N6-methyladenosine(m 6 A) is the most abundant post-transcriptional RNA modification in eukaryotes. However, little is known about its role in pancreatic adenocarcinoma (PAAD). The aim of our study was to identify gene signatures and prognostic values of m 6 A regulators in PAAD. Patients from 3 different datasets with complete genomic and transcriptomic sequencing data were enrolled. Survival analysis for different gene alterations was performed using log-rank tests and Cox regression model. The association between alteration of m 6 A regulators and clinicopathological characteristics was examined using chi-square test. Results showed a high frequency of copy number alterations (CNAs) of m 6 A regulatory genes in PAAD patients, but somatic mutations were rarely happened. CNAs and mutations of m 6 A regulatory genes was associated with patient’s gender, pathologic stage and resected tumor size. Patients with “gain of function” for m 6 A “reader” genes combined with copy number loss of “writers” or “erasers” had worse overall survival (OS) compared with other patterns. Moreover, copy number gain of m 6 A “reader” gene insulin growth factor 2 binding protein 2 ( IGF2BP2) was an independent risk factor for OS (HR = 2.392, 95%CI: 1.392-4.112, p<0.001) and disease-free survival (DFS) (HR = 2.400, 95%CI: 1.236-4.659, p=0.010). Gene Set Enrichment Analysis (GSEA) indicated that IGF2BP2 was correlated with multiple biological processes associated with cancer, of which the most significant processes were relevant to cancer cell cycle, cell immortalization and tumor immunity. To sum up, a significant relationship was found between m 6 A genomic alterations and worse clinical outcomes. These innovative findings are expected to guide further research on the mechanism of m 6 A in PAAD.
Millions of years of evolution have allowed animals to develop unusual locomotion capabilities. A striking example is the legless-jumping of click beetles and trap-jaw ants, which jump more than 10 times their body length. Their delicate musculoskeletal system amplifies their muscles’ power. It is challenging to engineer insect-scale jumpers that use onboard actuators for both elastic energy storage and power amplification. Typical jumpers require a combination of at least two actuator mechanisms for elastic energy storage and jump triggering, leading to complex designs having many parts. Here, we report the new concept of dynamic buckling cascading, in which a single unidirectional actuation stroke drives an elastic beam through a sequence of energy-storing buckling modes automatically followed by spontaneous impulsive snapping at a critical triggering threshold. Integrating this cascade in a robot enables jumping with unidirectional muscles and power amplification (JUMPA). These JUMPA systems use a single lightweight mechanism for energy storage and release with a mass of 1.6 g and 2 cm length and jump up to 0.9 m, 40 times their body length. They jump repeatedly by reengaging the latch and using coiled artificial muscles to restore elastic energy. The robots reach their performance limits guided by theoretical analysis of snap-through and momentum exchange during ground collision. These jumpers reach the energy densities typical of the best macroscale jumping robots, while also matching the rapid escape times of jumping insects, thus demonstrating the path toward future applications including proximity sensing, inspection, and search and rescue.
Background and purposeStress hyperglycemia ratio (SHR), which is used to assess stress hyperglycemia, is associated with the functional outcome of ischemic stroke (IS). IS can induce the inflammatory response. Neutrophil counts and neutrophil-to-lymphocyte ratio (NLR) as good and easily available inflammatory biomarkers, the relationship between neutrophil counts and NLR and SHR were poorly explored in IS. We aimed to systemically and comprehensively explore the correlation between various blood inflammation markers (mainly neutrophil counts and NLR) and SHR.MethodsData from 487 patients with acute IS(AIS) in Xiangya Hospital were retrospectively reviewed. High/low SHR groups according to the median of SHR (≤1.02 versus >1.02). Binary logistic regression analysis was used to evaluate the correlation between neutrophil counts and NLR and high SHR group. Subgroup analyses were performed in the TOAST classification and functional prognosis.ResultsThe neutrophil counts and NLR were all clearly associated with SHR levels in different logistic analysis models. In the subgroup analysis of TOAST classification, the higher neutrophil counts and NLR were the independent risk factors for high SHR patients with large-artery atherosclerosis (LAA) (neutrophil: adjusted OR:2.047, 95% CI: 1.355-3.093, P=0.001; NLR: adjusted OR:1.315, 95% CI: 1.129-1.530, P<0.001). The higher neutrophil counts were the independent risk factor for high SHR patients with cardioembolism (CE) (adjusted OR:2.413, 95% CI: 1.081-5.383, P=0.031). ROC analysis showed that neutrophil counts was helpful for differentiating high SHR group with CE and low SHR group with CE (neutrophil: AUC =0.776, P=0.002). However, there were no difference in levels of neutrophil counts and NLR between patients with SVO and without SVO. The higher neutrophil counts and NLR independently associated with high SHR patients with mRS ≤2 at 90 days from symptom onset, (neutrophil: adjusted OR:2.284, 95% CI: 1.525-3.420, P<0.001; NLR: adjusted OR:1.377, 95% CI: 1.164-1.629, P<0.001), but not in patients with mRS >2.ConclusionsThis study found that the neutrophil counts and NLR are positively associated with SHR levels in AIS patients. In addition, the correlation between neutrophil counts and NLR and different SHR levels are diverse according to TOAST classification and functional prognosis.
Glioma is the most common type of primary brain cancer in adults. Accumulating studies have reported that long non-coding RNAs (lncRNAs) serve a significant role in the initiation and development of glioma. lncRNA small nucleolar RNA host gene 7 (SNHG7) has been previously demonstrated to serve a role in numerous glioma biological processes, including cell proliferation, invasion and migration. The present study aimed to investigate the role of SNHG7 in glioma through reverse transcription-quantitative PCR, western blotting and cell function assays. The results revealed that SNHG7 expression was upregulated in glioma tissues and cell lines, while microRNA (miR)-138-5p expression was downregulated. Moreover, the knockdown of SNHG7 expression decreased the proliferation of glioma cells. Mechanistic studies demonstrated that SNHG7 downregulated miR-138-5p expression, which subsequently affected the expression levels of its target gene, enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). In conclusion, the results of the present study suggested that SNHG7 may act as a competing endogenous RNA to sponge miR-138-5p and modulate EZH2 expression. Thus, SNHG7 may enhance glioma proliferation via modulating the miR-138-5p/EZH2 signaling axis.
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