The inhibition of Beclin1-dependent autophagy sensitizes PTC cells to ABT737-induced death.

ABT737 is used as a specific BCL2 inhibitor, which can treat papillary thyroid carcinoma (PTC). However, the effect of ABT737 on PTC cell apoptosis is limited. Moreover, BCL2 inhibition causes the activation of Beclin1-dependent autophagy. Our study aimed to explore the effects of autophagy and Beclin1 on ABT737 efficacy in PTC. The experimental data showed that ABT737 synchronously enhanced autophagic activity and apoptosis level in PTC cells. ABT737 also promoted the dissociation of BCL2-Beclin1 and BCL2-Bax complexes. Autophagy inhibitors, Bafilomycin A1 and 3-MA, enhanced the inhibitory effect of ABT737 on the survival and function in PTC cells. Consistently, autophagy inhibition with Beclin1 pharmacological inhibitor (spautin-1) also enhanced the efficacy of ABT737. Additionally, ABT737 at low-dose promoted LC3 conversion in PTC cells, and did not affect PTC cell apoptosis and survival. However, The efficacy of low-dose of ABT737 in PTC cell apoptosis and survival was displayed with the addition of Bafilomycin A1, 3-MA or spautin-1. In conclusion, the limited role of ABT737 in PTC cell apoptosis is attributed to its promoting effect on Beclin1-dependent autophagy. Therefore, autophagy inhibition based on Beclin1 downregulation can enhance the sensitivity of PTC cells to ABT737-induced death.

TAT-Beclin 1 represses the carcinogenesis of DUSP4-positive PTC by enhancing autophagy.

BACKGROUND: DUSP4 is a pro-tumorigenic molecule of papillary thyroid carcinoma (PTC). DUSP4 also exists as an autophagic regulator. Moreover, DUSP4, as a negative regulator of MAPK, can prevent Beclin 1 from participating in autophagic response. This study aimed to explore whether TAT-Beclin 1, a recombinant protein of Beclin 1, could inhibit the tumorigenesis of DUSP4-positive PTC by regulating autophagy. METHODS: First, we divided PTC tissues into three groups according to DUSP4 expression levels by immunohistochemical analyses, and evaluated the relationship between autophagic molecules (Beclin 1 and LC3II) and DUSP4 using Western blotting assays. After overexpression of DUSP4 by lentiviral transduction, the in vitro and in vivo roles of TAT-Beclin 1 on DUSP4-overexpressed PTC cells were assessed (including autophagic activity, cell survival and function, and tumor growth). The roles of TAT-Beclin 1 in the survival of DUSP4-silenced PTC cells were also evaluated. RESULTS: Our results showed that the expression levels of autophagic proteins decreased with the increase of DUSP4 expression in PTC tissues. In PTC cells, DUSP4 overexpression-inhibited autophagic activity (including Beclin 1 expression, LC3 conversion rate and LC3-puncta formation) and -promoted cell proliferation and migration were reversed by TAT-Beclin 1 administration. In vivo assays also showed that DUSP4-overexpressed PTC cells had stronger tumorigenic ability and weaker autophagic activity, which was blocked by TAT-Beclin 1 administration. CONCLUSION: TAT-Beclin 1, as an autophagic promoter, could repress the carcinogenesis of DUSP4-positive PTC, which implies that the use of TAT-Beclin 1 for the PTC patients' treatment might be determined according to the DUSP4 level in their tumors.

Mitochondrial Uncouplers Confer Protection by Activating AMP-Activated Protein Kinase to Inhibit Neuroinflammation Following Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is a disease with high disability and mortality rates. Currently, the efficacy of therapies available for ICH is limited. Microglia-mediated neuroinflammation substantially exacerbates brain damage following ICH. Here, we investigated whether mitochondrial uncouplers conferred protection by suppressing neuroinflammation following ICH. To mimic ICH-induced neuroinflammation in vitro, we treated microglia with red blood cell (RBC) lysate. RBC lysate enhanced the expression of pro-inflammatory cytokines in microglia. A clinically used uncoupler, niclosamide (Nic), reduced the RBC lysate-induced expression of pro-inflammatory cytokines in microglia. Moreover, Nic ameliorated brain edema, decreased neuroinflammation, and improved neurological deficits in a well-established mouse model of ICH. Like niclosamide, the structurally unrelated uncoupler carbonyl cyanide p-triflouromethoxyphenylhydrazone (FCCP) reduced brain edema, decreased neuroinflammation, and improved neurological deficits following ICH. It has been reported that mitochondrial uncouplers activate AMP-activated protein kinase (AMPK). Mechanistically, Nic enhanced AMPK activation following ICH, and AMPK knockdown abolished the beneficial effects of Nic following ICH. In conclusion, mitochondrial uncouplers conferred protection by activating AMPK to inhibit microglial neuroinflammation following ICH.

[Finite Element Analysis of Biomechanics of Cervical Spine after Dynamic Cervical Implant Surgery].

This study aims to investigate the range of motion(ROM)and the stress variation in the intervertebral disc and the vertebral body on adjacent segments and the influence of force transmission mode after the dynamic cervical implant(DCI)surgery.Two types of surgery,DCI implantation and interbody fusion were used to establish the finite element model of the cervical C5,6segment degeneration treatment.The ROM and the adjacent discs and vertebral body stresses of two procedures under flexion,extension,lateral bending and axial rotation working conditions were analyzed.The results showed that ROM of the surgical segment in DCI model was well preserved and could restore to the normal ROM distributions(reduction of the amplitude was less than 25%),and the kinetic characteristics of adjacent segments was less affected.In fusion surgery model,however,ROM of the surgical segment was reduced by 86%-91%,while ROM,disc stress and vertebral stress of adjacent segments were increased significantly,and stress of the C5 vertebral body was increased up to 171.21%.Therefore DCI surgery has relatively small influence on cervical ROM and stress.The study provides a theoretical basis for DCI and fusion surgery in clinic.

[Genetic Diversity and Genetic Relationship of Different Forms of Trichosanthes kirilowii from Shandong Province].

OBJECTIVE: To investigate the genetic diversity and genetic relationship of different forms of Trichosanthes kirilowii from Shandong Province. METHODS: Different forms of Trichosanthes kirilowii from the same planting base were detected by random amplified polymorphic DNA( RAPD) with eight random primers. The amplified bands were detected and the fingerprint was drawn by Biosens Gel Imaging System software. The Jaccard coefficient was worked out by using NTSYS-pc software, and a cluster dendrogram of different samples was established based on unweighted pair-group method with arithmetic means (UPGMA). RESULTS: The eight primers produced 56 bands, among which, 32 bands were polymorphic. The cluster dendrogram displayed there was some differences of genetic relationship of different samples. CONCLUSION: There is similar genetic material basis of Trichosanthes kirilowii from the same planting base, but also there is apparent individual differences.

Comprehensive characterization of ERV-K (HML-8) in the chimpanzee genome revealed less genomic activity than humans.

Endogenous retroviruses (ERVs) originate from ancestral germline infections caused by exogenous retroviruses. Throughout evolution, they have become fixed within the genome of the animals into which they were integrated. As ERV elements coevolve with the host, they are normally epigenetically silenced and can become upregulated in a series of physiological and pathological processes. Generally, a detailed ERV profile in the host genome is critical for understanding the evolutionary history and functional performance of the host genome. We previously characterized and cataloged all the ERV-K subtype HML-8 loci in the human genome; however, this has not been done for the chimpanzee, the nearest living relative of humans. In this study, we aimed to catalog and characterize the integration of HML-8 in the chimpanzee genome and compare it with the integration of HML-8 in the human genome. We analyzed the integration of HML-8 and found that HML-8 pervasively invaded the chimpanzee genome. A total of 76 proviral elements were characterized on 23/24 chromosomes, including detailed elements distribution, structure, phylogeny, integration time, and their potential to regulate adjacent genes. The incomplete structure of HML-8 proviral LTRs will undoubtedly affect their activity. Moreover, the results indicated that HML-8 integration occurred before the divergence between humans and chimpanzees. Furthermore, chimpanzees include more HML-8 proviral elements (76 vs. 40) and fewer solo long terminal repeats (LTR) (0 vs. 5) than humans. These results suggested that chimpanzee genome activity is less than the human genome and that humans may have a better ability to shape and screen integrated proviral elements. Our work is informative in both an evolutionary and a functional context for ERVs.

PHACTR1 promotes the mobility of papillary thyroid carcinoma cells by inducing F-actin formation.

Papillary thyroid carcinoma (PTC) limits effective biomarkers for predicting prognosis and targeted therapy. Phosphatase and actin regulator 1 (PHACTR1) is a mobility-promoting molecule due to its regulation on F-actin formation, which is valuable for the investigation of PTC. Our study aimed to investigate the relationship between PHACTR1 and PTC carcinogenesis, especially mobility. Our results displayed that PHACTR1 expression was elevated in metastatic or larger PTC tissues. In addition, PTC cells K1 with more obvious mobility had higher PHACTR1 expression whereas weakly mobile cells TPC-1 was contrary. Moreover, PHACTR1 silencing inhibited the invasion, migration and tumorigenicity of K1 cells, while PHACTR1 overexpression promoted the invasion, migration and tumorigenicity in TPC-1 cells. Furthermore, PHACTR1 overexpression increased the fluorescent intensity of F-actin in TPC-1 cells. Importantly, the enhanced invasion and migration in TPC-1 cells caused by PHACTR1 overexpression were significantly reversed by the disruption of F-actin assembly with swinholide A. In conclusion, PHACTR1 can promote the mobility of PTC cells, which results in the carcinogenesis of PTC. PHACTR1-regulated F-actin formation determines the mobility of PTC cells. Therefore, PHACTR1 can function as a potential biomarker for predicting prognosis and targeting therapy in PTC.

Irradiance penetration distribution and flashing light frequency simultaneously affected with microalgal cell absorption and CO2 bubble scattering in a raceway pond.

In order to investigate light penetration and flashing light frequency for microalgal cell-CO2 bubble culture system in a raceway pond, user-defined function for CO2 mass transfer and bubble scattering models coupled with discrete ordinates radiation model were adopted to clarify simultaneous effects of microalgal cell absorption and CO2 bubble scattering. Light intensity along the microalgal suspension depth attenuated more rapidly with increased biomass concentration, decreased bubble generation diameter, increased CO2 gas content and incident light intensity. Ratio of light zone decreased from 81.13 % to 20.00 % when biomass concentration increased from 0 to 0.4 g/L because of light absorption and shading effects of microalgae. When bubble generation diameter increased from 0.1 to 1.6 mm, ratio of light zone increased from 37.95 % to 42.64 %, while microalgal flashing light cycle first decreased to a valley of 1.81 s at 0.8 mm and then increased. Local light intensity in the upper layers was more enhanced due to lots of CO2 bubbles gathering and reflecting more light with decreased bubble diameter and increased gas content. Light attenuated more rapidly in microalgal suspension with decreased bubble generation diameter and increased CO2 gas content because of increased bubble diffraction coefficient and contact area. When initial CO2 volume fraction increased from 0.02 to 0.2, flashing light frequency of microalgal cells decreased from 0.55 to 0.29 Hz and light zone time ratio φ decreased from 36.90 % to 18.40 %. At a biomass concentration of 0.1 g/L and a bubble flow rate of 0.1 m/s, the maximum light penetration and microalgal growth rate was achieved when bubble diameter, incident light intensity and gas content were optimally at 0.8 mm, 200 W/m2 and 0.02, respectively. This work provides data support and theoretical guidance for photobioreactor design and optimization of light energy utilization.

The Pro-Tumor Biological Function of IL-36α Plays an Important Role in the Tumor Microenvironment of HCC.

Purpose: To investigate the role of IL-36 in the tumorigenesis of hepatocellular carcinoma (HCC). IL-36 composed of a natural antagonist (IL-36Ra) and three agonists (IL-36α, -ß, -γ) that stimulate inflammation by binding to a common receptor consisting of IL-36R and IL-1RAcP. HCC is a common malignancy associated with high morbidity and mortality, often diagnosed at later stages. Although the exact role of IL-36α in HCC remains controversial, it is hypothesized that it may play a significant role in the development and progression of this cancer. Materials and Methods: In the current study, we measured both circulating and intrahepatic levels of IL-36α from HCC patients and healthy controls, using ELISA. The association between IL-36 and the differentiation of HCC was determined. Furthermore, the role IL-36 in both HCC and non-HCC cell lines was evaluated in vitro. Results: Circulating and intra-hepatic IL-36α was inversely correlated with differentiation of HCC, suggesting that IL-36α contribute to protection during the development of HCC. Based on bioinformatics, miR-27b-3p is closely related to downstream IL-36α. Thus, we determined miR-27b-3p expression in HCC tissues, showing upregulated miR-27b-3p was inversely correlated with IL-36α in HCC, perhaps via CXCL1 in HCC cells. It was confirmed that IL-36α inhibited HCC proliferation, viability and migration in vitro, consistent with reduced the expression of cytokines IL-1ß, IL-18, implying that IL-36α inhibited the possible involvement of pyroptosis. Conclusion: Our data suggests that IL-36α may be a potential therapeutic target and a prediction biomarker for the management of HCC.

MiR-379-5p inhibits the proliferation, migration, and invasion of breast cancer by targeting KIF4A.

BACKGROUND: Many studies have shown that microRNAs (miRNAs) play an essential role in gene regulation and tumor development. This study aimed to explore the expression of miR-379-5p and its mechanisms of affecting proliferation, migration, and invasion in breast cancer (BC). METHODS: MiRNAs and mRNAs expression data of BC and normal breast tissue samples were downloaded from the TCGA and GEO databases. qRT-PCR was used to detect the expression of miR-379-5p in human normal breast epithelial cell lines and human BC cell lines. The proliferation ability of transfected cells was detected by colony formation and EdU assays. The mobility and invasion ability of transfected cells was measured by wound healing and transwell assays. The relative protein expression of transfected cells was detected by western blot. Dual luciferase reporter assay was performed to identify the targeted binding of miR-379-5p and KIF4A. RESULTS: MiR-379-5p was lowly expressed in BC tissue samples and BC cell lines. The target genes of miR-379-5p were involved in many cancer-related signaling pathways. PPI analysis and the cytoHubba algorithm of Cytoscape identified 10 genes as the hub genes. Survival analysis showed that only KIF4A expression in 10 hub genes was significantly associated with the prognosis of BC patients and was significantly upregulated in BC. Overexpression of miR-379-5p inhibited proliferation, migration, and invasion in the BC cell line MDA-MB-231, which could be reversed by KIF4A. CONCLUSIONS: MiR-379-5p inhibits proliferation, migration, and invasion of BC by targeting KIF4A.

[Research Progress of Pharmacological Therapy and Nutritional Support for Cachexia 
in Lung Cancer Patients].

Cachexia is a common complication in patients with lung cancer. It aggravates the toxic and side effects of chemotherapy, hinders the treatment plan, weakens the responsiveness of chemotherapy, reduces the quality of life, increases complications and mortality, and seriously endangers the physical and mental health of patients with lung cancer. The causes and pathogenesis of tumor cachexia are extremely complex, which makes its treatment difficult and complex. Controlling cachexia in lung cancer patients requires many means such as anti-tumor therapy, inhibition of inflammatory response, nutritional support, physical exercise, and relief of symptoms to exert the synergistic effect of multimodal therapy against multiple mechanisms of tumor cachexia. To date, there has been a consensus within the discipline that no single therapy can control the development of cachexia. Some therapies have made some progress, but they need to be implemented in combination with multimodal therapy after fully assessing the individual characteristics of lung cancer patients. This article reviews the application of drug therapy and nutritional support in lung cancer patients, and looks forward to the research direction of cachexia control in lung cancer patients.
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Using Iron Tailings for Phosphate Removal in Cemented Phosphogypsum (PG) Backfill.

Compared with the post-treatment of pollutants, such as the removal of phosphate from wastewater, it is more important to develop effective emission control strategies to reduce phosphate pollution. Phosphogypsum (PG) is a typical solid waste byproduct of phosphate production and contains high amounts of residual phosphate. In order to control the phosphate emissions during the recycling of PG aggregates for cemented backfill, another solid waste product­iron tailings (ITs)­was added during the preparation of backfill slurry. The results showed that the ITs effectively accelerated the phosphate removal in cemented PG backfill, enabling the quick reduction in the phosphate concentration to the discharge standard (<0.5 mg/L) within 15 min. This means that the emissions of phosphate to bleeding water were effectively controlled. The adsorption experiment showed that phosphate was adsorbed by the ITs, and the adsorption data fitted well with the Langmuir adsorption model (R2 = 0.98) and pseudo-second-order kinetic model (R2 = 0.99), indicating that the phosphate adsorption of ITs was a monolayer chemical adsorption. Furthermore, an unconfined compressive strength (UCS) test was performed on the backfill with the addition of ITs. Compared to the control group (without ITs), the UCS of backfill with 20% ITs increased from 1.08 MPa to 1.33 MPa, indicating that the addition of solid waste could be beneficial to the strength development of the backfill by mitigating the interference of phosphate with the hydration process. The backfill cured for 28 d was selected for the toxic leaching test, and the phosphate concentration in the leachates was always below 0.02 mg/L, indicating that ITs can effectively immobilize phosphate in backfill for a long time.

Formation and dynamics of capillary-flow-induced colloidal rings.

We have directly observed the ring formation of colloidal particles of 1 µm diameter at the contact lines of air, water, and oil using a laser scanning confocal microscope. Colloidal rings form and grow through the transport of particles induced by capillary flow due to water evaporation. In addition, we observe the sudden "jump in" of particles into the ring and the "depletion" of particles in the ring. Particle-tracking experiment shows that the particles within the ring exhibit 1D-like motion along the circular ring geometry, and the pair correlation function of the ring configuration suggests an equilibrium interparticle distance of approximately 2.8 µm. It is also found that the structure and formation speed of the colloidal rings can be controlled by accelerating water evaporation by the addition of methanol as a cosolvent.

Thermoresponsiveness of integrated ultra-thin silicon with poly(N-isopropylacrylamide) hydrogels.

Stimuli-sensitive polymer materials have limited device functionality, design and manufacturing flexibility although they are pushed to enable smart device applications. Here we demonstrate the capability of integrating thermoresponsive poly(N-isopropylacrylamide) (PNIPAAm) hydrogels with silicon nanoribbons, and enable the stiff silicon ribbons to become adaptive and drivable by the soft environmentally sensitive substrate, such as becoming mechanically stretched and compressed on temperature change. These and related soft/hard smart devices and systems may open new opportunities in biomedical applications.

miR­122­5p suppresses the oncogenesis of PTC by inhibiting DUSP4 expression.

MicroRNAs (miRNAs or miRs) play an important role in regulating the occurrence and development of papillary thyroid carcinoma (PTC). miR­122­5p is widely considered a tumour inhibitor, which has not been fully explored in PTC. Bioinformatics analysis identified dual specificity phosphatase 4 (DUSP4), a tumour promoter gene for PTC, as a downstream target of miR­122­5p. The aim of the present study was to investigate the role and molecular mechanism of miR­122­5p in PTC oncogenesis. In this study, the expression pattern of miR­122­5p in PTC cancer tissues and PTC cell lines was investigated via reverse transcription­quantitative PCR. Furthermore, the roles of miR­122­5p in PTC were explored using gain­of­function and loss­of­function assays. The results revealed that the expression of miR­122­5p was significantly lower in PTC cancer tissues, especially in cancer tissues with significant invasion or metastasis. Overexpression of miR­122­5p caused by miR­122­5p mimics inhibited the proliferation, invasion, and migration of the PTC cell line K1, while knockdown of miR­122­5p by miR­122­5p inhibitors exhibited the opposite effect. Furthermore, in vivo assays revealed that miR­122­5p overexpression inhibited tumour growth. In addition, miR­122­5p was negatively correlated with DUSP4 expression in PTC cancer tissues. miR­122­5p overexpression inhibited DUSP4 expression in K1 cells, while miR­122­5p downregulation produced the inverse effect. Specifically, a luciferase reporter assay confirmed the binding sites of miR­122­5p on the 3'­UTR of DUSP4, demonstrating the targeting effect of miR­122­5p on DUSP4. miR­122­5p inhibited the oncogenesis of PTC by targeting DUSP4, revealing the potential application value of miR­122­5p in the diagnosis and treatment of PTC.

Orange light spectra filtered through transparent colored polyvinyl chloride sheet enhanced pigment content and growth of Arthrospira cells.

Microalgae are significantly affected by the spectra composition with various wavelengths. The development of light harvesting pigments can be controlled with specific wavelength of filtered light received by microalgae. Coverage of open raceway pond using transparent colored polyvinyl chloride sheets (PVCS) to filter light spectra, was assessed for the capacity to enhance biomass growth rate. Results showed that orange PVCS filtered light spectra at wavelengths from 480 to 665 nm, increased biomass dry weight (3.3 g/L) by 61% compared with control condition (white PVCS = 350-750 nm). Light spectra filtered through orange PVCS were more easily absorbed by the light harvesting pigment protein complex (phycobilisome) of Arthrospira platensis cells and subsequently transferred to intracellular photosynthesis reaction centers. Therefore, A. platensis cells cultivated with light spectra filtered through orange PVCS contained 62.7 mg/L chlorophyll-a and 23.5 mg/L carotenoid, which were 40% and 29% higher than control condition (with white PVCS).

Developing staggered woven mesh aerator with three variable-micropore layers in recycling water pipeline to enhance CO2 conversion for improving Arthrospira growth.

A staggered woven mesh (SWM) aerator equipped with three variable-micropore layers was developed to enhance the CO2 conversion into HCO3- in a recycling water pipeline for promoting CO2 utilization efficiency and Arthrospira growth in large-scale raceway ponds. The input CO2 gas was broken into smaller bubbles (0.78- 2.43 mm) through the first-stage shear with axial rectangles, second-stage shear with radial rectangles (equivalent pore diameter = 150 µm), and third-stage shear with uniform micropores. A high-speed camera (MotionXtra HG-100K CMOS) and an Image J image processing software were employed to capture the bubble pictures. Compared to the traditional steel pipe (TSP) aerator, the bubble generation diameter and time in the SWM aerator reduced by 72.3% and 48.6%, respectively. The optimized structure (ε = 14, pore = 23 µm) of the SWM aerator promoted the carbonization efficiency and HCO3- conversion efficiency into biomass by 78.6% and 64.6% than the TSP aerator. Further, the chlorophyll fluorescence and biomass measurements showed an increase in the actual photochemical efficiency (analyzed by Hansatech FMS1 chlorophyll fluorescence instrument) and biomass yield by 1.8 times and 80.1%.

miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis.

BACKGROUND: The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis. miR-183-5p, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of miR-183-5p in migration, invasion and aerobic glycolysis in HCC remains unclear. PURPOSE: To elucidate whether miR-183-5p affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism. METHODS: We attempted to observe the effects of miR-183-5p on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of miR-183-5p on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression. RESULTS: Our results show that miR-183-5p promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (PKM2, HK2, LDHA, GLUT1) expression in HepG2 cells. Further experiments indicated that miR-183-5p could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells. CONCLUSION: These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling.

Two-particle interfacial microrheology at polymer-polymer interfaces.

We continue to develop two-particle interfacial microrheology and have applied the technique to study the interfacial viscoelastic properties of immiscible poly(dimethylsiloxane) (PDMS)-poly(ethylene glycol) (PEG) interfaces. The interfacial storage and loss moduli are measured over a wide frequency range: at low frequencies, the interfaces are dominated by viscous responses whereas elasticity dominates at high frequencies. The zero-shear interfacial viscosity, estimated following the Cox-Merz rule and Cross model, falls between the bulk viscosities of the two individual polymers. Surprisingly, the interfacial relaxation time, calculated from the crossover of the storage and loss moduli, is observed to be an order of magnitude larger than that of the PDMS bulk polymers. The effects of tracer particle surface chemistry and size have also been investigated and show minimum influences on two-particle interfacial microrheology.

Understanding nanoparticle diffusion and exploring interfacial nanorheology using molecular dynamics simulations.

We have studied the dynamics of nanoparticles at polydimethylsiloxane (PDMS) oil-water interfaces using molecular dynamics (MD) simulations. The diffusion of nanoparticles in pure water and low-viscosity PDMS oil is found to be reasonably consistent with the prediction by the Stokes-Einstein equation. In addition, we have calculated the shear moduli and viscosities of bulk oil and water, as well as oil-water interfaces from single nanoparticle tracking and demonstrated the potential of probing nanorheology from an MD simulation approach. Surprisingly, we found that the lateral diffusion of nanoparticles as well as apparent interfacial nanorheology at the PDMS oil (low viscosity)-water interface are independent of the position of the nanoparticle at the interface.