ACS Applied Electronic Materials最新文献

Intensive longitudinal data (ILD) has been collected to capture the dynamic fluctuations of procrastination; however, researchers have typically measured daily procrastination by modifying trait measures (e.g., adding a time reference "today") without adequately testing their reliabilities. The main purpose of this study was to use an advanced approach, dynamic structural equation modeling, to assess the between- and within-person reliabilities of a widely used six-item measure of daily procrastination. A total of 252 participants completed retrospective measures of various types of trait procrastination and daily measures of procrastination over 34 consecutive days. The results showed that the entire scale for daily procrastination and five of its six items had high between- and within-person reliabilities, but one item had much lower reliabilities, suggesting that this item may be inappropriate in everyday contexts. Furthermore, we found moderate to strong associations between the latent trait factor of procrastination and trait measures of procrastination. In addition, we identified substantial between-person variation in person-specific reliabilities and explored its relevant factors. Overall, this study assessed the reliabilities of a daily measure of procrastination, which facilitated future studies to obtain more reliable and consistent results and to better estimate the reliability of ILD.

Estrogen‑related receptor (ERR) is an orphan nuclear receptor structurally akin to the estrogen receptor. ERR is expressed in tissues with active energy metabolism and regulates intracellular metabolic functions. Additionally, ERRs are known to be strongly expressed in the epidermis of skin tissue, but their functions are unknown. The present study investigated the function of ERRα in human skin fibroblasts. ERRα expressed in human dermal fibroblast TIG113 was knocked down using small interfering (si)RNA and gene expression was comprehensively analyzed using microarrays 48 h later. Pathway analysis was performed using Wikipathways on genes exhibiting expression changes of ≥1.5‑fold. Expression of cell cycle‑related and apoptosis‑related genes was compared using reverse transcription‑quantitative PCR. After treating TIG113 cells with siERRα for 72 h, cell proliferation was assessed using the Cell Counting Kit‑8 or a scratch wound healing assay and apoptotic cells were measured using the Poly Caspase Assay Kit. Cell cycle analysis was performed using flow cytometry. The expression of the ERRα gene was suppressed by siRNA. The expression of genes associated with cell cycle‑related pathways were decreased while that of those associated with apoptosis‑related pathways increased. Furthermore, the expression of cell cycle‑related genes such as cell division cycle 25C, cyclin E and cyclin B1 was decreased and the expression of apoptosis‑related genes such as caspase3 and Fas cell surface death receptor was increased. Cell proliferation was suppressed and the number of apoptotic cells increased ~2‑fold in ERRα‑knockdown TIG113 cells. Cell cycle analysis revealed that the number of cells in the Sub‑G₁ phase increased and that in the S and G₂/M phases decreased. The present study suggested that ERRα is an essential for the survival of human skin fibroblasts.

Cells rely on autophagy for the degradation and recycling of damaged proteins and organelles. Chaperone-mediated autophagy (CMA) is a selective process targeting proteins for degradation through the coordinated function of molecular chaperones and the lysosome‑associated membrane protein‑2A receptor (LAMP2A), pivotal in various cellular processes from signal transduction to the modulation of cellular responses under stress. In the present review, the intricate regulatory mechanisms of CMA were elucidated through multiple signaling pathways such as retinoic acid receptor (RAR)α, AMP‑activated protein kinase (AMPK), p38‑TEEB‑NLRP3, calcium signaling‑NFAT and PI3K/AKT, thereby expanding the current understanding of CMA regulation. A comprehensive exploration of CMA's versatile roles in cellular physiology were further provided, including its involvement in maintaining protein homeostasis, regulating ferroptosis, modulating metabolic diversity and influencing cell cycle and proliferation. Additionally, the impact of CMA on disease progression and therapeutic outcomes were highlighted, encompassing neurodegenerative disorders, cancer and various organ‑specific diseases. Therapeutic strategies targeting CMA, such as drug development and gene therapy were also proposed, providing valuable directions for future clinical research. By integrating recent research findings, the present review aimed to enhance the current understanding of cellular homeostasis processes and emphasize the potential of targeting CMA in therapeutic strategies for diseases marked by CMA dysfunction.

Lung cancer remains a leading cause of global cancer‑related deaths, therefore the identification of prognostic factors for lung cancer is critical. Casein kinase 2 alpha (CK2α) is one of the driver kinases in various cancers, and it was previously demonstrated that CK2α localization was associated with a poor prognosis in invasive breast cancer. In the present study, the importance of CK2α in the nucleolus was explored as a potential prognostic marker for surgically resected early‑stage lung adenocarcinoma. The present study included 118 patients who underwent pulmonary lobectomy between 2014 and 2018 in Fukushima Medical University Hospital (Fukushima, Japan), and in whom CK2α localization in tumor samples was assessed by immunohistochemistry. Patient and tumor characteristics, including pathological stage, histological type and histological grade, were analyzed. Recurrence‑free survival (RFS) and overall survival were evaluated in relation to nucleolar CK2α staining. CK2α staining in the nucleoli was observed in 50.8% of lung adenocarcinoma tumors. Positive nucleolar CK2α staining was independent of pathological stage, histological type and histological grade. Patients with positive nucleolar CK2α staining exhibited significantly worse RFS compared with patients with negative staining. Multivariate analysis identified nucleolar CK2α staining and lymph node metastasis as independent poor prognostic factors. The results of the present study suggested that nucleolar CK2α staining is a novel and independent prognostic factor in surgically resected early‑stage lung adenocarcinoma. These findings indicated the potential of nucleolar CK2α as a predictive biomarker for future recurrence, and a guide to treatment decisions. Further research is required, particularly in understanding the molecular mechanisms linking nucleolar CK2α to recurrence.

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the flow cytometric plots shown in Fig. 5A and B on p. 2572, each figure part contained a pair of duplicated data panels; specifically, the panels depicting the 'NC/5‑FU' and the 'shTRIM11/Gemcitabine' experiments in Fig 5A (MCF‑7 cells), and the 'NC/Paclitaxel' and 'shTRIM11/Adriamycin' experi-ments in Fig. 5B (MDA‑MB‑231 cells), were apparently identical. The authors were able to re‑examine their original data files, and realize that this figure was inadverently assembled incorrectly. The revised version of Fig. 5, now showing the correct data for the 'shTRIM11/Gemcitabine' experiment in Fig 5A and the 'NC/Paclitaxel' experiment in Fig. 5B, is shown on the next page. Note that the revisions made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 41: 2567‑2574, 2019; DOI: 10.3892/or.2019.7015].

This study evaluated symptoms assessed in common measures of eating disorder pathology and tested overlap to evaluate the extent to which measures may be interchangeable. Six measures were included: Bulimia Test-Revised, Eating Attitudes Test-26, Eating Disorder Diagnostic Scale, Eating Disorder Examination Questionnaire, Eating Pathology Symptoms Inventory, and Questionnaire for Eating Disorder Diagnoses. Content overlap was quantitatively estimated using the Jaccard Index. Mean overlap was low (.195), likely due to the wide range of symptoms (87) assessed. The mean overlap of each measure with all others was .117 - .267, and the overlap among individual measures was .083 - .382. Implications of low overlap among measures include variable characterization of eating disorder phenotypes and the risk for lower generalizability of findings due to measurement variability.

Significance: Standardization of fluorescence molecular imaging (FMI) is critical for ensuring quality control in guiding surgical procedures. To accurately evaluate system performance, two metrics, the signal-to-noise ratio (SNR) and contrast, are widely employed. However, there is currently no consensus on how these metrics can be computed.

Aim: We aim to examine the impact of SNR and contrast definitions on the performance assessment of FMI systems.

Approach: We quantified the SNR and contrast of six near-infrared FMI systems by imaging a multi-parametric phantom. Based on approaches commonly used in the literature, we quantified seven SNRs and four contrast values considering different background regions and/or formulas. Then, we calculated benchmarking (BM) scores and respective rank values for each system.

Results: We show that the performance assessment of an FMI system changes depending on the background locations and the applied quantification method. For a single system, the different metrics can vary up to $\sim 35\mathrm{dB}$ (SNR), $\sim 8.65a.u$ . (contrast), and $\sim 0.67a.u$ . (BM score).

Conclusions: The definition of precise guidelines for FMI performance assessment is imperative to ensure successful clinical translation of the technology. Such guidelines can also enable quality control for the already clinically approved indocyanine green-based fluorescence image-guided surgery.

Incidence of a number of liver diseases has increased. Gut microbiota serves a role in the pathogenesis of hepatitis, cirrhosis and liver cancer. Gut microbiota is considered 'a new virtual metabolic organ'. The interaction between the gut microbiota and liver is termed the gut‑liver axis. The gut‑liver axis provides a novel research direction for mechanism of liver disease development. The present review discusses the role of the gut‑liver axis and how this can be targeted by novel treatments for common liver diseases.

Long non‑coding RNAs serve a crucial role in autophagy of vascular smooth muscle cells (VSMCs). The present study aimed to investigate the effect of small nucleolar RNA host gene 1 (SNHG1) on autophagy in VSMCs and the associated underlying mechanisms. Rapamycin was used to induce autophagy in VSMCs and the effects of SNHG1 on the proliferation and migration of VSMCs and the change in phenotype were tested following overexpression and silencing of SNHG1. The target gene of SNHG1 was predicted and validated. SNHG1‑regulated autophagy of VSMCs via C‑type lectin domain family 7 member A (CLEC7A) was determined by combined silencing of SNHG1 and overexpression of CLEC7A. Rapamycin‑induced autophagy in VSMCs changed the cell phenotype from contractile to synthetic, with decreased expression of α‑smooth muscle actin and smooth muscle protein 22a and increased expression of osteopontin. Overexpression of SNHG1 caused the same change in phenotype while the opposite change was observed following SNHG1 silencing. Overexpression of SNHG1 promoted the proliferation and migration of VSMCs. CLEC7A was identified as a target gene of SNHG1 and a direct binding relationship between them was confirmed by RNA immunoprecipitation and RNA pull‑down assays. Overexpression of SNHG1 increased the expression of CLEC7A. The expression of both SNHG1 and CLEC7A was increased during autophagy of VSMCs. Overexpression of SNHG1 promoted autophagy of VSMCs and silencing of CLEC7A reduced this effect of SNHG1. In conclusion, SNHG1 and CLEC7A were increased in VSMCs following autophagy. SNHG1 promotes the conversion of VSMCs from a contractile phenotype to a synthetic phenotype by facilitating CLEC7A expression.

In a recent study, Reinforcement Learning (RL) used in combination with many-objective search, has been shown to outperform alternative techniques (random search and many-objective search) for online testing of Deep Neural Network-enabled systems. The empirical evaluation of these techniques was conducted on a state-of-the-art Autonomous Driving System (ADS). This work is a replication and extension of that empirical study. Our replication shows that RL does not outperform pure random test generation in a comparison conducted under the same settings of the original study, but with no confounding factor coming from the way collisions are measured. Our extension aims at eliminating some of the possible reasons for the poor performance of RL observed in our replication: (1) the presence of reward components providing contrasting feedback to the RL agent; (2) the usage of an RL algorithm (Q-learning) which requires discretization of an intrinsically continuous state space. Results show that our new RL agent is able to converge to an effective policy that outperforms random search. Results also highlight other possible improvements, which open to further investigations on how to best leverage RL for online ADS testing.