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BackgroundSerum carcinoembryonic antigen (CEA) is an important biomarker for diagnosis, prognosis, recurrence, metastasis monitoring, and the evaluation of the effect of chemotherapy in colorectal cancer (CRC). However, few studies have focused on the role of early postoperative CEA in the prognosis of stage II CRC.MethodsPatients with stage II CRC diagnosed between January 2007 and December 2015 were included. Receiver operating characteristic (ROC) curves were used to obtain the cutoff value of early postoperative CEA, CEA ratio and CEA absolute value. The areas under curves (AUCs) were used to estimate the predictive abilities of the CEA and T stage. The stepwise regression method was used to screen the factors included in the Cox regression analysis. Before and after propensity score (PS) - adjusted Cox regression and sensitivity analysis were used to identify the relationship between early postoperative CEA and prognosis. Meta-analysis was performed to verify the results. Kaplan-Meier survival curves were used to estimate the effects of CEA on prognosis.ResultsWe included 1081 eligible patients. ROC curves suggested that the cutoff value of early postoperative CEA was 3.66 ng/ml (P 0.05). Patients with a CEA ratio ≤0.55 or CEA absolute value ≤-0.98 had a worse prognosis (all P-values were < 0.001). Survival analysis suggested that adjuvant chemotherapy for stage II CRC patients with elevated early postoperative CEA may improve the CSS (P = 0.040).ConclusionsEarly postoperative CEA was a better biomarker for prognosis of stage II CRC patients than T stage and preoperative CEA, and has the potential to become a high-risk factor to guide the prognosis and treatment of stage II CRC patients.

C2N-ring-based molecular chains were designed at the molecular level and theoretically demonstrated to show distinctive and valuable electron transport properties that were superior to the parent carbonaceous system and other similar nanoribbon-based molecular chains. This new -type molecular chain presented an exponential attenuation of the conductance and electron transmission with the length. Essentially, the molecular chain retained the electron-resonant tunneling within 7 nm and the dominant transport orbital was the LUMO. Shorter molecular chains with stronger conductance anomalously possessed a larger tunnel barrier energy, attributing to the compensation of a much smaller HOMO–LUMO gap, and these two internal factors codetermined the transport capacity. Some influencing factors were also studied. In contrast to the common O impurity with a tiny effect on electron transmission of the C2N rings chain, the common H impurity clearly improved it. When the temperature was less than 400 K, the electron transmission varied with temperature within a narrow range, and the structural disorder deriving from proper heating did not greatly modify the transmission possibility and the exponentially decreasing tendency with the length. In a non-equilibrium condition, the current increased overall with the bias but the growth rate varied with size. A valuable negative differential resistance (NDR) effect appeared in longer molecular chains with an even number of big carbon–nitrogen rings and strengthened with size. The emergence of such an effect originated from the reduction in transmission peaks. The conductance of longer molecular chains was enhanced with the voltage but the two shortest ones presented completely different trends. Applying the bias was demonstrated to be an effective way for C2N-ring-based molecular chains to slow down the conductance decay constant and affect the transport regime. C2N-ring-based molecular chains show a perfect application in tunneling diodes and controllable molecular devices. [ABSTRACT FROM AUTHOR]

Van der Waals heterojunctions of two-dimensional atomic crystals are widely used to build functional devices due to their excellent optoelectronic properties, which are attracting more and more attention, and various methods have been developed to study their structure and properties. Here, density functional theory combined with the nonequilibrium Green's function technique has been used to calculate the transport properties of graphene/WS2 heterojunctions. It is observed that the formation of heterojunctions does not lead to the opening of the Dirac point of graphene. Instead, the respective band structures of both graphene and WS2 are preserved. Therefore, the heterojunction follows a unique Ohm's law at low bias voltages, despite the presence of a certain rotation angle between the two surfaces within the heterojunction. The transmission spectra, the density of states, and the transmission eigenstate are used to investigate the origin and mechanism of unique linear I–V characteristics. This study provides a theoretical framework for designing mixed-dimensional heterojunction nanoelectronic devices. [ABSTRACT FROM AUTHOR]

The effective implementation of quantization depends not only on the specific task but also on the hardware resources. This article presents a hardware-aware customized quantization method for convolutional neural networks. We propose a learnable parameter soft clipping full integer quantization (LSFQ), which includes weight and activation quantization with the learnable clipping parameters. Moreover, the LSFQ accelerator architecture is customized on the field-programmable gate array (FPGA) platform to verify the hardware awareness of our method, in which DSP48E2 is designed to realize the parallel computation of six low-bit integer multiplications. The results showed that the accuracy loss of LSFQ is less than 1% compared with the full-precision models including VGG7, mobile-net v2 in CIFAR10, and CIFAR100. An LSFQ accelerator was demonstrated at the 57th IEEE/ACM Design Automation Conference System Design Contest (DAC-SDC) and won the championship at the FPGA track. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease (PD) is the second most common neurodegenerative disease. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) has been demonstrated as an important regulator in PD pathology. However, the functional mechanisms played by SNHG14 in PD remain largely unclear. Methods: We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP+) to establish PD mouse and cell models. The levels of SNHG14, miR-214-3p, and Krüppel-like factor 4 (KLF4) were gauged by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot analysis. Cell viability and apoptosis were determined using the Cell Counting-8 Kit (CCK-8) assay and flow cytometry, respectively. The levels of inflammatory cytokines were evaluated by ELISA. The relationships among SNHG14, miR-214-3p, and KLF4 were confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that SNHG14 was upregulated and miR-214-3p was downregulated in PD models. SNHG14 knockdown ameliorated MPP+-stimulated damage in SK-N-SH cells, as evidenced by the enhancement in cell viability and the suppression in cell apoptosis and pro-inflammatory cytokine production. Mechanistically, SNHG14 directly targeted miR-214-3p via binding to miR-214-3p, and SNHG14 knockdown protected SK-N-SH cell from MPP+-stimulated cytotoxicity by upregulating miR-214-3p. KLF4 was a direct target of miR-214-3p, and SNHG14 regulated KLF4 expression by acting as a miR-214-3p sponge. Furthermore, miR-214-3p overexpression alleviated MPP+-stimulated damage in SK-N-SH cells by downregulating KLF4. Conclusion: Our current study first demonstrated the protective effect of SNHG14 knockdown on MPP+-stimulated cytotoxicity in SK-N-SH cells at least partially by targeting the miR-214-3p/KLF4 axis, illuminating a promising target for PD intervention and treatment. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is one of the most common neurodegenerative disorders. Long non‐coding RNAs have important regulatory values in various human diseases. Non‐coding RNA Activated by DNA Damage (NORAD) was reported to regulate PD progression in vitro, but its functional mechanism is fully unknown. We used 1‐methyl‐4‐phenylpyridinium (MPP+) to establish the cell‐based PD model. NORAD, microRNA‐204‐5p (miR‐204‐5p), and solute carrier family 5 member 3 (SLC5A3) levels were quantified using the quantitative real‐time polymerase chain reaction. Cell viability and apoptosis were determined by Cell Counting Kit‐8 and flow cytometry, respectively. The protein levels were analyzed via western blot. Cytotoxicity was assessed by the released lactate dehydrogenase level in cell supernatant. Oxidative stress and inflammation were measured by the standard indicators. Dual‐luciferase reporter and RNA immunoprecipitation assays were performed for intergenic combination. First, we found that NORAD was obviously reduced in MPP+‐treated neuroblastoma cells and lightened the MPP+‐induced cytotoxicity, oxidative stress, and inflammatory response. Then, NORAD was shown to be a miR‐204‐5p sponge and avoided the injury induced by MPP+ in neuroblastoma cells via targeting miR‐204‐5p. SLC5A3 was a miR‐204‐5p target and could be regulated by NORAD/miR‐204‐5p axis. SLC5A3 knockdown assuaged the anti‐miR‐204‐5p‐induced protection for neuroblastoma cells from MPP+. Altogether, NORAD played a neuroprotective role against the progression of MPP+‐induced PD model in neuroblastoma cells relying on the miR‐204‐5p/SLC5A3 axis. This study afforded the clear elaboration on the PD pathomechanism concerning NORAD. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease (PD) is the second most common neurodegenerative disease. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) has been demonstrated as an important regulator in PD pathology. However, the functional mechanisms played by SNHG14 in PD remain largely unclear., Methods: We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP + ) to establish PD mouse and cell models. The levels of SNHG14, miR-214-3p, and Krüppel-like factor 4 (KLF4) were gauged by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot analysis. Cell viability and apoptosis were determined using the Cell Counting-8 Kit (CCK-8) assay and flow cytometry, respectively. The levels of inflammatory cytokines were evaluated by ELISA. The relationships among SNHG14, miR-214-3p, and KLF4 were confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays., Results: Our data indicated that SNHG14 was upregulated and miR-214-3p was downregulated in PD models. SNHG14 knockdown ameliorated MPP + -stimulated damage in SK-N-SH cells, as evidenced by the enhancement in cell viability and the suppression in cell apoptosis and pro-inflammatory cytokine production. Mechanistically, SNHG14 directly targeted miR-214-3p via binding to miR-214-3p, and SNHG14 knockdown protected SK-N-SH cell from MPP + -stimulated cytotoxicity by upregulating miR-214-3p. KLF4 was a direct target of miR-214-3p, and SNHG14 regulated KLF4 expression by acting as a miR-214-3p sponge. Furthermore, miR-214-3p overexpression alleviated MPP + -stimulated damage in SK-N-SH cells by downregulating KLF4., Conclusion: Our current study first demonstrated the protective effect of SNHG14 knockdown on MPP + -stimulated cytotoxicity in SK-N-SH cells at least partially by targeting the miR-214-3p/KLF4 axis, illuminating a promising target for PD intervention and treatment., (Copyright © 2020 Zhou, Zhang, Guo, Zhang and Chen.)