A bilayer CoSi2/TiN has been grown on (100)Si, starting from a (100) p-type Si wafer deposited with thin layers of Ti followed by Co metal, through a two-stage annealing in a nitrogen environment and an intervening etch. In this process, Co and Ti switch places to form CoSi2 covered with TiN on Si. Cross-section transmission electron microscopy, and Rutherford backscattering/channeling spectrometry were used to characterize the bilayer sample. The CoSi2 was found to be single crystal, fully coherent, and epitaxial with (100)Si, whereas the TiN at the top of CoSi2 was polycrystalline. The stress in the CoSi2/TiN layer was found to be 1.9×1010 dynes/cm2. The planar (100) CoSi2/Si interface was interrupted with {111} ledges which are believed to be structural ledges present to maintain the coherency at the interface.
Many epithelial-mesenchymal transition (EMT)-promoting transcription factors have been implicated in tumorigenesis and metastasis, as well as chemoresistance of cancer. However, the underlying mechanisms mediating these processes are unclear. Here we report that Foxq1, a forkhead box-containing transcription factor and EMT-inducing gene, promotes stemness traits and chemoresistance in mammary epithelial cells. Using an expression profiling assay, we identified Twist1, Zeb2, and PDGFRα and β as Foxq1 downstream targets. We further show that PDGFRα and β can be directly regulated by Foxq1 or indirectly regulated through the Foxq1/Twist1 axis. Knockdown of both PDGFRα and β results in more significant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown of either PDGFRα or β alone. In addition, PDGFRβ is a more potent mediator of Foxq1-promoted stemness traits than PDGFRα. Finally, pharmacological inhibition or gene silencing of PDGFRs sensitizes mammary epithelial cells to chemotherapeutic agents in vitro and in vivo. These findings collectively implicate PDGFRs as critical mediators of breast cancer oncogenesis and chemoresistance driven by Foxq1, and may have important implications for the development of novel combinational therapeutics against breast cancer. Note: This abstract was not presented at the meeting. Citation Format: Fanyan Meng, Cecilia Speyer, Bin Zhang, Yongzhong Zhao, Wei Chen, David Gorski, Fred R. Miller, Guojun Wu. PDGFRα and β play critical roles in mediating Foxq1-driven breast cancer stemness and chemoresistance. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4092. doi:10.1158/1538-7445.AM2015-4092
Background Active surveillance (AS) with delayed intervention has gained acceptance as a management strategy for small renal masses (SRMs). However, during AS, there is a risk of tumor growth. Thus, we aim to investigate whether tumor growth in patients with SRMs leads to tumor progress. Methods In this study, we enrolled 16,070 patients from the Surveillance, Epidemiology, and End Results database with T1a renal cell carcinoma (RCC) between 2004 and 2017. The 16,070 patients were divided into three groups: 10,526 in the partial nephrectomy (PN) group, 2768 in the local ablation (LA) group, and 2776 in the AS group. Associations of tumor size with all‐cause and cancer‐specific mortality were evaluated using Kaplan–Meier analyses and Cox regression models. Results Four tumor size categories were delineated (≤1, >1–2, >2–3, and > 3–4 cm in diameter), and 10‐year all‐cause and cancer‐specific mortality both significantly increased with increasing tumor size in the PN, LA, and AS groups (all p < 0.05). Tumors were substaged based on diameter: T1aA (≤2 cm) and T1aB (>2–4 cm). All‐cause and cancer‐specific mortality were significantly higher in T1aB tumors than T1aA tumors in each group (hazard ratio = 1.395 and 1.538, respectively; all p < 0.05). Conclusions Tumor growth relates to worse prognosis of T1a RCC, and 2 cm serves as a size threshold that is prognostically relevant for patients with T1a RCC. Because of the lack of accurate predictors of tumor growth rate, AS for patients with SRMs incurs a risk of tumor progression.
Background Preoperative deep vein thrombosis (DVT) of the lower extremities delays surgery in patients with femoral shaft fractures and impairs functional recovery. However, studies on preoperative DVT in patients with femoral shaft fractures are still rare. This study was aimed to retrospectively analyze the preoperative incidence, location and risk factors associated with DVT in patients with femoral shaft fractures. Methods Data of patients with femoral shaft fractures and treated with surgery at the Third Hospital of Hebei Medical University were retrospectively collected from January 2013 to December 2019. The information collected included demographic data, comorbidities, injury-related data and laboratory tests. Patients were divided into DVT and non-DVT groups. Univariate and multivariate logistic regression analyses were performed to determine independent risk factors. Results A total of 432 patients were included in this study, of whom 114 (26.4%) patients were diagnosed with preoperative DVT (all asymptomatic) and injured extremities of 78.1% (89/114) were investigated. Multivariate analysis showed that older age (increase in each 10 years), delay time from injury to operation (in each day), FIB > 4 g/L were independent risk factors for preoperative DVT. Conclusion Patients with femoral shaft fractures (especially the elderly and patients with the above-mentioned conditions) are at the risk of DVT right from admission to surgery hence should be intensively monitored and provided with prompt treatment to prevent DVT.
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