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Background Construction of networks from cross-sectional biological data is increasingly common. Many recent methods have been based on Gaussian graphical modeling, and prioritize estimation of conditional pairwise dependencies among nodes in the network. However, challenges remain on how specific paths through the resultant network contribute to overall ‘network-level’ correlations. For biological applications, understanding these relationships is particularly relevant for parsing structural information contained in complex subnetworks. Results We propose the pair-path subscore (PPS), a method for interpreting Gaussian graphical models at the level of individual network paths. The scoring is based on the relative importance of such paths in determining the Pearson correlation between their terminal nodes. PPS is validated using human metabolomics data from the Hyperglycemia and adverse pregnancy outcome (HAPO) study, with observations confirming well-documented biological relationships among the metabolites. We also highlight how the PPS can be used in an exploratory fashion to generate new biological hypotheses. Our method is implemented in the R package , available at https://github.com/nathan-gill/pps. Conclusions The PPS can be used to probe network structure on a finer scale by investigating which paths in a potentially intricate topology contribute most substantially to marginal behavior. Adding PPS to the network analysis toolkit may enable researchers to ask new questions about the relationships among nodes in network data.

Background Whether differences in circulating long chain acylcarnitines (LCAC) are seen in heart failure (HF) patients with and without diabetes mellitus (DM), and whether these biomarkers report on exercise capacity and clinical outcomes, remains unknown. The objective of the current study was to use metabolomic profiling to identify biomarkers that report on exercise capacity, clinical outcomes, and differential response to exercise in HF patients with and without DM. Methods Targeted mass spectrometry was used to quantify metabolites in plasma from participants in the heart failure: a controlled trial investigating outcomes of exercise training (HF-ACTION) trial. Principal components analysis was used to identify 12 uncorrelated factors. The association between metabolite factors, diabetes status, exercise capacity, and time to the primary clinical outcome of all-cause mortality or all-cause hospitalization was assessed. Results A total of 664 participants were included: 359 (54%) with DM. LCAC factor levels were associated with baseline exercise capacity as measured by peak oxygen consumption (beta 0.86, p = 2 × 10−7, and were differentially associated in participants with and without DM (beta 1.58, p = 8 × 10−8 vs. 0.67, p = 9 × 10−4, respectively; p value for interaction = 0.012). LCAC levels changed to a lesser extent in participants with DM after exercise (mean ∆ 0.09, p = 0.24) than in those without DM (mean ∆ 0.16, p = 0.08). In univariate and multivariate modeling, LCAC factor levels were associated with time to the primary outcome (multivariate HR 0.80, p = 2.74 × 10−8), and were more strongly linked to outcomes in diabetic participants (HR 0.64, p = 3.21 × 10−9 v. HR 0.90, p = 0.104, p value for interaction = 0.001). When analysis was performed at the level of individual metabolites, C16, C16:1, C18, and C18:1 had the greatest associations with both exercise capacity and outcomes, with higher levels associated with worse outcomes. Similar associations with time to the primary clinical outcome were not found in a control group of patients without HF from the CATHeterization GENetics (CATHGEN) study. Conclusions LCAC biomarkers are associated with exercise status and clinical outcomes differentially in HF patients with and without DM. Impaired fatty acid substrate utilization and mitochondrial dysfunction both at the level of the skeletal muscle and the myocardium may explain the decreased exercise capacity, attenuated response to exercise training, and poor clinical outcomes seen in patients with HF and DM. Trial Registration clinicaltrials.gov Identifier: NCT00047437.

We sought to determine if novel plasma biomarkers improve traditionally defined metabolic health (MH) in predicting risk of cardiovascular disease (CVD) events irrespective of weight. Poor MH was defined in CATHGEN biorepository participants (n > 9300), a follow-up cohort (> 5600 days) comprising participants undergoing evaluation for possible ischemic heart disease. Lipoprotein subparticles, lipoprotein-insulin resistance (LP-IR), and GlycA were measured using NMR spectroscopy (n = 8385), while acylcarnitines and amino acids were measured using flow-injection, tandem mass spectrometry (n = 3592). Multivariable Cox proportional hazards models determined association of poor MH and plasma biomarkers with time-to-all-cause mortality or incident myocardial infarction. Low-density lipoprotein particle size and high-density lipoprotein, small and medium particle size (HMSP), GlycA, LP-IR, short-chain dicarboxylacylcarnitines (SCDA), and branched-chain amino acid plasma biomarkers were independently associated with CVD events after adjustment for traditionally defined MH in the overall cohort (p = 3.3 × 10−4–3.6 × 10−123), as well as within most of the individual BMI categories (p = 8.1 × 10−3–1.4 × 10−49). LP-IR, GlycA, HMSP, and SCDA improved metrics of model fit analyses beyond that of traditionally defined MH. We found that LP-IR, GlycA, HMSP, and SCDA improve traditionally defined MH models in prediction of adverse CVD events irrespective of BMI.

AIMS/HYPOTHESIS: We aimed to determine the association of maternal metabolites with newborn adiposity and hyperinsulinaemia in a multi-ethnic cohort of mother–newborn dyads. METHODS: Targeted and non-targeted metabolomics assays were performed on fasting and 1 h serum samples from a total of 1600 mothers in four ancestry groups (Northern European, Afro-Caribbean, Mexican American and Thai) who participated in the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study, underwent an OGTT at ~28 weeks gestation and whose newborns had anthropometric measurements at birth. RESULTS: In this observational study, meta-analyses demonstrated significant associations of maternal fasting and 1 h metabolites with birthweight, cord C-peptide and/or sum of skinfolds across ancestry groups. In particular, maternal fasting triacylglycerols were associated with newborn sum of skinfolds. At 1 h, several amino acids, fatty acids and lipid metabolites were associated with one or more newborn outcomes. Network analyses revealed clusters of fasting acylcarnitines, amino acids, lipids and fatty acid metabolites associated with cord C-peptide and sum of skinfolds, with the addition of branched-chain and aromatic amino acids at 1 h. CONCLUSIONS/INTERPRETATION: The maternal metabolome during pregnancy is associated with newborn outcomes. Maternal levels of amino acids, acylcarnitines, lipids and fatty acids and their metabolites during pregnancy relate to fetal growth, adiposity and cord C-peptide, independent of maternal BMI and blood glucose levels.

Heat-assisted magnetic recording (HAMR) relies on careful management of heat flow at the nanoscale. This article describes the heat-transfer aspects of such a system that must be considered above and beyond standard Fourier’s Law-based heat conduction. A background on nanoscale heat transport is provided that discusses energy carriers and the role of interfaces and microstructure in nanoscale conduction. These heat-transport concepts are applied to the key components of the HAMR system—the head (principally, the near-field transducer [NFT]) and the magnetic medium. This analysis frames the central challenge of thermal engineering for a HAMR system—getting the medium hot enough while maintaining a NFT that it is cool enough to avoid degradation over time. Of particular note are discussions on the role of the interface thermal conductance in the NFT and the importance of thermal anisotropy in the medium due to its granular microstructure.

Growth failure during infancy is a major global problem that has adverse effects on long-term health and neurodevelopment. Preterm infants are disproportionately affected by growth failure and its effects. Herein we found that extremely preterm infants with postnatal growth failure have disrupted maturation of the intestinal microbiota, characterized by persistently low diversity, dominance of pathogenic bacteria within the Enterobacteriaceae family, and a paucity of strictly anaerobic taxa including Veillonella relative to infants with appropriate postnatal growth. Metabolomic profiling of infants with growth failure demonstrated elevated serum acylcarnitines, fatty acids, and other byproducts of lipolysis and fatty acid oxidation. Machine learning algorithms for normal maturation of the microbiota and metabolome among infants with appropriate growth revealed a pattern of delayed maturation of the microbiota and metabolome among infants with growth failure. Collectively, we identified novel microbial and metabolic features of growth failure in preterm infants and potentially modifiable targets for intervention.

Maternal obesity increases the risk for large-for-gestational-age birth and excess newborn adiposity, which are associated with adverse long-term metabolic outcomes in offspring, probably due to effects mediated through the intrauterine environment. We aimed to characterise the maternal metabolic milieu associated with maternal BMI and its relationship to newborn birthweight and adiposity.Fasting and 1 h serum samples were collected from 400 European-ancestry mothers in the Hyperglycaemia and Adverse Pregnancy Outcome Study who underwent an OGTT at ∼28 weeks gestation and whose offspring had anthropometric measurements at birth. Metabolomics assays were performed using biochemical analyses of conventional clinical metabolites, targeted MS-based measurement of amino acids and acylcarnitines and non-targeted GC/MS.Per-metabolite analyses demonstrated broad associations with maternal BMI at fasting and 1 h for lipids, amino acids and their metabolites together with carbohydrates and organic acids. Similar metabolite classes were associated with insulin resistance with unique associations including branched-chain amino acids. Pathway analyses indicated overlapping and unique associations with maternal BMI and insulin resistance. Network analyses demonstrated collective associations of maternal metabolite subnetworks with maternal BMI and newborn size and adiposity, including communities of acylcarnitines, lipids and related metabolites, and carbohydrates and organic acids. Random forest analyses demonstrated contribution of lipids and lipid-related metabolites to the association of maternal BMI with newborn outcomes.Higher maternal BMI and insulin resistance are associated with broad-based changes in maternal metabolites, with lipids and lipid-related metabolites accounting, in part, for the association of maternal BMI with newborn size at birth.

One major challenge in efficiently implementing neuromorphic networks is the need for a large number of variable synaptic connections. Networks that use emerging resistive memories as synapses have been proposed to tackle this problem, but interfacing with these devices is still inefficient in deeply-scaled CMOS. Oscillatory Neural Networks (ONNs) use a different paradigm than most analog hardware implementations, and may be able to interface more efficiently with RRAM neurons. Previous work on ONNs, however, has not considered the effects of actual hardware implementation realities, such as delay in the network. In this work, the first reported IC implementation of an oscillatory neural network is designed and fabricated. Modifications are made to the ONN architecture based on theoretical analysis to allow for proper operation in real-world conditions. One modification is changing the PLL-type, giving the system a different dynamic trajectory which is robust to global delays. Additionally, circuitry is added to control the transport delay of the neuron output signals. A chip with the modified ONN architecture is designed and tested in 28 nm CMOS and estimated power and area figures are reported.

Background: Few studies have investigated the effects of exercise on modulation of host factors in cancer patients. We investigated the efficacy of chronic aerobic training on multiple host-related effector pathways in patients with solid tumours. Patients and Methods: Paired peripheral blood samples were obtained from 44 patients with solid tumours receiving cytotoxic therapy and synthetic erythropoietin (usual care; n=21) or usual care plus supervised aerobic training (n=23) for 12 weeks. Samples were characterised for changes in immune, cytokine and angiogenic factors, and metabolic intermediates. Aerobic training consisted of three supervised cycle ergometry sessions per week at 60% to 100% of peak oxygen consumption (VO2peak), 30–45 min per session, for 12 weeks following a nonlinear prescription. Results: The between-group delta change in cardiopulmonary function was +4.1 ml kg −1 min−1, favouring aerobic training (P

The muscle-specific ubiquitin ligases MuRF1, MuRF2, MuRF3 have been reported to have overlapping substrate specificities, interacting with each other as well as proteins involved in metabolism and cardiac function. In the heart, all three MuRF family proteins have proven critical to cardiac responses to ischemia and heart failure. The non-targeted metabolomics analysis of MuRF1-/-, MuRF2-/-, and MuRF3-/- hearts was initiated to investigate the hypothesis that MuRF1, MuRF2, and MuRF3 have a similarly altered metabolome, representing alterations in overlapping metabolic processes. Ventricular tissue was flash frozen and quantitatively analyzed by GC/MS using a library built upon the Fiehn GC/MS Metabolomics RTL Library. Non-targeted metabolomic analysis identified significant differences (via VIP statistical analysis) in taurine, myoinositol, and stearic acid for the three MuRF-/- phenotypes relative to their matched controls. Moreover, pathway enrichment analysis demonstrated that MuRF1-/- had significant changes in metabolite(s) involved in taurine metabolism and primary acid biosynthesis while MuRF2-/- had changes associated with ascorbic acid/aldarate metabolism (via VIP and t-test analysis vs. sibling-matched wildtype controls). By identifying the functional metabolic consequences of MuRF1, MuRF2, and MuRF3 in the intact heart, non-targeted metabolomics analysis discovered common pathways functionally affected by cardiac MuRF family proteins in vivo. These novel metabolomics findings will aid in guiding the molecular studies delineating the mechanisms that MuRF family proteins regulate metabolic pathways. Understanding these mechanism is an important key to understanding MuRF family proteins' protective effects on the heart during cardiac disease.

Magnetoresistance having a field and current dependence like that of GMR (but a rather small magnitude) has been observed in Co70Fe30/GeTe and Co70Fe30/Ge2Sb2Te5 granular films. Film stacks were fabricated using tandem (multilayer) deposition and annealing was required for the films to develop the GMR-type response. This GMR-type behavior is distinct from AMR, which is observed before annealing. With films having the structure [CoFe 4 nm/GeTe 6 nm]10, a magnetoresistance (MR) of 0.19 %, which has the GMR-type character can be observed after an optimal annealing temperature of 450 °C. TEM and X-ray reflectometry suggest that columnar granules with layered Fe form during deposition and with annealing. Magnetoresistive transport is believed to be between the discontinuous layers in each columnar grain. These discontinuous layers are observed to be superparamagnetic in SQUID ZFC-FC measurements measured from 5–300 K. Magnetoresistance can be fitted by the quadratic relation appropriate for GMR in granular films, especially at higher GeTe compositions. When Ge2Sb2Te5 is used instead of GeTe, higher anneal temperatures are required before the MR with GMR character appears. This GMR type response does not appear when pure Fe is used instead of the CoFe alloy, with the samples showing only AMR in this case. This is due to the absence of Co which seems to cause a more granular growth.

Older patients are more likely to acquire and die from acute respiratory distress syndrome (ARDS) and muscle weakness may be more clinically significant in older persons. Recent data implicate muscle ring finger protein 1 (MuRF1) in lung injury-induced skeletal muscle atrophy in young mice and identify an alternative role for MuRF1 in cardiac metabolism regulation through inhibition of fatty acid oxidation. To develop a model of lung injury-induced muscle wasting in old mice and to evaluate the skeletal muscle metabolomic profile of adult and old acute lung injury (ALI) mice. Young (2 month), adult (6 month) and old (20 month) male C57Bl6 J mice underwent Sham (intratracheal H2O) or ALI [intratracheal E. coli lipopolysaccharide (i.t. LPS)] conditions and muscle functional testing. Metabolomic analysis on gastrocnemius muscle was performed using gas chromatography-mass spectrometry (GC–MS). Old ALI mice had increased mortality and failed to recover skeletal muscle function compared to adult ALI mice. Muscle MuRF1 expression was increased in old ALI mice at day 3. Non-targeted muscle metabolomics revealed alterations in amino acid biosynthesis and fatty acid metabolism in old ALI mice. Targeted metabolomics of fatty acid intermediates (acyl-carnitines) and amino acids revealed a reduction in long chain acyl-carnitines in old ALI mice. This study demonstrates age-associated susceptibility to ALI-induced muscle wasting which parallels a metabolomic profile suggestive of altered muscle fatty acid metabolism. MuRF1 activation may contribute to both atrophy and impaired fatty acid oxidation, which may synergistically impair muscle function in old ALI mice.

Chronic hypersecretion of the 37 amino acid amylin is common in type 2 diabetics (T2D). Recent studies implicate human amylin aggregates cause proteotoxicity (cell death induced by misfolded proteins) in both the brain and the heart. Identify systemic mechanisms/markers by which human amylin associated with cardiac and brain defects might be identified. We investigated the metabolic consequences of amyloidogenic and cytotoxic amylin oligomers in heart, brain, liver, and plasma using non-targeted metabolomics analysis in a rat model expressing pancreatic human amylin (HIP model). Four metabolites were significantly different in three or more of the four compartments (heart, brain, liver, and plasma) in HIP rats. When compared to a T2D rat model, HIP hearts uniquely had significant DECREASES in five amino acids (lysine, alanine, tyrosine, phenylalanine, serine), with phenylalanine decreased across all four tissues investigated, including plasma. In contrast, significantly INCREASED circulating phenylalanine is reported in diabetics in multiple recent studies. DECREASED phenylalanine may serve as a unique marker of cardiac and brain dysfunction due to hyperamylinemia that can be differentiated from alterations in T2D in the plasma. While the deficiency in phenylalanine was seen across tissues including plasma and could be monitored, reduced tyrosine was seen only in the brain. The 50 % reduction in phenylalanine and tyrosine in HIP brains is significant given their role in supporting brain chemistry as a precursor for catecholamines (dopamine, norepinephrine, epinephrine), which may contribute to the increased morbidity and mortality in diabetics at a multi-system level beyond the effects on glucose metabolism.

Insulin resistance (IR) improves with weight loss, but this response is heterogeneous. We hypothesised that metabolomic profiling would identify biomarkers predicting changes in IR with weight loss.Targeted mass spectrometry-based profiling of 60 metabolites, plus biochemical assays of NEFA, β-hydroxybutyrate, ketones, insulin and glucose were performed in baseline and 6 month plasma samples from 500 participants who had lost ≥4 kg during Phase I of the Weight Loss Maintenance (WLM) trial. Homeostatic model assessment of insulin resistance (HOMA-IR) and change in HOMA-IR with weight loss (∆HOMA-IR) were calculated. Principal components analysis (PCA) and mixed models adjusted for race, sex, baseline weight, and amount of weight loss were used; findings were validated in an independent cohort of patients (n = 22).Mean weight loss was 8.67 ± 4.28 kg; mean ∆HOMA-IR was -0.80 ± 1.73, range -28.9 to 4.82). Baseline PCA-derived factor 3 (branched chain amino acids [BCAAs] and associated catabolites) correlated with baseline HOMA-IR (r = 0.50, p0.0001) and independently associated with ∆HOMA-IR (p0.0001). ∆HOMA-IR increased in a linear fashion with increasing baseline factor 3 quartiles. Amount of weight loss was only modestly correlated with ∆HOMA-IR (r = 0.24). These findings were validated in the independent cohort, with a factor composed of BCAAs and related metabolites predicting ∆HOMA-IR (p = 0.007).A cluster of metabolites comprising BCAAs and related analytes predicts improvement in HOMA-IR independent of the amount of weight lost. These results may help identify individuals most likely to benefit from moderate weight loss and elucidate novel mechanisms of IR in obesity.

A model that describes the homogeneous migration of oxygen vacancies as a function of electric field, temperature, and activation energy of diffusion was used to investigate the resistance switching and retention characteristics of memristive SrTiO3 Schottky devices. Numerical simulations suggest that, though ionic motion results in switching, it is not possible to meet the criteria of fast switching and long retention simultaneously; conditions that lead to sufficiently fast switching also lead to unacceptably fast decays of programmed states. However, an operational window is found when a term accounting for local enhancement of electric field in the dielectric is included. A discussion of the appropriateness of this inclusion is provided.

Background Mechanisms involved in regulating metabolic reprogramming in cancer cells are not fully understood. Acetylation is emerging as a major regulator of mitochondrial metabolism and may contribute to metabolic derangements that occur in cancer cells. Sirtuin-3, (SIRT3), is the main mitochondrial deacetylase and it serves to maintain mitochondrial energy homeostasis by deacetylating and activating mitochondrial proteins. Loss of SIRT3 leads to altered cellular metabolism including reduced ATP production and decreased fatty acid oxidation [1]. Remarkably, reduced SIRT3 expression is associated with cancer in patients and Sirt3 knockout mice [2]. However, the mechanism of mitochondrial protein hyperacetylation and the sub-sequent increased susceptibility to tumor formation remains unknown.

Thin film stresses are important in many areas of technology. In the semiconductor industry, metal interconnects are prone to stress voiding and hillock formation. Stresses in passivation layers can lead to excessive substrate curvature which can cause alignment difficulty in subsequent lithographic processing. In other thin film applications, stresses can cause peeling from mechanical failure at the film-substrate interface. Beyond these issues of reliability, stress and the resulting strain can be used to tune the properties of thin film materials. For instance, strain, coupled with the magnetostrictive effect, can be utilized to induce the preferred magnetization direction. Also, epitaxial strains can be used to adjust the bandgap of semiconductors. Finally, the anomalous mechanical properties of multilayered materials are thought to be partially due to the extreme strain states in the constituents of these materials. To fully optimize thin film performance, a fundamental understanding of the causes and effects of thin film stress is needed. These studies in turn rely on detailed characterization of the stress and strain state of thin films.X-ray diffraction and the elastic response of materials provide a powerful method for determining stresses. Stresses alter the spacing of crystallographic planes in crystals by amounts easily measured by x-ray diffraction. Each set of crystal planes can act as an in-situ strain gauge, which can be probed by x-ray diffraction in the appropriate geometry. Hence it is not surprising that x-ray diffraction is one of the most widely used techniques for determining stress and strain in materials. (For reviews of this topic, see References 5–7.) This article is a tutorial on the use of x-ray diffraction to extract the stress state and the unstrained lattice parameter from thin films. We present a handbook of useful results that can be widely applied and should be mastered by anyone seriously interested in stresses in crystalline thin films with a crystallographic growth texture.

The heteropitaxial growth of (111) Pt on (0001) sapphire and of (0001) Co on (111) Pt on (0001) sapphire has been observed in-situ using grazing incidence x-ray scattering (GIXS). The in-plane lattice parameters of the Pt and Co phases have been measured as a function of film thickness in the regime from two monolayers to 200 monolayers, Relaxation of elastic strain with thickness has been quantified. X-ray reflections consistent with stacking faults in the Co films have been observed and monitored as a function of thickness, giving a measure of the stacking fault density. A distinct Co phase was observed at two monolayers of Co on a thick Pt layer, indicating an incoherent interface between the Co and Pt, even at this very early stage of deposition.

Structural features in magnetic multilayer films such as interfacial sharpness and in-plane stress are regarded as responsible for the perpendicular magnetic anisotropy observed in these films. The Multilayers often consist of alternating magnetic and non-Magnetic layers, and the degree of interfacial sharpness between the two is a critical component in producing perpendicular anisotropy. Additionally, in-plane stress affects the anisotropy through Magnetostriction. In this work, we measure both the composition modulation and the stress in multilayers of Pt/CO with x-ray diffraction. Quantitative information about the composition modulation is extracted by recursively fitting a model of multilayer diffraction to the high angle superlattice lines. The Model incorporates a composition modulation of variable amplitude, along with a statistical description of the layer thickness fluctuations.

The strain relaxation of sputter-deposited epitaxial Fe on Cu(001)/MgO(001) was observed in-situ for coverages of I to 200 equivalent monolayers of Fe. Grazing incidence x-ray scattering (GIXS) with synchrotron radiation allowed the precise determination of the in-plane strain in the Fe film. The highest observed elastic strain for the Fe was -10.3% which is in agreement with the lattice parameter mismatch between Fe and Cu for both (001)- and {211}-oriented growth. In-plane rocking curves revealed a bifurcation of the Fe(110) and Fe(220) peaks which is due to the rotation of islands to reduce strain energy. The angle of rotation of these islands was found to depend upon the amount of strain relaxation that had occurred in each island, in agreement with a simple theory for strain relaxation via the creation of a misfit dislocation network. The absence of Fe(200) intensity at small Fe thicknesses, coupled with out-of-plane symmetric and pole figure scans, suggest that Fe islands are tilted out of the plane of the sample about the Fe axes by an angle consistent with Fe{211}-oriented growth. At larger thicknesses Fe(001) growth becomes dominant.

We consider the anisotropies due to coherency strains and the inilioliogcliotis stratlus associated with misfit dislocations, both of which give rise to anisotropy through maguctostrictive coupling. Coherency strains can give rise to anl apparent surface anisotrnpy due to the decrease in coherency strain with the film thickness. This anisotropy is comparable in magnitude to that observed experimentally for Fe [110] epitaxial thiut films on W [110]. The strain field associated with misfit dislocations produces a. surface anisotropy which is also comparable in magnitude to experimentally observed anisotropies. Dislocatioms along the inplane [001] and [110] directions both produce the same preferred direction of maguctization orientation.

Strain measurements were performed on multilayer films of Mo/Ni using x-ray diffraction with the scattering vector at varying degrees of inclination to the surface normal. In-plane variations in the lattice parameters confirm that there are coherency stresses between the Mo and Ni layers. Assuming the Nishiama-Wasserman orientation for the planes of Ni and Mo allowed the calculation of the complete stress state in both materials. The in-plane lattice parameter, the perpendicular lattice parameter and the unstrained lattice parameter have also been derived from the data. The substrate interaction stress which would be necessary to provide a force balance between the layers was calculated. This was found to be in good agreement with the global stress measured from wafer curvature. Preliminary results of modelling of the high angle superlattice lines to extract interfacial roughness in the growth direction are also presented.

The interfacial structure of Pt/Nb and Pt/Ni sputtered multilayer films was studied using x-ray diffraction in symmetric, asymmetric, and grazing incidence modes. The grazing incidence and asymmetric diffraction were used to distinguish alloying effects on the lattice spacing from strain in the films. This strain was shown to be consistent with semi-coherent interfaces in the Pt/Ni but not in the Pt/Nb in which another strain generating mechanism dominates.