Through-the-thickness fatigue crack closure behavior in an aluminum alloy

The variation in fatigue crack closure behavior across the thickness of aluminum alloy specimens was investigated. The specimen geometries examined were the middle crack tension M(T) and compact tension C(T). The fatigue crack closure behavior was determined using remote displacement and strain gages, near tip strain gages, and fatigue striations. A hybrid experimental/numerical method was also used to infer the crack opening loads. The results indicate a variation in crack opening load, of 0.2 in the specimen interior to 0.4 to 0.5 at the surface

Fatigue analysis of multiple site damage at a row of holes in a wide panel

This paper is concerned with predicting the fatigue life of unstiffened panels which contain multiple site damage (MSD). The initial damage consists of through-the-thickness cracks emanating from a row of holes in the center of a finite width panel. A fracture mechanics analysis has been developed to predict the growth, interaction, and coalescence of the various cracks which propagate in the panel. A strain-life analysis incorporating Neuber's rule for notches, and Miner's rule for cumulative damage, is also employed to predict crack initiation for holes without initial cracking. This analysis is compared with the results of a series of fatigue tests on 2024-T3 aluminum panels, and is shown to do an excellent job of predicting the influence of MSD on the fatigue life of nine inch wide specimens. Having established confidence in the ability to analyze the influence of MSD on fatigue life, a parametric study is conducted to examine the influence of various MSD scenarios in an unstiffened panel. The numerical study considered 135 cases in all, with the parametric variables being the applied cyclic stress level, the lead crack geometry, and the number and location of MSD cracks. The numerical analysis provides details for the manner in which lead cracks and MSD cracks grow and coalesce leading to final failure. The results indicate that MSD located adjacent to lead cracks is the most damaging configuration, while for cases without lead cracks, MSD clusters which are not separated by uncracked holes are most damaging

Strongly interacting 2D electron systems: Evidence for enhanced 1D edge-channel coupling

We observe nearly vanishing Hall resistances for integer filling factors in a counterflow (CF) experiment on a density balanced 2D bilayer system. Filling factor dependent equilibration lengths demonstrate enhanced 1D coupling via edge-channels. Due to the narrow barrier the edge-modes of the two 2DEGs are in close proximity allowing for 1D excitonic correlations. Electron drag measurements confirm the observed quantum state selective coupling between the layers

Determination of the carrier concentration in InGaAsN∕GaAs single quantum wells using Raman scattering

Raman scattering from longitudinal optical phonon-plasmon coupled mode was observed in a series of InGaAsN∕GaAs single quantum well samples grown by metalorganic vapor phase epitaxy. The phonon-plasmon mode spectra were fitted with the dielectric constant function based on Drude model that contains contributions from both lattice vibrations and conduction electrons. The carrier concentration is calculated directly from the plasmon frequency, which is obtained from the fitting procedure. An empirical expression for the electron concentration, [n], in InGaAsN∕GaAs samples is determined as [n]≈{2.35×1016(ωm−502)}cm−3, where ωm is the peak of the upper frequency branch, L+, of the phonon-plasmon mode measured in unit of cm−1. The phonon-plasmon coupled mode was also investigated in rapid thermally annealed samples

Differential inflammasome activation predisposes to acute-on-chronic liver failure in human and experimental cirrhosis with and without previous decompensation

OBJECTIVE Systemic inflammation predisposes acutely decompensated (AD) cirrhosis to the development of acute-on-chronic liver failure (ACLF). Supportive treatment can improve AD patients, becoming recompensated. Little is known about the outcome of patients recompensated after AD. We hypothesise that different inflammasome activation is involved in ACL F development in compensated and recompensated patients. DESIGN 249 patients with cirrhosis, divided into compensated and recompensated (previous AD), were followed prospectively for fatal ACL F development. Two external cohorts (n=327) (recompensation, AD and ACL F) were included. Inflammasome-driving interleukins (ILs), IL-1α (caspase-4/11-dependent) and IL-1β (caspase-1- dependent), were measured. In rats, bile duct ligationinduced cirrhosis and lipopolysaccharide exposition were used to induce AD and subsequent recompensation. IL-1α and IL-1β levels and upstream/downstream gene expression were measured. RESULTS Patients developing ACL F showed higher baseline levels of ILs. Recompensated patients and patients with detectable ILs had higher rates of ACL F development than compensated patients. Baseline CLIF-­C (European Foundation for the study of chronic liver failure consortium) AD, albumin and IL-1α were independent predictors of ACL F development in compensated and CLIF-­C AD and IL-1β in recompensated patients. Compensated rats showed higher IL-1α gene expression and recompensated rats higher IL-1β levels with higher hepatic gene expression. Higher IL-1β detection rates in recompensated patients developing ACL F and higher IL-1α and IL-1β detection rates in patients with ACL F were confirmed in the two external cohorts. CONCLUSION Previous AD is an important risk factor for fatal ACL F development and possibly linked with inflammasome activation. Animal models confirmed the results showing a link between ACL F development and IL-1α in compensated cirrhosis and IL-1β in recompensated cirrhosi

Cardiodynamic state is associated with systemic inflammation and fatal acute‐on‐chronic liver failure

Background & Aims: Acute-on-chronic liver failure (ACLF) is characterized by high short-term mortality and systemic inflammation (SI). Recently, different cardiodynamic states were shown to independently predict outcomes in cirrhosis. The relationship between cardiodynamic states, SI, and portal hypertension and their impact on ACLF development remains unclear. The aim of this study was therefore to evaluate the interplay of cardiodynamic state and SI on fatal ACLF development in cirrhosis. Results: At inclusion, hemodynamic measures including cardiac index (CI) and hepatic venous pressure gradient of 208 patients were measured. Patients were followed prospectively for fatal ACLF development (primary endpoint). SI was assessed by proinflammatory markers such as interleukins (ILs) 6 and 8 and soluble IL-33 receptor (sIL-33R). Patients were divided according to CI (4.2 L/min/m2) in hypo- (n = 84), normo- (n = 69) and hyperdynamic group (n = 55). After a median follow-up of 3 years, the highest risk of fatal ACLF was seen in hyperdynamic (35%) and hypodynamic patients (25%) compared with normodynamic (14%) (P =.011). Hyperdynamic patients showed the highest rate of SI. The detectable level of IL-6 was an independent predictor of fatal ACLF development. Conclusions: Cirrhotic patients with hyperdynamic and hypodynamic circulation have a higher risk of fatal ACLF. Therefore, the cardiodynamic state is strongly associated with SI, which is an independent predictor of development of fatal ACLF

Altered postprandial motility in chronic pancreatitis: role of malabsorption

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