Combined effects of surface oxidation and interfacial intermetallic compound growth on solderability degradation of electrodeposited tin thin films on copper substrate due to isothermal ageing

© 2018 Elsevier Ltd We report new insights into the solder wettability degradation of Sn thin films on Cu under 155 °C isothermal ageing. A multiscale wettability degradation model was established, reflecting quantitatively the surface oxidation and interfacial intermetallic compound (IMC) growth, on the basis of solder wetting behaviour. The thermal oxidation of Sn exhibited heterogeneous inward thickening, lateral expanding and outward platelet-like growth, forming nanocrystalline, oxygen-deficient SnO2with pronounced voiding/cracking propensity. Unlike a commonly held belief that the initial wettability loss is due to surface-exposing and oxidation of IMCs, it was found from dual combined effects of inward surface oxidation and outward IMC growth

Focused ion beam preparation of microbeams for in situ mechanical analysis of electroplated nanotwinned copper with probe type indenters

A site‐specific xenon plasma focused ion beam preparation technique for microcantilever samples (1 μm ‐ 20 μm width and 1:10 aspect ratio) is presented. The novelty of the methodology is the use of a chunk lift‐out onto a clean silicon wafer to facilitate easy access of a low‐cost probe type indenter which provides bending force measurement. The lift‐out method allows sufficient room for the indenter and a line of sight for the electron beam to enable displacement measurement. An electroplated nanotwinned copper (NTC) was cut to a 3 × 3 × 25 μm micro‐beam and in‐situ mechanically tested using the developed technique. It demonstrated measured values of Youngs modulus of 78.7 ± 11 GPa and flow stress of 0.80 ± 0.05 GPa, which is within the ranges reported in the literature

In situ transformation from P phase to μ phase in rhenium-containing single-crystal superalloy during thermal exposure

<p>An <i>in situ</i> phase transformation from P to μ in a rhenium-containing superalloy during high-temperature exposure has been investigated by transmission electron microscopy. The orientation relationship between the phases is found as (1–12)_μ // (1 0 0)_P and [2 4 1]_μ // [0 1 1]_P. An atomic model of the μ/P interface was built to reveal a perfectly coherent interface with lattice misfits of only 0.421 and 1.098%. Considering the small lattice distortions and the similar elemental composition of the phases, it is concluded that the phase transformation from P to μ is favourable.</p

Reaction Pathways and Kinetics of a Cyanobacterial Neurotoxin β‑<i>N</i>‑Methylamino‑<i>L</i>‑Alanine (BMAA) during Chlorination

<i>β-N</i>-Methylamino-<i>L</i>-alanine (BMAA), a probable cause of the amyotrophic lateral sclerosis/parkinsonism–dementia complex (ALS/PDC), or Alzheimer’s disease, has been identified in more than 20 cyanobacterial genera. However, its removal and fate in drinking water has never been reported before. In this study, the reaction of BMAA with chlorine, a common drinking-water oxidant/disinfectant, was investigated. A liquid chromatograph coupled with a triple quadrupole mass spectrometer was employed to quantify BMAA and its intermediates. Upon chlorination, four chlorinated intermediates, each with one or two chlorines, were identified. The disappearance of BMAA caused by chlorine follows a second-order reaction, with the rate constant <i>k</i>₁ is 5.0 × 10⁴ M^–1 s^–1 at pH ∼7.0. The chlorinated intermediates were found to further react with free chlorine, exhibiting a second-order rate constant <i>k</i>₃ = 16.8 M^–1 s^–1. After all free chlorine was consumed, the chlorinated intermediates autodecomposed slowly with a first order rate constant <i>k</i>₂ = 0.003 min^–1; when a reductant was added, these chlorinated intermediates were then reduced back to BMAA. The results as described shed a useful light on the reactivity, appearance, and removal of BMAA in the chlorination process of a drinking-water system

The loss rate of mitochondrial membrane phospholipids in lymphocytes of VMD patients.

<p>*P<0.05 vs. controls; ^#P<0.01 vs. controls.</p><p>The loss rate of mitochondrial membrane phospholipids in lymphocytes of VMD patients.</p

MtDNA deletion rate in myocardium of VMD patients (mean ± SEM).

<p>MtDNA deletion rate in myocardium of VMD patients (mean ± SEM).</p

The correlation curves of mtDNA deletion rate between myocardium and skeletal muscle, and mitochondrial membrane phospholipids loss rate between myocardium and skeletal muscle in VMC mice.

<p>The correlation of mitochondrial membrane phospholipids normal localization between myocardium and skeletal muscle in VMC mice was described in part b, R = 0.959, p<0.001; the correlation of partial loss of mitochondrial membrane phospholipids was described in part c, R = 0.886, p = 0.03; the correlation of most or complete loss was described in part d, R = 0.951, p = 0.001.</p

The structure of mitochondria in cardiomyocyte of VMC mice (magnification 10,000X).

<p>(<b>a</b>) Cardiomyocyte of normal mouse. The mitochondria were circle or elliptical with legible and densely packed cristae. There were also sporadic glycogen granules between the myofibrils. (<b>b</b>) Cardiomyocyte of mice 3 days after virus infection. The mitochondria proliferated and swelled, with pyknosis, vesicle and the decreased matrix; glycogen granule decreased or disappeared. (<b>c</b>) Cardiomyocyte of mice 11 days after virus infection. The mitochondria proliferated and swelled, with the fusion of mitochondrial membrane and merged to huge mitochondria; glycogen granule decreased; inhomogeneous myofibril dissolved, and the sarcomere disappeared. (<b>d</b>) Cardiomyocyte of mice 24 days after virus infection. The mitochondria significantly proliferated and swelled, the cristae became vague; glycogen granule decreased, and sarcoplasmic reticulum dilated.</p

The loss rate of mitochondrial membrane phospholipids in myocardium and skeletal muscle of VMC mice (mean ± SEM).

<p>^*P<0.05 vs. controls; ^#P<0.05 vs. 3d after viral infection.</p><p>The loss rate of mitochondrial membrane phospholipids in myocardium and skeletal muscle of VMC mice (mean ± SEM).</p

PCR result of myocardial mtDNA in VMC mice.

<p>Lane 1: myocardial mtDNA of 3 days after viral injection; lane 2: myocardial mtDNA of 11 days after viral injection; lane 3: myocardial mtDNA of 24 days after viral injection; lane 4: myocardial mtDNA of control mouse. M: DNA marker; N: negative control.</p