Kristoffersenlynn2468

The past decade has witnessed the preliminary development of pre-hospital emergency. We analyzed the scientific output related to pre-hospital emergency in the past two decades, aiming to evaluate the publication status of the literature related to pre-hospital emergency through bibliometrics analysis, and hope to provide enlightenment of trends and hotspots for the development of pre-hospital emergency.

By web of science, all literature on pre-hospital emergency from 2000 to 2 October 2020 was retrieved and screened by two researchers. Excel, Social Sciences Statistics Package (SPSS, version 24) and software GraphPad Prism 8 were used to analyze the publication trend in related fields. Besides, VOSviewer, Citespace were also applied to visualize the research trends and study the co-occurring keywords in pre-hospital emergency.

As of 2 October 2020, a total of 1839 pre-hospital emergency publications with total citation of 32800 times were identified. The United States accounted for the largest number os increased rapidly. However, the related articles were mainly published in developed countries, the United States has absolute advantages especially. Moreover, first-aid studies may become hotspots in the near future.Adenoid cystic carcinoma (AdCC) of the head and neck originates from salivary glands, with high risks of recurrence and metastasis that account for the poor prognosis of patients. The purpose of this research was to identify key genes related to AdCC for further investigation of their diagnostic and prognostic significance. In our study, the AdCC sample datasets GSE36820, GSE59702 and GSE88804 from the Gene Expression Omnibus (GEO) database were used to explore the abnormal coexpression of genes in AdCC compared with their expression in normal tissue. A total of 115 DEGs were obtained by screening with GEO2R and FunRich software. According to functional annotation analysis using Enrichr, these DEGs were mainly enriched in the SOX2, AR, SMAD and MAPK signaling pathways. A protein-protein network of the DEGs was established by the Search Tool for the Retrieval of Interacting Genes (STRING) and annotated through the WEB-based Gene SeT AnaLysis Toolkit (WebGestalt) and was shown to be enriched with proteins involdered to have a potential influence on AdCC but have not been studied in this disease. The analysis results promote our understanding of the molecular mechanisms and biological processes of AdCC, which might be useful for targeted therapy or diagnosis.

Currently, there is no favorable treatment plan for inflammatory pain, so exploring new analgesics is still a research hotspot in this area. Cyclin-dependent protein kinase 5 (Cdk5) is a pain-related protein kinase, but its mechanism in inflammatory pain has not been clarified. This research aimed to explore the mechanism of Cdk5-synaptophysin (Syn)-soluble N-ethylmaleimide-sensitivity factor (NSF) attachment protein receptor (SNARE) in acute and chronic inflammatory pain.

Rat models of acute and chronic inflammatory pain were induced by formalin and complete Freund's adjuvant (CFA), separately, and some rats injected with normal saline through intraplantar injection were divided into a control group. Momelotinib cost Thirty minutes before modeling, rats were given Cdk5 inhibitor (Roscovitine, Ros), SNARE scavenger (botulinum toxin A, BTTA), glutamate receptor inhibitor (MK801), and dimethyl sulfoxide (DMSO) through spinal canals, and the paw withdrawal threshold (PWT) and thermal withdrawal latency (PWL) at difference time points were compared.

Compared with rats in the control group, those in the rat models of acute and chronic inflammatory pain showed lower PWT and PWL, higher Cdk5 enzyme level, tight correlation of Cdk5 with Syn, SNARE, p25 proteins, and higher levels of Cdk5, Syn and SNARE. And the above situation was dramatically reversed under intervention of Ros, BTTA and MK801.

Cdk5-Syn-SNARE pathway is a therapeutic target for inflammatory pain. Blocking the activation of this pathway is beneficial to exert analgesic effect.

Cdk5-Syn-SNARE pathway is a therapeutic target for inflammatory pain. Blocking the activation of this pathway is beneficial to exert analgesic effect.

To investigate the effects of miR-24 and HMOX1 on the inflammatory response and neurological function in rats with cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH).

Fifteen Sprague-Dawley rats were randomly assigned to the sham group (sham operation, treated with normal saline). Rat model of SAH-induced CVS was established in 90 rats, and these rats were randomly divided into the model, miR-24 NC (treated with miR-24-NC vector), miR-24 inhibitor (treated with miR-24 inhibitor vector), HMOX-NC (treated with HMOX1-NC vector), oe-HMOX1 (treated with HMOX1 overexpression vector), and miR-24 inhibitor + si-HMOX1 (treated with miR-24 inhibitor and si-HMOX1 vectors) groups. Adenoviral vectors containing the target sequences were injected into the hippocampus of the rats in the corresponding groups. Dual-luciferase reporter assay was conducted to verify the relationship between miR-24 and HMOX1. The learning and memory abilities, neurological function, cerebral edema, permeability of blood-brain barrier, myeloperoxidase activity, and levels of miR-24, HMOX1, interleukin-6, tumor necrosis factor-α, superoxide dismutase, and malondialdehyde in rats were examined.

miR-24 could negatively regulate HMOX1 expression. SAH-induced CVS was accompanied with increased miR-24 expression and decreased HMOX1 expression. Inhibiting miR-24 expression or enhancing the expression of its down streaming target, HMOX1, could partly reverse the increased oxidation and inflammation as well as functional deficits in the rats. Moreover, the effects of miR-24 inhibitor could be reversed by inhibiting HMOX1 expression.

miR-24 downregulation can promote HMOX1 expression, thereby decreasing the inflammatory response and improving the neurological function of rats with CVS after SAH.

miR-24 downregulation can promote HMOX1 expression, thereby decreasing the inflammatory response and improving the neurological function of rats with CVS after SAH.

Immune checkpoint inhibitors (ICI) has achieved remarkable clinical benefit in advanced lung adenocarcinoma (LUAD). However, effective clinical use of ICI agents is encumbered by the high rate of innate resistance. The aim of our research is to identify significant gene mutations which can predict clinical benefit of immune checkpoint inhibitors in LUAD.

The "mafComapre" function of "MafTools" package was used to screen the differentially mutated genes between durable clinical benefit (DCB) group and no durable clinical benefit (NDB) group based on the somatic mutation data from NSCLc_PD1_mSK_2018. Machine learning was performed to select significantly mutated genes to accurately classify patients into DCB group and NDB group. A nomogram model was constructed based on the significantly mutated genes to predict the susceptibility of patients to ICI. Finally, we explored the correlation between two classifications of immune cell infiltration, PD-1 and PD-L1 expression, tumor mutational burden (TMB) and prognosis.

Through utilize machine learning, 6 significantly mutated genes were obtained from 8 differentially mutated genes and used to accurately classify patients into DCB group and NDB group. The DCA curve and clinical impact curve revealed that the patients can benefit from the decisions made based on the nomogram model. Patients highly sensitive to ICI have elevated immune activity, higher expression of PD-1 and PD-L1, increased TMB, and well prognosis if they accept ICI treatment.

Our research selected 6 significantly mutated genes that can predict clinical benefit of ICI in LUAD patients.

Our research selected 6 significantly mutated genes that can predict clinical benefit of ICI in LUAD patients.

Long non-coding RNA (lncRNA) SNHG17 has been shown to modulate the biological behavior of multiple cancers (e.g., colorectal and lung cancers). However, its involvement in pancreatic cancer (PC) has not been explored; therefore, in the present study, we sought to examine this involvement.

First, the mRNA expression levels of various genes were quantified in PC tissues and cell lines using quantitative reverse-transcription PCR (qRT-PCR). The interaction between SNHG17 and miR-942 was explored by bioinformatics prediction as well as a dual luciferase reporter assay. The proliferation and viability of pancreatic carcinoma cells were examined using cell counting kit-8 and MTT assays, respectively. Cellular migratory and invasive properties were evaluated using transwell migration and wound healing assays. Cell death was measured using flow cytometry. Protein expression was quantified by western blotting.

SNHG17 expression was markedly higher in human PC specimens and cell lines than in normal healthy tissues and pancreatic epithelial cells. MiR-942 expression displayed the opposite trend. Bioinformatics prediction and a dual luciferase reporter assay confirmed that SNHG17 serves as a sponge for miR-942. Loss-of-function assay revealed that SNHG17 silencing reduced the proliferation and viability of PC cells, impaired their migratory and invasive capacities, and led to their apoptosis. All these changes could be reversed by miR-942 inhibition. Further mechanical studies showed that SNHG17 silencing decreased the expression of several tumor modulators, including XXX, and this decrease was countered by miR-942 inhibition.

Our study provides experimental evidence for an interaction between SNHG17 and miR-942, which may unveil a new approach for PC pharmacotherapy.

Our study provides experimental evidence for an interaction between SNHG17 and miR-942, which may unveil a new approach for PC pharmacotherapy.

Recent studies have proven that there is a relationship between long non-coding RNAs (lncRNAs) and malignant tumor hepatocellular carcinoma (HCC). However, the function of RUSC1-AS1 and its relative regulators in HCC remains unknown.

studies, CCK-8 assays, colony formation assays, transwell assays, and wound healing tests were carried out to evaluate the proliferation, migration, and invasion of HCC cells. The correlation between RUSC1-AS1 expression with tumor size or weight was studied in nude mice. Bioinformatics analysis, dual luciferase, quantitative Real-Time PCR (qRT-PCR), and Western blot analysis aimed to discover the relevance between miR-340-5p and RUSC1-AS1 or cAMP responsive element binding protein 1 (CREB1).

When compared with normal groups, RUSC1-AS1 expression in HCC tissues and HCC cell lines was higher. We also found that knockdown of RUSC1-AS1 inhibited HCC cell progression, including proliferation, migration, and invasion, and suppressed tumorigenesis

. Further studies demonstrated that the expression of RUSC1-AS1 negatively correlated with miR-340-5p expression in HCC cells. In addition, miR-340-5p was identified as a direct target of RUSC1-AS1 and tightly associated with the prevention of tumor progression. Moreover, miR-340-5p bound directly to CREB1. CREB1 overexpression reversed the impact of miR-340-5p on HCC cells. Together, lncRNA RUSC1-AS1 plays a regulatory role in the PI3K/AKT signaling pathway in HCC cells.

We demonstrated that lncRNA RUSC1-AS1 influenced HCC cell progression by modulating its downstream target miR-340-5p/CREB1 axis via the PI3K/AKT signaling pathway, which may be a potential prognostic and therapeutic target for treating HCC.

We demonstrated that lncRNA RUSC1-AS1 influenced HCC cell progression by modulating its downstream target miR-340-5p/CREB1 axis via the PI3K/AKT signaling pathway, which may be a potential prognostic and therapeutic target for treating HCC.