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Solder joints of electronic packaging devices are used as mechanical fixation and electrical interconnection between chips and circuit boards, which provides protection for the normal operation of electronic equipment. Therefore, real-time monitoring of the status of solder joints is essential for predictive maintenance of equipment. In this paper, we propose a digital twin based on semi-supervised learning for diagnosing faults in chip interconnection solder joints. In order to achieve maximum generalization of limited label information, the interdependence between sample labels with similar feature distributions is fully exploited by semi-supervised learning. Additionally, we use real-time monitoring data to update the learning model, and reveal the evolution of solder joint failure under different loads through diagnostic results of model. A dynamic model is formed by stimulated fault evolution characteristics into a solder joint failure model to form a diagnose fault dynamic model in a virtual space. Finally, we designed a thermal-vibration coupling experiment to verify the effectiveness of the digital twin-based solder joint failure diagnosis model. The results show that the digital twin maintains good consistency with the performance degradation process of the solder joint throughout its life cycle. Moreover, the diagnostic accuracy of the digital twin model can reach 85%, which proves that our method can monitor the service status of physical entities online, and intelligently predict the failure mode and life cycles under load conditions.

Background: Approximately 30–40% of growth hormone-secreting pituitary adenoma (GHPA) harbor somatic mutations in the GNAS (α subunit of the stimulatory G protein) gene. However, the latent functional role of the mutations and relative molecular mechanism in GHPA remain unknown. Methods: The GNAS gene mutations were detected in GHPAs using a standard PCR-sequencing procedure. The mutation-associated MEG3 expression was measured by RT-qPCR. MEG3 was manipulated in GH3 cells using a lentiviral expression system. Alterations in mRNA profiles in the MEG3-overexpressed cells were analyzed by RNA-seq. The cell invasion ability was measured using a Transwell assay, and the EMT-associated proteins were quantified by immunofluorescence and western blot. Finally, a tumor cell xenograft mouse model was applied to verify the effect of MEG3 on tumor growth and invasiveness. Results: The percentage of invasive tumors was significantly declined in GNAS-mutated GHPA tumors with the GNAS mutations compared to those tumors with the wild-type of GNAS. Consistently, the GH3 cell invasion capacity was decreased by expressing the mutant GNAS. MEG3 is uniquely expressed at high levels in GHPA harboring the mutated GNAS gene. Accordingly, the upregulation of MEG3 resulted in inhibiting cell invasion; and vice versa, the downregulation of MEG3 led to enhancing cell invasion. Mechanistically, the high level of MEG3 in mutated GNAS cells prevented the cell invasion via inactivation of the Wnt/β-catenin signaling pathway, which was further validated in vivo. Conclusion: The GNAS mutations inhibit the invasiveness of GHPA cells via inactivation of the MEG3/Wnt/β-catenin signaling pathway.

Approximately 30–40% of growth hormone-secreting pituitary adenoma (GHPA) harbor somatic mutations in the GNAS (α subunit of the stimulatory G protein) gene. However, the latent functional role of the mutations and relative molecular mechanism in GHPA remain unknown. The GNAS gene mutations were detected in GHPAs using a standard PCR-sequencing procedure. The mutation-associated MEG3 expression was measured by RT-qPCR. MEG3 was manipulated in GH3 cells using a lentiviral expression system. Alterations in mRNA profiles in the MEG3-overexpressed cells were analyzed by RNA-seq. The cell invasion ability was measured using a Transwell assay, and the EMT-associated proteins were quantified by immunofluorescence and western blot. Finally, a tumor cell xenograft mouse model was applied to verify the effect of MEG3 on tumor growth and invasiveness. The percentage of invasive tumors was significantly declined in GNAS-mutated GHPA tumors with the GNAS mutations compared to those tumors with the wild-type of GNAS. Consistently, the GH3 cell invasion capacity was decreased by expressing the mutant GNAS. MEG3 is uniquely expressed at high levels in GHPA harboring the mutated GNAS gene. Accordingly, the upregulation of MEG3 resulted in inhibiting cell invasion; and vice versa, the downregulation of MEG3 led to enhancing cell invasion. Mechanistically, the high level of MEG3 in mutated GNAS cells prevented the cell invasion via inactivation of the Wnt/β-catenin signaling pathway, which was further validated in vivo. The GNAS mutations inhibit the invasiveness of GHPA cells via inactivation of the MEG3/Wnt/β-catenin signaling pathway.

Background: Osteoarthritis (OA) is a debilitating disease that inflicts intractable pain, a major problem that humanity faces, especially in aging populations. Stem cells have been used in the treatment of many chronic diseases, including OA. Cartilage progenitor cells (CPCs) are a type of stem cells with the ability to self- renew and differentiate. They hold a promising future for the understanding of the progression of OA and for its treatment. Previous studies have reported the relationship between mitochondrial dynamics and mesenchymal stem cell (MSC) proliferation, differentiation and aging. Mitochondrial dynamic and morphology change during stem cell differentiation. Methods: This study was performed to access the relationship between mitochondrial dynamics and chondrogenic differentiation of CPCs. Mitochondrial fusion and fission levels were measured during the chondrogenic differentiation process of CPCs. After that, we used mitochondrial fusion promoter to induce fusion in CPCs and then the chondrogenic markers were measured. Using Transmission Elecron Microscopy (TEM) and confocal microscopy to capture the mass and fusion status of mitochondria. Lentiviruses were used to detect the role of mitofusin 2 (MFN2) in CPC chondrogenic differentiation. In vivo, MNF2 was over-expressed in sheets of rCPCs, which were then injected intra-articularly into the knees of rats. Results: Mitochondrial fusion markers were upregulated during the chondrogenic induction process of CPCs. The mass of mitochondria was higher in differentiated CPC and the fusion status was obvious relative to un-differentiated CPC. Chondrogenesis of CPCs was upregulated with the induction by mitochondrial fusion promoter. MFN2 over-expression significantly increased chondrocyte-specific gene expression and reversed OA through Notch2 signal pathway.Conclusions: Our study demonstrated that the mitochondrial fusion promotes chondrogenesis differentiation of CPCs. MFN2 accelerates the chondrogenesis differentiation of CPCs through Notch2. In vivo, MNF2-OE in sheets of rCPCs ameliorated OA in the rat model.

Although bromocriptine (BRC) as first-line drugs are recommended for treating patients with prolactinoma, a minority of patients with prolactinoma resistance to BRC. Moreover, our previous study showed that the difference in drug sensitivity in BRC- treated rat prolactinoma cells, MMQ cells are more resistant to BRC, and GH3 cells are more sensitive to BRC. Curcumin (Cur) has been shown to inhibit proliferation of prolactinoma cell lines. The aim of this study is to further investigate whether Cur could enhance the growth-inhibitory effect of BRC resistance on prolactinoma cell lines and its possible mechanism. CCK-8 kit was used to test cell growth. Cell-cycle analysis and apoptosis was performed by flow cytometry. Electron microscopy was used to test autophagosome. The mRNA expression profiles were analysed using the Affymetrix Gene-Chip array. Western blotting was used to test protein expression. Our data showed that Cur enhanced the growth-inhibitory effect of BRC on GH3 and MMQ cell proliferation. BRC and Cur both induced cell apoptosis, and Cur could significantly increase the apoptosis of BRC on pituitary adenoma cells through the ERK/EGR1 signaling pathway. Moreover, Cur could enhance the autophagic cell death (ACD) of BRC on tumor cell by inhibiting the AKT/GSK3β signaling pathway. The same results were confirmed in vivo study. Taken together, Cur sensitizes rat pituitary adenoma cell to BRC by activating the ERK/EGR1 and inhibiting AKT/GSK3β signaling pathway.

Background: Despite improvements reported in diagnosis and treatments in recent decades, pancreatic cancer still characterized with poor prognosis and low survival rate among solid tumors. Intensive interests have grown in exploring novel predictive biomarkers, aiming to enhance the efficiency in early detection and treatment prognosis.Methods: In this study, we identified the differentially expressed genes (DEGs) in pancreatic cancer through analyzed five gene expression profiles, and established the functional modules according to the functional interaction (FI) network between DEGs.Results: Significant upregulation of the selected DEG, IFITM1, was evaluated in several bioinformatics online tools and verified with immunohistochemistry staining from 90 pancreatic cancer patients’ samples. Prognostic data showed that high expression of IFITM1 associated with poor survival and multivariate Cox regression analysis showed that IFITM1 was one of independent prognostic factor for the overall survival. Meanwhile, significant correlations of the expression of IFITM1 and the infiltration of immune cells were found by TIMER. Furthermore, higher level of IFITM1 was assessed in pancreatic cancer cell lines compared to normal human pancreatic duct epithelial cell and silencing IFITM1 in tumor cells remarkedly inhibited the cancer tumorigenicity.Conclusion: Collectively, our findings suggested that IFITM1 might have promising clinical utility for pancreatic cancer.

Background The application of neuroendoscopy in intraventricular hemorrhage (IVH) has attracted more and more attention in recent years. Studies have shown that the use of neuroendoscopy for IVH evacuation has advantages over external ventricular drainage (EVD) alone. However, the cases of most current research are small and all of them are retrospective studies. The aim of this study is to explore the prognosis of patients with moderate to severe IVH who undergo endoscopic IVH evacuation surgery versus those who undergo EVD alone. Methods The study is a prospective, randomized, controlled, multi-center clinical trial. Nine hundred and fifty-six subjects with moderate to severe IVH across four tertiary hospitals in China will be randomly assigned (1:1) to receive either endoscopic IVH evacuation surgery or EVD. The primary objective is to compare patients’ survival rate at 12 months after surgery. Discussion The trial is designed to investigate the prognostic benefits of endoscopic IVH evacuation surgery for patients with moderate to severe IVH. Currently, it has never been investigated in a prospective randomized controlled clinical trial. Trial registration ClinicalTrials.gov, NCT04037267. Registered on 26 July 2019.