Dynamic observation: The rapid oxidative redispersion of large Pt nanoparticles supported on ceria‐based oxide in autoexhaust catalysts is demonstrated in the absence of Cl by in situ XANES analysis. An atomic migration model accounts for the observed redispersion through the trapping of Pt species at sites on the Ce support that exhibit strong interactions between the Pt oxide and the support.

In recent years, circular RNAs (circRNAs) have been identified to be essential regulators of various human cancers. However, knowledge of the functions of circRNAs in prostate cancer remains very limited. The correlation between circABCC4 and human cancer is largely unknown. This study aims to investigate the biological functions of circABCC4 in prostate cancer progression and illustrate the underlying mechanism. We found that circABCC4 was remarkably up‐regulated in prostate cancer tissues and cell lines and promoted FOXP4 expression by sponging miR‐1182 in prostate cancer cells. CircABCC4 knockdown markedly suppressed prostate cancer cell proliferation, cell‐cycle progression, migration and invasion in vitro. Furthermore, silencing of the circRNA also delayed tumor growth in vivo. Taken together, our findings indicated that circABCC4 facilitates the malignant behaviour of prostate cancer by promoting FOXP4 expression through sponging of miR‐1182. The circABCC4–miR‐1182‐FOXP4 regulatory loop may be a promising therapeutic target for prostate cancer intervention.

Human oocyte maturation is a precondition for fertilization and ensuing embryonic development. Previously, we identified TUBB8 variants as a genetic determinant of human oocyte maturation arrest and showed that these variants cause variable and mixed phenotypes in oocyte maturation and early embryo development. We also estimated that rare inherited or de novo variants in the TUBB8 gene accounted for 30% of individuals in a small cohort of patients affected by oocyte maturation arrest. In the present study, we recruited a further 87 patients from unrelated families diagnosed with oocyte maturation or early embryonic arrest and identified 30 patients carrying TUBB8 variants. The corresponding phenotypes not only include oocyte maturation arrest, failure of fertilization, and early embryonic arrest, but also extend to the new phenotype of failure of embryo implantation. These observations provide the most detailed mutational and phenotypic spectrum of TUBB8, further extend the spectrum of variants and dysfunctional oocyte and embryo phenotypes caused by TUBB8 variants, and confirm previous findings for a critical role of TUBB8 during oocyte maturation and early embryonic development. Thus, TUBB8 mutation screening might not only be a genetic diagnostic marker for patients with oocyte maturation arrest, but might also have clinical implications for evaluating the competence of patients' functional oocytes with first polar body (PB1).

Dedicated to the Catalysis Society of Japan on the occasion of its 50th Anniversary Supported precious metals, such as platinum (Pt), rhodium (Rh), and palladium (Pd), are used to facilitate many industrial catalytic processes. Pt in particular is found at the core of catalysts used throughout the petrochemical industry: from bifunctional catalysts (isomerization/dehydrogenation) used for refining of hydrocarbon fuel stocks, to three-way (CO and hydrocarbon oxidation/NO x reduction) conversions within car exhausts. In this latter, ubiquitous applicationcommercialized in the USA and Japan in 1977 [1] -Pt has always been a pivotal component in the abatement of harmful gas emissions from gasoline-or diesel-driven engines. The ever-increasing appreciation of the damage that noxious gas emissions are doing to our environment and the finite availability of noble metals provide strong drivers for the continued study and optimization of the behavior of Pt-based three-way catalysts (TWCs). Central to technological progress in this area is a fundamental understanding of how these materials behave, which may allow us to stop them degrading or deactivating during operation.

We report the first application of high-frequency threedimensional power Doppler ultrasound imaging in a genetically engineered mouse (GEM) prostate cancer model. We show that the technology sensitively and specifically depicts functional neoangiogenic blood flow because little or no flow is measurable in normal prostate tissue or tumors smaller than 2-3 mm diameter, the neoangiogenesis ''switch-on'' size. Vascular structures depicted by power Doppler were verified using Microfil-enhanced micro-computed tomography (micro-CT) and by correlation with microvessel distributions measured by immunohistochemistry and enhanced vascularity visualized by confocal microscopy in two GEM models [transgenic adenocarcinoma of the mouse prostate (TRAMP) and PSP94 gene-directed transgenic mouse adenocarcinoma of the prostate (PSP-TGMAP)]. Four distinct phases of neoangiogenesis in cancer development were observed, specifically, (a) an early latent phase; (b) establishment of a peripheral capsular vascular structure as a neoangiogenesis initiation site; (c) a peak in tumor vascularity that occurs before aggressive tumor growth; and (d) rapid tumor growth accompanied by decreasing vascularity. Microsurgical interventions mimicking local delivery of antiangiogenesis drugs were done by ligating arteries upstream from feeder vessels branching to the prostate. Microsurgery produced an immediate reduction of tumor blood flow, and flow remained low from 1 h to 2 weeks or longer after treatment. Power Doppler, in conjunction with micro-CT, showed that the tumors recruit secondary blood supplies from nearby vessels, which likely accounts for the continued growth of the tumors after surgery. The microsurgical model represents an advanced angiogenic prostate cancer stage in GEM mice corresponding to clinically defined hormone-refractory prostate cancer. Three-dimensional power Doppler imaging is completely noninvasive and will facilitate basic and preclinical research on neoangiogenesis in live animal models. [Cancer Res 2007;67(6):2830-9]

Objects To evaluate prognostic factors and treatment outcomes of primary squamous cell carcinoma in thyroid (PSCCTh) over the past decades using a large national database. Methods All patients diagnosed with PSCCTh between 1973 and 2015 were identified with the Surveillance, Epidemiology, and End Results Program (SEER) 18‐registry database. Relevant clinical data were collected, and prognostic factors of overall survival (OS) and disease‐specific survival (DSS) were analyzed. Results This cohort study included 242 patients, accounting for 0.12% of all primary thyroid carcinomas from 1973 to 2015 nationwide. Of the patients with PSCCTh, 75% were older than 60 years at diagnosis. Patient age older than 60 years (HR 2.242, 95% CI 1.367–3.676, P = 0.001) and a tumor size larger than or equal to 50 mm (HR 1.479, 95% CI 1.011–2.165, P = 0.044) were independent negative prognostic factors. The univariate analysis suggested that the morphological subtype (OS, P = 0.033; DSS, P = 0.048), clinical treatment modality (OS, P < 0.0001; DSS, P < 0.0001), and T stage (OS, P = 0.004; DSS, P = 0.001) were important predictive factors for OS and DSS. In contrast, gender, race, year of diagnosis, geographic location, N stage, and M stage were not prognostic factors. Conclusions PSCCTh is a rare malignancy with an aggressive nature and poor prognosis. Survival is predicted by the treatment modality, patient age, T stage, tumor size, and morphological subtypes. This study showed that early diagnosis and complete surgical resection plus adjuvant radiation therapy were associated with a better outcome.

Context Metabolic reprogramming is a common feature of tumorigenesis. It remains unknown concerning the expression pattern of metabolism-associated genes in dedifferentiated thyroid cancer (DDTC). Objective This study aimed to identify a useful signature to indicate dedifferentiation of papillary thyroid cancer (PTC). Design and Setting We used one discovery and two validation cohorts to screen out aberrant metabolic genes in DDTC, and further used The Cancer Genome Atlas (TCGA) cohort to search for independent risk factors for the low-differentiated phenotype of PTC as a signature of dedifferentiation. The prediction of the signature for DDTC was validated in the TCGA cohort and the combined Gene Expression Omnibus cohort. We also analyzed the correlations of the signature risk score with clinicopathological features of PTC. Gene set enrichment analyses were performed in the TCGA cohort. Results Significant enrichment of metabolic pathways correlated with differentiation status of PTC. A signature of metabolic genes including LPCAT2, ACOT7, HSD17B8, PDE8B, and ST3GAL1 was discovered and validated across three cohorts. The signature was not only predictive of DDTC but also significantly associated with BRAFV600E mutation (P < 0.001), T3/T4 stage (P < 0.001), extrathyroidal extension (P < 0.001), lymph node metastasis (P < 0.001), and tumor/lymph node/metastasis III/IV stage (P < 0.001) in PTC. Downregulations of LPCAT2 expression (P = 0.009) and ST3GAL1 expression (P = 0.005) increased risks of decreased disease-free survival for patients. Furthermore, the signature was implicated in a number of oncogenic biological pathways. Conclusions Our findings suggest that metabolic deregulations mediate dedifferentiation of PTC, and that the metabolic gene signature can be used as a biomarker for DDTC.

The expression pattern and detailed roles of long noncoding RNA LINC00511 in clear cell renal cell carcinoma (ccRCC) remain unknown. We measured LINC00511 expression in ccRCC. We clarified the clinical characteristics associated with LINC00511 in ccRCC. We examined the biological roles of LINC00511 in the progression of ccRCC, and we identified the potential mechanisms involved. LINC00511 was upregulated in ccRCC tissues and cell lines. High LINC00511 expression significantly correlated with TNM classification, lymph node metastasis, and short overall survival among patients with ccRCC. Additionally, LINC00511 knockdown restricted ccRCC cell proliferation, colony formation, and metastasis in vitro; accelerated cell cycle arrest at G0–G1 and apoptosis in vitro; and decreased tumor growth in vivo. Investigation of the mechanism revealed that LINC00511 directly interacted with microRNA-625 (miR-625), and the inhibitory effects of the LINC00511 knockdown on malignant characteristics were neutralized by miR-625 silencing. Furthermore, cyclin D1 (CCND1) was identified as a direct target of miR-625 in ccRCC cells. The tumor-suppressive activity of miR-625 upregulation on ccRCC cells was reversed by CCND1 reintroduction. In conclusion, LINC00511 serves as a competing endogenous RNA that regulates CCND1 expression by sponging miR-625 in ccRCC. Hence, the LINC00511/miR-625/CCND1 pathway might be a promising therapeutic target in ccRCC.