Commercial gadolinium-based
materials have been widely used as
contrast agents for magnetic resonance imaging (MRI), but the high
toxicity of leaking free Gd3+ ions still raises biosafety
concerns. Here, we develop a novel, safe, and efficient MRI contrast
agent based on a stable Fe(III) complex of fluorine and nitrogen co-doped
carbon dots (F,N-CDs) that was prepared from glucose and levofloxacin
by a simple microwave-assisted thermal decomposition method. The obtained
Fe3+@F,N-CD complex exhibits higher longitudinal relaxivity
(r
1 = 5.79 mM–1·s–1) than that of the control samples of the Fe3+@CD complex (r
1 = 4.23 mM–1 s–1) and free Fe3+ (r
1 = 1.59 mM–1 s–1)
in aqueous solution, as assessed by a 1.5 T NMR analyzer. More importantly,
the Fe3+@F,N-CD complex is very stable with a large coordination
constant of 1.06 × 107 in aqueous medium. While incubated
with HeLa cells, the Fe3+@F,N-CD complex shows clear MR
images, demonstrating that it has potential to be an excellent MRI
contrast agent. Furthermore, in vivo MRI experiments indicate that
the Fe3+@F,N-CD complex provides high-resolution MRI pictures
of 4T1 tumor bearing BALB/c mice 15 min after injection and can be
completely excreted 2 h after administration. No cytotoxicity was
observed with F,N-CDs and Fe concentration up to 0.2 mg/mL and 0.3
mM in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide
cell proliferation assay, respectively. The possible mechanism of
the enhanced MRI effect of the Fe3+@F,N-CD complex is therefore
proposed. The extremely low toxicity, high r
1 relaxivity, strong photoluminescence, and low synthetic cost
enable the Fe3+@F,N-CD complex to be a safe and promising T
1-weighted MRI contrast agent for clinical applications.
A single-atom metal doped on carbonaceous nanomaterials has attracted increasing attention due to its potential applications as high-performance catalysts. However, few studies focus on the applications of such nanomaterials as nanotheranostics for simultaneous bioimaging and cancer therapy. Herein, it is pioneeringly demonstrated that the single-atom Gd anchored onto graphene quantum dots (SAGd-GQDs), with dendrite-like morphology, was successfully prepared. More importantly, the as-fabricated SAGd-GQDs exhibits a robustly enhanced longitudinal relaxivity (r 1 = 86.08 mM −1 s −1 ) at a low Gd 3+ concentration of 2 μmol kg −1 , which is 25 times higher than the commercial Gd-DTPA (r 1 = 3.44 mM −1 s −1 ). In vitro and in vivo studies suggest that the obtained SAGd-GQDs is a highly potent and contrast agent to obtain high-definition MRI, thereby opening up more opportunities for future precise clinical theranostics.
Minimally invasive esophagectomy is now accepted as a regular treatment modality for esophageal cancer. Upper gastrointestinal (GI) bleeding is a common postoperative adverse event of esophagectomy. However, there are very few reports in the literature on endoscopic management of early upper GI bleeding after an esophagectomy. Here, we report the successful management of such an early case of GI bleeding after thoracolaparoscopic esophagectomy by the use of endoscopic intrathoracic anastomosis.
Background
Influenza A virus (IAV) triggers acute exacerbation of chronic obstructive pulmonary disease (AECOPD), but the molecular mechanisms remain unclear. In this study, we investigated the role of IAV induced NLRP3 inflammasome activation to increase airway inflammation response in the progression of AECOPD.
Methods
Human bronchial epithelial cells were isolated and cultured from normal and COPD bronchial tissues and co-cultured with IAV. The NLRP3 inflammasome associated genes were identified using RNA sequencing, and the expressions of NLRP3 inflammasome components were measured using qRT-PCR and western blot after cells were transfected with siRNA and treated with MCC950. Moreover, IAV-induced COPD rat models were established to confirm the results; 37 AECOPD patients were included to measure the serum and bronchoalveolar lavage fluid (BALF) of interleukin (IL)-18 and IL-1β.
Results
Increased levels of NLRP3 inflammasome components were not seen until 6 h post-inoculation in normal cells. However, both cell groups reached peak NLRP3 level at 12 h post-inoculation and maintained it for up to 24 h. ASC, Caspase-1, IL-1β and IL-18 were also elevated in a similar time-dependent pattern in both cell groups. The mRNA and protein expression of the NLRP3 inflammasome components were decreased when COPD cells treated with siRNA and MCC950. In COPD rats, the NLRP3 inflammasome components were elevated by IAV. MCC950 alleviated lung damage, improved survival time, and reduced NLRP3 inflammasome components expression in COPD rats. Additionally, the serum and BALF levels of IL-1β and IL-18 were increased in AECOPD patients.
Conclusions
NLRP3 inflammasome is activated in COPD patients as a pre-existing condition that is further exacerbated by IAV infection.
Esophageal cancer is a widespread cancer of the digestive system that has two main subtypes: esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EA). In the diverse range of cancer therapy schemes, the side effects of conventional treatments remain an urgent challenge to be addressed. Therefore, the pursuit of novel drugs with multiple targets, good efficacy, low side effects, and low cost has become a hot research topic in anticancer therapy. Based on this, epigenetics offers an attractive target for the treatment of esophageal cancer, where major mechanisms such as DNA methylation, histone modifications, non-coding RNA regulation, chromatin remodelling and nucleosome localization offer new opportunities for the prevention and treatment of esophageal cancer. Recently, research on epigenetics has remained at a high level of enthusiasm, focusing mainly on translating the basic research into the clinical setting and transforming epigenetic alterations into targets for cancer screening and detection in the clinic. With the increasing emergence of tumour epigenetic markers and antitumor epigenetic drugs, there are also more possibilities for anti-esophageal cancer treatment. This paper focuses on esophageal cancer and epigenetic modifications, with the aim of unravelling the close link between them to facilitate precise and personalized treatment of esophageal cancer.
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