Search

We aimed to examine the correlation of T-cell immunoglobulin and ITIM domain (TIGIT)-expressing CD3 + CD56 + cells (TNKS) with coronary artery disease (CAD), atherosclerotic lesion progression, and inflammatory environment. A total of 199 subjects, including 98 patients with acute coronary syndrome (ACS), 52 patients with chronic coronary syndrome (CCS), and 49 control subjects, were recruited in the study. The TIGIT-expressing TNKS were quantified by flow cytometric analysis; the severity of coronary artery lesions was evaluated by the Gensini score. Whole blood cells were stimulated with interleukin-2 (IL-2), interleukin-7 (IL-7), and interleukin-15 (IL-15) in presence or absence of STAT, PI3K, and P38 MAPK inhibitors, respectively. The TIGIT-expressing TNKS was significantly increased in patients with CAD, ACS, and CCS compared to the control group (P < 0.05). The TIGIT-expressing TNKS were independent predictors of CAD, ACS and CCS (P < 0.05). The TIGIT-expressing TNKS were positively associated with Gensini score (P < 0.05). The TIGIT-expressing TNKS was positively correlated with age, and being male (P < 0.05). The inflammatory microenviroment with increased IL-2, IL-7, and IL-15 contributed to upregulation of TIGIT expression in TNKS. PI3K and P38 MAPK inhibitors could inhibit the upregulation of TIGIT expression in TNKS induced by IL-2, IL-7, and IL-15. The TIGIT-expressing TNKS may be involved in common pathogenesis of ACS and CCS, and atherosclerotic lesion progression. Meanwhile, the increased TIGIT-expressing TNKS might be associated with a proatherogenic microenvironment or inflammatory microenvironment. PI3K and P38 MAPK signaling pathways were involved in the regulation of TIGIT expression. [ABSTRACT FROM AUTHOR]

Background: The association of Apolipoprotein A‐I (APOAI) with T cell subsets and interferon‐ү (IFN‐γ) in patients with coronary artery disease (CAD) has been not reported. Thus, this study aimed to investigate the association of APOAI with T cell subsets and IFN‐γ in CAD. Methods: This study included a total of 107 patients with CAD including acute coronary syndrome and chronic coronary syndrome. T cell subsets, and CD3‐CD56+ natural killer cells were quantified by flow cytometric analysis. The serum concentrations of IFN‐ү were measured by enzyme‐linked immunosorbent assay. Lipid profiles, C‐reactive protein (CRP), and fibrinogen were measured in the clinical laboratory. Clinical data was obtained duration hospitalization. Results: The CD4+ T cells were higher in patients of the low‐APOAI group (.05). The high‐density lipoprotein cholesterol (HDL‐C) was also inversely associated with CD4+ T cells (p <.05), and positively associated with CD8+ T cells (p <.05). Lastly, APOA1 and HDL‐C did not correlated with fibrinogen and CRP (p >.05). Conclusion: The present study demonstrated the correlation of APOAI with T cell subsets and IFN‐γ in CAD. These results provided novel information for the regulatory action between APOAI and T cell subsets and inflammatory immunity in CAD. [ABSTRACT FROM AUTHOR]

1D-structure perovskite materials have gradually attracted people's attention due to the flexibility of their crystal structures and their strong stability to environments such as water and humidity. In this work, 1D/3D mixed-dimensional perovskite materials were achieved by adding large cation tBA+. The Cs+ doped high quality perovskite films (CstBAMAFA) were prepared by a two-step solution method, and the photoelectrical properties and stability of perovskite solar cells (PSCs) were systematically analyzed. The photoelectric conversion efficiency (PCE) of the champion Cs+ doped 1D/3D PSCs reached 17.08%, and the stability was significantly improved compared with the control group. The PCE of unencapsulated PSCs could retain 80% of the initial value after 197 days of storage in Ar glove box, and 69.3% of the initial value after 20 days of storage at 30 °C with a relative humidity of 50–60%. The improved efficiency and stability of Cs+ doped 1D/3D PSCs are attributed to the filling of the grain boundaries by the 1D phase. [Display omitted] • Larger tert-butylamine cation (tBA+) replaces MA+ to form a 1D/3D structure. • tBA+ regulates the size of the grain in the novel 1D/3D perovskite solar cell. • Multiple cations doped 1D/3D perovskites improve efficiency and stability. [ABSTRACT FROM AUTHOR]

Interfacial passivation of perovskite films is an effective way to further improve the power conversion efficiency (PCE) and long-term stability of perovskite solar cells (PSCs). In this work, the combination of ionic liquid (IL) BMIMBF 4 and isopropanol (IPA) are used as green mixed anti-solvent. The existence of ionic liquids can delay the crystallization of perovskite and obtain dense perovskite films, because the non-volatile characteristics of BMIMBF 4 is left on the surface of perovskite, which is used for interfacial passivation. The perovskite film, which is prepared by mixed anti-solvent, can effectively reduce surface defects and significantly inhibit non-radiative recombination. Comparing with IPA as single anti-solvent, the PCE increased from 14.49% to 16.25%. In addition, the perovskite film with mixed anti-solvent still retains 76.8% of the initial efficiency after the unpacked PSCs are soaked in 100 mW/cm2 light for 20 days, and it retains 72.6% of the initial efficiency after 20 days of aging in an air atmosphere with 50∼60% relative humidity. The significant improvement of stability shows that the mixed green anti-solvent which combining BMIMBF 4 with IPA is an effective strategy for preparing stable PSCs by one-step method. [Display omitted] • Combining IL BMIMBF 4 with IPA are used as green mixed anti-solvent. • BMIMBF 4 left on the surface of perovskite is used for interfacial passivation. • Stability is significantly improved using the green mixed anti-solvent. [ABSTRACT FROM AUTHOR]

Autophagy is critical for myocardial ischemia-reperfusion (I/R) injury. However, there is still considerable debate over its protective and deleterious effects. The purpose of this study was to determine the involvement of the proprotein convertase subtilisin/Kexin type 9 (PCSK9) and its inhibitor in myocardial ischemia-reperfusion injury autophagy (MRI). Nine groups of eighty rats were used: sham, I/R2 h, I/R4 h, I/R6 h, I/R8 h, I/R1 d, and I/R2 d. A 30-min coronary artery blockage was used to produce myocardial IR. The time required for reperfusion rose linearly with the time gradient, from 2 h to 2 days. Following the determination of the best reperfusion period, three groups were formed: sham, I/R, and I/R + P (PCSK9 inhibitor (evolocumab) 10 mg/kg diluted in 2 ml sterile injection water was administered subcutaneously 1 week and half an hour before to surgery. Each group's infarction area was determined by electrocardiography (ECG), cardiac function, and 2,3,5-triphenyltetrazolium chloride (TTC) /Evan Blue (EB) staining. To detect morphological alterations in myocardial cells in each group, hematoxylin and eosin (HE) staining was used. Meanwhile, western blotting, immunohistochemistry, and Masson trichrome staining were utilized to quantify myocardial fibrosis and PCSK9 and autophagy protein expression. The results indicated that PCSK9 expression levels increased significantly in MRI, as indicated by increased levels of the autophagy regulatory protein light chain 3 (LC3) and Beclin-1, which activated autophagy in cardiomyocytes, exacerbated myocardial injury, and increased the size of myocardial infarcts. Meanwhile, PCSK9 regulates mitophagy via the Bcl-2/adenovirus E1B 19-kDa interacting protein (BNIP3) pathway, which controls myocardial infarction MRI throughout. Additionally, the PCSK9 inhibitor significantly decreased autophagy, enhanced cardiac function, and reduced the extent of reperfusion injury, consequently reducing myocardial infarct size expansion. PCSK9 is upregulated in the myocardial ischemia-reperfusion injury hearts and regulates mitophagy via the BNIP3 pathway, which in turn contributes to reperfusion injury after myocardial infarction. PCSK9 inhibition protects against myocardial ischemia-reperfusion injury via suppressing autophagy. • the expression levels of PCSK9 and autophagy markers rose in a proportional ratio with increasing reperfusion time, peaking at 1 day of reperfusion and thereafter decreased. Meanwhile, we believe that PCSK9 regulation of mitophagy peaked at 1 day after reperfusion, boosting autophagosome formation, intensifying mitochondrial damage, and exacerbating reperfusion injury development. (2) In response to MRI, we discovered a gradual rise in PCSK9 in reperfused hearts, which contributes to scar growth and cardiac dysfunction. • Data demonstrated that elevated PCSK9 expression hastened the progression of myocardial infarction by triggering mitochondrial apoptosis in cardiomyocytes after passing through the BNIP3 pathway. It causes more severe reperfusion injury, which increases the extent of the myocardial infarction. • Pretreatment with PCSK9 inhibitors reduced PCSK9 expression, slowed autophagy formation, and reduced myocardial ischemia-reperfusion injury, enhancing ventricular remodeling and improve cardiac function, resulting in a smaller myocardial infarction. • We believe PCSK9 has a role in the evolution of myocardial infarction, and ischemia-reperfusion damage. • PCSK9 is up-regulated in the hearts with myocardial ischemia-reperfusion injury and regulates mitophagy through the BNIP3 pathway, thus promoting reperfusion injury after myocardial infarction. PCSK9 inhibition protects against myocardial ischemia-reperfusion injury via suppressing autophagy. [ABSTRACT FROM AUTHOR]

The facile approach combined the halide mixture of chloride and bromide anions with the exchange of short-chain ligand Phenethylamine (PEA) was used to prepare hybrid perovskite PEA-MAPbBr 3-x Cl x quantum dots (PEA-QDs-Cl), which realized blue emissive quantum dots light-emitting diode (QLED) with wider gamut of Commission Internationale de l'Eclairage (CIE) coordinates (Δx = −0.04, Δy = 0.03) than National Television Systems Committee (NTSC) TV color standard. Compared to pristine MAPbBr 3 quantum dots (pristine-QDs) prepared by conventional long-chain ligands, the size of PEA-QDs-Cl was manipulated from 9 nm to 3 nm characterized by HRTEM, emissive spectra were blue shifted from 528 nm to 469 nm measured by photoluminescence (PL). Meanwhile, time-resolved PL (TRPL) decay lifetimes of perovskite quantum dots doped with chloride anions (QDs-Cl) were improved from 10.3 ns to 13.9 ns, because short-chain ligands were introduced to passivate defects on the surface of QDs-Cl. Furthermore, XPS results showed that the chloride content was decreased from 34.7% to 33.7% through chloride vacancies on the surface of QDs-Cl were passivated by PEA. [Display omitted] • Perovskite quantum dots prepared by halide mixture of chloride and bromide anions. • Introducing short-chain ligands to passivate the defects on the surface of QDs-Cl. • Sizes of QDs-Cl were manipulated from 9 nm to 3 nm by anion exchange method. • PL shows color tunable emissive spectra were blue shifted from 528 nm to 469 nm. • Blue emissive perovskite QLEDs with wider gamut of CIE coordinates than NTSC. [ABSTRACT FROM AUTHOR]