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Quan Kuai,1 Xueping Jian2 1Department of Plastic Surgery, Guangxi Weimei Cosmetology Hospital, Nanning, People’s Republic of China; 2Department of Oral and Maxillofacial Surgery and Plastic Surgery, the Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, People’s Republic of ChinaCorrespondence: Xueping Jian, Department of Oral and Maxillofacial Surgery and Plastic Surgery, the Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, People’s Republic of China, Tel +86-0791-86362541, Email 541180666@qq.comPurpose: Accumulating evidence has reported that microRNAs (miRNAs) play a critical role in the mechanism of keloid formation, and recent research found that miR-23b-3p was upregulated in keloid fibroblasts (KFs). Herein, we explored the potential effect of miR-23b-3p on fibroblasts in keloid.Materials and Methods: Clinical tissues, primary KFs and KEL FIB cells were used to detect the expression of miR-23b-3p by performing qRT-PCR. Gene knockdown was carried out to evaluate the molecular and biological changes of primary KFs and KEL FIB cells by conducting CCK-8 assay, flow cytometry and Western blot. The online databases and luciferase reporter assay were utilized to screen and identify the potential target of miR-23b-3p.Results: Upregulation of miR-23b-3p was detected in keloid tissues, primary KFs and KF cell line KEL FIB cells, and inhibition of miR-23b-3p promoted apoptosis and suppressed proliferation and the expression of collagen I, collagen III and fibronectin of primary KFs and KEL FIB cells. Further investigation revealed that TNFAIP3, the ubiquitin-editing enzyme A20, was the direct target of miR-23b-3p, and inhibition of miR-23b-3p promoted the expression of A20 in primary KFs and KEL FIB cells. The in vitro assays indicated that A20 suppression inhibited apoptosis and facilitated proliferation and the expression of collagen I, collagen III and fibronectin of miR-23b-3p inhibitor-transfected primary KFs and KEL FIB cells. Finally, we found that miR-23b-3p inhibitor reduced the expression of receptor interacting serine/threonine protein kinase 1 (RIPK1), which was partially reversed by A20 inhibition.Conclusion: These findings suggested that inhibition of miR-23b-3p/A20/RIPK1 axis induced apoptosis, limited proliferation and decreased extracellular matrix of KFs, providing a potential therapeutic target for treatment of keloid.Keywords: keloid fibroblasts, proliferation, apoptosis, extracellular matrix, MiR-23b-3p

Evidence increasingly indicated that lung cancer incidence in female individuals continue to rise, and women have a higher risk to develop adenocarcinoma than men. Male and female individuals differ in their innate and adaptive immune responses, and there are sex differences in response to the PD-1/PD-L1-dependent blocking immunotherapy. Whether the differential expression of PD-1 between genders affect the response to blocking treatment is currently unknown. In this study, we examined sex differences in serum sPD-1, mPD-1 expression on T cells, and sex hormone levels in non-small cell lung cancer (NSCLC) patients. Our results revealed a higher level of sPD-1 and expression of PD-1 on CD4+T cell in female patients than in male patients; we identified that serum sPD-1 level and the expression of mPD-1 on T cells were significantly reduced in NSCLC; we also found that serum testosterone level increased in female patients compared with control subjects and that increased testosterone downregulated the expression of mPD-1 on T cell. These findings provide a better understanding of the differences in PD-1 expression between genders in NSCLC patients and the effect of sex hormones on PD-1 expression and supply evidence for early lung cancer diagnosis and responsiveness to immune checkpoint inhibitors.

Qiuling Wang,1,* Jingxin Han,1,* Pu Xu,1 Xinchun Jian,1,2 Xieshan Huang,1 Deyu Liu1 1Stomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People’s Republic of China; 2Department of Oral and Maxillofacial Surgery, Xiangya Hospital, Central South University, Central South University, Changsha, Hunan, 410008, People’s Republic of China*These authors contributed equally to this workCorrespondence: Deyu LiuStomatology Center, Affiliated Haikou Hospital, Xiangya Medical College, Central South University, Renmin Road No. 43, Haikou, Hainan, 570208, People’s Republic of ChinaEmail mant3345@163.comBackground: Targeting the long non-coding RNAs (LncRNAs)-microRNAs (miRNAs)-mRNA competing endogenous RNA (ceRNA) networks has been proved as an effective strategy to treat multiple cancers, including oral squamous cell carcinoma (OSCC). Based on this, the present study identified a novel LncRNA SNHG16/miR-17-5p/CCND1 signaling pathway that played an important role in regulating the pathogenesis of OSCC.Methods: The expression levels of cancer-associated genes were examined by Real-Time qPCR and Western Blot at transcriptional and translated levels, respectively. CCK-8 assay was performed to determine cell proliferation, and cell apoptosis ratio was measured by the Annexin V-FITC/PI double staining assay. Transwell assay was performed to examine cell migration, and dual-luciferase reporter gene system assay was used to validate the ceRNA networks.Results: LncRNA SNHG16 and CCND1 were upregulated, while miR-17-5p was downregulated in OSCC tissues and cell lines, compared to their normal counterparts. Also, miR-17-5p negatively correlated with both LncRNA SNHG16 and CCND1 mRNA, but LncRNA SNHG16 was positively relevant to CCND1 mRNA in OSCC tissues. By performing the gain- and loss-of-function experiments, we noticed that LncRNA SNHG16 overexpression aggravated the malignant phenotypes, such as cell proliferation, viability, migration and epithelial-mesenchymal transition (EMT) in OSCC cells, while LncRNA SNHG16 knock-down had opposite effects. Furthermore, our dual-luciferase reporter gene system evidenced that LncRNA SNHG16 sponged miR-17-5p to upregulate CCND1 in OSCC cells, and the inhibiting effects of LncRNA SNHG16 ablation on OSCC progression were abrogated by both downregulating miR-17-5p and overexpressing CCND1. Finally, the xenograft tumor-bearing mice models were established, and our data validated that LncRNA SNHG16 served as an oncogene to promote tumorigenicity of OSCC cells in vivo.Conclusion: Taken together, targeting the LncRNA SNHG16/miR-17-5p/CCND1 axis hindered the development of OSCC, and this study provided potential diagnostic and therapeutic biomarkers for OSCC in clinic.Keywords: oral squamous cell carcinoma, competing endogenous RNA, LncRNA SNHG16, MiR-17-5p, cyclin D1

Background: A majority of hospice care is delivered at home, with significant caregiver involvement. Identifying factors associated with caregiver-reported quality measures could help improve hospice care in the United States. Objectives: To identify correlates of caregiver-reported quality measures: burden, satisfaction, and quality of end-of-life (EoL) care in home hospice care. Design: A cross-sectional study was conducted from April 2017 through February 2018. Setting/Subjects: A nonprofit, urban hospice organization. We recruited caregivers whose patients were discharged from home hospice care. Eligible caregiver participants had to be 18 years or older, English-speaking, and listed as a primary caregiver at the time the patient was admitted to hospice. Measures: The (1) short version of the Burden Scale for Family Caregivers; (2) Family Satisfaction with Care; and (3) Caregiver Evaluation of the Quality of End-Of-Life Care. Results: Caregivers (n?=?391) had a mean age of 59 years and most were female (n?=?297, 76.0%), children of the patient (n?=?233, 59.7%), and non-Hispanic White (n?=?180, 46.0%). The mean age of home hospice patients was 83 years; a majority had a non-cancer diagnosis (n?=?235, 60.1%), were female (n?=?250, 63.9%), and were non-Hispanic White (n?=?210, 53.7%). Higher symptom scores were significantly associated with greater caregiver burden and lower satisfaction with care; but not lower quality of EoL care. Caregivers who were less comfortable managing patient symptoms during the last week on hospice had higher caregiver burden, lower caregiver satisfaction, and lower ratings of quality of EoL care. Conclusion: Potentially modifiable symptom-related variables were correlated with caregiver-reported quality measures. Our study reinforces the important relationship between the perceived suffering/symptoms of patients and caregivers' hospice experiences.

Xiaoying Wang, 1 Xiao Jian, 1 Jun Dou, 2 Zicheng Wei, 3 Fengshu Zhao 2 1Wuxi School of Medicine, Jiangnan University, Wuxi, People’s Republic of China; 2Department of Pathogenic Biology and Immunology, School of Medicine, Southeast University, Nanjing, People’s Republic of China; 3Department of Stomatology Affiliated Hospital of Jiangnan University, Wuxi, People’s Republic of ChinaCorrespondence: Jun Dou; Fengshu ZhaoDepartment of Pathogenic Biology and Immunology, Medical School, Southeast University, 87 Dingjiaqiao Road, Nanjing 210009, People’s Republic of ChinaTel +86-25-83272454; +86-25-83272506Email njdoujun@seu.edu.cn; Fengshu_zhao@126.comBackground: The microtubule actin cross-linking factor 1 (MACF1) is involved in cellular migration, adhesion, and invasion processes. Its abnormal expression initiates tumor cell proliferation and metastasis in numerous cancer types.Methods: In this study, we utilized short hair-pin RNA interference of MACF1 to assess the inhibitory effects on the metastatic potential of B16F10 melanoma cells both in vitro and in vivo a mouse model.Results: The MACF1 expression was increased in B16F10 cells-induced tumor tissues; while the down-regulation of MACF1 impacted the B16F10 melanoma cell metastatic behavior by decreasing the ability of colony formation and invasion in vitro as well as inhibiting B16F10 cells-induced tumor growth and lung metastasis in vivo. The results of Western blot and immunohistochemistry indicated that the expression of E-cadherin and Smad-7 was significantly increased whereas the expression of N-cadherin and TGF-β 1 was significantly decreased in tumor tissue of mice challenged with the B16F10/MACF1-RNAi cells when compared with the B16F10 cells challenged mice.Conclusion: The data presented in this study demonstrated that down-regulated MACF1 expression decreased B16F10 melanoma metastasis in mice by inhibiting the epithelial to mesenchymal transition program. Thus, MACF1 may be a novel target for melanoma therapy.Keywords: melanoma, microtubule actin cross-linking factor 1, metastasis, epithelial to mesenchymal transition

Photochromic molecules offer the unique opportunity to demonstrate multifunctional devices with light-tunable electrical characteristics. Gobbi et al. build light-switchable electronic heterojunctions based on atomically precise, photo-reversible molecular superlattices on graphene and MoS2.

Two-dimensional material heterostructures enable unique electronic features by introducing periodic potentials. Here, Gobbiet al. use a monolayer supramolecular lattice with a tunable one-dimensional periodic potential to modify the electronic structure of graphene.

We report on the observation of spatially asymmetric turbulent structures with a long radial correlation length in the core of high-collisionality H -mode plasmas on DIII-D tokamak. These turbulent structures develop from shorter wavelength turbulence and have a radially elongated structure. The envelope of turbulence spans a broad radial range in the mid-radius region, leading to streamer-like transport events. The underlying turbulence is featured by intermittency, long-term memory effect, and the characteristic spectrum of self-organized criticality. The amplitude and the radial scale increase substantially when the shearing rate of the mean flow is reduced below the turbulent scattering rate. The enhanced long-radial-range-correlated (LRRC) transport events are accompanied by apparent degradation of normalized energy confinement time. The emergence of such LRRC transport events may serve as a candidate explanation for the degrading nature of H-mode core plasma confinement at high collisionality on DIII-D tokamak. [ABSTRACT FROM AUTHOR]

Limited lignocellulose degradation is the primary obstacle to feed digestion efficiency in ruminant animals. Low-quality forage with high levels of fibrous components can favor the proliferation of fibrolytic bacteria, but whether this can result a profound microbial shift after dietary intervention remains unclear. In this study, we monitored the microbial communities in the rumens of five ruminally cannulated Hu sheep through dietary transition from alfalfa hay (AH, pre-CS) to corn stover (CS, post-CS) and then back to AH (post-AH), with each treatment lasting for 14 days. The CS intervention significantly increased the relative abundance of microorganisms involved in lignocellulose degradation, including Fibrobacter and Treponema. When the diet was switched back to AH, the microbial community did not completely return to a pre-CS treatment state. In the post-AH microbial community, the relative abundances of Fibrobacter and Treponema were persistently high, and were similar to those in the post-CS community. Meanwhile, the diversity of the microbial community increased after dietary transition from AH to CS and remained significantly higher after transition from CS to AH compared to those under the original AH diet. Enzyme activity measurement verified significant increase of carboxymethyl cellulase (CMCase) and xylanase catalytic activities in the rumen. Microbial functional predictions using Tax4Fun revealed that this microbial persistence may enhance the carbohydrate metabolism pathway in the rumen. In summary, persistence of Fibrobacter and Treponema can be enhanced through a low-quality forage intervention at least for 2 weeks, which may enlighten the reprogram of microbial population in the rumen in the future.

A dimensionless collisionality scan has been performed in H-mode plasmas on DIII-D tokamak, with detailed measurements of intermediate-to-high wavenumber turbulence using Doppler backscattering systems. It is found that the shorter wavelength turbulence develops into spatially asymmetric turbulent structures with a long-radial-range correlation (LRRC) in the mid-radius region of high collisionality discharges. Linear cgyro simulations indicate that the underlying turbulence is likely driven by the electron-temperature-gradient mode. The LRRC transport events are highly intermittent and show a power spectrum of S n ̃ (k ⊥) ∝ k ⊥ − 1 for density fluctuations, which is often associated with self-organized criticality. The magnitude and the radial scale of those turbulent structures increase significantly when the E r × B mean flow shearing rate decreases at higher collisionality. The enhanced LRRC transport events appear to be correlated with the degraded energy confinement time. The emergence of such LRRC transport events may serve as a candidate explanation for the degrading nature of H-mode core plasma confinement at high collisionality. [ABSTRACT FROM AUTHOR]

The original version of this article incorrectly listed an affiliation of Sara Bonacchi as ‘Present address: Institut National de la Recherche Scientifique (INRS), EMT Center, Boulevard Lionel-Boulet, Varennes, QC, J3X 1S2, 1650, Canada’, instead of the correct ‘Present address: Department of Chemical Sciences - University of Padua - Via Francesco Marzolo 1 - 35131 Padova - Italy’. And an affiliation of Emanuele Orgiu was incorrectly listed as ‘Present address: Department of Chemical Sciences, University of Padua, Via Francesco Marzolo 1, Padova, 35131, Italy’, instead of the correct ‘Present address: Institut National de la Recherche Scientifique (INRS), EMT Center, Boulevard Lionel-Boulet, Varennes, QC, J3X 1S2, 1650, Canada’. This has been corrected in both the PDF and HTML versions of the article.

Aging associated changes in liver include reduced hepatic blood flow, increased number of stellate cells, and collagen deposits in perisinusoidal space. We tested the possibility of mitigating these changes with caloric restriction. Two-month-old mice were subjected to 30 percent caloric restriction for 12 months and then examined for the effect of caloric restriction on the sinusoidal network, collagen deposition, and the number of stellate cells. Using intravital fluorescence microscopy, assessments were made on sinusoidal diameter, density, volumetric flow, perfusion index, and autofluorescence of vitamin A that was primarily stored with lipid droplets in stellate cells. A significant effect was observed in the vitamin A autofluorescence of stellate cells; stellate cell associated fluorescence was diminished in terms of number and size of fluorescent spots. Caloric restriction reduced collagen deposits in liver sections and lowered the gene expression of α1-(I) collagen but not α-smooth muscle actin. No differences were detected in sinusoidal dimension measurements. Our results showed that caloric restriction was effective in ameliorating the increase in stellate cells and the mild fibrosis in old mice. However, caloric restriction had no impact on stellate cell activity level as indicated by the unaffected α-smooth muscle actin expression.