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Long non-coding RNAs (lncRNAs) are emerging as important players in gene regulation and cardiovascular diseases. However, the roles of lncRNAs in atherosclerosis are poorly understood. In the present study, we found that the levels of NIPA1-SO were decreased while those of NIPA1 were increased in human atherosclerotic plaques. Furthermore, NIPA1-SO negatively regulated NIPA1 expression in human umbilical vein endothelial cells (HUVECs). Mechanistically, NIPA1-SO interacted with the transcription factor FUBP1 and the NIPA1 gene. The effect of NIPA1-SO on NIPA1 protein levels was reversed by the knockdown of FUBP1. NIPA1-SO overexpression increased, whilst NIPA1-SO knockdown decreased BMPR2 levels; these effects were enhanced by the knockdown of NIPA1. The overexpression of NIPA1-SO reduced while NIPA1-SO knockdown increased monocyte adhesion to HUVECs; these effects were diminished by the knockdown of BMPR2. The lentivirus-mediated-overexpression of NIPA1-SO or gene-targeted knockout of NIPA1 in low-density lipoprotein receptor-deficient mice reduced monocyte-endothelium adhesion and atherosclerotic lesion formation. Collectively, these findings revealed a novel anti-atherosclerotic role for the lncRNA NIPA1-SO and highlighted its inhibitory effects on vascular inflammation and intracellular cholesterol accumulation by binding to FUBP1 and consequently repressing NIPA1 expression.

The ultrasound diagnosis imaging report reflects the sum of a radiologist's synthesis and judgement into a patient's condition. It is also an important product that is generated by radiologists to help the patients. In spite of the importance of clear and effective report writing, radiologists usually receive little or no formal reporting education. There are key principles when reporting the ultrasound findings, impression, and recommendations to promote report quality and reading experience. The findings should emphasize short and factual observations while avoiding redundancy. The impression is the thoughtful synthesis of findings leading to a diagnosis, a differential diagnosis and management recommendations. Improved report writing is achieved only after persistent learning, follow up and summaries.

Peyton's four-step teaching method is widely used in education of clinical skills. At the present study, this method was introduced into musculoskeletal ultrasound training, and the effect of this training strategy was evaluated. Problems which may occur in the process were also searched in order to improve this method. Compared to traditional method, students accepted Peyton's four-step teaching method, namely demonstration, deconstruction, comprehension and performance all achieved better scores in both theory and skill tests. Peyton's four-step teaching method also stimulated students′ learning interest and improved their teaching skill. However, one-to-one teaching is inefficient and few mutual discussion and inspiration among group members. The modified Peyton's four-step method with group teaching will be optimized and applied in future research and application.

Gliomas are the most aggressive and common type of malignant brain tumor, with limited treatment options and a dismal prognosis. Angiogenesis, a hallmarks of cancer, is one of two critical events in the progression of gliomas. Accumulating evidence has demonstrated that in glioma dysregulated molecules like long noncoding RNAs (lncRNAs), are closely linked to tumorigenesis and prognosis. However, the effects of and mechanisms of action of lncRNAs during tumor angiogenesis are poorly understood. The effect of lncRNA RP11-732M18.3 on angiogenesis was elucidated through an intracranial orthotopic glioma model, immunohistochemistry, and an in vitro angiogenesis assay. Co-culture experiments and cell migration assays were performed to investigate the function of lncRNA RP11-732M18.3 in vitro. lncRNA RP11-732M18.3 increased CD31+ microvessel density, and overexpression of lncRNA RP11-732M18.3 resulted in poor mouse survival. lncRNA RP11-732M18.3 promoted endothelial cell migration and tube formation. Nomogram and Kaplan-Meier survival analyses indicated that higher VEGFA is correlated with a poor prognosis. Mechanistically, lncRNA RP11-732M18.3 promotes angiogenesis by increasing the nuclear level of EP300 and facilitating the transcription and secretion of VEGFA. Our study contributes to the latest understanding of glioma angiogenesis and prognosis. lncRNA RP11-732M18.3 may be a potential treatment target in glioma.

Objective To compare the learning outcomes of “interactive anatomical teaching” combined with “peer education” with traditional teaching in shoulder joint ultrasound training. Methods Two groups of refresher doctors were given shoulder joint ultrasound training, using “interactive anatomical teaching” combined with “peer education” (combined teaching group) and traditional teaching (traditional teaching group)respectively. Before and after the training, selected-response examination, practical operation and film reading ability were evaluated. After the training, a questionnaire survey was conducted to refresher doctors, including comprehensive course evaluation and satisfaction with personal capacity building. Results After the training, there was no statistically significant difference in Objective examination questions between the two groups. The score of combined teaching group was significantly higher than that of traditional teaching group on practical operation and film reading ability (P＜0.05). The comprehensive course evaluation and satisfaction with personal ability improvement in combined teaching group was significantly higher than that of traditional teaching group(P＜0.05). Conclusions The“interactive anatomical teaching” combined with “peer education” enable the refresher doctors to master the theoretical knowledge, operation skills and diagnosis of shoulder joint ultrasound tecnhology, which is believed to be a better teaching and training method than traditional approaches.

Background: Oxidative stress is an early event in the development of Alzheimer's disease (AD) and maybe a pivotal point of interaction governing AD pathogenesis; oxidative stress contributes to metabolism imbalance, protein misfolding, neuroinflammation and apoptosis. Excess reactive oxygen species (ROS) are a major contributor to oxidative stress. As vital sources of ROS, mitochondria are also the primary targets of ROS attack. Seeking effective avenues to reduce oxidative stress has attracted increasing attention for AD intervention. Methods: We developed liposome‐packaged Ligustilide (LIG) and investigated its effects on mitochondrial function and AD‐like pathology in the APPswe/PS1dE9 (APP/PS1) mouse model of AD, and analyzed possible mechanisms. Results: We observed that LIG‐loaded liposome (LIG‐LPs) treatment reduced oxidative stress and β‐amyloid (Aβ) deposition and mitigated cognitive impairment in APP/PS1 mice. LIG management alleviated the destruction of the inner structure in the hippocampal mitochondria and ameliorated the imbalance between mitochondrial fission and fusion in the APP/PS1 mouse brain. We showed that the decline in cAMP‐dependent protein kinase A (PKA) and A‐kinase anchor protein 1 for PKA (AKAP1) was associated with oxidative stress and AD‐like pathology. We confirmed that LIG‐mediated antioxidant properties and neuroprotection were involved in upregulating the PKA/AKAP1 signaling in APPswe cells in vitro. Conclusion: Liposome packaging for LIG is relatively biosafe and can overcome the instability of LIG. LIG alleviates mitochondrial dysfunctions and cognitive impairment via the PKA/AKAP1 signaling pathway. Our results provide experimental evidence that LIG‐LPs may be a promising agent for AD therapy. [ABSTRACT FROM AUTHOR]

Background: Long noncoding RNAs (lncRNAs) have been identified as regulators of a number of developmental and tumorigenic processes. However, the functions of most lncRNAs in glioma remain unknown and the mechanisms governing the proliferation of tumor cells remain poorly defined. Methods: Both in vitro and in vivo assays were performed to investigate the roles of lncRNAs in the pathophysiology of gliomas. lncRNA arrays were used to identify differentially expressed lncRNAs. Subcutaneous tumor formation and a brain orthotopic tumor model in nude mice were used to investigate the functions of lncRNAs in vivo. The in vitro functions of lncRNAs were analyzed by fluorescence-activated cell sorting, colony formation, and western blot analyses. RNA fluorescence in situ hybridization and immunoprecipitation were used to explore the underlying mechanisms. Findings: Here, we describe the newly discovered noncoding RNA RP11-732M18.3, which is highly overexpressed in glioma cells and interacts with 14-3-3β/α to promote glioma growth, acting as an oncogene. Overexpression of lncRNA RP11-732 M18.3 was associated with the proliferation of glioma cells and tumor growth in vitro and in vivo. Remarkably, lncRNA RP11-732M18.3 promoted cell proliferation and G1/S cell cycle transition. lncRNA RP11-732M18.3 is predominately localized in the cytoplasm. Mechanistically, the interaction of lncRNA RP11-732M18.3 with 14-3-3β/α increases the degradation of the p21 protein. lncRNA RP11-732M18.3 promoted the recruitment of ubiquitin-conjugating enzyme E2 E1 to 14-3-3β/α and the binding of 14-3-3β/α with ubiquitin-conjugating enzyme E2 E1 (UBE2E1) promoted the degradation of p21. Interpretation: Overall these data demonstrated that lncRNA RP11-732M18.3 regulates glioma growth through a newly described lncRNA-protein interaction mechanism. The inhibition of lncRNA RP11-732M18.3 could provide a novel therapeutic target for glioma treatment. Keywords: lncRNA RP11-732M18.3, 14-3-3β/α, p21, Tumorigenesis, Glioma

MnC40H40N10O12, monoclinic, P21/c (no. 14), a = 8.252(6) Å, b = 18.144(10) Å, c = 13.580(8) Å, β = 97.61(3)°, V = 2015(2) Å3, Z = 2, Rgt(F) = 0.0390, wRref(F2) = 0.1027, T = 120 K.