PurposeThe purpose of this paper is to evaluate the application of an acoustic micro‐imaging (AMI) inspection technique in monitoring solder joints through lifetime performance and demonstrate the robustness of the monitoring through analysis of AMI data.Design/methodology/approachAccelerated thermal cycling (ATC) test data on a flip chip test board were collected through AMI imaging. Subsequently, informative features and parameters of solder joints in acoustic images were measured and analysed. Through analysing histogram distance, mean intensity and grey area of the solder joints in acoustic images, cracks between the solder bump and chip interface were tracked and monitored. The results are in accord with associated Finite Element (FE) prediction.FindingsAt defective bumps, the formation of a crack causes a larger acoustic impedance mismatch which provides a stronger ultrasound reflection. The intensity of solder joints in the acoustic image increase according to the level of damage during the ATC tests. By analysing the variation of intensity and area, solder joint fatigue failure was monitored. A failure distribution plot shows a normal distribution pattern, where corner joints have the lowest reliability and are more likely to fail first. A strong agreement between AMI monitoring test data and FE prediction was observed, demonstrating the feasibility of through lifetime monitoring of solder joints using AMI.Originality/valueThe paper indicates the feasibility of the novel application of AMI inspection to monitor solder joint through lifetime performance non‐destructively. Solder joints' real life conditions can be tracked by an AMI technique, hence solder joint fatigue failure cycles during the ATC tests can be monitored and analysed non‐destructively.
microRNAs (miRNAs) perform various oncogenic or tumor suppressor functions in carcinogenesis. Currently, the underlying mechanisms of miRNAs in osteosarcoma (OS) are poorly understood. In the present study, it is demonstrated that expression of miR-544 was markedly upregulated in OS cells and clinical tissues. Furthermore, overexpression of miR-544 enhanced OS cell proliferation in vitro. Bioinformatics analysis indicated that miR-544 may target the 3′-untranslated region of axis formation inhibitor 2, which was validated using luciferase reporter gene assays. The present study demonstrated a vital role for miR-544 in promoting OS cell proliferation, indicating that it may represent a novel prognostic factor or therapeutic target for OS.
Post‐stroke depression, a common complication after stroke, severely affects the recovery and quality of life of patients with stroke. Owing to its complex mechanisms, post‐stroke depression treatment remains highly challenging. Hippocampal synaptic plasticity is one of the key factors leading to post‐stroke depression; however, the precise molecular mechanisms remain unclear. Numerous studies have found that neurotrophic factors, protein kinases and neurotransmitters influence depressive behaviour by modulating hippocampal synaptic plasticity. This review further elaborates on the role of hippocampal synaptic plasticity in post‐stroke depression by summarizing recent research and analysing possible molecular mechanisms. Evidence for the correlation between hippocampal mechanisms and post‐stroke depression helps to better understand the pathological process of post‐stroke depression and improve its treatment.
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