Optimum mask and source patterns to print a given shape

Proceedings of S P I E - the International Society for OpticalNew degrees of freedom can be optimized in mask shapes when the source is also adjustable, because required image symmetries can be provided by the source rather than the collected wavefront. The optimized mask will often consist of novel sets of shapes that are quite different in layout from the target IC patterns. This implies that the optimization algorithm should have good global convergence properties, since the target patterns may not be a suitable starting solution. We have eveloped an algorithm that can optimize mask and source without using a starting design. Examples are shown where the process window obtained is between 2 and 6 times larger than that achieved with standard RET methods. The optimized masks require phase shift, but no trim mask is used. Thus far we have only optimized 2D patterns over small fields (periodicities of 1im or less). We also discuss mask optimization with fixed source, source optimization with fixed mask, and the re-targeting of designs in different mask regions to provide a common exposure level.published_or_final_versio

Optimum mask and source patterns to print a given shape

New degrees of freedom can be optimized in mask shapes when the source is also adjustable, because required image symmetries can be provided by the source rather than the collected wave front. The optimized mask will often consist of novel sets of shapes that are quite different in layout from the target integrated circuit patterns. This implies that the optimization algorithm should have good global convergence properties, since the target patterns may not be a suitable starting solution. We have developed an algorithm that can optimize mask and source without using a starting design. Examples are shown where the process window obtained is between two and six times larger than that achieved with standard reticle enhancement techniques (RET). The optimized masks require phase shift, but no trim mask is used. Thus far we can only optimize two-dimensional patterns over small fields (periodicities of ;1 mm or less), though patterns in two separate fields can be jointly optimized for maximum common window under a single source. We also discuss mask optimization with fixed source, source optimization with fixed mask, and the retargeting of designs in different mask regions to provide a common exposure level. © 2002 Society of Photo-Optical Instrumentation Engineers.published_or_final_versio

Encoding optical control in LCK kinase to quantitatively investigate its activity in live cells.

LCK is a tyrosine kinase that is essential for initiating T-cell antigen receptor (TCR) signaling. A complete understanding of LCK function is constrained by a paucity of methods to quantitatively study its function within live cells. To address this limitation, we generated LCK*, in which a key active-site lysine is replaced by a photocaged equivalent, using genetic code expansion. This strategy enabled fine temporal and spatial control over kinase activity, thus allowing us to quantify phosphorylation kinetics in situ using biochemical and imaging approaches. We find that autophosphorylation of the LCK active-site loop is indispensable for its catalytic activity and that LCK can stimulate its own activation by adopting a more open conformation, which can be modulated by point mutations. We then show that CD4 and CD8, T-cell coreceptors, can enhance LCK activity, thereby helping to explain their effect in physiological TCR signaling. Our approach also provides general insights into SRC-family kinase dynamics

STIM2 regulates PKA-dependent phosphorylation and trafficking of AMPARs

STIMs (STIM1 and STIM2 in mammals) are transmembrane proteins that reside in the endoplasmic reticulum (ER) and regulate store-operated Ca2+ entry (SOCE). The function of STIMs in the brain is only beginning to be explored, and the relevance of SOCE in nerve cells is being debated. Here we identify STIM2 as a central organizer of excitatory synapses. STIM2, but not its paralogue STIM1, influences the formation of dendritic spines and shapes basal synaptic transmission in excitatory neurons. We further demonstrate that STIM2 is essential for cAMP/PKA-dependent phosphorylation of the AMPA receptor (AMPAR) subunit GluA1. cAMP triggers rapid migration of STIM2 to ER–plasma membrane (PM) contact sites, enhances recruitment of GluA1 to these ER-PM junctions, and promotes localization of STIM2 in dendritic spines. Both biochemical and imaging data suggest that STIM2 regulates GluA1 phosphorylation by coupling PKA to the AMPAR in a SOCE-independent manner. Consistent with a central role of STIM2 in regulating AMPAR phosphorylation, STIM2 promotes cAMP-dependent surface delivery of GluA1 through combined effects on exocytosis and endocytosis. Collectively our results point to a unique mechanism of synaptic plasticity driven by dynamic assembly of a STIM2 signaling complex at ER-PM contact sites

Outlook for inverse design in nanophotonics

Recent advancements in computational inverse design have begun to reshape the landscape of structures and techniques available to nanophotonics. Here, we outline a cross section of key developments at the intersection of these two fields: moving from a recap of foundational results to motivation of emerging applications in nonlinear, topological, near-field and on-chip optics.Comment: 13 pages, 6 figure

The node of Ranvier in CNS pathology.

Healthy nodes of Ranvier are crucial for action potential propagation along myelinated axons, both in the central and in the peripheral nervous system. Surprisingly, the node of Ranvier has often been neglected when describing CNS disorders, with most pathologies classified simply as being due to neuronal defects in the grey matter or due to oligodendrocyte damage in the white matter. However, recent studies have highlighted changes that occur in pathological conditions at the node of Ranvier, and at the associated paranodal and juxtaparanodal regions where neurons and myelinating glial cells interact. Lengthening of the node of Ranvier, failure of the electrically resistive seal between the myelin and the axon at the paranode, and retraction of myelin to expose voltage-gated K(+) channels in the juxtaparanode, may contribute to altering the function of myelinated axons in a wide range of diseases, including stroke, spinal cord injury and multiple sclerosis. Here, we review the principles by which the node of Ranvier operates and its molecular structure, and thus explain how defects at the node and paranode contribute to neurological disorders