Development of a Cost-Effective 3D-Printed Airway Suction Simulator for Respiratory Therapy Students.

BACKGROUND: Three-dimensional (3D)-printed models are cost-effective and can be customized by trainers. This study designed a 3D-printed airway suction simulator for use by respiratory therapy (RT) students. The objective was to demonstrate the cost-effectiveness and application of 3D-printed models in respiratory care training, aiming to enhance the educational experience for RT students. METHODS: This study developed a 3D-printed airway suction simulator that was cost-effective. A randomized controlled trial was conducted involving RT students to compare effectiveness in a 3D-model group and a control group. Skill assessments and written examinations were used to evaluate the participants' knowledge and skills. RESULTS: A total of 38 second-year RT students were randomly assigned to either the 3D-model group (n = 19) or the control group (n = 19). One participant in the 3D-model group was lost to follow-up during the planned direct observation of procedural skills (DOPS) assessment and satisfaction questionnaire completion. The posttest written examination scores were significantly higher in the 3D-model group than in the control group (100% vs 80%, P = .02). The scores from the DOPS and satisfaction questionnaire were comparable in the 2 groups. CONCLUSIONS: This study demonstrated that 3D printing can be used to create a safe and cost-effective airway suction simulator for use by RT students, with potential to enhance training methods. Further research is necessary.

Cytoplasmic Polyadenylation Element Binding Protein 1 and Atherosclerosis: Prospective Target and New Insights.

The ribonucleic acid (RNA)-binding protein Cytoplasmic Polyadenylation Element Binding Protein 1 (CPEB1), a key member of the CPEB family, is essential in controlling gene expression involved in both healthy physiological and pathological processes. CPEB1 can bind to the 3'- untranslated regions (UTR) of substrate messenger ribonucleic acid (mRNA) and regulate its translation. There is increasing evidence that CPEB1 is closely related to the pathological basis of atherosclerosis. According to recent investigations, many pathological processes, including inflammation, lipid metabolism, endothelial dysfunction, angiogenesis, oxidative stress, cellular senescence, apoptosis, and insulin resistance, are regulated by CPEB1. This review considers the prevention and treatment of atherosclerotic heart disease in relation to the evolution of the physiological function of CPEB1, recent research breakthroughs, and the potential participation of CPEB1 in atherosclerosis.

History and Development of ABCA1.

ATP-binding cassette protein A1 (ABCA1) is a key protein in the transport of intracellular cholesterol to the extracellular and plays an important role in reducing cholesterol accumulation in surrounding tissues. Bibliometric analysis refers to the cross-science of quantitative analysis of a variety of documents by mathematical and statistical methods. It combines an analysis of structural and temporal patterns in scholarly publications with a description of topic concentration and types of uncertainty. This paper analyzes the history, hotspot, and development trend of ABCA1 through bibliometrics. It will provide readers with the research status and development trend of ABCA1 and help the hot research in this field explore new research directions. After screening, the research on ABCA1 is still in a hot phase in the past 20 years. ABCA1 is emerging in previously unrelated disciplines such as cancer. There were 551 keywords and 6888 breakout citations counted by CiteSpace. The relationship between cancer and cardiovascular disease has been linked by ABCA1. This review will guide readers who are not familiar with ABCA1 research to quickly understand the development process of ABCA1 and provide researchers with a possible future research focus on ABCA1.

Apelin-13: A Protective Role in Vascular Diseases.

Vascular disease is a common problem with high mortality all over the world. Apelin-13, a key subtype of apelin, takes part in many physiological and pathological responses via regulating many target genes and target molecules or participating in many signaling pathways. More and more studies have demonstrated that apelin-13 is implicated in the onset and progression of vascular disease in recent years. It has been shown that apelin-13 could ameliorate vascular disease by inhibiting inflammation, restraining apoptosis, suppressing oxidative stress, and facilitating autophagy. In this article, we sum up the progress of apelin-13 in the occurrence and development of vascular disease and offer some insightful views about the treatment and prevention strategies of vascular disease.

A Potential Role of NFIL3 in Atherosclerosis.

Nuclear factor interleukin-3 (NFIL3), a proline- and acidic-residue-rich (PAR) bZIP transcription factor, is called the E4 binding protein 4 (E4BP4) as well, which is relevant to regulate the circadian rhythms and the viability of cells. More and more evidence has shown that NFIL3 is associated with different cardiovascular diseases. In recent years, it has been found that NFIL3 has significant functions in the progression of atherosclerosis (AS) via the regulation of inflammatory response, macrophage polarization, some immune cells and lipid metabolism. In this overview, we sum up the function of NFIL3 during the development of AS and offer meaningful views how to treat cardiovascular disease related to AS.

Protein tyrosine phosphatase non-receptor type 2 as the therapeutic target of atherosclerotic diseases: past, present and future.

Tyrosine-protein phosphatase non-receptor type 2(PTPN2), an important member of the protein tyrosine phosphatase family, can regulate various signaling pathways and biological processes by dephosphorylating receptor protein tyrosine kinases. Accumulating evidence has demonstrated that PTPN2 is involved in the occurrence and development of atherosclerotic cardiovascular disease. Recently, it has been reported that PTPN2 exerts an anti-atherosclerotic effect by regulating vascular endothelial injury, monocyte proliferation and migration, macrophage polarization, T cell polarization, autophagy, pyroptosis, and insulin resistance. In this review, we summarize the latest findings on the role of PTPN2 in the pathogenesis of atherosclerosis to provide a rationale for better future research and therapeutic interventions.

LncRNA HOTAIR Enhances Epithelial-to-mesenchymal Transition to Promote the Migration and Invasion of Liver Cancer by Regulating NUAK1 via Epigenetic Inhibition miR-145-5p Expression.

LncRNA HOTAIR play important roles in the epigenetic regulation of carcinogenesis and progression in liver cancer. Previous studies suggest that the overexpression of HOTAIR predicts poor prognosis. In this study, through transcriptome sequencing data and in vitro experiments, we found that HOTAIR were more highly expressed and there is significantly positive relationship between HOTAIR and NUAK1 in liver cancer tissues and cell lines. miR-145-5p was downregulated and showed negative correlation with HOTAIR and NUAK1. Transfect Sh-HOTAIR, LZRS-HOTAIR, miR-145 mimic, miR-145 inhibitor to change the expression of HOTAIR and miR-145-5p. The addition of HTH-01-015 inhibits the expression of NUAK1. HOTAIR knockdown, miR-145-5p upregulation and NUAK1 inhibition all repressed migration, invasion and metastasis and reversed the epithelial-to-mesenchymal transition in SNU-387 and HepG2 cells. We also showed that HOTAIR recruiting and binding PRC2 (EZH2) epigenetically represses miR-145-5p, which controls the target NUAK1, thus contributing to liver cancer cell-EMT process and accelerating tumor metastasis. Moreover, it is demonstrated that HOTAIR crosstalk with miR-145-5p/NUAK1 during epigenetic regulation. Our findings indicate that HOTAIR/miR-145-5p/NUAK1 axis acts as an EMT regulator and may be candidate prognostic biomarker and targets for new therapies in liver cancer.

CUI-Net: a correcting uneven illumination net for low-light image enhancement.

Uneven lighting conditions often occur during real-life photography, such as images taken at night that may have both low-light dark areas and high-light overexposed areas. Traditional algorithms for enhancing low-light areas also increase the brightness of overexposed areas, affecting the overall visual effect of the image. Therefore, it is important to achieve differentiated enhancement of low-light and high-light areas. In this paper, we propose a network called correcting uneven illumination network (CUI-Net) with sparse attention transformer and convolutional neural network (CNN) to better extract low-light features by constraining high-light features. Specifically, CUI-Net consists of two main modules: a low-light enhancement module and an auxiliary module. The enhancement module is a hybrid network that combines the advantages of CNN and Transformer network, which can alleviate uneven lighting problems and enhance local details better. The auxiliary module is used to converge the enhancement results of multiple enhancement modules during the training phase, so that only one enhancement module is needed during the testing phase to speed up inference. Furthermore, zero-shot learning is used in this paper to adapt to complex uneven lighting environments without requiring paired or unpaired training data. Finally, to validate the effectiveness of the algorithm, we tested it on multiple datasets of different types, and the algorithm showed stable performance, demonstrating its good robustness. Additionally, by applying this algorithm to practical visual tasks such as object detection, face detection, and semantic segmentation, and comparing it with other state-of-the-art low-light image enhancement algorithms, we have demonstrated its practicality and advantages.

A purified membrane protein from Akkermansia muciniphila blunted the sepsis-induced acute lung injury by modulation of gut microbiota in rats.

The gut microbiota has been implicated in the pathogenesis and progression of sepsis. Akkermansia muciniphila is considered to be a promising probiotic with reduced abundance in cecal ligation and puncture (CLP)-induced sepsis model, and its specific outer membrane protein (Amuc_1100) can partially recapitulate the probiotic function of Akkermansia muciniphila. However, its role in sepsis is unclear. This study aimed to investigate the effect of Amuc_1100 on the gut microbiota of septic rats, thereby improving the prognosis of septic acute lung injury (ALI). A total of 42 adult Sprague-Dawley (SD) rats were randomly divided into three groups: the sham control (SC group), the septic ALI induced by CLP method (CLP group), and administered Amuc_1100 by oral gavage (3 µg/d) for 7 d before the CLP procedure (AMUC group). The survival of the three groups was recorded and the feces and lung tissues of rats were collected 24 h after treatment for 16S rRNA sequencing and histopathological evaluation. Oral administration of Amuc_1100 improved the survival rate and alleviated lung histopathological damage induced by sepsis. Serum levels of pro-inflammatory cytokines and chemokines were substantially attenuated. Amuc_1100 significantly increased the abundance of some beneficial bacteria in septic rats. Additionally, the Firmicutes/Bacteroidetes ratio was low in septic rats, which was partially corrected by increasing Firmicutes and decreasing Bacteroidetes after oral administration of Amuc_1100 (p < 0.05). In addition, Escherichia-Shigella, Bacteroides, and Parabacteroides were relatively enriched in septic rats, while in the AMUC group, their abundance was restored to levels similar to that of the healthy group. Amuc_1100 protects against sepsis by enhancing beneficial bacteria and reducing potential pathogenic bacteria. These findings indicate that Amuc_1100 can blunt CLP-induced ALI through the modulation of gut microbiota, thereby providing a new promising therapeutic target in sepsis.

Sterol carrier protein 2: A promising target in the pathogenesis of atherosclerosis.

Atherosclerosis, the underlying pathophysiological basis of cardiovascular disease, has been recognized as a lipid-driven chronic inflammatory disease. Sterol carrier protein 2 (SCP-2) is a 13-kDa non-specific lipid-transfer protein expressed by various tissues and cells, such as liver, heart, vascular smooth muscle cells (VSMCs), and macrophages. SCP-2 has an extensive role in cardiovascular and metabolic diseases. Recently, SCP-2 was reported to promote the development of atherosclerosis by regulating lipid metabolism and peroxidation, endocannabinoid metabolism, vascular inflammation, and fatty acid metabolism. In this review, we summarized the recent advances regarding the role of SCP-2 in the pathogenesis of atherosclerosis and tried to provide a rationale for future investigation and a better understanding of the biological functions of SCP-2 in atherosclerotic cardiovascular disease.

Retraction notice to "Betulinic acid downregulates expression of oxidative stress-induced lipoprotein lipase via PKC/ERK/c-Fos pathways in RAW264.7 macrophages" [Biochimie 119C (2015) 192-203].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Concerns raised by Dr. Sander Kersten in PubPeer pointed out that Figs. 6.1B and 6.2B of this paper were different figures but the legends and Western blots were identical; the quantification was also seen to be different between the two figures. Shortly afterwards, the authors asked to publish a corrigendum for part B of Fig. 6.1, including images of western blots and associated bar plots. Subsequently, the journal conducted an investigation and found evidence that there had been improper manipulation and duplication of images in Fig. 2 E, 6.2 B, 5 A and and 6.2 D, as shown by the reuse of several western blot bands with approximately 180° rotation in each case. After raising the complaint with the authors, the corresponding author agreed that the paper should be retracted. The authors apologise to the readers of the journal.

Corrigendum: Helmet ventilation for pediatric patients during the COVID-19 pandemic: A narrative review.

[This corrects the article DOI: 10.3389/fped.2022.839476.].

Role and therapeutic potential of gelsolin in atherosclerosis.

Atherosclerosis is the major pathophysiological basis of a variety of cardiovascular diseases and has been recognized as a lipid-driven chronic inflammatory disease. Gelsolin (GSN) is a member of the GSN family. The main function of GSN is to cut and seal actin filaments to regulate the cytoskeleton and participate in a variety of biological functions, such as cell movement, morphological changes, metabolism, apoptosis and phagocytosis. Recently, more and more evidences have demonstrated that GSN is Closely related to atherosclerosis, involving lipid metabolism, inflammation, cell proliferation, migration and thrombosis. This article reviews the role of GSN in atherosclerosis from inflammation, apoptosis, angiogenesis and thrombosis.

Effectiveness of high-flow nasal cannulae compared with noninvasive positive-pressure ventilation in preventing reintubation in patients receiving prolonged mechanical ventilation.

Many intensive care unit patients who undergo endotracheal extubation experience extubation failure and require reintubation. Because of the high mortality rate associated with reintubation, postextubation respiratory management is crucial, especially for high-risk populations. We conducted the present study to compare the effectiveness of oxygen therapy administered using high-flow nasal cannulae (HFNC) and noninvasive positive pressure ventilation (NIPPV) in preventing reintubation among patients receiving prolonged mechanical ventilation (PMV). This single-center, prospective, unblinded randomized controlled trial was at the respiratory care center (RCC). Participants were randomized to an HFNC group or an NIPPV group (20 patients in each) and received noninvasive respiratory support (NRS) administered using their assigned method. The primary outcome was reintubation within7 days after extubation. None of the patients in the NIPPV group required reintubation, whereas 5 (25%) of the patients in the HFNC group required reintubation (P = 0.047). The 90-day mortality rates of the NIPPV and HFNC groups (four patients [20%] vs. two patients [10%], respectively) did not differ significantly. No significant differences in length of RCC stay, length of hospital stay, time to liberation from NRS, and ventilator-free days at 28-day were identified. The time to event outcome analysis also revealed that the risk of reintubation in the HFNC group was higher than that in the NIPPV group (P = 0.018). Although HFNC is becoming increasingly common as a form of postextubation NRS, HFNC may not be as effective as NIPPV in preventing reintubation among patients who have been receiving PMV for at least 2 weeks. Additional studies evaluating HFNC as an alternative to NIPPV for patients receiving PMV are warranted.ClinicalTrial.gov ID: NCT04564859; IRB number: 20160901R.Trial registration: ClinicalTrial.gov ( https://clinicaltrials.gov/ct2/show/NCT04564859 ).

CTRP1: A novel player in cardiovascular and metabolic diseases.

Cardiovascular diseases (CVDs) are a series of diseases induced by inflammation and lipid metabolism disorders, among others. Metabolic diseases can cause inflammation and abnormal lipid metabolism. C1q/TNF-related proteins 1 (CTRP1) is a paralog of adiponectin that belongs to the CTRP subfamily. CTRP1 is expressed and secreted in adipocytes, macrophages, cardiomyocytes, and other cells. It promotes lipid and glucose metabolism but has bidirectional effects on the regulation of inflammation. Inflammation can also inversely stimulate CTRP1 production. A vicious circle may exist between the two. This article introduces CTRP1 from the structure, expression, and different roles of CTRP1 in CVDs and metabolic diseases, to summarize the role of CTRP1 pleiotropy. Moreover, the proteins which may interact with CTRP1 are predicted through GeneCards and STRING, speculating their effects, to provide new ideas for the study of CTRP1.

Characteristics and local risk factors of community-acquired and health-care-associated Staphylococcus aureus pneumonia.

This study aims at identifying characteristics, risk factors and mortality of community-acquired (CAP) and health-care-associated pneumonia (HCAP) by Staphylococcus aureus (S. aureus). We retrieved adults with S. aureus CAP or HCAP diagnosed by blood or pleural effusion culture in 2.6 years, and compared with those of Streptococcus pneumoniae (S. pneumoniae) CAP or HCAP diagnosed by blood or respiratory culture, or urine antigen. We found 18 patients with CAP and 9 HCAP due to S. aureus (female 33%, 66.6 ± 12.4 years-old), and 48 patients with CAP and 15 HCAP due to S pneumoniae (female 41%, 69.5 ± 17.5 years). Diabetes mellitus (52% vs. 24%, p = 0.019), hemodialysis (11% vs. 0%, p = 0.046), skin lesions (44% vs. 0%, p < 0.001), cavitary nodules (37% vs. 1.6%, p < 0.001) and pleural effusions (48% vs. 18%, p = 0.007) were more common in staphylococcal than pneumococcal group. Three patients with staphylococcal pneumonia had acute myocardial infarction. Pneumonia severity index (139 ± 52 vs. 109 ± 43, p = 0.005) and 30-day mortality (41% vs. 9.5%, p = 0.001) were higher in staphylococcal group. Multivariate analysis showed underlying disease (especially cancer and cirrhosis), risk class 4/5, altered mentality, shock and bilateral pneumonia were risk factors for 30-day mortality.