- bonds. Interestingly, the NTH-mB8 films fumed by trifluoroacetic acid (TFA)/triethylamine (TEA) (or standing at room temperature) vapors show reversible fluorescence on/off switching property. The cast film of NTH-mB8 exhibited almost no fluorescence. The NTH-mB8 film fumed by TFA vapor exhibited intensive cyan emission, which was quickly quenched by TEA vapor. The reversible remarkable fluorescence on/off switching properties suggested that the organic solution of NTH-mB8 could be used as security ink without needing a covering reagent in information security protection.

Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis.

BACKGROUND: Recently, LINC00665 has been reported to be a pivotal regulator in kinds of malignancy, such as lung cancer and liver cancer. However, the functions and underlying mechanisms of LINC00665 in gastric cancer (GC) remain unclear. MATERIALS AND METHODS: We recruited 49 paired GC tissue to explore LINC00665 expression by qRT-PCR. In vitro function assays were used to explore the roles of LINC00665 in GC progression. Moreover, the interaction among LINC00665, miR-149-3p and RNF2 was explored by bioinformatics analysis and luciferase reporter assay. RESULTS: In the present study, we found that LINC00665 expression was significantly elevated in GC tissues and cell lines. High LINC00665 expression was associated with TNM stage, histological grade, and poor prognosis of GC patients. Function assays showed that LINC00665 suppression significantly reduced GC cells viability and invasion ability in vitro. Mechanistic analysis showed that LINC00665 might serve as a ceRNA for miR-149-3p to regulate the expression of RNF2. CONCLUSION: Our current study revealed the LINC00665/miR-149-3p/RNF2 axis was involved in GC progression, providing novel insights into the treatment for GC.