Polarity-Mediated Antisolvent Control Enables Efficient Lanthanide-Based near-Infrared Perovskite LEDs.

Alloying lanthanide ions (Yb3+) into perovskite quantum dots (Yb3+:CsPb(Cl1-xBrx)3) is an effective method to achieve efficient near-infrared (NIR) luminescence (>950 nm). Increasing the Yb3+ alloying ratio in the perovskite matrix enhances the luminescence intensity of Yb3+ emission at 990 nm. However, high Yb3+ alloying (>15%) results in vacancy-induced inferior material stability. In this work, we developed a polarity-mediated antisolvent manipulation strategy to resolve the incompatibility between a high Yb3+ alloying ratio and inferior stability of Yb3+:CsPb(Cl1-xBrx)3. Precise control of solution polarity enables increased uniformity of the perovskite matrix with fewer trap densities. Employing this strategy, we obtain Yb3+:CsPb(Cl1-xBrx)3 with the highest Yb3+ alloying ratio of 30.2% and a 2-fold higher electroluminescence intensity at 990 nm. We lever the engineered Yb3+:CsPb(Cl1-xBrx)3 to fabricate NIR-LEDs, achieving a peak external quantum efficiency (EQE) of 8.5% at 990 nm: this represents the highest among perovskite NIR-LEDs with an emission wavelength above 950 nm.

Lyophilization enhances the stability of Panax notoginseng total saponins-loaded transfersomes without adverse effects on ex vivo/in vivo skin permeation.

Transfersomes (TFSs) have been extensively investigated to enhance transdermal drug delivery. As a colloidal dispersion system, TFSs are prone to problems such as particle aggregation and sedimentation, oxidation and decomposition of phospholipids. To enhance the stability of panax notoginseng saponins (PNS)-loaded transfersomes (PNS-TFSs) without adverse influences on their skin permeation, we prepared lyophilized PNS-loaded transfersomes (PNS-FD-TFSs), clarified their physicochemical characteristics and investigated their in vitro drug release, ex vivo skin permeation/deposition and in vivo pharmacokinetics. In this study, a simple, fast and controllable process was developed for preparing lyophilized PNS-TFSs. In the optimized PNS-FD-TFS formulation, sucrose and trehalose were added to the PNS-TFS dispersion with a mass ratio of trehalose, sucrose, and phospholipid of 3:2:1, and the mixture was frozen at -80 °C for 12 h followed by lyophilization at -45 °C and 5 Pa for 24 h. The optimized formulation of PNS-FD-TFSs was screened based on the appearance and reconstitution time of the lyophilized products, vesicle size, and PDI of the freshly reconstituted dispersions. It maintained stable physicochemical properties for at least 6 months at 4 °C. The vesicle size of PNS-FD-TFSs was below 100 nm and homogenous with a polydispersity index of 0.2 after reconstitution. The average encapsulation efficiencies of the five index saponins notoginsenoside R1 (NGR1), ginsenoside Rg1 (GRg1), ginsenoside Re (GRe), ginsenoside Rb1 (GRb1) and ginsenoside Rd (GRd) in PNS-FD-TFSs were 68.41 ± 5.77%, 68.95 ± 6.08%, 65.46 ± 10.95%, 91.50 ± 5.62% and 95.78 ± 1.70%, respectively. The reconstituted dispersions of PNS-FD-TFSs were similar to PNS-TFSs in in vitro release, ex vivo skin permeation, and deposition. The pharmacokinetic studies showed that, compared with the PNS liposomes (PNS-LPS), the PNS-FD-TFS-loaded drug could permeate through the skin and enter the blood rapidly. It can be concluded that the lyophilization process can effectively improve the stability of PNS-TFSs without compromising their transdermal absorption properties.

Thickness-variation-insensitive near-infrared quantum dot LEDs.

In terms of tunable luminescence and high quantum efficiency, colloidal quantum dots (CQDs) are promising semiconductors for constructing near-infrared light-emitting diodes (NIR-LEDs). However, currently available NIR-LEDs are susceptible to variations in the emission layer thickness (EMLT), the highest external quantum efficiency (EQE) decreases to below 50% (relative to peak EQE) when the EMLT varies out of a narrow range of (±30 nm). This is due to the thickness-dependent carrier recombination rate and current density variation, resulting in batch-to-batch EQE fluctuations that limit LED reproducibility. Here we report efficient NIR-LEDs that exhibit EQE variations of less than 15% (relative to the champion EQE) over an EMLT range of 40-220 nm; the highest achievable EQE of ∼11.5% was obtained by encapsulating a 212 nm-thick CQD within a type-I inorganic shell to enhance the radiative recombination in the dots, resulting in a high photoluminescence quantum yield of 80%, and by post-treating the films with a bifunctional linking agent to improve and balance the hole and electron mobilities in the entire film (electron mobility: 8.23 × 10-3 cm2 V-1 s-1; hole mobility: 7.0 × 10-3 cm2 V-1 s-1). This work presents the first NIR-LEDs that exhibit EMLT-invariant EQE over an EMLT range of 40-220 nm, which represents the highest EQE among reported CQD NIR-LEDs with a QD thickness exceeding 100 nm.

Iodotrimethylsilane as a Reactive Ligand for Surface Etching and Passivation of Perovskite Nanocrystals toward Efficient Pure-red to Deep-red LEDs.

Resurfacing perovskite nanocrystals (NCs) with tight-binding and conductive ligands to resolve the dynamic ligands-surface interaction is the fundamental issue for their applications in perovskite light-emitting diodes (PeLEDs). Although various types of surface ligands have been proposed, these ligands either exhibit weak Lewis acid/base interactions or need high polar solvents for dissolution and passivation, resulting in a compromise in the efficiency and stability of PeLEDs. Herein, we report a chemically reactive agent (Iodotrimethylsilane, TMIS) to address the trade-off among conductivity, solubility and passivation using all-inorganic CsPbI3 NCs. The liquid TMIS ensures good solubility in non-polar solvents and reacts with oleate ligands and produces in situ HI for surface etching and passivation, enabling strong-binding ligands on the NCs surface. We report, as a result, red PeLEDs with an external quantum efficiency (EQE) of ≈23 %, which is 11.2-fold higher than the control, and is among the highest CsPbI3 PeLEDs. We further demonstrate the universality of this ligand strategy in the pure bromide system (CsPbBr3 ), and report EQE of ≈20 % at 640, 652, and 664 nm. This represents the first demonstration of a chemically reactive ligand strategy that applies to different systems and works effectively in red PeLEDs spanning emission from pure-red to deep-red.

Advances in Solution-Processed Blue Quantum Dot Light-Emitting Diodes.

Quantum dot light-emitting diodes (QLEDs) have been identified as a next-generation display technology owing to their low-cost manufacturing, wide color gamut, and electrically driven self-emission properties. However, the efficiency and stability of blue QLEDs still pose a significant challenge, limiting their production and potential application. This review aims to analyse the factors leading to the failure of blue QLEDs and presents a roadmap to accelerate their development based on the progress made in the synthesis of II-VI (CdSe, ZnSe) quantum dots (QDs), III-V (InP) QDs, carbon dots, and perovskite QDs. The proposed analysis will include discussions on material synthesis, core-shell structures, ligand interactions, and device fabrication, providing a comprehensive overview of these materials and their development.

A Novel Prognostic Model for Patients with Primary Gastric Diffuse Large B-Cell Lymphoma.

Objectives: Primary gastric diffuse large B-cell lymphoma (PG-DLBCL) is a common phenotype of extranodal non-Hodgkin's lymphoma (NHL). This research aims to identify a model for predicting overall survival (OS) and cancer-specific survival (CSS) in PG-DLBCL. Methods: A total of 1716 patients diagnosed with PG-DLBCL between 1975 and 2017 were obtained from the SEER database and further randomly divided into the training and validating cohorts at a ratio of 7 : 3. Univariate and multivariate cox analyses were conducted to determine significant variables for the construction of nomogram. The performance of the model was then assessed by the concordance index (C-index), the calibration plot, and the area under the receiver operating characteristic (ROC) curve (AUC). Results: Multivariate analysis revealed that age, race, insurance status, Ann Arbor stage, marital status, chemotherapy, and radiation therapy all showed a significant association with OS and CSS. These characteristics were applied to build a nomogram. In the training cohort, the discrimination of nomogram for OS and CSS prediction was excellent (C-index = 0.764, 95% CI, 0.744-0.784 and C-index = 0.756, 95% CI, 0.732-0.780). The AUC of the nomogram for predicting 3- and 5-year OS was 0.779 and 0.784 and CSS was 0.765 and 0.772. Similar results were also observed in the internal validation set. Conclusions: We have successfully established a novel nomogram for predicting OS and CSS in PG-DLBCL patients with good accuracy, which can help physicians to quickly and accurately complete the evaluation of survival probability, risk stratification, and therapeutic strategy at diagnosis.

Relaxin-3 Ameliorates Diabetic Cardiomyopathy by Inhibiting Endoplasmic Reticulum Stress.

Background: This study is aimed at investigating whether relaxin-3 exhibits protective effects against cardiomyopathy in diabetic rats by suppressing ERS. Methods: Eighty male SD rats were randomly divided into two groups: controls (n = 20) and diabetes (n = 60). The streptozotocin-treated rats were randomly divided into three groups: diabetic group (DM), low-dose relaxin-3 group (0.2 µg/kg/d), and high-dose relaxin-3 group (2 µg/kg/d). The myocardial tissues and collagen fiber were observed by hematoxylin and eosin (H&E) and Masson staining. Serum brain natriuretic peptide (BNP), troponin (TNI), myoglobin, interleukin (IL-17), interleukin (IL)-1α, and tumor necrosis factor (TNF)-α were determined by ELISA. The protein expression of glucose regulatory protein 78 (GRP78) and C/EBP homologous protein (CHOP) in the heart tissue of each group was detected by Western blot analysis. Results: (1) HE and Masson staining indicated that relaxin-3 could attenuate myocardial lesions and myocardial collagen volume fraction. (2) BNP, TnI, and myoglobin in the DM group at four and eight weeks were significantly higher than in the controls (P < 0.01). The relaxin-3-treated groups showed significantly reduced serum BNP, TnI, and myoglobin levels compared with the DM group (P < 0.05). (3) IL-17, IL-1α, and TNF-α levels in the DM rats at 4 weeks were higher than in the controls (P < 0.05). Low or high dose of relaxin-3-treated groups showed reduced serum IL-17 and TNF-α levels compared with the DM group at four and eight weeks (P < 0.05). (4) CHOP and GRP78 protein expression was increased in the DM group at four and eight weeks compared with the controls (P < 0.01), and small and large doses of relaxin-3 significantly reduced GRP78 and CHOP protein expression. Conclusions: Exogenous relaxin-3 ameliorates diabetic cardiomyopathy by inhibiting ERS in diabetic rats.

Overlapping anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis with neuromyelitis optica spectrum disorders: a case report.

BACKGROUND: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis can coexist with neuromyelitis optica spectrum disorder (NMOSD). Patients with overlapping anti-NMDAR encephalitis with positive NMDAR antibodies and aquaporin 4 immunoglobulin G (AQP4-IgG)-seropositive NMOSD are rare but should not be ignored. CASE PRESENTATION: This report describes a unique case of anti-NMDAR encephalitis coexisting with NMOSD. A 27-year-old male presented with blurred vision, cognitive impairment, psychosis, dysphagia, gait instability and urinary incontinence. Brain magnetic resonance imaging (MRI) showed abnormal signals in the right cerebellar hemisphere, temporal lobe, and corpus callosum. NMDAR antibodies were positive in the CSF. AQP4-IgG antibodies were positive in the serum. The patient's condition was stable following intravenous gamma globulin, corticosteroids, immunosuppressants and symptomatic treatments. CONCLUSIONS: This case provides further evidence for the occurrence of anti-NMDAR encephalitis overlapping NMOSD with AQP4-IgG-seropositive in a Chinese patient. However, the mechanisms underlying the occurrence of double-positive antibodies remain elusive.

MicroRNA-34a Promotes Ischemia-Induced Cardiomyocytes Apoptosis through Targeting Notch1.

Myocardial apoptosis occurs during myocardial ischemia. This study aimed to determine the effect of microRNA-34a (miR-34a) in ischemia-induced myocardial apoptosis. Mainly, SD rats were subjected to myocardial ischemia by ligaturing the left anterior descending branch of coronary artery. After rats had myocardial infarction, HE staining and TUNEL staining confirmed a significant increase in apoptosis. The expression of miR-34a was noticeably upregulated, while the expression of Notch1 was downregulated. An increase in caspase-3 and a decrease in Bcl-2/Bax ratio were observed in myocardium. Similar results were observed in the in vitro model of cardiomyocyte ischemia and anoxia of this study. When rat cardiomyocytes were administered with serum starvation and microaerophilic system, apoptosis-related proteins were significantly increased. However, transfecting the miR-34a inhibitor into the cardiomyocyte before the serum starvation and hypoxia treatment could increase the ratio of Bcl-2/Bax and downregulate the expression of caspase-3, as well as prevent cardiomyocytes from apoptosis. As opposed to the abovementioned points, the upregulation of miR-34a expression by transfecting miR-34a mimics induced Notch1 reduce and apoptosis-related proteins increase apparently, while upregulation of Notch1 could stimulate apoptosis attributed to miR-34a. Mechanistically, we demonstrated that Notch1 is a direct target of miR-34a. In conclusion, our current results suggested that miR-34a significantly stimulates ischemia-induced cardiomyocytes apoptosis by targeting Notch1.

Gold-Trisoctahedra-Coated Capillary-Based SERS Platform for Microsampling and Sensitive Detection of Trace Fentanyl.

A cost-effective and highly reproducible capillary-based surface-enhanced Raman scattering (SERS) platform for sensitive, portable detection and identification of fentanyl is presented. Through encapsulating gold trisoctahedra (Au TOH) in the capillary tube for the first time, the SERS platform was constructed by combining the superior SERS properties of Au TOH and the advantages of capillaries in SERS signal amplification, facile sample extraction, and portable trace analysis. The effects of the size and density of Au TOH on the SERS performance were investigated by experiments and simulations, which showed that the maximum SERS enhancement was obtained for Au TOH with the size of 75 nm when particle density reached 74.54 counts/µm2. The proposed SERS platform possesses good reproducibility with a relative standard deviation (RSD) of less than 5%. As a demonstration, the platform was applied to detect fentanyl spiked in aqueous solution and serum samples with a limit of detection (LOD) as low as 1.86 and 40.63 ng/mL, respectively. We also validated the feasibility of the designed platform for accurate identification of trace fentanyl adulterated in heroin at mass concentration down to 0.1% (10 ng in 10 µg total). Overall, this work advances more explorations on capillary-based SERS platform to benefit portable trace analysis.

Association Analysis Between HLA-DQA1 Loci and Neuromyelitis Optica Spectrum Disorder in a Han Chinese Population.

BACKGROUND: Genome-wide association studies for neuromyelitis optica spectrum disorder (NMOSD) have established an association between HLA-DQ alpha 1 (DQA1) and risk for NMOSD. Though ethnicity is generally considered a major influencing factor in genetic analyses, little is known regarding the association of HLA-DQA1 polymorphisms with NMOSD in the Han population, especially the single-nucleotide polymorphisms (SNPs) at HLA-DQA1 . METHODS: We genotyped SNP at loci rs28383224 in a case-control study consisting of 137 subjects (51 patients with NMOSD and 86 unrelated controls were recruited) of Han ethnicity. Logistic regression was used to test the association of SNP with NMOSD susceptibility, the sex and age were adjusted, odds ratios and 95% confidence intervals were estimated. RESULTS: The rs28383224 polymorphism and susceptibility to NMOSD were not statistically associated ( P >0.05) in the Han population in the current study. No significant difference was found in allelic frequencies or genotypic distributions among different subsets of NMOSD patients ( P >0.05). CONCLUSION: In the current study, there is no evidence that polymorphism of rs28383224 in the HLA-DQA1 gene is associated with the risk of NMOSD in the Han Chinese population.

A near-infrared light triggered fluormetric biosensor for sensitive detection of acetylcholinesterase activity based on NaErF4: 0.5 % Ho3+@NaYF4 upconversion nano-probe.

Acetylcholinesterase (AChE), as an important neurotransmitter, is widely present in the peripheral and central nervous systems. The aberrant expression of AChE could cause diverse neurodegenerative diseases. Herein, we developed a facile and interference-free fluorimetric biosensing platform for highly sensitive AChE activity determination based on a NaErF4: 0.5 % Ho3+@NaYF4 nano-probe. This nano-probe exhibits a unique property of emitting bright monochromic red (650 nm) upconversion (UC) emission under multiband (~808, ~980, and ~1530 nm) near-infrared (NIR) excitations. The principle of this detection relies on the quenching of the strong monochromic red UC emission by oxidization products of 3,3',5,5'-tetramethylbenzidine generated through AChE-modulated cascade reactions. This system shows a great sensing performance with a detection limit (LOD) of 0.0019 mU mL- 1 for AChE, as well as good specificity and stability. Furthermore, we validated the potential of the nano-probe in biological samples by determination of AChE in whole blood with a LOD of 0.0027 mU mL-1, indicating the potential application of our proposed platform for monitoring the progression of AChE-related disease.

Effect of Peptidylarginine Deiminase 4 on Endothelial Progenitor Cell Function in Peripheral Arterial Disease.

At present, the global prevalence of peripheral arterial disease is increasing year by year, and it has become a worldwide disease. Studies have shown that transplanting endothelial progenitor cells (EPCs) into ischemic tissues can improve the tissue ischemia, thereby having a therapeutic effect on peripheral arterial diseases. This indicates that EPCs play a therapeutic effect in peripheral arterial disease. Recent studies have shown that peptidylarginine deiminase (PAD) is involved in the regulation of epigenetics and its inhibitor Cl-amidine can improve endothelium-dependent vasodilation and significantly reduce the formation of arterial thrombosis. It can also play a role in hematopoietic stem cells that share the same origin with EPCs. Therefore, we speculate that PAD4 may also have an effect on EPCs through a similar mechanism, thereby participating in the damage and repair of peripheral arterial disease. Therefore, we first detected the expression of PAD4 in EPCs of peripheral arterial disease and detected changes in the number and function of endothelial progenitor cells in peripheral blood after injecting the PAD4 inhibitor Cl-amidine into mice. A mouse model of lower limb ischemia was established to explore the effect of PAD4 on the function of EPCs in peripheral arterial disease. The results show that PAD4 is highly expressed in peripheral arterial diseases and the PAD4 inhibitor Cl-amidine can increase the number of EPCs and can treat peripheral arterial diseases by improving the proliferation, migration, and vascularization of EPCs.

Ultrasensitive detection of SARS-CoV-2 spike protein in untreated saliva using SERS-based biosensor.

Early diagnosis and monitoring of SARS-CoV-2 virus is essential to control COVID-19 outbreak. In this study, we propose a promising surface enhanced Raman scattering (SERS)-based COVID-19 biosensor for ultrasensitive detection of SARS-CoV-2 virus in untreated saliva. The SERS-immune substrate was fabricated by a novel oil/water/oil (O/W/O) three-phase liquid-liquid interfaces self-assembly method, forming two layers of dense and uniform gold nanoparticle films to ensure the reproducibility and sensitivity of SERS immunoassay. The detection was performed by an immunoreaction between the SARS-CoV-2 spike antibody modified SERS-immune substrate, spike antigen protein and Raman reporter-labeled immuno-Ag nanoparticles. This SERS-based biosensor was able to detect the SARS-CoV-2 spike protein at concentrations of 0.77 fg mL-1 in phosphate-buffered saline and 6.07 fg mL-1 in untreated saliva. The designed SERS-based biosensor exhibited excellent specificity and sensitivity for SARS-CoV-2 virus without any sample pretreatment, providing a potential choice for the early diagnosis of COVID-19.

Catechin relieves hypoxia/reoxygenation-induced myocardial cell apoptosis via down-regulating lncRNA MIAT.

BACKGROUND: Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R-induced myocardial cell apoptosis is largely unknown. OBJECTIVE: This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R-induced myocardial cells. METHODS: LncRNA MIAT expression was detected by qRT-PCR. Cell viability of H9C2 cells was detected using CCK-8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual-luciferase reporter gene assay and ChIP assay. RESULTS: In MI/R rats, catechin improved heart function and down-regulated lncRNA MIAT expression in myocardial tissue. In H/R-induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up-regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk-3ß activation. In addition, MIAT inhibited Akt/Gsk-3ß activation and promoted cell apoptosis in H/R-induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk-3ß activation through inhibiting MIAT expression in H/R-induced H9C2 cells. CONCLUSION: Catechin relieved H/R-induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk-3ß pathway.

Association of Hyperhomocysteinemia with Increased Coronary Microcirculatory Resistance and Poor Short-Term Prognosis of Patients with Acute Myocardial Infarction after Elective Percutaneous Coronary Intervention.

BACKGROUND: This study aims to investigate the coronary microcirculatory resistance and prognosis of patients with acute myocardial infarction (AMI) concomitant with hyperhomocysteinemia (HHcy) after an elective percutaneous coronary intervention (PCI). METHODS: A total of 101 patients that underwent elective PCI between May 2015 and July 2018 due to AMI were consecutively enrolled in this study. Patients were divided into a HHcy group (53) and a normal Hcy group (control; 48) based on their plasma homocysteine concentration. The characteristics of coronary angiography, the index of microcirculatory resistance (IMR) of infarct-related vessels (IRV), changes in left ventricular end diastolic diameter (LVEDd) and left ventricular ejection fraction (LVEF) before and after PCI, and the incidence of major adverse cardiovascular events (MACE) three months after PCI were compared between these groups. RESULTS: Compared to the results from the Hcy group, the HHcy group had a higher IMR. The HHcy group had significantly higher LVEDd and a lower LVEF than the Hcy group 3 months after PCI. Additionally, the incidence of MACE at three months after PCI was higher in the HHcy group than in the Hcy group. Pearson correlation analysis revealed a positive correlation with IMR in the HHcy group. Furthermore, there was a difference in the LVEDd measured at one day after PCI and at three months after PCI in the HHcy group. CONCLUSION: AMI patients concomitant with HHcy that undergo elective PCI are prone to coronary microcirculatory dysfunction and have a poor cardiac function and poor prognosis at three months after PCI.

Crown ether-appended calix[2]triazolium[2]arene as a macrocyclic receptor for the recognition of the H2PO4- anion.

A crown ether-appended calix[2]triazolium[2]arene, which exhibits excellent selectivity for H2PO4- compared to other anions, has been designed and synthesized. The selectivity of the prepared receptor for H2PO4- is caused by the stabilization of H2PO4- by the neighboring triazolium hydrogen bond donors and crown ether hydrogen bond acceptors.

Ellagic acid inhibits proliferation and migration of cardiac fibroblasts by down-regulating expression of HDAC1.

Cardiac fibroblasts (CFs) could be activated after myocardial infarction (MI). Thus, it is necessary to explore effective drugs to suppress the activation of CFs following MI. This study was designed to investigate the impacts of ellagic acid on CFs and the underlying mechanisms. The expression of histone deacetylases (HDACs) and fibrosis-related genes was detected by qRT-PCR and western blot. The Masson's Trichrome Staining assay was used to evaluate the area of cardiac fibrosis. The proliferation and migration of CFs were measured by CCK8 Kit and Transwell assay, respectively. Our results showed that ellagic acid significantly reduced protein expression of HDAC1, mRNA expression of collagen I, collagen III, MMP-2 and MMP-9 and the area of cardiac fibrosis in MI rats. In Ang II-stimulated CFs, ellagic acid (60 µmol/L) decreased the protein expression of HDAC1, collagen I, collagen III, MMP-2 and MMP-9, and inhibited cell proliferation and migration. Further, HDAC1 over-expression reversed the inhibitor effects of ellagic acid on proteins expression (collagen I, collagen III, MMP-2 and MMP-9) and proliferation and migration of CFs. The present results suggested that ellagic acid suppressed proliferation and migration of CFs by down-regulating expression of HDAC1.

The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model.

BACKGROUND The role of miR-181a in the development of cardiac disease and in particular, myocardial fibrosis following myocardial infarction (MI) remains unknown. The aim of this study was to explore the role of miR-181a in myocardial fibrosis in a rat model of MI and the expression of TGF-ß receptor III (TßRIII). MATERIAL AND METHODS Forty adult male Wistar rats were randomly divided into an MI model group (n=30) and a control group with (n=10). The rat MI model involved ligating the left anterior descending (LAD) coronary artery in the model group; the control group was treated with a sham operation. Cardiac function was assessed using cardiac ultrasound. Myocardial fibroblasts were extracted from the rat hearts and transfected with a miR-mimic or miR-inhibitor, and cell growth was measured using an MTT assay. The level of miR-181a expression was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blots. RESULTS miR-181a expression was significantly increased during the progression of MI (P<0.05). Over-expression of miR-181a was associated with increased deposition of extracellular matrix (ECM) components, collagen I and fibronectin. This effect was reversed with the use of a miR-181a inhibitor (P<0.05). Upregulation of miR-181a suppressed the expression of TGF-ß receptor III (TßRIII) by binding with 3'-UTR. CONCLUSIONS In this rat model of MI, the findings were that miR-181a had a role in the progression of myocardial fibrosis. The findings require further studies to determine whether miR-181a might provide a novel therapeutic target to limit myocardial fibrosis following MI.

Inflammatory cytokines in cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation.

BACKGROUND: To investigate the changes of inflammatory cytokines in cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation and the effects of metoprolol on them. METHODS: A total of 92 cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation in our hospital from April 2015 to March 2017 were selected and randomly divided into the control group and the observation group, with 46 cases in each group. Three months after pacemaker implantation, the control group was treated with aspirin, the observation group was treated with metoprolol on the basis of aspirin, and the curative effects were compared between the two groups. After treatment, the heart rate, the frequency and duration of atrial fibrillation and the atrial fibrillation load were observed. P-wave dispersion (PD) and cardiac function of the two groups of patients at 6 months after treatment were compared. The changes of serum levels of tumor necrosis factor-α (TNF-α), high sensitive C-reactive protein (Hs-CRP) and interleukin-6 (IL-6) in patients were compared before treatment and at 1, 3 and 6 months after treatment. The quality of life of the two groups of patients was observed. RESULTS: After treatment, the effective rate of treatment in the observation group was significantly higher than that in the control group (P<0.05). After treatment, the average heart rate and atrial fibrillation load in the observation group were significantly improved compared with those in the control group, and the frequency and duration of atrial fibrillation were significantly lower than those in the control group (P<0.05). After treatment, the maximum P-wave duration (Pmax), the minimum P-wave duration (Pmin) and PD in the observation group were significantly lower than those in the control group (P<0.05). The left ventricular ejection fraction (LVEF) in the observation group was significantly higher than that in the control group, and the left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and E/A in the observation group were significantly lower than those in the control group (P<0.05). After treatment, the levels of TNF-α, Hs-CRP and IL-6 in the two groups of patients were decreased significantly, and those in the observation group were significantly lower than those in the control group (P<0.05). The quality of life score in the observation group was significantly higher than that in the control group (P<0.05). CONCLUSIONS: Metoprolol can effectively reduce the incidence of atrial fibrillation, atrial fibrillation loadand inflammatory cytokine levels in cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation, and improve cardiac function of the patients and their quality of life. It has an important clinical significance.