Ultrasonography in the intensive care unit: a bibliometrics analysis.

Background: Ultrasonography is widely used in critical care practice. The status of related studies remains unclear. The purpose of this study is to analyze current literature investigating the use of ultrasound in critical care units by using bibliometric analysis. Methods: The Science Citation Index Expanded (SCI-E) database was used for data retrieval. The search formula for literature retrieval was "ultrasound" OR "ultrasonography" AND "intensive care unit" OR "critical care unit" OR "intensive care" OR "critical care". The bibliometric software package of R software was used to analyze the results. Information of related literatures were analyzed. Results: Finally, 3,715 articles were included. The number of published articles and the number of references increased annually. The research fields included medical imaging, critical care medicine, cardiology, etc. The United States has published more documents in this field than other countries and has shown the highest rate of cooperation with other countries. Among the top 10 research institutions with the largest number of publications, 5 are from France and 3 are from the United States. There are many authors from China in the top 10 published studies. Among the top 10 journals with the largest number of published articles, 5 journals are top journals in the field of critical care medicine. Among the top 10 keywords, there are 5 of ultrasound specialty and 2 of critical care medicine. Conclusions: Researches on the use of ultrasound in critical care units are mainly concentrated in several developed countries in Europe and the United States. Chinese research institutions should perform more studies in this field and increase cooperation with institutions from other countries.

Exosomal ERBB2IP contributes to tumor growth via elevating PSAT1 expression in non-small cell lung carcinoma.

BACKGROUND: Both exosomes and circular RNAs (circRNAs) are involved in tumor growth. Hsa_circ_0001492 (circERBB2IP) has been reported to be overexpressed in plasma exosomes from patients with lung adenocarcinoma, but the biological role of exosomal circERBB2IP in non-small cell lung carcinoma (NSCLC) is indistinct. METHODS: Exosomes isolated from serums and medium samples were validated by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blotting. Relative expression of circERBB2IP was detected by RT-qPCR. Loss-of-function was done to determine the effect of circERBB2IP on NSCLC cell proliferation and migration. Molecular mechanisms associated with circERBB2IP were predicted by bioinformatic analysis and validated by dual-luciferase reporter, RIP, and RNA pulldown assays. In vivo experiments were performed to identify the function of circERBB2IP in NSCLC. RESULTS: We discovered that circERBB2IP expression was correlated with TNM grade, lymph node metastasis and tumor size of NSCLC patients. Upregulation of circERBB2IP was observed in exosomes derived from NSCLC patient's serum and circERBB2IP might be a potential diagnostic biomarker for NSCLC. CircERBB2IP was transmitted between carcinoma cells through exosomes. Knockdown of circERBB2IP lowered cell growth in mouse models and restrained NSCLC cell proliferation and migration. CircERBB2IP could mediate PSAT1 expression via sponging miR-5195-3p. CONCLUSION: In conclusion, circERBB2IP may drive NSCLC growth by the miR-5195-3p/PSAT1 axis in NSCLC, shedding light on a diagnostic biomarker and therapeutic target for NSCLC.

[Myocardial cells and mitochondrial autophagy in sepsis mice induced by lipopolysaccharide].

OBJECTIVE: To investigate the alterations in the level of myocardial cells and mitochondrial autophagy during myocardial injury in lipopolysaccharide (LPS)-induced septic animal models. METHODS: Male C57BL/J mice were randomly divided into negative control group (NC), LPS treatment groups (6, 12, 24, 36 hours). The LPS treatment groups were subjected to LPS (10 mg/kg) injection intraperitoneally, and the NC group was injected intraperitoneally with the same amount of saline. The mice were sacrificed at the above time points to collect blood and heart tissues. Cytoplasmic protein, mitochondria and mitochondrial proteins were extracted from the myocardial tissue, and other myocardial tissue was frozen for next analysis. Cardiac troponin I (cTnI) levels in sera were evaluated by ELISA; mitochondrial membrane potential (MMP) was tested by JC-1 staining and fluorescence cytometry at different time points after LPS intraperitoneal injection. Furthermore, the levels of autophagy-related proteins such as microtubule-associated protein 1 light chain 3 (LC3), PTEN-induced kinase 1 (pink1), E3-ubiquitin ligase parkin were measured by Western blotting and fluorescent immunohistochemistry. RESULTS: Compared with the control group, the serum levels of cTnI induced by LPS were significantly higher as 6 hours, while the MMP was significantly lower in the LPS treatment groups, and the lowest was in the 12-hour group. The expression of autophagy-related protein LC3-II/LC3-I significantly increased in the LPS 12-hour treatment group, pink1/parkin was significantly elevated in the LPS 6-hour treatment group, and they then gradually decreased. CONCLUSION: The autophagy stress is activated in myocardium during myocardial injury induced by LPS treatment and it probably happens earlier at myocardial mitochondria.

[Construction of PPENK-MIDGE-NLS gene vector and the expression in rat].

Increasing the production and secretion of endogenous opioid peptide by immune cell can significantly induce myocardial protective effects against ischemia-reperfusion injury. Gene therapy is promising to increase endogenous enkephalin (ENK). However, classical viral and plasmid vectors for gene delivery are hampered by immunogenicity, gene recombination, oncogene activation, the production of antibacterial antibody and changes in physiological gene expression. Minimalistic immunologically defined gene expression (MIDGE) can overcome all the deficients of viral and plasmid vectors. The exon of rat's preproenkephalin (PPENK) gene was amplified by PCR and the fragments were cloned into pEGFP-N1 plasmids. The recombined plasmids were digested with enzymes to obtain a linear vector contained promoter, preproenkephalin gene, RNA stable sequences and oligodesoxy nucleotides (ODNs) added to both ends of the gene vector to protect gene vector from exonuclease degradation. A nuclear localization sequence (NLS) was attached to an ODN to ensure the effective transport to the nucleus and transgene expression. Flow cytometry, laser confocal microscopy and Western blotting demonstrated that PPENK-MIDGE-NLS can transfect leukocyte of rat in vivo, increase the expression of proenkephalin (PENK) in tissue, and the transfection efficiency depends on gene vector's dosage. These results indicate that PPENK-MIDGE-NLS could be an innovative method to protect and treatment of myocardial ischemia-reperfusion injury.