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In advanced technological nodes, the photoresist absorbs light, which is reflected by underlying topography during optical lithography of implantation layers. Anti-reflective coating (ARC) helps to suppress the reflections, but ARC removal may damage transistors, not to mention its relatively high cost. Therefore ARC is usually not used, and topography modeling becomes obligatory for printing implantation shapes. Furthermore, presence of Fin Field Effect Transistors (FinFETs) makes modeling of non-uniform substrate reflections exceptionally challenging. In realistic designs, the same implantation shape may be found in a vertical or in a rotated horizontal orientation. This creates two types of relationships between the critical dimension (CD) and FinFET, namely parallel to and perpendicular to the fins. The measurement data shows that CDs differ between these two orientations. This discrepancy is also revealed by our Rigorous Optical Topography simulator. Numerical experiments demonstrate that the shape orientation may introduce CD differences of up to 45 nm with a 248 nm illumination for 14 nm technology. These differences are highly dependent on the enclosure (distance between implantation shape and active area). One of the major causes of the differences is that in the parallel orientation the shape is facing solid sidewalls of fins, while the perpendicular oriented shape “sees” only perforated sidewalls of the fin structure, which reflect much less energy. Meticulously stated numerical experiments helped us to thoroughly understand anisotropic behavior of CD measurement. This allowed us to more accurately account for FinFET-related topography effects in the compact implantation modeling for optical proximity corrections (OPC). This improvement is validated against wafer measurement data.

Molecular dynamic simulation of nano imprint lithography (NIL) in which nanoscale patterned stamp is pressed onto amorphous polyethylene (PE) surface is performed to study the deformation behavior of polymer resist. Force fields including bond, angle, torsion, and Lennard Jones potential are used to describe the inter-molecular and intra-molecular forces of PE molecules and stamp. Periodic boundary condition is used in horizontal direction and canonical NVT ensemble is employed to control the system temperature. Using the simulation results, the behavior of polymer resist is investigated during the imprinting process. The mechanism of resist deformation is analyzed by considering various parameters including the surface geometry, atom distribution, and density. Especially, the density in the bottom (emboss) region is found to be larger than the top (cavity) region due to compression of polymer molecules. The result indicates that small scale patterning of polymer resist largely depends on compression rather than the flow of molecules. The numerical results are compared with the local density measurement data using the atomic force microscope (AFM). They exhibit a similar behavior at least in a qualitative sense. Additional simulations, where the stamp geometry and molecular mobility are varied and are performed to investigate the deformation characteristics of polymer resist. From these simulations, important elements for understanding of NIL process are obtained.

Patients with end-stage renal disease (ESRD) are known to have impaired immune function. Dendritic cells (DCs) are the major antigen-presenting cells that initiate primary immune responses, linking innate and adaptive immunity. Although suboptimal immune responses to vaccination, as frequently observed in ESRD patients, might suggest the presence of impaired DC function, the precise nature of altered DC function is not fully understood.In the current study, we compared the maturation status, viability, and function of monocyte-derived DCs (moDCs) of patients on hemodialysis (HD) with healthy controls.Surface expression of major histocompatibility complex class II, CD83, and CD86, and chemokine receptor CCR7 in moDCs was not different between HD patients and healthy controls. No significant difference was detected in the viability of moDCs determined by expression of annexin V and propidium iodide between two groups. However, moDCs from HD patients produced significantly higher amounts of IL-6 when stimulated by cytokine cocktails compared to healthy controls. In addition, mature moDCs from HD patients showed significantly enhanced allogeneic T-cell proliferation compared to healthy controls.Our data demonstrate aberrant DC function in HD patients and suggest that this might contribute to impaired immune responses.

End-stage renal disease patients are known to be in a state of chronic low-grade inflammation and to have high infection-related morbidity and mortality. However, the precise mechanisms are not understood. The purpose of this study was to determine the mechanisms underlying chronic low-grade inflammation and defects in innate immune responses in hemodialysis (HD) patients.In 33 HD patients, we measured the basal status of toll-like receptor 4 (TLR4) positivity in the CD14-positive monocyte population in the peripheral blood (not strong, i.e., CD14(low)), with plasma levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β, IL-6, IL-8, IL-10, and IL-12p70 compared with 22 healthy controls. After stimulation by lipopolysaccharide (LPS), the plasma cytokine response was also compared.In the basal state, the percentage of peripheral blood TLR4(+)CD14(low) monocytes and plasma cytokines were significantly higher in HD patients (p 0.05), suggesting that preactivated primed monocytes might be responsible for the chronic inflammatory state in HD patients. However, upon LPS challenge, the fold increase in plasma cytokine response was significantly reduced in HD patients (p 0.05) compared with controls. More importantly, the fold increase of these cytokines showed a positive correlation with plasma albumin (p 0.05) and a negative correlation with C-reactive protein (CRP) (p 0.05), suggesting the presence of a possible link between chronic low-grade inflammation and suboptimal innate immune response.Chronic low-grade inflammation due to preactivated peripheral blood CD14(+) leukocyte subset might be a mechanism for impaired innate immune responses, thus resulting in the high rates of infection-related morbidity and mortality observed in HD patients.

As the industry progresses toward smaller patterning nodes with tighter CD error budgets and narrower process windows, the ability to control pattern quality becomes a critical, yield-limiting factor. In addition, as the feature size of design layouts continues to decrease at 32nm and below, optical proximity correction (OPC) technology becomes more complex and more difficult. From a lithographic point of view, it is the most important that the patterns are printed as designed. However, unfavorable localized CD variation can be induced by the lithography process, which will cause catastrophic patterning failures (i.e. ripple effects, and severe necking or bridging phenomenon) through process variation. It is becoming even more severe with strong off-axis illumination conditions and other resolution enhancement techniques (RETs). Traditionally, it can be reduced by optimizing the rule based edge fragmentation in the OPC setup, but this fragmentation optimization is very dependent upon the engineer's skill. Most fragmentation is based on a set of simple rules, but those rules may not always be robust in every possible design shape. In this paper, a model based approach for solving these imaging distortions has been tested as opposed to a previous rule based one. The model based approach is automatic correction techniques for reducing complexity of the OPC recipe. This comes in the form of automatically adjusting fragments lengths along with feedback values at every OPC iterations for a better convergence. The stability and coverage for this model based approach has been tested throughout various layout cases.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a prototypic halogenated aromatic hydrocarbon (HAH), is known as one of the most potent toxicants. At least a part of its toxic effects appears to be derived from its ability to induce TNF-alpha production. However, the signaling pathway of TCDD that leads to TNF-alpha expression has not been elucidated. In this study, we investigated the signaling mechanism of TCDD-induced TNF-alpha expression in PMA-differentiated THP-1 macrophages. TCDD induced both mRNA and protein expression of TNF-alpha in a dose- and time-dependent manner. Alpha-naphthoflavone (NF), an aryl hydrocarbon receptor (AhR) inhibitor, prevented the TCDD-induced expression of TNF-alpha at both mRNA and protein levels. Genistein, a protein tyrosine kinase (PTK) inhibitor, and PD153035, an EGFR inhibitor, also blocked the increase of TNF-alpha expression by TCDD, indicating the role of EGFR in TCDD-induced TNF-alpha expression. On the other hand, PP2, a c-Src specific inhibitor, did not affect TCDD-induced TNF-alpha expression. EGFR phosphorylation was detected as early as 5 min after TCDD treatment. TCDD-induced EGFR activation was AhR-dependent since co-treatment with alpha-NF prevented it. ERK was found to be a downstream effector of EGFR activation in the signaling pathway leading to TNF-alpha production after TCDD stimulation. Activation of ERK was observed from 30 min after TCDD treatment. PD98059, an inhibitor of the MEK-ERK pathway, completely prevented the TNF-alpha mRNA and protein expression induced by TCDD, whereas inhibitors of JNK and p38 MAPK had no effect. PD153035, an EGFR inhibitor, as well as alpha-NF significantly reduced ERK phosphorylation, suggesting that ERK activation by TCDD was mediated by both EGFR and AhR. These results indicate that TNF-alpha production by TCDD in differentiated THP-1 macrophages is AhR-dependent and involves activation of EGFR and ERK, but not c-Src, JNK, nor p38 MAPK. A signaling pathway is proposed where TCDD induces sequential activation of AhR, EGFR and ERK, leading to the increased expression of TNF-alpha.

Density variation of nanoscale patterns in thermal nanoimprint lithography was studied both by experiments and molecular dynamics simulations. A simple soft imprinting technique was used to fabricate various nanopatterns (70nm and 600nm lines and 150nm dots) over a large area (2×3cm2). Local density was measured by the relative magnitude of van der Waals interactions between a sharp tip and the patterned surface. In order to investigate the mechanism of density variation, molecular dynamic simulations were performed. Experimental and simulation results demonstrated that the density of the pressed region (valleys) was higher than that of the cavity region (hills) when a simple amorphous polymer is thermally imprinted with a patterned mold.