Many crystals, such as those of metals, can transform from one symmetry into another having lower free energy via a diffusionless transformation. Here we create binary colloidal crystals consisting of polymer microspheres, pulled together by DNA bridges, that induce specific, reversible attractions between two species of microspheres. Depending on the relative strength of the different interactions, the suspensions spontaneously form either compositionally ordered crystals with CsCl and CuAu-I symmetries, or disordered, solid solution crystals when slowly cooled. Our observations indicate that the CuAu-I crystals form from CsCl parent crystals by a diffusionless transformation, analogous to the Martensitic transformation of iron. Detailed simulations confirm that CuAu-I is not kinetically accessible by direct nucleation from the fluid, but does have a lower free energy than CsCl. The ease with which such structural transformations occur suggests new ways of creating unique metamaterials having structures that may be otherwise kinetically inaccessible.

• Hindered diffusion becomes the dominant force of molecular movement in a thrombus.• The thrombus core acts as a selective molecular prison.Hemostatic thrombi formed after a penetrating injury have a heterogeneous architecture in which a core of highly activated, densely packed platelets is covered by a shell of lessactivated, loosely packed platelets. In the first manuscript in this series, we show that regional differences in intrathrombus protein transport rates emerge early in the hemostatic response and are preserved as the thrombus develops. Here, we use a theoretical approach to investigate this process and its impact on agonist distribution. The results suggest that hindered diffusion, rather than convection, is the dominant mechanism responsible for molecular movement within the thrombus. The analysis also suggests that the thrombus core, as compared with the shell, provides an environment for retaining soluble agonists such as thrombin, affecting the extent of platelet activation by establishing agonist-specific concentration gradients radiating from the site of injury. This analysis accounts for the observed weaker activation and relative instability of platelets in the shell and predicts that a failure to form a tightly packed thrombus core will limit thrombin accumulation, a prediction tested by analysis of data from mice with a defect in clot retraction. (Blood.

During thrombotic or hemostatic episodes, platelets bind collagen and release ADP and thromboxane A 2 , recruiting additional platelets to a growing deposit that distorts the flow field. Prediction of clotting function under hemodynamic conditions for a patient's platelet phenotype remains a challenge. A platelet signaling phenotype was obtained for 3 healthy donors using pairwise agonist scanning, in which calcium dye-loaded platelets were exposed to pairwise combinations of ADP, U46619, and convulxin to activate the P2Y 1 /P2Y 12 , TP, and GPVI receptors, respectively, with and without the prostacyclin receptor agonist iloprost. A neural network model was trained on each donor's pairwise agonist scanning experiment and then embedded into a multiscale Monte Carlo simulation of donor-specific platelet deposition under flow. The simulations were compared directly with microfluidic experiments of whole blood flowing over collagen at 200 and 1000/s wall shear rate. The simulations predicted the ranked order of drug sensitivity for indomethacin, aspirin, MRS-2179 (a P2Y 1 inhibitor), and iloprost. Consistent with measurement and simulation, one donor displayed larger clots and another presented with indomethacin resistance (revealing a novel heterozygote TP-V241G mutation). In silico representations of a subject's platelet phenotype allowed prediction of blood function under flow, essential for identifying patientspecific risks, drug responses, and novel genotypes. IntroductionDuring a clotting event, platelets respond to combinatorial stimuli, including collagen, adenosine diphosphate (ADP), thromboxane A 2 (TXA 2 ), thrombin, epinephrine, and serotonin, as well as endothelialderived inhibitors such as nitric oxide and prostacyclin (PGI 2 ). Excessive platelet buildup at the site of cardiovascular disease and plaque rupture causes more than 1 million heart attacks and strokes in the United States each year. Excessive thrombus formation after plaque rupture remains difficult to predict and can be linked to hyperactive platelet function. 1,2 Therefore, low-dose aspirin to inhibit platelet cyclooxygenase-1 (COX-1) and clopidogrel to inhibit platelet P2Y 12 signaling are used widely in patients with cardiovascular risks, although patient response to these drugs can vary.Interindividual variations in platelet reactivity, even in the healthy population, have been associated with several factors, including female sex, fibrinogen level, ethnicity, inherited variations, and polymorphisms. 3,4 Similarly, platelet dysfunction or antiplatelet therapy can be associated with bleeding risks. [5][6][7] Furthermore, the function of blood is highly dependent on hemodynamic forces; examples include shear-induced platelet activation at Ͼ 5000/s shear rate, 8,9 requirement of VWF in arterial thrombosis, 10-12 shear effects on VWF structure/function and GPIb-VWF A1 domain-bonding dynamics, 13-17 RBC-dependent platelet migration toward the wall, 18,19 and convection-enhanced mass transfer to and from local zones of clotting or bleeding....

DNA is the premier material for directing nanoscale self-assembly, having been used to produce many complex forms. Recently, DNA has been used to direct colloids and nanoparticles into novel crystalline structures, providing a potential route to fabricating meta-materials with unique optical properties. Although theory has sought the crystal phases that minimize total free energy, kinetic barriers remain essentially unstudied. Here we study interfacial equilibration in a DNA-directed microsphere self-assembly system and carry out corresponding detailed simulations. We introduce a single-nucleotide difference in the DNA strands on two mixed microsphere species, which generates a free-energy penalty for inserting 'impurity' spheres into a 'host' sphere crystal, resulting in a reproducible segregation coefficient. Comparison with simulation reveals that, under our experimental conditions, particles can equilibrate only with a few nearest neighbours before burial by the growth front, posing a potential impediment to the growth of complex structures.

A model is presented and analyzed for the dynamics of intrinsic point defects, vacancies, and self -interstitials, in single-crystal silicon. Computations and asymptotic analysis are used to describe the appearance of the oxidation-induced stacking-fault ring (OSF ring) created during the cooling of silicon crystals in the Czochralski growth process. The model predicts that the OSF ring separates an inner region supersaturated with vacancies from a self-interstitial rich outer region. The OSF ring corresponds to a region of no net excess of either point defect. Simulations of the dynamics of the OSF ring with changes in the crystal growth rate ( 17) and the axial temperature gradient at the melt/crystal interface (G) accurately predict experimental data for a wide range of growth conditions when point defect thermophysical properties (equilibrium concentrations and diffusivities) are fit to a single set of experimental data. The point defect properties determined this way are within the range of values reported in the literature. Asymptotic analysis of the point defect dynamics model gives a simple mechanistic picture for the development of the point defect supersaturations and yields a closed-form expression for the critical value of (V/G) for the location of the OSF ring. This expression is in excellent agreement with the predictions of simulation and with the empirical correlation determined from experiments. InfroductionWafers of crystalline silicon, grown by the Czochralski (CZ) crystal growth method are used as substrates in almost all of today's microelectronic devices. Already very high, the demands on the purity and crystalline perfection for silicon wafers are becoming increasingly stringent, as the linewidth used in microelectronic devices decreases toward a 0.1 I.Lm design rule. Although Czochralski-grown silicon is free of continuous dislocations, the material contains a myriad of crystallographic imperfections. Besides distributions of point defects, vacancies, and self -interstitials, and concentrations of impurities, CZ-silicon contains grown-in microdefects. These microdefects, such as precipitates, voids, and dislocation loops, are formed in the crystal from the aggregation of point defects and impurities during crystal growth and subsequent annealing and device processing. The key to increasing the qual-

Future optical materials promise to do for photonics what semiconductors did for electronics, but the challenge has long been in creating the structure they require—a regular, three-dimensional array of transparent microspheres arranged like the atoms in a diamond crystal. Here we demonstrate a simple approach for spontaneously growing double-diamond (or B32) crystals that contain a suitable diamond structure, using DNA to direct the self-assembly process. While diamond symmetry crystals have been grown from much smaller nanoparticles, none of those previous methods suffice for the larger particles needed for photonic applications, whose size must be comparable to the wavelength of visible light. Intriguingly, the crystals we observe do not readily form in previously validated simulations; nor have they been predicted theoretically. This finding suggests that other unexpected microstructures may be accessible using this approach and bodes well for future efforts to inexpensively mass-produce metamaterials for an array of photonic applications.

An internally consistent model is presented for the dynamic formation of microdefects in single‐crystal silicon. The model is built on the dynamics of point defects, vacancies and self‐interstitials, and is extended to include the growth of clusters of these point defects into microdefects. A hybrid finite‐element/finite‐difference numerical method is used to solve the coupled system of partial differential equations, which includes sets of discrete rate equations for small clusters and Fokker‐Planck equations for larger ones. As described previously by a point defect dynamics model [J. Electrochem. Soc., 145, 303 (1998)], the oxidation‐induced stacking fault (OSF)‐ring position delineates the vacancy‐rich region inside from the external interstitial‐rich crystal. In Czochralski silicon, the radial position of the OSF‐ring correlates well with the expression V/G false(ROSFfalse)=1.34×10−3 cm2 min−1 K−1 . Simulations are used to explore the formation of voids in the vacancy‐rich region inside the OSF‐ring. Predictions of the total concentration of observable voids and the dependence of this concentration on the cooling rate agree with experiments and point to the importance of the axial temperature profile in the crystal from the melting point (1685 K) down to about 1150 K in setting the number and size of voids. The total number of voids correlates with V 〈G〉 where 〈G〉 is a measure of the temperature gradient in the temperature range 1173 K ≤ T ≤ 1685 K. The appearance of the OSF‐ring is explained qualitatively in terms of the residual vacancy concentration remaining in the crystal after aggregation has ceased. © 1999 The Electrochemical Society. All rights reserved.

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