Sandwiched film of graphene/silver nanowire conductive layer reinforced by hydroxyethyl cellulose bond layer.

Multilayer nanocomposite film made of different materials has multifunctional properties and is applied in the field of flexible electronic devices. Herein, hydroxyethyl cellulose (HEC) and boron nitride nanosheets (BNNS) were used as the matrix and thermal conductivity material of the HEC/BNNS (HB) insulation layer and were combined with conductive blade structure graphene/silver nanowires (GA) film to prepare a three-layer HB/GA20/HB film. Using the high mechanical properties of the HEC based film, the tensile strength of the three-layer film is increased to 22.0 MPa, 633 % higher than that of the pure conductive film. The sensor prepared by multilayer film has good bending sensing performance (1500 cycles) and electromagnetic shielding performance (29.3 dB). The heating temperature of HB/GA20/HB film heater is up to 107.9 °C at 20 V. In the HB/GA20/HB film, the external HB layer provides insulation, thermal conductivity and physical support, and the internal GA layer with good conductive and sensing properties is combined to build a multi-functional sensor, which can be applied as a mobile sensor, heater and electromagnetic shielding material in the flexible wearable field.

Paroxetine protects against bleomycin-induced pulmonary fibrosis by blocking GRK2/Smad3 pathway.

G protein-coupled receptor kinase-2 (GRK2) is involved in TGF-ß1-induced activation of lung fibroblasts, which could give rise to the pathogenesis of pulmonary fibrosis. Paroxetine (PRXT) serves as a selective GRK2 inhibitor which is widely used to treat anxiety and depression for several decades. However, whether PRXT could inhibit TGF-ß1-induced activation of lung fibroblasts and combat bleomycin-induced pulmonary fibrosis remains unclear. Here, we investigated the effects of PRXT on pulmonary fibrosis in C57/BL6 caused by bleomycin as well as on the activation of murine primary lung fibroblasts stimulated with TGF-ß1. The results demonstrated that PRXT markedly improved the pulmonary function and 21-day survival in bleomycin-induced mice. Meanwhile, PRXT significantly decreased collagen deposition, inflammation, and oxidative stress in lung tissues from bleomycin-induced mice. Furthermore, we found that PRXT could inhibit the protein and mRNA expression of GRK2 and Smad3 in lung tissues from bleomycin-induced mice. In vitro experiments also PRXT could inhibit cell activation and collagen synthesis in a concentration-dependent manner in TGF-ß1-induced lung fibroblasts. In addition, we found that Smad3 overexpression by adenovirus transfection could offset anti-fibrotic and antioxidative effects from PRXT in TGF-ß1-induced lung fibroblasts, which showed no effects on the protein expression of GRK2. In conclusion, PRXT mediates the inhibition of GRK2, which further blocks the transcription of Smad3 in TGF-ß1-induced lung fibroblasts, providing an attractive therapeutic target for pulmonary fibrosis.

AAV9-Tspyl2 gene therapy retards bleomycin-induced pulmonary fibrosis by modulating downstream TGF-ß signaling in mice.

Idiopathic pulmonary fibrosis (IPF) is a devastating fibrotic lung disease characterized by scarring and destruction of the lung architecture, with limited treatment options. Targeted gene therapy to restore cell division autoantigen-1 (CDA1) expression may be a potential treatment approach to delay the progression of pulmonary fibrosis (PF). Here, we focused on CDA1, which was significantly decreased in human IPF, in a mouse model of bleomycin (BLM)-induced PF, and in transforming growth factor (TGF-ß)-challenged lung fibroblasts. In vitro, CDA1 overexpression by lentivirus infection in human embryonic lung fibroblasts (HFL1 cells) inhibited the production of pro-fibrotic and pro-inflammatory cytokines, lung fibroblast-to-myofibroblast transition, and extracellular matrix protein expression induced by exogenous TGF-ß1 treatment, whereas CDA1 knockdown with small interfering RNA promoted this effect. CDA1 overexpression also inhibited cell proliferation and migration. In a mouse model of BLM-induced PF, we provided novel evidence that the intratracheal delivery of adeno-associated virus serotype 9 carrying the mouse Tspyl2 gene reduced lung tissue inflammation and fibrosis. Mechanistically, CDA1, as a transcription regulator, could repress the TGF-ß signal transduction in vivo and in vitro. In conclusion, our results show that Tspyl2 gene therapy plays an antifibrotic role by inhibiting the lung fibroblast-to-myofibroblast transition and downstream TGF-ß/Smad3 signaling transduction in BLM-induced PF in mice, suggesting that CDA1 is an appropriate and promising therapeutic target for PF.

In Situ Loading of Polypyrrole onto Aramid Nanofiber and Carbon Nanotube Aerogel Fibers as Physiology and Motion Sensors.

Nanocomposite conductive fiber has been newly developed as a lightweight material with high flexibility and strong weavability, which can meet the requirements of flexible wearable devices. Herein, lightweight porous aramid nanofibers (ANF) and carbon nanotube (CNT) aerogel fibers coated with polypyrrole (PPy) layers are prepared by a wet spinning method for motion detection and information transmission. The ANF/CNT/PPy aerogel fiber with low density (56.3 mg/cm3), conductivity (6.43 S/m), and tensile strength (2.88 MPa) were used as motion sensors with high sensitivity (0.12) and long life (1000 cycles). At the same time, the differential conductivity of aerogel fibers is utilized to reduce the information transmission time (up to 46%). High- and low-temperature-resistant (-196 to 100 °C) aerogel fibers are also available as a quick heater and ionic solution detector. In summary, the prepared ANF/CNT/PPy aerogel fiber can be used as a multifunctional sensor for human-health detection and motion monitoring.

Artificial Intelligence for COVID-19: A Systematic Review.

Background: Recently, Coronavirus Disease 2019 (COVID-19), caused by severe acute respiratory syndrome virus 2 (SARS-CoV-2), has affected more than 200 countries and lead to enormous losses. This study systematically reviews the application of Artificial Intelligence (AI) techniques in COVID-19, especially for diagnosis, estimation of epidemic trends, prognosis, and exploration of effective and safe drugs and vaccines; and discusses the potential limitations. Methods: We report this systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We searched PubMed, Embase and the Cochrane Library from inception to 19 September 2020 for published studies of AI applications in COVID-19. We used PROBAST (prediction model risk of bias assessment tool) to assess the quality of literature related to the diagnosis and prognosis of COVID-19. We registered the protocol (PROSPERO CRD42020211555). Results: We included 78 studies: 46 articles discussed AI-assisted diagnosis for COVID-19 with total accuracy of 70.00 to 99.92%, sensitivity of 73.00 to 100.00%, specificity of 25 to 100.00%, and area under the curve of 0.732 to 1.000. Fourteen articles evaluated prognosis based on clinical characteristics at hospital admission, such as clinical, laboratory and radiological characteristics, reaching accuracy of 74.4 to 95.20%, sensitivity of 72.8 to 98.00%, specificity of 55 to 96.87% and AUC of 0.66 to 0.997 in predicting critical COVID-19. Nine articles used AI models to predict the epidemic of the COVID-19, such as epidemic peak, infection rate, number of infected cases, transmission laws, and development trend. Eight articles used AI to explore potential effective drugs, primarily through drug repurposing and drug development. Finally, 1 article predicted vaccine targets that have the potential to develop COVID-19 vaccines. Conclusions: In this review, we have shown that AI achieved high performance in diagnosis, prognosis evaluation, epidemic prediction and drug discovery for COVID-19. AI has the potential to enhance significantly existing medical and healthcare system efficiency during the COVID-19 pandemic.

Polyvinyl alcohol-mediated splitting of Kevlar fibers and superior mechanical performances of the subsequently assembled nanopapers.

In this work, a composite of aramid nanofibers (ANFs) and polyvinyl alcohol (PVA) was prepared by PVA-assisted splitting of macro Kevlar fibers, which assures the uniform wrapping of PVA chains on the surface of ANFs, thus leading to an enhanced interfacial bonding strength between ANFs and PVA. The morphological characterizations manifest the enhanced diameters of the ANFs after PVA wrapping. The subsequently assembled ANFs/PVA paper shows a strength of 283.25 MPa and a toughness of 32.41 MJ m-3, which are increased by 57% and 152% compared to the pure ANF paper, respectively. The superior mechanical properties are attributed to the strong interfacial bonding strength, enhanced hydrogen bonding interactions, the densification of the materials, and curved fracture paths. Meanwhile, the ANFs/PVA paper also shows robust UV shielding and visible transparency properties, as well as excellent environmental stabilities, especially at high and low temperatures.

Clinical Characteristics and Prognostic Analysis of Patients With Pulmonary Tuberculosis and Type 2 Diabetes Comorbidity in China: A Retrospective Analysis.

Background: Tuberculosis (TB) is one of the leading communicable diseases, with significant morbidity and mortality. Diabetes can increase the risk of developing TB and the related adverse outcomes. This study retrospectively analyzed the clinical characteristics and prognosis of patients with pulmonary TB and type 2 diabetes comorbidity. Methods: About 282 cases with pulmonary TB and type 2 diabetes comorbidity were identified from West China Hospital between January 1, 2010, and December 31, 2016, and were followed up for at least 3 years. We further used Kaplan-Meier methods and COX regression analysis to identify the influence factors for all-cause death. Results: Compared to the survival patients, patients who died were older, exhibited significantly lower albumin and hemoglobin levels, but higher Charlson Comorbidity Index (CCI) score at admission, and had a lower usage rate of metformin. The all-cause mortality rates at 1 and 5 years were 5.67 and 20.59%, separately. For 1-year all-cause death, higher albumin level (HR = 0.90, 95% CI: 0.81-0.99) was the independently protective factor, but older age (HR = 1.07, 95% CI: 1.01-1.13) and CCI score ≥3 (HR = 6.77, 95% CI: 1.40-32.69) were the independent risk factors. For long-term all-cause death, higher albumin level (HR = 0.94, 95% CI: 0.88-1.00), the use of metformin (HR = 0.21, 95% CI: 0.07-0.59), insulin (HR = 0.27, 95% CI: 0.10-0.74), or sulfonylureas (HR = 0.23, 95% CI: 0.07-0.74) were the independently protective factors, but older age (HR = 1.03, 95% CI: 1.00-1.07) and CCI score ≥3 (HR = 7.15, 95% CI: 2.56-19.92) were the independent risk factors. Conclusions: The lower albumin level, older age, and CCI score ≥3 were predictors of all-cause death in patients with pulmonary TB and type 2 diabetes comorbidity. In the long run, patients who use metformin, insulin, or sulfonylureas as hypoglycemic agents may have a lower incidence of death.

Highly compressible, heat-insulating and self-extinguishing cellulose nanofiber/aramid nanofiber nanocomposite foams.

Foam as a kind of burgeoning materials with laminated porous 3D structure was realized multifunctional application in diversified fields. In this work, we aimed to prepare a highly compressible and self-extinguishing multifunctional nanocomposite foam with anisotropic porous 3D structure through a green aqueous freeze-drying method. In order to address the inflammable property and brittleness issue of high-loading cellulose nanofiber foam, aramid nanofiber was incorporated into cellulose nanofiber framework, forming the multicomponent and multilevel honeycomb structure of the nanocomposite foam. Herein, the compression cycle properties of the nanocomposite foam could be significantly improved by adding 50 wt.% aramid nanofiber and at 20% stress recovered by 100 % even if cyclically compressed 200 times. The total heat release of the nanocomposite foam was as low as 2.12 MJ/m2 which also had low thermal conductivity about 28.8 mW/m ·â€¯K. The ANF improved the flame retardancy of the composite foam.

Improved mechanical and ultraviolet shielding performances of hydroxyethyl cellulose film by using aramid nanofibers as additives.

Recently, aramid nanofibers (ANFs) have drawn the attention of scientist due to the high mechanical strength, high-temperature resistance, and high electrical and thermal insulation properties. In this work, we aimed at improving the mechanical and ultraviolet shielding properties of hydroxyethyl cellulose (HEC) film by using ANFs as additives. Mechanical results show that the 1.0 % ANFs could improve the tensile strength of pure HEC film by 176.6 %. Meanwhile, the ANFs additives can also enable the HEC film excellent ultraviolet (UV) shielding and visible light transmittance, as well as high UV radiation resistance ability. It is believed that the high mechanical strength of the HEC/ANFs composites is derived from the rearrangement of HEC chains along the tensile direction after the addition of hard ANFs and the enhanced hydrogen bonds between HEC and ANFs.

Fisetin Alleviated Bleomycin-Induced Pulmonary Fibrosis Partly by Rescuing Alveolar Epithelial Cells From Senescence.

Idiopathic pulmonary fibrosis is an aging-associated disease, satisfactory therapies are not yet available. Accelerated senescence of alveolar epithelial cells plays an important part in Idiopathic pulmonary fibrosis pathogenesis. Fisetin (FIS) is a natural non-toxic flavonoid, which has many pharmacological functions. However, the role of FIS in pulmonary fibrosis has not been established. In this study, we found that FIS treatment apparently alleviated BLM-induced weight loss, inflammatory cells infiltration, inflammatory factors expression, collagen deposition and alveolar epithelial cell senescence, along with AMPK activation and the down regulation of NF-κB and TGF-ß/Smad3 in vivo. In vitro, FIS administration significantly inhibited the senescence of alveolar epithelial cells and senescence-associated secretory phenotype, followed by reduced transdifferentiation of fibroblasts to myofibroblasts as well as collagen deposition in fibroblasts, which was blocked by an AMPK inhibitor, Compound C. Together, these results suggest that FIS can alleviate the development of BLM-induced pulmonary fibrosis, which is related to the inhibition of TGF-ß/Smad3 signaling and the reduction of alveolar epithelium cell senescence by regulating AMPK/NF-κB signaling pathway. FIS may be a promising candidate for patients with pulmonary fibrosis.

The association between osteopontin and tuberculosis: A systematic review and meta-analysis.

OBJECTIVE: We examined the data reported in the studies for comparison of osteopontin (OPN) levels in tuberculosis and healthy participants, and to discuss whether OPN could be extended to disease diagnosis, severity assessment and therapeutic effect monitering. METHODS: A systematic literature search was conducted in PubMed, EMBASE, Scopus, the Cochrane Library, Web of Science, the China National Knowledge Infrastructure (CNKI) and WanFang databases. The pooled risk estimates were shown in standardized mean difference (SMD) with 95% confidence interval (CI) for OPN levels. The random effect model was used according to the test of heterogeneity among studies. Subgroup analyses and meta-regression models were performed to identify the possible sources of heterogeneity. RESULTS: 17 retrospective studies with 933 tuberculosis participants and 786 healthy controls were finally included in this article. In the primary meta-analysis, higher serum/plasma OPN levels were found in tuberculosis patients (SMD = 2.58, 95%CI = 2.09~3.08, P<0.001). Besides, pooled results from positive acid-fast bacilli (AFB) staining and imaging-severe tuberculosis group demonstrated higher OPN concentrations (SMD = 0.90, 95%CI = 0.58~1.21, P<0.001; SMD = 1.11, 95%CI = 0.90~1.33, P<0.001; respectively), and OPN levels decreased after two months of standard anti-tuberculosis therapy (SMD = 2.10, 95%CI = 1.36~2.85, P<0.001). CONCLUSIONS: Elevated serum/plasma OPN levels may be associated with an increased risk of tuberculosis, while further well-designed studies are needed. Moreover, OPN could be considered as a potential biomarker for tuberculosis surveillance and severity assessment.

Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice.

Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal, and chronic lung disease. There are no effective drug therapies for IPF. Hyperoside, a flavonoid glycoside, has been proven to have anti-inflammatory, anti-fibrosis, antioxidant, and anti-cancer effects. The aim of this study was to explore the role of hyperoside in bleomycin-induced pulmonary fibrosis development in mice. We established the pulmonary fibrosis model by a single intratracheal aerosol injection of bleomycin. Seven days after the bleomycin treatment, the mice were intraperitoneally administered with hyperoside for 14 days. We found that hyperoside treatment ameliorated fibrotic pathological changes and collagen deposition in the lungs of mice with bleomycin-induced pulmonary fibrosis. Hyperoside treatment also reduced the levels of MDA, TNF-α, and IL-6 and increased the activity of SOD. In addition, hyperoside might inhibit the epithelial-mesenchymal transition (EMT) via the AKT/GSK3ß pathway. Based on these findings, hyperoside attenuated pulmonary fibrosis development by inhibiting oxidative stress, inflammation, and EMT in the lung tissues of mice with pulmonary fibrosis. Therefore, hyperoside might be a promising candidate drug for the treatment of pulmonary fibrosis.

All cellulose composites prepared by hydroxyethyl cellulose and cellulose nanocrystals through the crosslink of polyisocyanate.

In this work, all cellulose composite (ACC) films were prepared through a blocked polyisocyanate (BPIC) induced cross-linking of hydroxyethyl cellulose (HEC) and cellulose nanocrystals (CNC). The chemical characterization indicates that the covalent bonds have been formed between HEC and CNC. Mechanical test shows that the addition of 4 % CNC into the HEC matrix improves the tensile strength by 120.2 % compared to the neat HEC film. The further incorporation of 10 % BPIC into the above ACC film can enhance the tensile strength by 280.2 %. The water contact angles of the ACC film that constituted by 4 % CNC and 10 % BPIC is increased to 100.1° while the thermal decomposition temperature is up to 210 °C. The morphological analysis suggests that the CNC is beneficial to the dispersion of the cross-linked HEC, which increases the elongation at break and maintains the excellent tensile strength meanwhile.

Ultrathin MXene/aramid nanofiber composite paper with excellent mechanical properties for efficient electromagnetic interference shielding.

MXenes, new two-dimensional compounds with hydrophilic surfaces and high metallic conductivity, have attracted significant interest in the electromagnetic interference shielding field in recent years. Nevertheless, poor mechanical properties and brittle nature are bottlenecks for their commercial application. Herein, one-dimensional ANFs were designed as the intermolecular cross-linker between d-Ti3C2Tx flakes and MXene (d-Ti3C2Tx)/aramid nanofiber (ANF) composite paper with a multi-layered structure was fabricated via the vacuum-assisted filtration approach. Further investigation revealed that the ANFs and MXene displayed good combination by hydrogen bonding, and MXene/ANF composite papers exhibited excellent mechanical properties and superior electrical conductivity. The MXene/ANF composite paper possessed a favorable shielding effectiveness (SE) which reached ∼28 dB in 8.2-12.4 GHz (X band) with an ultra-thin thickness ∼17 µm and showed potential application prospects as an advanced composite in sensitive electronic products.

Identification of gene and microRNA changes in response to smoking in human airway epithelium by bioinformatics analyses.

Smoking is a substantial risk factor for many respiratory diseases. This study aimed to identify the gene and microRNA changes related to smoking in human airway epithelium by bioinformatics analysis.From the Gene Expression Omnibus (GEO) database, the mRNA datasets GSE11906, GSE22047, GSE63127, and microRNA dataset GSE14634 were downloaded, and were analyzed using GEO2R. Functional enrichment analysis of the differentially expressed genes (DEGs) was enforced using DAVID. The protein-protein interaction (PPI) network and differentially expressed miRNAs (DEMs)- DEGs network were executed by Cytoscape.In total, 107 DEGs and 10 DEMs were determined. Gene Ontology (GO) analysis revealed that DEGs principally enriched in oxidation-reduction process, extracellular space and oxidoreductase activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway demonstrated that DEGs were principally enriched in metabolism of xenobiotics by cytochrome P450 and chemical carcinogenesis. The PPI network revealed 15 hub genes, including NQO1, CYP1B1, AKR1C1, CYP1A1, AKR1C3, CEACAM5, MUCL1, B3GNT6, MUC5AC, MUC12, PTGER4, CALCA, CBR1, TXNRD1, and CBR3. Cluster analysis showed that these hub genes were associated with adenocarcinoma in situ, squamous cell carcinoma, cell differentiation, inflammatory response, oxidative DNA damage, oxidative stress response and tumor necrosis factor. Hsa-miR-627-5p might have the most target genes, including ITLN1, TIMP3, PPP4R4, SLC1A2, NOVA1, RNFT2, CLDN10, TMCC3, EPHA7, SRPX2, PPP1R16B, GRM1, HS3ST3A1, SFRP2, SLC7A11, and KLHDC8A.We identified several molecular changes induced by smoking in human airway epithelium. This study may provide some candidate genes and microRNAs for assessing the risk of lung diseases caused by smoking.

Identification of Gene Changes Induced by Dexamethasone in the Anterior Segment of the Human Eye Using Bioinformatics Analysis.

BACKGROUND Glucocorticoids (GCs)-induced glaucoma is a common adverse effect of prolonged GCs use. To better understand the effects of GCs on aqueous humor (AH) outflow, we analyzed the dataset GSE37474 using bioinformatics analysis to identify gene changes and pathways in the anterior segment of the human eye induced by dexamethasone (DEX). MATERIAL AND METHODS The GSE37474 dataset downloaded from the Gene Expression Omnibus (GEO) database was examined in this study. GEO2R was utilized to analyze data and identify differentially expressed genes (DEGs). Gene Ontology (GO) enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were constructed using the DAVID database followed by construction of a protein-protein interaction (PPI) network performed using Cytoscape software. Finally, modules and hub genes were screened out using MCODE and cytoHubba plugin, respectively. RESULTS A set of 252 DEGs were screened. Among the DEGs, 143 genes were upregulated and 109 were downregulated. GO analysis indicated that some of the DEGs participated in extracellular matrix (ECM) organization and cholesterol homeostasis. Additionally, KEGG pathways were predominantly enriched in tyrosine metabolism and ECM-receptor interaction. From the PPI network, 2 modules were identified, and 10 hub genes were screened out, including CCL2, FOS, IGF1, PTGS2, CCL5, EDN1, IL11, F3, PMCH, and BDKRB1. The 2 module genes primarily participate in the TNF signaling pathway, cytokine-cytokine receptor interaction, and the Jak-STAT signaling pathway. CONCLUSIONS The present study identified some significant DEGs, hub genes, pathways, and modules in the human anterior segment induced by DEX. These results demonstrate that DEX changes the expression of certain genes and pathways to resist aqueous humor outflow, which could be new targets for developing novel and more effective approaches of diagnosis and therapy for GCs-induced glaucoma.

Respiratory Fluoroquinolones Monotherapy vs. ß-Lactams With or Without Macrolides for Hospitalized Community-Acquired Pneumonia Patients: A Meta-Analysis.

Background: The choice of empirical antibiotic treatment for patients with community-acquired pneumonia (CAP) who are admitted to non-intensive care unit (ICU) hospital wards is complicated by the limited availability of evidence. We systematically reviewed the efficacy and safety of strategies of empirical treatment with respiratory fluoroquinolone monotherapy and ß-lactam with or without macrolide for non-ICU hospitalized CAP patients. Methods: We searched databases including PubMed, the Cochrane Library (Issue11, 2018), EMbase, China National Knowledge Internet (CNKI), WanFang Data, VIP, and China Biology Medicine disc (CBMdisc) to identify randomized controlled trials (RCTs) involving the comparison of respiratory fluoroquinolone monotherapy and ß-lactam with or without macrolide for the non-ICU hospitalized patients with CAP up to November 2018. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data, and assessed the risk of bias of the included studies. A meta-analysis was performed with the outcomes. Results: A total of 22 studies involving 6,235 patients were included. The results of the meta-analysis showed a non-significant trend toward an advantage to the respiratory fluoroquinolone in overall mortality (RR 0.82, 95% CI 0.65-1.02). No significant difference was found between the two strategies in clinical success (the intention-to-treat population: RR 1.03, 95% CI 0.99-1.08; the clinically evaluable population: RR 1.03, 95% CI 0.999-1.055; the population in which it was unclear whether intention-to-treat or per-protocol analysis was used: RR 1.04, 95% CI 0.99-1.09), microbiological treatment success (RR 1.04, 95% CI 0.997-1.092), and length of stay (SMD -0.06, 95% CI -0.16 to 0.04). The advantage of respiratory fluoroquinolone was statistically significant on the drug-related adverse events (RR 0.87, 95% CI 0.77-0.97). Conclusions: Current evidence shows that fluoroquinolone monotherapy has similar efficacy and favorable safety compared with ß-lactam with or without macrolide for non-ICU hospitalized CAP patients. Since the limitation of region, quantity and quality of included studies, more RCTs with large scale and high quality are needed to verify the above conclusion.

Association between the mannose-binding lectin (MBL)-2 gene variants and serum MBL with pulmonary tuberculosis: An update meta-analysis and systematic review.

In recent years, many studies have demonstrated that the MBL-2 gene polymorphisms may be associated with pulmonary tuberculosis (PTB) susceptibility. Moreover, some studies have shown that serum MBL levels were influenced by the MBL-2 gene polymorphisms and that it plays an important role in tuberculosis infection. However, the results of these studies were inconsistent and underpowered. The current meta-analysis and systematic review aimed to evaluate the association between the MBL-2 gene polymorphisms and serum MBL levels with PTB. Finally, 30 eligible articles were included in the study. The overall results indicated that the MBL-2 rs1800450 (54 A/B) and rs5030737 (52 A/D) polymorphisms were risk factors for PTB, but the MBL-2 rs1800451 (57 A/C) and rs7095891 (+4 P/Q) polymorphisms as protective factors against PTB. No associations were found in the other three polymorphisms (exon 1, rs7096206 (-221 X/Y), and rs11003125 (-550 H/L) of the MBL-2 gene. In addition, we could not detect any significant differences between haplotypes among PTB patients and healthy controls. More important, the meta-analysis results indicated that the serum MBL levels in patients with PTB were significantly lower than those in healthy controls (SMD = 0.43, 95% CI = 0.33-0.52). This study suggested that the MBL-2 gene polymorphisms may be involved in the pathogenesis of PTB, and serum MBL may be a biomarker for the diagnosis of PTB. More rigorous research is needed in the future to confirm these findings further.

Triple Versus Double Therapy for the Treatment of Severe Infections Caused by Carbapenem-Resistant Enterobacteriaceae: A Systematic Review and Meta-Analysis.

INTRODUCTION: The role of combination treatment in the management of carbapenem-resistant Enterobacteriaceae infections (CRE) is still unclear. There have been no meta-analysis comparing the efficiency of triple therapy in treating CRE infections with that of double therapy. In this perspective, we conducted a meta-analysis to clarify whether triple therapy is superior to double therapy in treating patients with CRE infections. METHODS: We performed a systematic review, using PubMed and Embase without any restrictions until October 2019. Risk ratio (RR) with 95% CI were pooled to evaluate the effect of intervention. RESULTS: A total of 33 studies with 1,441 subjects were identified. Pooled analysis showed that triple therapy was not associated with a reduced mortality compared with double therapy (HR 0.99 95% CI 0.85-1.14, P = 0.85). CONCLUSIONS: This meta-analysis suggests that triple therapy is not superior to double therapy in the treatment of patients with CRE infections, although the quality of evidence is generally low based on current literatures. Future well-defined, randomized controlled trials will be required to elucidate the role of triple therapy in the treatment of CRE infections.

Blocking the ERK1/2 signal pathway can inhibit S100A12 induced human aortic smooth muscle cells damage.

Increased levels of S100A12 and activated matrix metalloproteinase 2/9 (MMP-2/9) produced by human aortic smooth muscle cells (HASMCs) have recently implicated in the development of thoracic aortic disease. In the present study, we investigated the effect of S100A12 on HASMCs and identified the intracellular signal pathways involved by Western blot. The results were shown that up-expression of S100A12 in HASMCs induced cell apoptosis and inhibited cell proliferation. Additionally, S100A12 significantly increased the expression of MMP-2, MMP-9, and VCAM-1 in HASMCs at translational levels. Furthermore, our results also showed that S100A12 induced HASMCs damage by increased related proteins expression was mediated by the activation of ERK1/2 signal pathway, whereas p38 MAPK had no effect on those processes. Blocked the activation of ERK1/2 could decrease S100A12 induced the apoptosis and inhibited cell proliferation of HASMCs. In conclusion, these results indicated that S100A12 could increase the expression of MMP-2, MMP-9, and vascular cell adhesion molecule 1 (VCAM-1) in HASMCs via activation of ERK1/2 signal pathway, which leads to injury of HASMCs. Therefore, antagonists of ERK1/2 may be useful for treating thoracic aortic dissection.