The synthesis of boron carbide filaments final report

Synthesis, strength, crystal structure, and composite material formation of boron carbide whisker

Test device prevents weld joint damage by eliminating axial pin forces on unpotted modules

Test device makes electrical connection to pins on unpotted electronic modules without introducing any displacing forces of the pins, thus preventing weld joint damage. The pins are spaced in a potting header, but are free to slide in and out except for restraint from welded wire joints

PD-L1 testing for lung cancer in the UK: recognizing the challenges for implementation.

A new approach to the management of non-small-cell lung cancer (NSCLC) has recently emerged that works by manipulating the immune checkpoint controlled by programmed death receptor 1 (PD-1) and its ligand programmed death ligand 1 (PD-L1). Several drugs targeting PD-1 (pembrolizumab and nivolumab) or PD-L1 (atezolizumab, durvalumab, and avelumab) have been approved or are in the late stages of development. Inevitably, the introduction of these drugs will put pressure on healthcare systems, and there is a need to stratify patients to identify those who are most likely to benefit from such treatment. There is evidence that responsiveness to PD-1 inhibitors may be predicted by expression of PD-L1 on neoplastic cells. Hence, there is considerable interest in using PD-L1 immunohistochemical staining to guide the use of PD-1-targeted treatments in patients with NSCLC. This article reviews the current knowledge about PD-L1 testing, and identifies current research requirements. Key factors to consider include the source and timing of sample collection, pre-analytical steps (sample tracking, fixation, tissue processing, sectioning, and tissue prioritization), analytical decisions (choice of biomarker assay/kit and automated staining platform, with verification of standardized assays or validation of laboratory-devised techniques, internal and external quality assurance, and audit), and reporting and interpretation of the results. This review addresses the need for integration of PD-L1 immunohistochemistry with other tests as part of locally agreed pathways and protocols. There remain areas of uncertainty, and guidance should be updated regularly as new information becomes available

Influence of anodizing process on fatigue life of a machined aluminium alloy

In order to investigate the coupled effects of machining and anodizing processes on fatigue life of alloy 7010-T7451, a series of rotating bending fatigue tests were conducted at 60Hz. In the as machined condition, test results showed that fatigue life is surface roughness dependent and that fatigue life decreases with an increase in surface roughness and this effect is found to be more pronounced in high cycle fatigue where major portion of fatigue life is consumed in nucleating the cracks. Effects of pretreatments, like degreasing and pickling employed prior to anodizing, on fatigue life of the given alloy were also studied. Results demonstrated that degreasing showed no change in fatigue life while pickling had negative impact on fatigue life of specimens. The small decrease in fatigue life of anodized specimens as compare to pickled specimens is attributed to brittle and microcracking of the coating. Scanning electron microscopic (SEM) examination revealed multi-site crack initiation for the pickled and anodized specimens. SEM examination showed that pickling solution attacked the grain boundaries and intermetallic inclusions present on the surface resulting in pits formation. These pits are of primary concern with respect to accelerated fatigue crack nucleation and subsequent anodized coating formation

Study of the growth parameters involved in synthesizing boron carbide filaments

Growth and deposition zone geometry effects on boron carbide whisker production, mechanical properties, and composite application

A fatigue multi-site cracks model using coalescence, short and long crack growth laws, for anodized aluminum alloys

It has been shown that decrease of the fatigue life of aluminium alloys treated with anodization can be explained by the degradation of surface condition due to pickling. In order to predict fatigue life of anodized aluminium alloys, a multi-site crack growth model is developed by considering the pickling pits sites as initial flaws from which fatigue cracks develop. A map of the pickled surface is built from topography measurement with a contact profilometer. Then the pits are detected and their sizes are defined (depth, length and width). At the beginning of the calculation, a short crack growth law is used for crack having depths less than grain size. Then Paris long crack growth law is used. The coalescence of cracks is considered when their lengths increased by its crack tip plastic zone are large enough to interact with other neighbouring short cracks. The fatigue life is calculated for Kmax achieving 70 % KIC

Age-related mitochondrial DNA depletion and the impact on pancreatic beta cell function

Type 2 diabetes is characterised by an age-related decline in insulin secretion. We previously identified a 50% age-related decline in mitochondrial DNA (mtDNA) copy number in isolated human islets. The purpose of this study was to mimic this degree of mtDNA depletion in MIN6 cells to determine whether there is a direct impact on insulin secretion. Transcriptional silencing of mitochondrial transcription factor A, TFAM, decreased mtDNA levels by 40% in MIN6 cells. This level of mtDNA depletion significantly decreased mtDNA gene transcription and translation, resulting in reduced mitochondrial respiratory capacity and ATP production. Glucose-stimulated insulin secretion was impaired following partial mtDNA depletion, but was normalised following treatment with glibenclamide. This confirms that the deficit in the insulin secretory pathway precedes K+ channel closure, indicating that the impact of mtDNA depletion is at the level of mitochondrial respiration. In conclusion, partial mtDNA depletion to a degree comparable to that seen in aged human islets impaired mitochondrial function and directly decreased insulin secretion. Using our model of partial mtDNA depletion following targeted gene silencing of TFAM, we have managed to mimic the degree of mtDNA depletion observed in aged human islets, and have shown how this correlates with impaired insulin secretion. We therefore predict that the age-related mtDNA depletion in human islets is not simply a biomarker of the aging process, but will contribute to the age-related risk of type 2 diabetes