Effect of intravenous and topical laryngeal lidocaine on sore throat after extubation: a prospective randomized controlled study.

OBJECTIVE: The present study aimed to compare the effect of topical laryngeal lidocaine with intravenous lidocaine before endotracheal intubation on the incidence and severity of postoperative sore throat, hoarseness, and cough. PATIENTS AND METHODS: This prospective randomized controlled study enrolled 144 patients undergoing laparoscopic cholecystectomy with endotracheal intubation. The patients were randomized to three groups and received 2% lidocaine by topical laryngeal spray (group T), intravenous 2% lidocaine (group I), and the equivalent volume of intravenous saline (group C) before intubation. The incidence and severity of sore throat, hoarseness, and cough reaction at 0.5, 1, 6, and 24 h after extubation were collected. RESULTS: The incidence of sore throat was significantly lower in group T than in groups I and C (6.4% vs. 37.2% and 86.7%, p < 0.001), respectively at 0.5 h after extubation, and it was significantly lower in group I than that in group C (37.2% vs. 86.7%, p < 0.001). Both the incidence of hoarseness and cough were significantly lower in group T than in group I and in group C (14.9% vs. 97.7% and 97.8%, p < 0.001, and 19.1% vs. 72.0% and 93.3%, p < 0.001), respectively. The severity of sore throat, hoarseness and cough in group T was significantly lower than that in group I and that in group C (p < 0.05), and it was significantly lower in group I than in group C (p < 0.05). CONCLUSIONS: Both topical laryngeal lidocaine and intravenous lidocaine before intubation have positive effects on preventing sore throat. Topical laryngeal route was superior to intravenous route. Chictr.org.cn ID: ChiCTR2100042442.

Identification of diagnostic biomarkers and immuno-infiltration analysis for rheumatoid arthritis based on biological information and WGCNA.

OBJECTIVE: Rheumatoid arthritis (RA), as an autoimmune disease, poses a huge social and economic burden worldwide. Although the diagnosis of RA has been gradually improved, there is still a need to discover accurate and rapid biomarkers for diagnosis and therapy with a precise understanding of the disease. This study aimed to screen diagnostic biomarkers and analyze immune infiltration in RA based on weighted gene co-expression network analysis (WGCNA). MATERIALS AND METHODS: Firstly, we screened the experimental and validation sets associated with RA from the GEO database. Crossover genes were obtained using differential genes (DEGs) and key modules in WGCNA. Subsequently, the crossover genes were constructed into protein-protein interaction (PPI) networks and screened to obtain hub genes. The receiver operating characteristic (ROC) curve assessment was performed to identify diagnostic biomarkers. In addition, we used the Cibersort algorithm for immuno-infiltration analysis and the DGidb database to search for drugs associated with diagnostic biomarkers. RESULTS: In the end, 377 DEGs were identified, and the enrichment analysis revealed significant associations with the immune system. Blue modules in the WGCNA analysis were positively associated with the disease and were identified as key modules. ROC curves evaluated the four hub genes, which significantly differentiated RA from healthy controls and could be used as diagnostic biomarkers. In further analysis, we found that RA is closely related to immunity, and the search identified multiple drugs that hold promise for treating RA. CONCLUSIONS: BCL2A1, PTGS2, FAS, and LY96 may be used as diagnostic biomarkers, which is significant for diagnosing and treating RA.

The value of microbiology rapid on-site evaluation of sepsis caused by pulmonary infection.

OBJECTIVE: This study aims to evaluate the value of microbial rapid on-site evaluation (M-ROSE) of sepsis, and septic shock caused by pulmonary infection. PATIENTS AND METHODS: Thirty-six patients with sepsis and septic shock due to hospital-acquired pneumonia were analyzed. Accuracy and time were compared with M-ROSE, traditional culture, and next-generation sequencing (NGS). RESULTS: A total of 48 strains of bacteria and 8 strains of fungi were detected by bronchoscopy in 36 patients. The accuracy rate of bacteria and fungi was 95.8% and 100%, respectively. M-ROSE took an average of 0.34±0.01 hours, much faster than NGS (22h±0.01 h, p<0.0001) and traditional culture time (67.50±0.91 h, p<0.0001). CONCLUSIONS: M-ROSE may quickly identify common bacteria and fungi, so it may be a useful method for the etiological diagnosis of sepsis and septic shock caused by pulmonary infection.

Ferroptosis in neurodegenerative diseases: inhibitors as promising candidate mitigators.

OBJECTIVE: Ferroptosis is a new form of iron-dependent programmed cell death, characterized by intracellular iron overload and lipid peroxidation. Several studies have revealed that ferroptosis is associated with the occurrence and development of various neurodegenerative diseases (NDs). Therefore, this paper reviews the mechanism and related genes of ferroptosis, focusing on the research of antiferroptosis drugs in NDs to provide theoretical support for future experimental research and clinical application. MATERIALS AND METHODS: This work focuses on ferroptosis, and the authors searched the literature on PubMed related to ferroptosis using the keywords "neurodegenerative diseases" and "neurons". All articles were from August 2022 and earlier, excluding irrelevant or retracted articles, and articles from the last five years were used as the main inclusion criteria. RESULTS: After collection and summary, it was found that ferroptosis in NDs was not only related to iron metabolism, lipid metabolism, and amino acid metabolism but also related to genes such as Nrf2, FSP1, VDACs, and p53. We also summarized drugs that inhibited ferroptosis in NDs and classified them according to their mechanism of action. CONCLUSIONS: Ferroptosis was involved in the progression of NDs through its production mechanism and related genes. Targeting ferroptosis might be a new strategy for treating NDs.

Killing two birds with one stone: miR-126 involvement in both cancer and atherosclerosis.

OBJECTIVE: Both cancer and atherosclerosis are the main causes of morbidity and mortality in the world, and some patients even suffer from both of them. Several studies have shown an association between the pathogenesis of cancer and atherosclerosis. It has been reported that miR-126 may participate in the pathological process of cancer and atherosclerosis. Therefore, we aimed to summarize the role of miR-126 in cancer and atherosclerosis respectively, as well as a possible association between them. MATERIALS AND METHODS: In this paper, "miR-126" and "microRNA-126" are used as the first group of keywords, "atheromatosis" and "atherosclerosis" are used as the second group of keywords, and "tumor" and "cancer" are used as the third group of keywords. In PubMed, the authors selected one of the first group and the second group of keywords to search the literature related to miR-126 and cancer, and one of the first group and the third group of keywords was selected to search the literature on miR-126 and atherosclerosis. All collected articles are from 2021 and before. Irrelevant, withdrawn and review articles were excluded, and the included literature was mainly in the recent five years. RESULTS: After collection and summary, miR-126 is found involved in cell apoptosis, proliferation, angiogenesis, inflammation, and other processes in both cancer and atherosclerosis by negatively targeting PI3K, VEGF, VCAM-1, EGFL7, CXCL12-CXCR4 axis, and LRP6. Moreover, we briefly review the prospects of miR-126 as a biomarker for the diagnosis and treatment of cancer and atherosclerosis in clinical applications. CONCLUSIONS: It has been demonstrated that miR-126 can influence cancer and atherosclerosis by affecting the same or different target genes. Therefore, it facilitates our understanding of the common prevention and treatment strategies of cancer and atherosclerosis by regulating the miR-126-target genes network.

Circ_0001982 accelerates the progression of colorectal cancer via sponging microRNA-144.

The article "Circ_0001982 accelerates the progression of colorectal cancer via sponging microRNA-144, by Q. Deng, C.-J. Wang, R. Hao, Q.-Y. Yang, published in Eur Rev Med Pharmacol Sci 2020; 24 (4): 1755-1762-DOI: 10.26355/eurrev_202002_20352-PMID: 32141543" has been withdrawn from the authors due to some inaccuracies about pictures and data (Figures 2C and 2D need to be further confirmed). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20352.

Circ_0001982 accelerates the progression of colorectal cancer via sponging microRNA-144.

OBJECTIVE: The aim of this study was to uncover the expression pattern and biological function of circ_0001982 in the progression of colorectal cancer (CRC). PATIENTS AND METHODS: Relative expression level of circ_0001982 in 66 paired CRC tissues and adjacent normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The association between circ_0001982 level and clinical indexes of CRC patients was assessed. The effect of circ_0001982 on cellular behaviors of HT29 and HCT-116 cells was evaluated in vitro. Dual-Luciferase reporter gene assay was conducted to verify the binding relation between circ_0001982 and microRNA-144. Finally, rescue experiments were performed to assess the role of the circ_0001982/microRNA-144 axis in mediating the progression of CRC. RESULTS: Circ_0001982 was significantly up-regulated in CRC tissues when compared with adjacent normal ones. CRC patients with a high expression level of circ_0001982 showed a significantly higher rate of distant metastasis and worse survival. Knockdown of circ_0001982 remarkably attenuated the proliferative, migratory, and invasive capacities of HCT-116 cells. However, opposite results were observed after the overexpression of circ_0001982 in HT29 cells. MicroRNA-144 was verified as a target gene of circ_0001982, which could be negatively regulated by circ_0001982. Furthermore, microRNA-144 was capable of reversing the regulatory effect of circ_0001982 on the proliferative, migratory, and invasive capacities of CRC cells. CONCLUSIONS: Up-regulated circ_0001982 was closely related to distant metastasis and poor prognosis of CRC. In addition, circ_0001982 attenuated the progression of CRC by negatively regulating microRNA-144.

Effect of NLK on the proliferation and invasion of laryngeal carcinoma cells by regulating CDCP1.

OBJECTIVE: The morbidity and mortality of laryngeal cancer are increasing rapidly, seriously threatening human health. There are several causes of laryngeal cancer, but the exact molecular mechanism is unclear. Finding the molecular targets of laryngeal cancer has become an emerging hot spot. Nemo-like kinase (NLK) is abnormally expressed in tumors, but its role in laryngeal cancer has not been reported. PATIENTS AND METHODS: Real Time PCR and Western blot were used to detect NLK mRNA and protein expression in cancer tissues and adjacent tissues of laryngeal cancer patients. The laryngeal carcinoma cell line Hep-2 cells were cultured in vitro and randomly divided into three groups: control group, NC group, and NLK siRNA group followed by the analysis of cell proliferation by MTT assay, Caspase3 activity, and cell invasion by the transwell chamber. MMP-9 and CDCP1 expression was measured by Western blot. RESULTS: NLK mRNA and protein expression was significantly increased in laryngeal carcinoma tissues compared with those in adjacent tissues (p<0.05). NLK siRNA transfection into Hep-2 cells significantly down-regulated NLK expression, inhibited Hep-2 cell proliferation and invasion, increased Caspase-3 activity with statistical differences compared to control group (p<0.05). Down-regulation of NLK expression in Hep-2 cells inhibited MMP-9 expression and decreased CDCP1 expression. CONCLUSIONS: NLK is expressed in tumor tissues of patients with laryngeal cancer. The down-regulation of NLK expression may play a role in the proliferation, apoptosis, and invasion of laryngeal carcinoma cells and it is possible by regulating MMP-9 and CDCP1 expression.

Brachial artery flow-mediated dilatation and carotid intima-media thickness in young ED patients with insulin resistance.

The evidence of a close relationship between cardiovascular disease and erectile dysfunction (ED) is well documented. The aim of this study is to investigate whether there is an early asymptomatic impairment of the peripheral vasculature in young ED patients without obvious cardiovascular disease. We studied a total of 261 ED patients (19-40 years old) and 40 age-matched healthy controls. All participants received questionnaires of cardiovascular risk factors and erectile function assessment, were subjected to lab tests of fasting blood sample, and underwent the ultrasonographic examination of brachial artery flow-mediated dilation (FMD) and carotid intima-media thickness (c-IMT). Insulin resistance (IR) was measured by the homeostasis model assessment of insulin resistance (HOMA-IR). Compared with normal human controls, FMD was significantly lower, whereas the average c-IMT was significantly greater in ED patients. An inverse correlation was found between FMD and mean c-IMT. The ED patients had significantly higher levels of fasting glucose, fasting insulin and HOMA-IR index, but showed relatively lower total testosterone and prolactin levels than the controls. Both FMD and c-IMT showed a significant correlation with International Index of Erectile Function-5 questionnaire (IIEF-5) score, age and HOMA-IR. Multivariate stepwise regression analysis demonstrated that age, HOMA-IR and IIEF-5 score were the risk factors associated with FMD and c-IMT. In conclusion, young ED patients in association with IR display diminished FMD and increased c-IMT. Furthermore, ED, HOMA-IR and age are independent predictors of the two subclinical atherosclerotic markers.

Prolyl isomerase Pin1 stabilizes and activates orphan nuclear receptor TR3 to promote mitogenesis.

Pin1 regulates a subset of phosphoproteins by isomerizing phospho-Ser/Thr-Pro motifs via a 'post-phosphorylation' mechanism. Here, we characterize TR3 as a novel Pin1 substrate, and the mitogenic function of TR3 depends on Pin1-induced isomerization. There are at least three phospho-Ser-Pro motifs on TR3 that bind to Pin1. The Ser95-Pro motif of TR3 is the key site through which Pin1 enhances TR3 stability by retarding its degradation. Pin1 can also catalyze TR3 through phospho-Ser431-Pro motif, which is phosphorylated by extracellular signal-regulated kinase 2 (ERK2), resulting in enhanced TR3 transactivation. Furthermore, Pin1 not only facilitates TR3 targeting to the promoter of cyclin D2, a novel downstream target of TR3, but also promotes TR3 to recruit p300, thereby inducing cell proliferation. Importantly, we found that Pin1 is indispensable for TR3 to promote tumor growth both in vitro and in vivo. Our study thus suggests that Pin1 has an important role in cell proliferation by isomerizing TR3.

Bioactive coumarins from Boenninghausenia sessilicarpa.

Bioassay guided fractionation of Boenninghausenia sessilicarpa (Rutaceae) resulted in the isolation of a new dimeric coumarin glucoside 9'-methoxyl rutarensin (1) and a cytotoxic compound rutamarin (4), as well as an antivirus component leptodactylone (8), together with six known coumarins. Their structures were elucidated by 1D- and 2D NMR spectroscopy and ESI-MS analyses, respectively. Rutamarin (4) showed significant inhibitory activities against A-549, Bel-7402, HepG-2 and HCT-8 tumour cell lines with IC50s of 1.318, 2.082, 2.306 and 2.497 microg/ml. In addition, leptodactylone (8) showed potent protective activity on cells infected by SARS-CoV with ratio of 60% at 100 microg/ml.