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40 (95% CI 1.35, 1.46) and OR 1.55 (95% CI 1.41, 1.70), respectively). Female sex, age, being divorced or never married, having only primary education or currently being under education, as well as being on welfare/transfer income increased odds of antidepressant use. Completing higher education and having high income were associated with lower odds.
In asthma, antidepressant use is significantly higher than in the background population. Even after adjusting for known risk factors, asthma remains a predictor of antidepressant use, signalling a psychologic burden related to living with asthma.
In asthma, antidepressant use is significantly higher than in the background population. Even after adjusting for known risk factors, asthma remains a predictor of antidepressant use, signalling a psychologic burden related to living with asthma.
The prognostic implications of the admission cTnI level and D2B time combined on in-hospital and 1-year heart failure (HF) and mortality in STEMI patients undergoing a primary percutaneous coronary intervention (PCI) are remain uncertain.
We divided the consecutive 1485 STEMI patients who underwent PCI from January 2015 to October 2019 at our hospital into three groups based on their admission cTnI levels normal group (<0.1 ng/mL), middle group (0.1 to less than 3 ng/mL), and high group (≥3 ng/mL) and into two groups by their D2B times >90 min (>90-D2B) and ≤90 min (≤90-D2B). During the in-hospital and 1-year follow-up periods, the incidence of composite clinical events increased significantly with the increase in the admission cTnI level (p < 0.05). In-hospital, the composite rate of death and HF events was significantly higher in the >90-D2B group compared to the ≤90-D2B group (p = 0.006), but its influence disappeared in the 1-year follow-up (p > 0.05). A multivariable logistic analysis revealed that, in the ≤90-D2B group, with the exception of the cTnI ≥3 ng/mL patients, the cTnI level had no effect on in-hospital or 1-year outcomes; in >90-D2B group, cTnI ≥3ng/mL increased outcomes in both periods.
High cTnI levels (≥3 ng/mL) on admission are independent of the D2B time for predicting in-hospital and 1-year cardiac events in STEMI patients undergoing PCI.
High cTnI levels (≥3 ng/mL) on admission are independent of the D2B time for predicting in-hospital and 1-year cardiac events in STEMI patients undergoing PCI.
The combination of sonodynamic therapy and oxygenation strategy is widely used in cancer treatment. However, due to the complexity, heterogeneity and irreversible hypoxic environment produced by hepatocellular carcinoma (HCC) tissues, oxygen-enhancing sonodynamic therapy (SDT) has failed to achieve the desired results. With the emergence of ferroptosis with reactive oxygen species (ROS) cytotoxicity, this novel cell death method has attracted widespread attention.
In this study, nanobubbles (NBs) were connected with the sonosensitizer Indocyanine green (ICG) to construct a 2-in-1 nanoplatform loaded with RAS-selective lethal (RSL3, ferroptosis promoter) (RSL3@O2-ICG NBs), combined with oxygen-enhanced SDT and potent ferroptosis. In addition, nanobubbles (NBs) combined with low-frequency ultrasound (LFUS) are called ultrasound-targeted nanobubble destruction (UTND) to ensure specific drug release and improve safety.
MDA/GSH and other related experimental results show that RSL3@O2-ICG NBs can enhance SDT t has been proven to be significant, revealing the prospect of 2-in-1 nanobubbles combined with SDT and ferroptosis in treating HCC.
The therapeutic effect of the in vitro synergistic treatment has been proven to be significant, revealing the prospect of 2-in-1 nanobubbles combined with SDT and ferroptosis in treating HCC.
Traumatic spinal cord injury (TSCI) induces a powerful inflammatory response that can significantly exacerbate the extent and severity of neural damage (termed as "secondary injury"). Thus, the suppression of inflammation is crucial for reducing neurological dysfunction following TSCI. However, the conventional anti-inflammatory drugs show limited efficacy because of poor penetration and release kinetics at the injury site. This study describes the design, synthesis, release kinetics, biosafety, and preclinical efficacy of minocycline (MC)-loaded poly(α-lipoic acid)-methylprednisolone (PαLA-MP) prodrug nanoparticles (NPs) for the combined anti-inflammatory treatment of TSCI.
NPs were produced by conjugating MP to PαLA and then loading MC. The NP structure was confirmed through
H nuclear magnetic resonance (
H NMR), Fourier transform infrared spectroscopy, ultraviolet-visible absorption spectroscopy, gel permeation chromatography, dynamic light scattering, and transmission electron microscopy. Drug-loadunction following experimental TSCI, which suggests their potential for clinical application.
The MC-PαLA-MP NPs can mitigate secondary inflammation and preserve motor function following experimental TSCI, which suggests their potential for clinical application.
Cancer vaccines are a promising therapeutic approach in cancer immunotherapy and can inhibit tumor growth and prevent tumor recurrence and metastasis by activating a sustained antitumor immunoprotective effect. However, the therapeutic effect of cancer vaccines is severely weakened by the low immunogenicity of cancer antigens and the immunosuppressive microenvironment in tumor tissues.
Here, we report a novel hybrid membrane nanovaccine, composed of mesoporous silica nanoparticle as a delivery carrier, hybrid cell membranes obtained from dendritic cells and cancer cells, and R837 as an immune adjuvant (R837@HM-NPs). We investigated the anti-tumor, tumor recurrence and metastasis prevention abilities of R837@HM-NPs and their mechanisms of action through a series of in vivo and ex vivo experiments.
R837@HM-NPs not only provide effective antigenic stimulation but are also a durable supply of the immune adjuvant R837. In addition, R837@HM-NPs promote antigen endocytosis into dendritic cells via various receptor-mediated pathways. Compared with HM-NPs or R837@HM-NPs, R837@HM-NPs in combination with an immune checkpoint blockade showed stronger antitumor immune responses in inhibiting tumor growth, thus eliminating established tumors, and rejecting re-challenged tumors by regulating the immunosuppressive microenvironment and immunological memory effect.
These findings suggest that the hybrid membrane nanovaccine in combination with immune checkpoint blockade is a powerful strategy to enhance antitumor immunotherapy without concerns of systemic toxicity.
These findings suggest that the hybrid membrane nanovaccine in combination with immune checkpoint blockade is a powerful strategy to enhance antitumor immunotherapy without concerns of systemic toxicity.
Modulating the inflammatory response of human gingival fibroblasts (hGFs) is important for the control of periodontal inflammation because it is a key event in the pathogenesis of periodontitis. Here, we aimed to determine whether polyglucose sorbitol carboxymethyl ether (PSC)-coated superparamagnetic iron oxide nanoparticles (SPIONs) protect hGFs against invasion and inflammatory stimulation by
(
).
First, we determined the cytotoxicity and antimicrobial activity of PSC-SPIONs. Then, their effects on invasion of hGFs by
were evaluated by counting invading
, fluorescence staining, and transmission electron microscopy. The effect of PSC-SPIONs on inflammation in hGFs induced by
lipopolysaccharide was evaluated by measurement of reactive oxygen species (ROS), and enzyme-linked immunosorbent assays, quantitative reverse transcription-polymerase chain reaction, and Western blotting of key indicator molecules. The effects of dimercaptosuccinic acid (DMSA)-coated SPIONs and the free form of PSC alone were also tested and compared with those of PSC-SPIONs.
PSC-SPIONs (25 μg/mL) are cytocompatible with hGFs and exhibit no antimicrobial effects on
. However, they inhibit invasion of hGFs by
at 15 μg/mL. Autophagy activator They also decrease ROS production and inflammatory cytokine secretion by hGFs at 5, 15, and 25 μg/mL, by downregulating activation of the nuclear factor-kappa B signaling pathway. Furthermore, PSC alone does not inhibit inflammation, while DMSA-SPIONs do. This indicates that the nanosize effects of PSC-SPIONs, rather than their coating material, play the dominant role in their anti-inflammatory activity.
PSC-SPIONs protect hGFs against
invasion and inflammatory stimulation. Thus, they have potential for clinical application in control of periodontal inflammation.
PSC-SPIONs protect hGFs against P. gingivalis invasion and inflammatory stimulation. Thus, they have potential for clinical application in control of periodontal inflammation.
WNT/β-catenin signal pathway is a potential hope for lung tissue repair. We investigated the levels of Dickkopf-1 (DKK1), an endogenous inhibitor of WNT/β-catenin signal pathway, in chronic obstructive pulmonary disease (COPD) patients and airway inflammation.
Collected the demographic and clinical characteristics of 36 healthy controls, 25 stable COPD patients and 10 acute exacerbation of COPD (AECOPD) patients, then performed pulmonary function and detected serum DKK1 levels. After over-expression of DKK1, detect the levels of DDK1, lipoprotein-related protein 6 (LRP6) and inflammatory factors in bronchial epithelial cells stimulated with cigarette smoke extract (CSE).
Serum DKK1 were reduced in stable COPD patients compared to healthy controls (3866.72 ± 775.33 pg/mL vs 5317.61 ± 1317.20 pg/mL, p<0.0001), but there was no significant difference between stable and acutely exacerbated patients (3866.72 ± 775.33 pg/mL vs 3482.10 ± 841.25 pg/mL, p>0.05). DKK1 was positively correlated with FEV1 (r biomarker pattern.
Smoking is the primary cause of chronic obstructive pulmonary disease (COPD); however, only 10-20% of smokers develop the disease suggesting possible genomic association in the causation of the disease. In the present study, we aimed to explore the whole genome transcriptomics of blood monocytes from COPD smokers (COPD-S), COPD Ex-smokers (COPD-ExS), Control smokers (CS), and Control Never-smokers (CNS) to understand the differential effects of smoking, COPD and that of smoking cessation.
Exploratory analyses in form of principal component analysis (PCA) and hierarchical component analysis (uHCA) were performed to evaluate the similarity in gene expression patterns, while differential expression analyses of different supervised groups of smokers and never smokers were performed to study the differential effect of smoking, COPD and smoking cessation. Differentially expressed genes among groups were subjected to post-hoc enrichment analysis. Candidate genes were subjected to external validation by quantitately separated from all smokers (COPDS, COPD-ExS, and CS), while amongst all smokers, control smokers had aggregated in a separate cluster. Smoking cessation appeared beneficial if started at an early stage as many genes altered due to smoking started reverting towards the baseline, whereas only a few COPD-related genes showed reversal after smoking cessation.
