Modeling Evaporation and Particle Assembly in Colloidal Droplets

Evaporation-induced assembly of nanoparticles in a drying droplet is of great importance in many engineering applications, including printing, coating, and thin film processing. The investigation of particle dynamics in evaporating droplets can provide fundamental hydrodynamic insight for revealing the processing–structure relationship in the particle self-organization induced by solvent evaporation. We develop a free-energy-based multiphase lattice Boltzmann method coupled with Brownian dynamics to simulate evaporating colloidal droplets on solid substrates with specified wetting properties. The influence of interface-bound nanoparticles on the surface tension and evaporation of a flat liquid–vapor interface is first quantified. The results indicate that the particles at the interface reduce surface tension and enhance evaporation flux. For evaporating particle-covered droplets on substrates with different wetting properties, we characterize the increase of evaporate rate via measuring droplet volume. We find that droplet evaporation is determined by the number density and circumferential distribution of interfacial particles. We further correlate particle dynamics and assembly to the evaporation-induced convection in the bulk and on the surface of droplet. Finally, we observe distinct final deposits from evaporating colloidal droplets with bulk-dispersed and interface-bound particles. In addition, the deposit pattern is also influenced by the equilibrium contact angle of droplet

Interfacial Targeting of Sessile Droplets Using Electrospray

We report on the use of electrospray atomization to deliver nanoparticles and surfactant directly to the surface of sessile droplets. The particles delivered to the target droplet remained adsorbed at its interface since they arrived solvent-free. Upon complete evaporation, the interface of the target drop was mapped to the underlying substrate, forming a nanoparticle deposit. The use of electrospray permitted the exploration of the interfacial particle transport and the role of surfactants in governing particle motion and deposit structure. When no surfactant was present in the sprayed solution, there was no observable convection of the interfacial particles. When Tween 80, a high-molecular-weight surfactant, was added to the sprayed solution, the surface flow was similarly suppressed. Only when small surfactants (e.g., sodium dodecyl sulfate) were present in the sprayed solution was Marangoni flow, directed toward the droplet apex, induced at the interface. This flow drove the interfacial particles to the apex of the target droplet, creating a particle-dense region at the center of the final deposit. We found that small surfactants were capable of desorbing from the interface at a sufficiently high rate relative to the evaporation time scale of the target droplet. Once inside the drop, the desorbed surfactant was convected to the contact line where it accumulated, inducing a surface tension gradient and a solutal Marangoni flow. Numerical modeling using the lattice Boltzmann–Brownian dynamics method confirmed this mechanism of particle transport and its relationship to deposit structure. The use of sacrificial targets combined with electrospray may provide a unique capability for building colloidal monolayers with organized structure in a scalable way

New Point Mutations in Surface and Core Genes of Hepatitis B Virus Associated with Acute on Chronic Liver Failure Identified by Complete Genomic Sequencing

<div><p>The objective of this study was to identify new viral biomarkers associated with acute on chronic liver failure (ACLF) by complete genomic sequencing of HBV. Hepatitis B virus mutations associated with ACLF were screened by Illumina high-throughput sequencing in twelve ACLF cases and twelve age-matched mild chronic hepatitis B patients, which were validated in 438 chronic hepatitis B patients (80 asymptomatic carriers, 152 mild chronic hepatitis B patients, 102 severe chronic hepatitis B patients and 104 ACLF patients) by direct sequencing. The results of Illumina sequencing showed that the mutations at 7 sites (T216C, G285A, A1846T, G1896A, C1913A/G, A2159G, and A2189C) of 12 ACLF patients were significantly higher than those of 12 controls. In the validation cohorts, a significantly higher ratio of genotype B to C was found in patients with ACLF than in patients with non-ACLF. Multivariate analysis showed that T216C, G1896A, C1913A/G and A2159G/C were independent risk factors for ACLF. C216 in any combination, A/G1913 in any combination, and G/C2159 in any combination had high specificity for ACLF. In summary, T216C and A2159G/C mutations were novel factors independently associated with ACLF. Combined mutations in hepatitis B cases could play important roles in ACLF development.</p></div

The risks of CHB-M, CHB-S, and ACLF cases with 7 site mutations on the basis of genotype B and genotype C as compared with ASCs, CHB-M and CHB-S respectively.

<p>ASC, asymptomatic hepatitis B surface antigen carriers; CHB-M, mild chronic hepatitis B; CHB-S, severe chronic hepatitis B; ACLF, acute on chronic liver failure; CI, confidence interval; AOR, adjusted odds ratio;</p><p>* compared with ASCs;</p><p>** compared with CHB-M;</p><p>*** compared with CHB-S.</p><p>^a<i>P</i> < 0.01, as compared with control.</p><p>^b<i>P</i> < 0.05, as compared with control.</p><p>The risks of CHB-M, CHB-S, and ACLF cases with 7 site mutations on the basis of genotype B and genotype C as compared with ASCs, CHB-M and CHB-S respectively.</p

The associations of seven mutations in hepatitis B virus (HBV) with asymptomatic hepatitis B surface antigen carriers, mild chronic hepatitis B, severe chronic hepatitis B, acute on chronic liver failure in genotypes B and C.

<p>The associations of seven mutations in hepatitis B virus (HBV) with asymptomatic hepatitis B surface antigen carriers, mild chronic hepatitis B, severe chronic hepatitis B, acute on chronic liver failure in genotypes B and C.</p

The risks of ACLF cases with 7 site mutations on the basis of genotype B and genotype C as compared with non-ACLF cases.

<p>ACLF, acute on chronic liver failure; CI, confidence interval; AOR, adjusted odds ratio.</p><p>^a<i>P</i> < 0.01, as compared with non-ACLF.</p><p>^b<i>P</i> < 0.05, as compared with non-ACLF.</p><p>The risks of ACLF cases with 7 site mutations on the basis of genotype B and genotype C as compared with non-ACLF cases.</p

Primers used for Illumina sequencing and direct PCR sequencing of HBV.

<p>Primers used for Illumina sequencing and direct PCR sequencing of HBV.</p

The results of stepwise multivariate regression analysis for independent risk factors associated with ACLF cases.

<p>ACLF, acute on chronic liver failure; CI, confidence interval; AOR, adjusted odds ratio.</p><p>^a<i>P</i><0.01, as compared with non-ACLF.</p><p>^b<i>P</i><0.05, as compared with non-ACLF.</p><p>The results of stepwise multivariate regression analysis for independent risk factors associated with ACLF cases.</p

The clinical data and HBV mutation profiles in 438 subjects.

<p>ALT, alanine aminotransferase; AST, aspartate aminotransferase; ASC, asymptomatic hepatitis B surface antigen carriers; CHB-M, mild chronic hepatitis B; CHB-S, severe chronic hepatitis B; ACLF, acute on chronic liver failure;</p><p>^a<i>P</i><0.01, as compared with ASC.</p><p>^b<i>P</i><0.01, as compared with CHB-M.</p><p>^c<i>P</i><0.01, as compared with CHB-S.</p><p>^d<i>P</i><0.05, as compared with ASC.</p><p>^e<i>P</i><0.05, as compared with CHB-M.</p><p>^f<i>P</i><0.05, as compared with CHB-S.</p><p>The clinical data and HBV mutation profiles in 438 subjects.</p

Sensitivity and specificity of specific mutation patterns of hepatitis B virus for ACLF.

<p>ACLF, acute on chronic liver failure; CI, confidence interval; —,not calculated.</p><p>^a<i>P</i><0.01, as compared with non-ACLF.</p><p>^b combinations with any 2 or more of T216C, G1896A, C1913A/G and A2159G/C.</p><p>Sensitivity and specificity of specific mutation patterns of hepatitis B virus for ACLF.</p