Perturbation-induced droplets for manipulating droplet structure and configuration in microfluidics

In this work, we mechanically perturb a liquid-in-liquid jet to manipulate the size and structure of the droplets formed from break-up of the jet. The induced break-up is relatively insensitive to fluctuations in the surrounding fluid flow. When the amplitude of perturbations is large and the interfacial tension of the liquid–liquid system is low, the size of the droplets can be precisely tuned by controlling the rate at which the liquid exits the tip of the dispensing nozzle through the frequency of perturbation. When applied to microfluidic devices with the appropriate geometry, our perturbation-induced droplet approach offers a strategy to manipulating droplet structures. We demonstrate that by varying the imposed perturbation frequency and phase lag, the structure of the multi-compartmental drops and the configuration of the resultant drops in the same flow condition can be manipulated. Moreover, after careful treatment of the wettability of the devices, we show that the structure of the droplets can be precisely controlled to change from single emulsion to double emulsion within the same device. The perturbation-induced droplet generation represents a new paradigm in the engineering of droplets, enhancing current droplet-based technologies for applications ranging from particle fabrication to confined micro-reactions.postprin

Effects of Rosiglitazone on the Expression of PPAR-&#947 and on the Production of IL-6 and IL-8 in Acute Lung Injury Model Using Human Pulmonary Epithelial Cells

Purpose: Peroxisome proliferator-activated receptor (PPAR)-γ ligand is known to repress the expression of pro-inflammatory mediators. However, it is unclear how it affects PPAR-γ expression and the inflammatory response in the human lung. We investigated the effects of rosiglitazone (synthetic PPAR-γ ligand) on the PPAR-γ expression and on the IL-6 and IL-8 production in acute lung injury model using human lung epithelial cells.Methods: A549 and Beas-2B cells were pre-treated with rosiglitazone and/or BADGE (selective PPAR-γ antagonist) and then treated with media control or cytokine mixture including TNF-α, IL-1β, and IFN-γ. PPAR-γ expression was analyzed in cell lysates by Western blot. IL-6 and IL-8 production was measured in the culture supernatants by ELISA.Results: PPAR-γ expression was identified in all experimental groups except for the control. The cytokine mixture-induced IL-6 and IL-8 production was significantly inhibited by pre-treatment with rosiglitazone (P<0.01). However, this inhibitory effect of rosiglitazone was not reversed by BADGE. Conclusion: These suggest that rosiglitazone induces the PPAR-γ expression and it may inhibit the cytokine mixture-induced IL-6 and IL-8 production through the PPAR-γ independent pathway. The inhibitory mechanisms of rosiglitazone on the cytokine mixture-induced IL-6 and IL-8 production in human alveolar, and bronchial epithelial cells remain to be further investigated.Keywords: Rosiglitazone, PPAR-γ expression, IL-6, IL-8, Acute lung injur

Effects of Rosiglitazone on the Expression of PPAR-&#947 and the Production of IL-6 and IL-8 in Acute Lung Injury Model Using Human Pulmonary Epithelial Cells

Purpose: Peroxisome proliferator-activated receptor (PPAR)-γ ligand is known to repress the expression of pro-inflammatory mediators. However, it is unclear how it affects PPAR-γ expression and the inflammatory response in the human lung. We investigated the effects of rosiglitazone (synthetic PPAR-γ ligand) on the PPAR-γ expression and on the IL-6 and IL-8 production in acute lung injury model using human lung epithelial cells.Methods: A549 and Beas-2B cells were pre-treated with rosiglitazone and/or BADGE (selective PPAR-γ antagonist) and then treated with media control or cytokine mixture including TNF-α, IL-1 β, and IFN-γ. PPAR-γ expression was analyzed in cell lysates by Western blot. IL-6 and IL-8 production was measured in the culture supernatants by ELISA.Results: PPAR-γ expression was identified in all experimental groups except for the control. The cytokine mixture-induced IL-6 and IL-8 production was significantly inhibited by pre-treatment with rosiglitazone (P<0.01). However, this inhibitory effect of rosiglitazone was not reversed by BADGE.Conclusion: These suggest that rosiglitazone induces the PPAR-γ expression and it may inhibit the cytokine mixture-induced IL-6 and IL-8 production through the PPAR-γ independent pathway. The inhibitory mechanisms of rosiglitazone on the cytokine mixture-induced IL-6 and IL-8 production in human alveolar and bronchial epithelial cells remain to be further investigated.Keywords: Rosiglitazone, PPAR-γ, IL-6, IL-8, Acute lung injur

Joint longitudinal and survival-cure models in tumour xenograft experiments

In tumour xenograft experiments, treatment regimens are administered, and the tumour volume of each individual is measured repeatedly over time. Survival data are recorded because of the death of some individuals during the observation period. Also, cure data are observed because of a portion of individuals who are completely cured in the experiments. When modelling these data, certain constraints have to be imposed on the parameters in the models to account for the intrinsic growth of the tumour in the absence of treatment. Also, the likely inherent association of longitudinal and survival‐cure data has to be taken into account in order to obtain unbiased estimators of parameters. In this paper, we propose such models for the joint modelling of longitudinal and survival‐cure data arising in xenograft experiments. Estimators of parameters in the joint models are obtained using a Markov chain Monte Carlo approach. Real data analysis of a xenograft experiment is carried out, and simulation studies are also conducted, showing that the proposed joint modelling approach outperforms the separate modelling methods in the sense of mean squared errors

Large enhancement of the photovoltaic effect in ferroelectric complex oxides through bandgap reduction

Tuning the bandgap in ferroelectric complex oxides is a possible route for improving the photovoltaic activity of materials. Here, we report the realization of this effect in epitaxial thin films of the ferroelectric complex oxide Bi3.25La0.75Ti3O12 (BLT) suitably doped by Fe and Co. Our study shows that Co (BLCT) doping and combined Fe, Co (BLFCT) doping lead to a reduction of the bandgap by more than 1 eV compared to undoped BLT, accompanied by a surprisingly more efficient visible light absorption. Both BLCT and BLFCT films can absorb visible light with a wavelength of up to 500 nm while still exhibiting ferroelectricity, whereas undoped BLT only absorbs UV light with a wavelength of less than 350 nm. Correlated with its bandgap reduction, the BLFCT film shows a photocurrent density enhanced by 25 times compared to that of BLT films. Density functional theory calculations indicate that the bandgap contraction is caused by the formation of new energy states below the conduction bands due to intermixed transition metal dopants (Fe, Co) in BLT. This mechanism of tuning the bandgap by simple doping can be applied to other wide-bandgap complex oxides, thereby enabling their use in solar energy conversion or optoelectronic applications

Gap modification of atomically thin boron nitride by phonon mediated interactions

A theory is presented for the modification of bandgaps in atomically thin boron nitride (BN) by attractive interactions mediated through phonons in a polarizable substrate, or in the BN plane. Gap equations are solved, and gap enhancements are found to range up to 70% for dimensionless electron-phonon coupling \lambda=1, indicating that a proportion of the measured BN bandgap may have a phonon origin

High Fidelity Tape Transfer Printing Based On Chemically Induced Adhesive Strength Modulation

Transfer printing, a two-step process (i.e. picking up and printing) for heterogeneous integration, has been widely exploited for the fabrication of functional electronics system. To ensure a reliable process, strong adhesion for picking up and weak or no adhesion for printing are required. However, it is challenging to meet the requirements of switchable stamp adhesion. Here we introduce a simple, high fidelity process, namely tape transfer printing(TTP), enabled by chemically induced dramatic modulation in tape adhesive strength. We describe the working mechanism of the adhesion modulation that governs this process and demonstrate the method by high fidelity tape transfer printing several types of materials and devices, including Si pellets arrays, photodetector arrays, and electromyography (EMG) sensors, from their preparation substrates to various alien substrates. High fidelity tape transfer printing of components onto curvilinear surfaces is also illustrated

Genetic variants of interferon regulatory factor 5 associated with chronic hepatitis B infection

Aim: To investigate possible effects of IRF5 polymorphisms in the 3’ UTR region of the IFR5 locus on susceptibility to hepatitis B virus (HBV) infection and progression of liver diseases among clinically classified Vietnamese patients.Methods: Four IFR5 SNPs (rs13242262A/T, rs77416878C/T, rs10488630A/G, and rs2280714T/C) were genotyped in clinically classified HBV patients [chronic hepatitis B (CHB). n = 99; liver cirrhosis (LC), n = 131; hepatocellular carcinoma (HCC), n = 149] and in 242 healthy controls by direct sequencing and TaqMan real-time PCR assays. Results: Comparing patients and controls, no significant association was observed for the four IFR5 variants. However, the alleles rs13242262T and rs10488630G contributed to an increased risk of liver cirrhosis (LC vs CHB: OR = 1.5, 95%CI: 1.1-2.3, adjusted P = 0.04; LC vs CHB: OR = 1.7, 95%CI: 1.1-2.6, adjusted P = 0.019). Haplotype IRF5*TCGT constructed from 4 SNPs was observed frequently in LC compared to CHB patients (OR = 2.1, 95%CI: 1.2-3.3, adjusted P = 0.008). Haplotype IRF5*TCAT occurred rather among CHB patients than in the other HBV patient groups (LC vs CHB: OR = 0.4, 95%CI: 0.2-0.8, adjusted P = 0.03; HCC vs CHB: OR = 0.3, 95%CI: 0.15-0.7, adjusted P = 0.003). The IRF5*TCAT haplotype was also associated with increased levels of ALT, AST and bilirubin. Conclusion: Our study shows that IFR5 variants may contribute as a host factor in determining the pathogenesis in chronic HBV infections