N G van Kampen 1981 Amsterdam: North-Holland xiv + 419 pp price Dfl 180 This is a book which, at a lower price, could be expected to become an essential part of the library of every physical scientist concerned with problems involving fluctuations and stochastic processes, as well as those who just enjoy a beautifully written book. It provides an extensive graduate-level introduction which is clear, cautious, interesting and readable.

https://iopscience.iop.org/article/10.1088/0031-9112/34/4/040/pdf

Stochastic Processes in Physics and Chemistry

Course Description This is an advanced course in which we explore the field of Statistical Optics. Topics covered include such subjects as the statistical properties of natural (thermal) and laser light, spatial and temporal coherence, effects of partial coherence on optical imaging instruments, effects on imaging due to randomly inhomogeneous media, and a statistical treatment of the detection of light. Development of this more comprehensive model of the behavior of light draws upon the use of tools traditionally available to the electrical engineer, such as linear system theory and the theory of stochastic processes.

http://ieeexplore.ieee.org/iel5/3/23094/01073023.pdf

Statistical optics

/pdf/the-black-swan-the-impact-of-the-highly-improbable-578rzpihbf.pdf

The Black Swan: The Impact of the Highly Improbable

Diffusion and Reactions in Fractals and Disordered Systems

Background: Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this. Objectives: To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids. Search methods: We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors. Selection criteria: We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake. Data collection and analysis: Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression. Main results: We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias. Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet. Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence), cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs), cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence), coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs), stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials) or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs). There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk. All evidence was of moderate GRADE quality, except as noted. Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence). However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT). Effects on stroke are unclear. Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection. LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes. There were no dose or duration effects in subgrouping or meta-regression. There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence). Authors' conclusions: This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.

/pdf/omega-3-fatty-acids-for-the-primary-and-secondary-prevention-1cmrctwm4e.pdf

Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease.

The shot noise, line edge roughness (LER) and quantum efficiency of EUV interaction with seven resists related to EUV-2D (SP98248B) are studied. These resists were identical to EUV-2D except were prepared with seven levels of added base while keeping all other resist variables constant. These seven resists were patterned with EUV lithography, and LER was measured on 100-200 nm dense lines. Similarly, the resists were also imaged using DUV lithography and LER was determined for 300-500 nm dense lines. LER results for both wavelengths were plotted against Esize. Both curves show very similar LER behavior-the resists requiring low doses have poor LER, whereas the resists requiring high doses have good LER. One possible explanation for the observed LER response is that the added base improves LER by reacting with the photogenerated acid to control the lateral spread of acid, leading to better chemical contrast at the line edge.
An alternative explanation to the observed relationship between LER and Esize is that shot-noise generated LER decreases as the number of photons absorbed at the line edge increases. We present an analytical model for the influence of shot noise based on Poisson statistics that preidicts that the LER is proportional to (Esize)-1/2. Indeed, both sets of data give straight lines when plotted this way (DUV r2 = 0.94; EUV r2 = 0.97). We decided to further evaluate this interpretation by constructing a simulation model for shot noise resulting from exposure and acid diffusion at the mask edge. In order to acquire the data for this model, we used the base titration method developed by Szmanda et al. to determine C-parameters and hence the quantum efficiency for producing photogenerated acid. This information, together with film absorptivity, allows the calculation of number and location of acid molecules generated at the mask edgte by assuming a stochastic distribution of individual photons corresponding to the aerial image function. The edge "roughness" of the acid molecule distribution in the film at the mask edge is then simulated as a function of acid diffusion length and compared to the experimental data. In addition, comparisoins between of the number of acid molecules generated and photons consumed leads to values of quantum efficiencies for these EUV resists.

Shot noise, LER, and quantum efficiency of EUV photoresists

Double patterning (DP) appears to be the most probable patterning technology for initial
32 nm node manufacturing. This work explores how it may be accurately simulated. In the first
instance, the process is approximated using two planar exposures in a commercial lithographic
simulation package. This work is then followed up by more accurate calculations using a
prototype simulator (based of Rigorous Coupled Wave Analysis propagation techniques) which
allows the topography generated from the first exposure pass to influence the light propagation in
the second exposure. The accuracy of the prototype simulator is demonstrated by validating its'
output against the vector model in PROLITH V10, for the planar topography case. Results from
the RCWA simulations show that for an example poly gate double patterning process, the
presence of the topography enhances the process window of the second exposure, in terms of
both exposure and focus latitude. The topography simulator is also used to study the robustness
of the second exposure process window to fluctuations in the CD printed during the first
exposure pass and of the influence of misalignment between the two passes.

The Modeling of Double Patterning Lithographic Processes

Lithography simulators have become a standard tool in industrial and governmental research and development departments. In contrast to the modeling approaches for the optical system and for the lithographic performance of i-line resists, there is still no consensus on the modeling of chemically amplified resists (CAR). Existing models differ in the description of the kinetics and the diffusion phenomena during post exposure bake (PEB) and in the specification of the development rate. A modeling approach was established, that combines the light induced generation of photoacid, in- and outdiffusion of acid or base components, a generalized deprotection kinetics, Fickian and non-Fickian diffusion of resist components and an arbitrary development rate model. Existing models such as the effective acid model and a standard deprotection model for CAR can be considered as special cases of the implemented model. To evaluate the importance of certain options of the model and of the model parameters we have evaluated the performance of the model by comparing simulated CD data and resist profiles with experimental data.

Comparison of simulation approaches for chemically amplified resists

Requirements of resist modeling strategies for EUV and low-k1 ArF nanolithography continue to become
more stringent. Resist designers are consistently faced with the task of reducing exposure dose and line
roughness while simultaneously improving exposure latitude, depth-of-focus and ultimate resolution.
In this work, we briefly discuss a next-generation resist model for the prediction of statistical resist
responses such as line-edge roughness, line-width roughness and CD variability, as well as base
lithographic responses such as exposure latitude. The model's parameterized fit to experimental data from a
state-of-the art polymer-bound PAG resist irradiated at ArF and EUV will be shown. The probabilistic
computation of acid generation at ArF and EUV will be discussed. The factors influencing the
hypothesized primary cause of resist roughness, acid shot noise, are discussed.

Statistical simulation of photoresists at EUV and ArF

Background The effect and association of omega-3 fatty acids (n-3 FA) intake and biomarker levels with cardiovascular (CV) clinical and intermediate outcomes remains controversial. We update prior Evidence Reports of n-3 FA and clinical and intermediate CV disease (CVD) outcomes. Objectives Evaluate the effect of n-3 FA on clinical and selected intermediate CV outcomes and the association of n-3 FA intake and biomarkers with CV outcomes. The n-3 FA under review include eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), stearidonic acid (SDA), and alphalinolenic acid (ALA). Data sources MEDLINE®, Embase®, the Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and CAB Abstracts from 2000 or 2002 to June 8, 2015, and eligible studies from the original reports and relevant existing systematic reviews. Review methods We included randomized controlled trials (RCTs) of any n-3 FA intake compared to no, lower, or other n-3 FA intake with an outcome of interest conducted in healthy adults, those at risk for CVD, or those with CVD. We also included prospective observational studies of the association between baseline n-3 FA intake or biomarker level and followup outcomes. We required 1 year or more of followup for clinical outcomes and 4 weeks for intermediate outcomes (blood pressure [BP] and lipids). Results From 11,440 citations (from electronic literature searches and existing systematic reviews), 829 abstracts met basic eligibility criteria; 61 RCTs and 37 longitudinal observational studies (in 147 articles) were included. Most RCTs and observational studies had few risk-of-bias concerns. Total n-3 FA: There is low strength of evidence (SoE) of no association between total n-3 FA intake and stroke death or myocardial infarction. There is insufficient evidence for other outcomes.Marine oils, total: There is moderate to high SoE that higher marine oil intake lowers triglycerides (Tg), raises high density lipoprotein cholesterol (HDL-c), and lowers the ratio of total cholesterol to HDL-c but raises low density lipoprotein cholesterol (LDL-c); also that higher marine oil intake does not affect major adverse CV events, all-cause death, total stroke, sudden cardiac death, coronary revascularization, atrial fibrillation, or BP. There is low SoE of associations between higher marine oil intake and decreased risk of CVD death, coronary heart disease (CHD), myocardial infarction, ischemic stroke, and congestive heart failure (CHF). There is low SoE of no association with CHD death or hemorrhagic stroke. There is insufficient evidence for other outcomes.Marine oil FA individually: There is low SoE of no associations between EPA or DHA intake (separately) and CHD, and between EPA or DPA and atrial fibrillation. There is low SoE of no association between EPA biomarkers and atrial fibrillation, but moderate SoE of no effect of purified DHA supplementation on BP or LDL-c. There is insufficient evidence for other specific marine oil FA and outcomes.ALA: There is moderate SoE of no effect of ALA intake on BP, LDL-c, HDL-c, or Tg. There is low SoE of no association between ALA intake or biomarker level and CHD, CHD death, atrial fibrillation, and CHF. There is insufficient evidence for other outcomes.Other n-3 FA analyses: There is insufficient evidence comparing n-3 FA with each other or for SDA.Subgroup analyses: Nineteen of 22 studies found no interaction of sex on any effect of n-3 FA. Likewise, 19 of 20 studies found no differential effect by statin co-use. Within 16 studies evaluating diabetes subgroups, 2 found statistically significant beneficial effects of n-3 FA in those with diabetes but not in those without diabetes, but no test of interaction was reported. Conclusions The 61 RCTs mostly compared marine oil supplements with placebo on CVD outcomes in populations at risk for CVD or with CVD, while the 37 observational studies mostly examined associations between various individual n-3 FA and long-term CVD events in generally healthy populations. Compared with the prior report on n-3 FA and CVD, there is more robust RCT evidence on ALA and on clinical CV outcomes; also, by design there are newly added data on associations between n-3 FA biomarkers and CV outcomes. However, conclusions regarding the effect of n-3 FA intake on CV outcomes or associations with outcomes remain substantially unchanged. Marine oils statistically significantly raise HDL-c and LDL-c by similar amounts (≤2 mg/dL), while lowering Tg in a dose-dependent manner, particularly in individuals with elevated Tg; they have no significant effect on BP. ALA has no significant effect on intermediate outcomes. Limited data were available from RCTs on the effect of n-3 FA on clinical CVD outcomes. Observational studies suggest that higher marine oil intake (including from dietary fish) is associated with lower risk of several CVD outcomes. No clear differences in effects or associations were evident based on population, demographic features, or cointerventions. Future RCTs would be needed to establish adequate evidence of the effect of n-3 FA on CVD outcomes or to clarify differential effects in different groups of people. However, future trials are unlikely to alter conclusions about the effects of n-3 FA supplementation on intermediate cardiovascular outcomes (BP, LDL-c, HDL-c, or Tg).

Stewart A. Robertson

Papers

Shot noise, LER, and quantum efficiency of EUV photoresists

The Modeling of Double Patterning Lithographic Processes

Comparison of simulation approaches for chemically amplified resists

Statistical simulation of photoresists at EUV and ArF

Omega-3 Fatty Acids and Cardiovascular Disease: An Updated Systematic Review.