Stress-induced Defects Research Articles

Stress-induced surface instabilities and defects in thin films sputter deposited on compliant substrates.

Existing analyses predict that thin metal films deposited on compliant substrates are subject to a variety of surface instabilities, such as wrinkles, folds, creases, etc., that become more prominent with increased compressive residual stress. Under compressive stress, cracks have been assumed to form only when the interfacial strength is weak, allowing the film to detach from the substrate. In this work, we demonstrate that cracks also form on surfaces under compressive mismatch strain when the interface is strong. In particular, we consider metal alloy films sputter deposited under bias on elastomers with different thicknesses, curing temperatures or surface treatments. The deposition parameters created residual compressive strains and strong adhesion in the bilayers. Samples without surface treatment formed wrinkles and through-thickness cracks at 0.25-0.4% mismatch strains. Only through-thickness cracks were observed in UV treated samples. The crack spacing was found to decrease by a factor of 4 when the surface was UV treated and by a factor of 3 as the elastomer thickness decreased from 30 to 6 μm. Cracks penetrated through the elastomer, 15-30 times deeper than the film thickness, and formed in all samples with a brittle coating. A numerical model was developed to explain the formation of through-thickness cracks and wrinkles under applied compressive mismatch strains. The model suggests that cracks can initiate from the peak of wrinkles when the critical fracture strength of the coating is exceeded. For the UV treated samples, through-thickness cracks are possibly impacted by the formation of an embrittled near surface PDMS layer.

Coronary calcification compromises myocardial perfusion irrespective of luminal stenosis

AimThe aim of this study was to evaluate the relationship between coronary artery calcification (CAC) assessed by multi-detector computed tomography (MDCT) and myocardial perfusion assessed by cardiac magnetic resonance imaging (CMR) in a group of symptomatic patients. MethodRetrospective analysis of 120 patients (age 65.1±8.9years, 88 males) who presented with atypical chest pain to Bethanien Hospital, Frankfurt, Germany, between 2007 and 2010 and who underwent CAC scoring using MDCT, CMR, and conventional coronary angiography. Patients were divided into those with high-grade (HG) stenosis (n=67, age 65.1±9.4 years) and those with no-HG stenosis (n=53, age 65.1±8.6 years). ResultsThere were more males with HG stenosis (82.1% vs. 62.3%, p=0.015), in whom the percentage and number of abnormal perfusion segments were higher at rest (37.3% vs. 17%, p=0.014) but not different with stress (p=0.83) from those with no-HG stenosis. Thirty-four patients had myocardial perfusion abnormalities at rest and 26 patients developed perfusion defects with stress. Stress-induced myocardial perfusion defects were 22.4% sensitive and 79.2% specific for detecting HG stenosis. The CAC score was lower in patients with no-HG stenosis compared to those with HG stenosis (p<0.0001). On the ROC curve, a CAC score of 293 had a sensitivity of 71.6% and specificity of 83% in predicting HG stenosis [(AUC 0.80 (p<0.0001)]. A CAC score of 293 or the presence of at least 1 segment myocardial perfusion abnormality was 74.6% sensitive and 71.7% specific in detecting HG stenosis, the respective values for the 2 abnormalities combined being 19.4% and 90.6%. The severity of CAC correlated with the extent of myocardial perfusion in the patient group as a whole with stress (r=0.22, p=0.015), particularly in those with no-HG stenosis (r=0.31, p=0.022). A CAC score of 293 was 31.6% sensitive and 87.3% specific in detecting myocardial perfusion abnormalities. ConclusionIn a group of patients with exertional angina, coronary calcification is more accurate in detecting high-grade luminal stenosis than myocardial perfusion defects. In addition, in patients with no stenosis, the incremental relationship between coronary calcium score and the extent of myocardial perfusion suggests coronary wall hardening as an additional mechanism for stress-induced angina other than luminal narrowing. These preliminary findings might have a clinical impact on management strategies of these patients other than conventional therapy.

Monitoring Stress-Induced Defects in HK/MG FinFETs Using Random Telegraph Noise

In this letter, we report on nFinFETs degradation during stress exploiting $I_{D}$ and $I_{G}$ noise analysis. We employed a stress/measure approach to monitor device characteristics at different levels of cumulative stress. $I_{G}$ – $V_{G}$ and $I_{D}$ – $V_{G}$ indicators suggest defects generation to occur away from the channel. This is confirmed by the quantitative analysis of $I_{D}$ and $I_{G}$ stationary RTN signals at operating conditions, which show no correlation as opposite to what reported for planar FETs. Moreover, we analyze for the first time the $I_{D}$ -t and $I_{G}$ -t non-stationary instabilities during stress. The results confirm that the generation of defects responsible for SILC occurs away from the channel. Only in highly stressed devices, $I_{D}$ - $t$ and $I_{G}$ - $t$ curves observed during stress exhibit anti-correlation, due to comparable values of the gate and drain current levels originated by the high defect density. Hence, in nFinFETs, $I_{D}$ and $I_{G}$ RTN/instabilities might originate from mechanisms involving different entities.

Rapamycin ameliorates chitosan nanoparticle-induced developmental defects of preimplantation embryos in mice.

Chitosan nanoparticles (CSNPs) are used as drug or gene delivery vehicles. However, a detailed understanding of the effects of CSNPs on embryonic development remains obscure. Here, we show that CSNPs can be internalized into mouse blastocysts, such as the zona pellucida, the perivitelline space, and the cytoplasm. Consequently, CSNPs-induced endoplasmic reticulum (ER) stress increases both of Bip/Grp78, Chop, Atf4, Perk, and Ire1a mRNAs expression levels, and reactive oxygen species. Moreover, CSNPs show double- and multi-membraned autophagic vesicles, and lead to cell death of blastocoels. Conversely, treatment with rapamycin, which plays an important role as a central regulator of cellular proliferation and stress responses, decreased CSNPs-induced mitochondrial Ca+2 overloading, apoptosis, oxidative stress, ER stress, and autophagy. In vivo studies demonstrated that CSNPs injection has significant toxic effect on primordial and developing follicles. Notably, rapamycin rescued oxidative stress-induced embryonic defects via modulating gene expression of sirtuin and mammalian target of rapamycin. Interestingly, CSNPs treatment alters epigenetic reprogramming in mouse embryos. Overall, these observations suggest that rapamycin treatment could ameliorate CSNPs-induced developmental defects in preimplantation embryos. The data from this study would facilitate to understand the toxicity of these CSNPs, and enable the engineering of safer nanomaterials for therapeutic applications.

An in vitro reproduction of stress-induced memory defects: Effects of corticoids on dendritic spine dynamics.

Previously, in organotypic slice culture of rodent hippocampus we found that three repeated inductions of LTP, but not a single induction, led to a slow-developing long-lasting enhancement of synaptic strength coupled with synapse formation. Naming this structural plasticity RISE (repetitive LTP-induced synaptic enhancement) and assuming it to be a potential in vitro reproduction of repetition-dependent memory consolidation, we are analyzing its cellular mechanisms. Here, we applied a glucocorticoid to the culture to mimic acute excess stress and demonstrated its blockade of RISE. Since excess stress interferes with behavioral memory consolidation, the parallelism between RISE in vitro and memory consolidation in vivo is supported. We recently reported that RISE developed after stochastic processes. Here we found that the glucocorticoid interfered with RISE by suppressing the increment of dendritic spine fluctuation that precedes a net increase in spine density. The present study provides clues for understanding the mechanism of stress-induced memory defects.

Review—Device Assessment of Electrically Active Defects in High-Mobility Materials

The stringent device performance specifications of advanced scaled down technologies necessitates the implementation of high mobility substrates such as SiGe, Strained Si (sSi), Ge, sGe and/or III-V materials like GaAs, InGaAs. The control of the stress-induced defects remains a key challenge. Simple device structures such as capacitors, diodes and transistors are used to assess the electrical activity of extended defects (dislocations; antiphase boundaries; …) in high-mobility channel materials. Beside junction current analyses and lifetime studies, also the use of low-frequency noise characterization is reported. Special case studies are discussed to illustrate the used methodology. The potential of TCAD studies to better understand the electrical defect activity is also briefly addressed.

Correlation between stress-induced leakage current and dielectric degradation in ultra-porous SiOCH low-k materials

Stress-Induced Leakage Current (SILC) behavior during the dielectric degradation of ultra-porous SiOCH low-k materials was investigated. Under high voltage stress, SILC increases to a critical value before final hard breakdown. This SILC increase rate is mainly driven by the injected charges and is negligibly influenced by temperature and voltage. SILC is found to be transient and shows a t−1 relaxation behavior, where t is the storage time at low voltages. This t−1 transient behavior, described by the tunneling front model, is caused by both electron charging of neutral defects in the dielectric close to the cathode interface and discharging of donor defects close to the anode interface. These defects have a uniform density distribution within the probed depth range, which is confirmed by the observed flat band voltage shift results collected during the low voltage storage. By applying an additional discharging step after the low voltage storage, the trap energies and spatial distributions are derived. In a highly degraded low-k dielectric, the majority of defects have a trap depth between 3.4 eV and 3.6 eV and a density level of 1 × 1018 eV−1 cm−3. The relation between the defect density N and the total amount of the injected charges Q is measured to be sub-linear, N ∼ Q0.45±0.07. The physical nature of these stress-induced defects is suggested to be caused by the degradation of the Si-O based skeleton in the low-k dielectric.

Compact Modeling of Total Ionizing Dose and Aging Effects in MOS Technologies

This paper presents a physics-based compact modeling approach that incorporates the impact of total ionizing dose (TID) and stress-induced defects into simulations of metal-oxide-semiconductor (MOS) devices and integrated circuits (ICs). This approach utilizes calculations of surface potential (ψ <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">s</sub> ) to capture the charge contribution from oxide trapped charge and interface traps and to describe their impact on MOS electrostatics and device operating characteristics as a function of ionizing radiation exposure and aging effects. The modeling approach is demonstrated for bulk and silicon-on-insulator (SOI) MOS device. The formulation is verified using TCAD simulations and through the comparison of model calculations and experimental I - V characteristics from irradiated devices. The modeling approach is suitable for simulating TID and aging effects in advanced MOS devices and ICs, and is compatible with modern MOSFET compact modeling techniques. A circuit-level demonstration is given for TID and aging effects in SRAM cells.

Physically-based extraction methodology for accurate MOSFET degradation assessment

This paper analyzes conventional parameter extraction methodologies applied to MOSFET devices subject to electrical stress and highlights the complexity to accurately get and separate both electrostatic and transport degradations. It is shown that an accurate Coulomb scattering assessment from the linear Id-Vg characteristics is mandatory whenever the amount of interface charges/traps becomes significant. Thus, this paper proposes a novel technique able to extract the electrostatic drift and the field-dependent mobility directly from the experimental data without any a priori assumption for the transport.Applied to MOSFETs experiencing Hot Carrier Stress, the proposed methodology provides deeper insights into the relationship between stress-induced defects location and their impact on electrostatic and transport degradations.

Antioxidant metallothionein alleviates endoplasmic reticulum stress-induced myocardial apoptosis and contractile dysfunction

Aims. Endoplasmic reticulum (ER) stress exerts myocardial oxidative stress, apoptosis, and contractile anomalies, although the precise interplay between ER stress and apoptosis remains elusive. This study was designed to examine the impact of the cysteine-rich free radical scavenger metallothionein on ER stress-induced myocardial contractile defect and underlying mechanisms. Methods and results. Wild-type friendly virus B and transgenic mice with cardiac-specific overexpression of metallothionein were challenged with the ER stress inducer tunicamycin (1 mg/kg, intraperitoneal, 48 h) prior to the assessment of myocardial function, oxidative stress, and apoptosis. Our results revealed that tunicamycin promoted cardiac remodeling (enlarged left ventricular end systolic/diastolic diameters with little changes in left ventricular wall thickness), suppressed fractional shortening and cardiomyocyte contractile function, elevated resting Ca2+, decreased stimulated Ca2+ release, prolonged intracellular Ca2+ clearance, and downregulated sarco(endo)plasmic reticulum Ca2+-ATPase levels, the effects of which were negated by metallothionein. Treatment with tunicamycin caused cardiomyocyte mitochondrial injury, as evidenced by decreased mitochondrial membrane potential (∆Ѱm, assessed by JC-1 staining), the effect of which was negated by the antioxidant. Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity. Interestingly, metallothionein transgene significantly alleviated tunicamycin-induced myocardial apoptosis. Conclusion. Taken together, our data favor a beneficial effect of metallothionein against ER stress-induced cardiac dysfunction possibly associated with attenuation of myocardial apoptosis.

Effect of film thickness on the temperature dependence of thermal conductivity for diamond/BeO composites

Polycrystalline diamond films of different thickness have been deposited on the surface of beryllium oxide (BeO) substrates by hot filament chemical vapor deposition (CVD). Thermal conductivity (κ value) of various samples has been measured. The biggest increase of 17.5% in thermal conductivity relative to the substrate is obtained in the composite with 5.0μm film at room temperature. The temperature dependence of the thermal conductivity for the composites with films of different thickness has been investigated. Comprehensive effect of film purity and residual stress is found to be responsible for the variation of temperature dependence for the composites. Stress-induced defects play an important role in the thermal conductivity at high temperature from our analysis. This work is of great significance on the preparation and thermal application of composites with CVD diamond in such a film/substrate structure.

All-systolic non-ECG-gated myocardial perfusion MRI: Feasibility of multi-slice continuous first-pass imaging.

To develop and test the feasibility of a new method for non-ECG-gated first-pass perfusion (FPP) cardiac MR capable of imaging multiple short-axis slices at the same systolic cardiac phase. A magnetization-driven pulse sequence was developed for non-ECG-gated FPP imaging without saturation-recovery preparation using continuous slice-interleaved radial sampling. The image reconstruction method, dubbed TRACE, used self-gating based on reconstruction of a real-time image-based navigator combined with reference-constrained compressed sensing. Data from ischemic animal studies (n = 5) was used in a simulation framework to evaluate temporal fidelity. Healthy subjects (n = 5) were studied using both the proposed approach and the conventional method to compare the myocardial contrast-to-noise ratio (CNR). Patients (n = 2) underwent adenosine stress studies using the proposed method. Temporal fidelity of the developed method was shown to be sufficient at high heart-rates. The healthy volunteers studies demonstrated normal perfusion and no dark-rim artifacts. Compared with the conventional scheme, myocardial CNR for the proposed method was slightly higher (8.6 ± 0.6 versus 8.0 ± 0.7). Patient studies showed stress-induced perfusion defects consistent with invasive angiography. The presented methods and results demonstrate feasibility of the proposed approach for high-resolution non-ECG-gated FPP imaging of 3 myocardial slices at the same systolic phase, and indicate its potential for achieving desirable image quality (high CNR and no dark-rim artifacts).

In situ study of mass loss, shrinkage and stress development during drying of cast colloidal films

During constrained drying of binder-assisted colloidal coatings on rigid substrates, drying stress-induced defects such as cracks and warpage can often be observed due to the lateral confinement of the film by the substrate. The purpose of the current work is to understand the origin of these drying defects and to develop strategies for their avoidance by the adjustment of slurry composition or processing parameters. In this paper, the time-dependent drying behavior of colloidal ceramic coatings was studied in situ by observation of mass loss, drying shrinkage and drying stress by different methods, such as transparent substrate deflection and beam deflection methods. The stress development and the critical moment, at which cracks form, were investigated in films of different compositions with respect to solvent, particle size, binder and plasticizer. The origins of the measured differences in drying shrinkage, crack formation as well as residual stresses after drying were discussed.

Pax3 and Pax7 Play Essential Safeguard Functions against Environmental Stress-Induced Birth Defects

Exposure to environmental teratogenic pollutant leads to severe birth defects. However, the biological events underlying these developmental abnormalities remain undefined. Here, we report a molecular link between an environmental stress response pathway and key developmental genes during craniofacial development. Strikingly, mutant mice with impaired Pax3/7 function display severe craniofacial defects. We show that these are associated with an upregulation of the signaling pathway mediated by the Aryl hydrocarbon receptor (AHR), the receptor to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), revealing a genetic interaction between Pax3 and AHR signaling. Activation of AHR signaling in Pax3-deficient embryos drives facial mesenchymal cells out of the cell cycle through the upregulation of p21 expression. Accordingly, inhibiting AHR activity rescues the cycling status of these cells and the facial closure of Pax3/7 mutants. Together, our findings demonstrate that the regulation of AHR signaling by Pax3/7 is required to protect against TCDD/AHR-mediated teratogenesis during craniofacial development.

Real-time cine first-pass perfusion imaging enables rapid detection of functionally significant high-grade coronary stenosis

Background Among the spectrum of patients with coronary artery disease (CAD), those suffering from high-grade stenosis are at a significantly elevated risk for adverse events [1]. Such high-grade disease may result in the so-called “coronary steal” phenomenon under vasodilator stress [2] thereby inducing wall-motion abnormalities (WMAs) in the affected territories, referred to as transient ischemic dilation. We developed a “real time” cine first-pass perfusion (FPP) CMR method for concurrent imaging of myocardial function and perfusion. We hypothesized that this method is capable of simultaneously capturing stress-induced perfusion defects and WMAs in a single ungated scan. Methods

Lurasidone exerts antidepressant properties in the chronic mild stress model through the regulation of synaptic and neuroplastic mechanisms in the rat prefrontal cortex.

Background:Major depression is associated with several alterations, including reduced neuronal plasticity and impaired synaptic function, which represent an important target of pharmacological intervention.Methods:In the present study, we have investigated the ability of the antipsychotic drug lurasidone to modulate behavioral and neuroplastic alterations in the chronic mild stress model of depression.Results:Rats that show reduced sucrose consumption after 2 weeks of chronic mild stress have reduced expression of the pool of Bdnf transcripts with the long 3′ untranslated region (3′-UTR) that may be targeted to the synaptic compartment, suggesting the contribution of the neurotrophin to the behavioral dysfunction produced by chronic mild stress. The downregulation of Bdnf expression persisted also after 7 weeks of chronic mild stress, whereas chronic lurasidone treatment improved anhedonia in chronic mild stress rats and restored Bdnf mRNA levels in the prefrontal cortex. Moreover, chronic lurasidone treatment was able to normalize chronic mild stress-induced defects of Psd95 and Gfap as well as changes in molecular regulators of protein translation at the synapse, including mTOR and eEF2.Conclusions:These results demonstrate that lurasidone shows antidepressant properties in the chronic mild stress model through the modulation of synaptic and neuroplastic proteins. Such changes may contribute to the amelioration of functional capacities, which are deteriorated in patients with major depression and stress-related disorders.

Right ventricular stress-induced perfusion defects and late gadolinium enhancement in coronary artery disease.

The assessment of right ventricular (RV) perfusion defects has remained challenging during vasodilator stress perfusion with cardiovascular magnetic resonance (CMR). The significance of RV signal abnormalities during vasodilator stress perfusion and late gadolinium-enhanced CMR is yet uncertain. Among 61 individuals who underwent adenosine CMR stress testing before cardiac catheterization, we assessed the severity of coronary artery stenoses, mortality, the presence of stress and rest perfusion defects, as well as the presence of late gadolinium enhancement (LGE). Right ventricular stress-induced perfusion defects were positively associated with left anterior descending artery and proximal right coronary artery stenoses but were negatively associated with left circumflex artery stenoses. The presence of RVLGE was associated with mortality, but 77% of those with RVLGE also had left ventricular LGE. Proximal right coronary artery and left anterior descending artery stenoses are positively associated, whereas left circumflex artery stenoses are negatively associated with RV stress-induced perfusion defects. Right ventricular LGE was associated with mortality, but further study is needed to determine whether this is independent of left ventricular LGE.

Broadband Microwave-Based Metrology Platform Development: Demonstration of In-Situ Failure Mode Diagnostic Capabilities for Integrated Circuit Reliability Analyses

In this paper, we discuss the use of broadband high frequency electromagnetic waves (RF) to non-destructively identify, classify and characterize performance-limiting defects in emerging nanoelectronic devices. As an illustration, the impact of thermal cycling on the RF signal characteristics (insertion loss (S21) and return loss (S11)) is used to infer thermo-mechanical stress-induced defects in metal interconnects. The inferred defects are supported with physical analytical data where possible.

Crystallization mechanisms occurring in the Se–Te glassy system

Crystallization kinetics, studied under non-isothermal conditions in dependence on particle size, is reviewed for the Se–Te glassy system, with particular focus on occurring macroscopic crystallization mechanisms. The observed complexity of the crystallization processes is explained in terms of the two previously identified mechanisms—bulk crystallization originating from nuclei randomly distributed in the volume of each glass particle (formation of these nuclei is consistent with the classical nucleation theory) and crystallization from surface/volume active centers, dislocations, structural defects, and heterogeneities originating from the mechanical damage of the material (e.g., during grinding and milling). In addition, a new crystallization mechanism, previously unobserved in this system, was revealed for hyperquenched Se95Te5 glass. The origin of this mechanism is suggested to be closely associated with the stress-induced defects contained in the highly strained structure of this glass. The strong compositional dependence of the occurrence of this mechanism then seems to be caused by the high cooperativity of the amorphous structure of the specific composition.

The impact of stress-induced defects on MOS electrostatics and short-channel effects

This paper investigates the influence of stress-induced oxide-trapped charge and interface traps on the electrostatics of metal–oxide–semiconductor (MOS) devices and its relation to short-channel effects (SCE). Interface trap and oxide-trapped charge densities are included in the derivation of scaling models that are based on solving Poisson’s equation in the depletion approximation (i.e., in weak inversion) using analytical approximations for the electrostatic potential. The impact of interface traps and oxide-trapped charge on the electrostatic potential profile, scaling, and short-channel effects are modeled analytically and verified with TCAD simulations. The theory and modeling approach is validated through comparisons with the experimental extraction of SCE in n-channel MOS field-effect transistors (MOSFETs) measured before and after hot-carrier stress.