冠心病患者人格特质的研究进展

冠心病是一种常见心血管疾病。有研究表明人格特质对冠心病发病及预后具有显著影响。本文就近年来对冠心病患者人格特质的相关研究进行综述,以期从心理学角度为冠心病的相关临床护理提供指导。     

Resveratrol ameliorates thoracic blast exposure-induced inflammation,endoplasmic reticulum stress and apoptosis in the brain through the Nrf2/Keap1 and NF-κB signaling pathway

Blast injuries include the various types of internal and external trauma caused by the impact force of high-speed blast waves with multiple mechanisms involved. Thoracic blast exposure could induce neurotrauma as well, but effective therapies are lacking. Resveratrol is a polyphenol flavonoid secreted by plants and has been shown to provide cardiovascular protection and play anti-inflammatory, anti-oxidation and anti-cancer roles. However, the effects of resveratrol on thoracic blast exposure-induced brain injury have not been investigated. To explore this, a mouse model of thoracic blast exposure-induced brain injury was established. Sixty C57BL/6 wild type mice were randomly divided equally into four groups (one control group, one model group, and model groups with 25 or 50 mg/kg resveratrol injected intraperitoneally). As traumatic brain injury often accompanied by mental symptoms, cognitive dysfunction and anxious behavior were evaluated by Y maze, elevated plus maze and open field test. We also examined the mice for histopathological changes by hematoxylin-eosin staining; the expressions of inflammatory-related factors by ELISA; endoplasmic reticulum stress in brain tissue via the generation of reactive oxygen species (ROS) and the expressions of inositol-requiring enzyme-α (IRE-α) and C/EBP homologous protein (CHOP); apoptosis by measuring levels of Bax, p53 and Bcl-2. In addition, proteins of related pathways were also studied by western blotting. We found that resveratrol significantly reduced the levels of inflammatory-related factors, including interleukin (IL)-1β, IL-4, and high mobility group box protein 1(HMGB1), and increased the level of anti-inflammatory-related factor, IL-10, under thoracic blast exposure (P < 0.05). Cognitive dysfunction and anxious behavior were also ameliorated by resveratrol. In brain tissue, resveratrol significantly attenuated thoracic blast exposure-induced generation of ROS and expressions of IRE-α and CHOP, lowered the expressions of Bax and p53, and maintained Bcl-2 expression (P < 0.05). Additionally, resveratrol significantly ameliorated thoracic blast exposure-induced increases of Kelch-like ECH-associated protein 1 (Keap1) and nuclear factor (NF)-κB and the decrease in nuclear factor erythroid 2-related factor 2(Nrf2) expression in the brain (P < 0.05). Our results indicate that resveratrol has a protective effect on thoracic blast exposure-induced brain injury that is likely mediated through the Nrf2/Keap1 and NF-κB signaling pathways.     

Curcumin relieves depressive-like behaviors via inhibition of the NLRP3 inflammasome and kynurenine pathway in rats suffering from chronic unpredictable mild stress

Increasing evidence suggests that inflammation is related to the pathophysiology of depression. Curcumin (CUR), which is a natural component extracted from the rhizome of Curcuma longa, seems to be efficacious in depression treatment. Hence, the present study aims to explore whether the anti-depressive effect of curcumin is connected to its anti-inflammatory features. Twenty-one SD rats were randomly divided into three groups, namely, control, CUMS (chronic unpredictable mild stress), and CUMS + CUR. After stress exposure for four weeks, the CUMS group showed depressive-like behaviors, and the curcumin treatment successfully corrected the depressive-like behaviors in stressed rats. Additionally, the curcumin could effectively decrease mRNA expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and suppress NF-κB activation. Curcumin also inhibited the stressed-induced P2X7R/NLRP3 inflammasome axis activation, along with the reduced transformation of pro-IL-1β to mature IL-1β. The stress-induced activation of indolamine-2, 3-dioxygenase (IDO) and an increased kynurenine/tryptophan ratio were also ameliorated by curcumin supplementation. In conclusion, the study revealed that curcumin relieves a depressive-like state through the inhibition of the NLRP3 inflammasome and kynurenine pathway.     

Unusual subcutaneous dedifferentiated liposarcoma exhibiting coexistence of meningothelial-like whorls and inflammatory myofibroblastic tumor-like structures

To explore the clinicopathological features of a rare dedifferentiated liposarcoma (DDLPS) with meningothelial-like whorls, we retrospectively analyzed 46 reported cases and 1 case that we encountered. Fluorescence in situ hybridization (FISH) analysis of the MDM2 amplification status of our case was also performed. Our case involved a 73-year-old male patient who had a mass in the upper part of his left arm for 10 years and was treated by surgical ablation of the tumor because of the mass' recent rapid enlargement. Microscopically, the tumor tissues showed coexistence of well-differentiated and dedifferentiated components, the latter of which included meningothelial-like whorls and inflammatory myofibroblastic tumor-like structures. The dedifferentiated components diffusely expressed vimentin, MDM2, CDK4, p16, and smooth muscle actin. They were also focally positive for desmin but negative for S-100, CD117, CD34, ALK, EMA, SOX-10, p53, and β-catenin. FISH detection showed MDM2 amplification. In conclusion, subcutaneous DDLPS with meningothelial-like whorls and inflammatory myofibroblastic tumor-like features is rare. This case broadens the histopathological lineage of DDLPS, and confirms DDLPS with myogenic differentiation. The use of the combination of MDM2, CDK4, p16, and FISH to detect MDM2 amplification is a reliable basis for the diagnosis of DDLPS with meningothelial-like whorls.     

Ms RED: A novel multi-scale residual encoding and decoding network for skin lesion segmentation

Computer-Aided Diagnosis (CAD) for dermatological diseases offers one of the most notable showcases where deep learning technologies display their impressive performance in acquiring and surpassing human experts. In such the CAD process, a critical step is concerned with segmenting skin lesions from dermoscopic images. Despite remarkable successes attained by recent deep learning efforts, much improvement is still anticipated to tackle challenging cases, e.g., segmenting lesions that are irregularly shaped, bearing low contrast, or possessing blurry boundaries. To address such inadequacies, this study proposes a novel Multi-scale Residual Encoding and Decoding network (Ms RED) for skin lesion segmentation, which is able to accurately and reliably segment a variety of lesions with efficiency. Specifically, a multi-scale residual encoding fusion module (MsR-EFM) is employed in an encoder, and a multi-scale residual decoding fusion module (MsR-DFM) is applied in a decoder to fuse multi-scale features adaptively. In addition, to enhance the representation learning capability of the newly proposed pipeline, we propose a novel multi-resolution, multi-channel feature fusion module (M²F²), which replaces conventional convolutional layers in encoder and decoder networks. Furthermore, we introduce a novel pooling module (Soft-pool) to medical image segmentation for the first time, retaining more helpful information when down-sampling and getting better segmentation performance. To validate the effectiveness and advantages of the proposed network, we compare it with several state-of-the-art methods on ISIC 2016, 2017, 2018, and PH². Experimental results consistently demonstrate that the proposed Ms RED attains significantly superior segmentation performance across five popularly used evaluation criteria. Last but not least, the new model utilizes much fewer model parameters than its peer approaches, leading to a greatly reduced number of labeled samples required for model training, which in turn produces a substantially faster converging training process than its peers. The source code is available at https://github.com/duweidai/Ms-RED.     

Downregulation of miR-21 modulates Ras expression to promote apoptosis and suppress invasion of Laryngeal squamous cell carcinoma

MiRNAs are small, noncoding RNA molecules that emerge as important regulators of cancer-related processes. The miR-21 microRNA is overexpressed in a wide variety of cancers and has been causally related to cellular proliferation and apoptosis. In this study, we found that miR-21 is overexpressed in Laryngeal squamous cell carcinoma (LSCC) and correlated with advanced stage. Inhibition of miR-21 by antisense oligonucleotides (ASO) led to decreased protein level of Ras and profound suppression of cell proliferation and invasion. Hep-2 cells exposed to miR-21 ASO exhibited cell cycle arrest at G1 phase and increased apoptosis. Furthermore, growth of LSCC xenograft tumours was significantly suppressed by repeated injection of ASO-miR-21 lentivirus and the Ras protein expression in LSCC xenograft tumours was also downregulate by ASO-miR-21. Taken together, our data suggest that miR-21 may play an oncogenic role in the cellular processes of LSCC and represent a novel target for effective therapies.     

Peri-implant crevicular fluid SIRT1 levels decrease in patients with peri-implant inflammatory: A prospective observational study

BackgroundA dental Implant is a prosthetic device made of alloplastic materials implanted into the bone to provide retention and support for a dental prosthesis. Sirtuin1 (SIRT1) molecule, a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase, regulates a variety of physiological and pathological processes, including oxidative stress, metabolism, cell proliferation, cell differentiation, inflammatory, and apoptosis. We explored whether the expression of SIRT1 correlates in patients receiving implants with peri-implant mucositis (PIM) and peri-implantitis (PI) in comparison to patients with healthy peri-implant area (PIH).MethodsA number of 198 patients with dentition defects were enrolled in the study after their implants were functional for at least 6 months. All 198 subjects were divided into 3 groups: 1) control patients with PIH healthy implants; 2) patients with PIM mucositis; and 3) patients with PI implantitis. To distinguish these three groups, peri-implant crevicular fluid (PICF) was collected by inserting a sterile paper strip into the gap around the implant and the levels of SIRT1 and cytokines were measured by the enzyme linked immunosorbent assay (ELISA). Demographic and clinical data included age, sex, Body Mass Index (BMI), probing depth (PD), plaque index (PLI), bleeding on probing (BOP), oral health impact profile (OHIP-14), history of periodontitis and the use time of implants.ResultsThe PD, PLI, OHIP-14 evaluation scores in patients with periodontitis of PIM mucositis and PI implantitis were all significantly higher than in patients with PIH healthy implants. Overall, the SIRT1 levels in PICF of the PIM and PI patients were significantly lower than of the PIH patients. In comparison with PIM patients, SIRT1 levels of the PI patients were remarkably lower than the PIH patients. Pearson's analysis showed that SIRT1 levels were negatively correlated with levels of interleukin (IL)-6, C-reactive protein (CRP) and IL-1β in patients with PIM and PI. We suggest that SIRT1 levels could serve as a potential diagnostic biomarker of PI or PIM. The PICF levels of SIRT1, CRP, IL-6, IL-1β and the history of periodontitis were the risk factors for patients with peri-implant inflammatory process.ConclusionThe measurement of SIRT1 expression in PICF may serve as a biomarker for the ongoing inflammatory process in patients with dental implants. The low SIRT1 levels correlated with PI implantitis and PIM mucositis as well as the elevated levels of pro-inflammatory cytokines (CRP, IL-6 and IL-1β).     

Involvement of plasma lncRNA GSEC in sepsis discrimination and prognosis,and its correlation with macrophage cell inflammation and proliferation

BackgroundDespite the dysregulation and function of G-quadruplex-forming sequence containing lncRNA (GSEC) have been widely reported in human cancers, there are few available data revealing its role in sepsis.ObjectiveTo assess the expression and function of GSEC in the development of sepsis and its potential molecular mechanism.Materials and methodsA total of 78 sepsis patients, 55 non-sepsis intensive care unit patients, and 42 healthy individuals were enrolled in this study. The expression of GSEC was evaluated in plasma and macrophage cells with polymerase chain reaction. The inflammation response of sepsis patients and macrophage cells was analyzed with an enzyme-linked immunosorbent assay. The diagnostic and prognostic value of GSEC in sepsis patients were estimated by receiver operator curve (ROC) and Cox analysis. The molecular mechanism underlying the function of GSEC was investigated in RAW264.7 cell with luciferase reporter assay and cell transfection.ResultsSignificant upregulation of GSEC was observed in sepsis patients’ plasma, which could discriminate sepsis patients from healthy and non-sepsis individuals. Upregulation of GSEC was positively correlated with inflammation cytokine levels and adverse prognosis of sepsis patients. In vitro, GSEC was found to modulate the expression level of miR-873-3p, which mediated the regulatory effect of GSEC on the inflammation and proliferation of RAW264.7.ConclusionUpregulated GSEC could serve as a biomarker of sepsis pathogenesis and development. GSEC regulates the inflammation and proliferation of macrophage cells through modulating miR-873-3p.