Ultrasensitive Upconversion Nanoparticle Immunoassay for Human Serum Cardiac Troponin I Detection Achieved with Resonant Waveguide Grating.

Selective detection of biomarkers at low concentrations in blood is crucial for the clinical diagnosis of many diseases but remains challenging. In this work, we aimed to develop an ultrasensitive immunoassay that can detect biomarkers in serum with an attomolar limit of detection (LOD). We proposed a sandwich-type heterogeneous immunosensor in a 3 × 3 well array format by integrating a resonant waveguide grating (RWG) substrate with upconversion nanoparticles (UCNPs). UCNPs were used to label a target biomarker captured by capture antibody molecules immobilized on the surface of the RWG substrate, and the RWG substrate was used to enhance the upconversion luminescence (UCL) of UCNPs through excitation resonance. The LOD of the immunosensor was greatly reduced due to the increased UCL of UCNPs and the reduction of nonspecific adsorption of detection antibody-conjugated UCNPs on the RWG substrate surface by coating the RWG substrate surface with a carboxymethyl dextran layer. The immunosensor exhibited an extremely low LOD [0.24 fg/mL (9.1 aM)] and wide detection range (1 fg/mL to 100 pg/mL) in the detection of cardiac troponin I (cTnI). The cTnI concentrations in human serum samples collected at different times during cyclophosphamide, epirubicin, and 5-fluorouracil (CEF) chemotherapy in a breast cancer patient were measured by an immunosensor, and the results showed that the CEF chemotherapy did cause cardiotoxicity in the patient. Having a higher number of wells in such an array-based biosensor, the sensor can be developed as a high-throughput diagnostic tool for clinically important biomarkers.

Immune checkpoint inhibitors: a new era for esophageal cancer.

Introduction: The poor prognosis for patients with esophageal cancer (EC) requires evolving current treatment regimens. Immune checkpoint inhibitors show clinical efficacy and a great safety profile in multiple tumors. And the monoclonal antibodies that target programmed death receptor-1/programmed death receptor ligand-1 or the cytotoxic T lymphocyte antigen-4 pathway has shown potential curable effect of EC. Areas covered: This review article covers the prognostic significance of immune checkpoint expression, the accumulating current clinical studies of checkpoint inhibitors in esophageal cancer patients, and future directions. Expert opinion: Many clinical studies have reported favorable survival results with manageable toxicity of anti-programmed death receptor-1/programmed death receptor ligand-1 and anti-cytotoxic T lymphocyte antigen-4 treatment. More results are expected from future clinical studies. It is believed that combining chemoradiotherapy and immune checkpoint inhibitors can induce safe and efficient anti-tumor immune responses and can be a promising therapeutic strategy.

TBS Predict Coronary Artery Calcification in Adults.

PURPOSE: This study analyzes the association between the bony microarchitecture score (trabecular bone score, TBS) and coronary artery calcification (CAC) in adults undergoing health exams. MATERIALS AND METHODS: We retrospectively collected subjects (N = 81) who underwent coronary computed tomography and bone mineral density studies simultaneously. CAC was categorized to three levels (Group 0, G0, no CAC, score = 0, N = 45; Group 1, G1, moderate CAC, score = 1-100, N = 17; Group 2, G2, high CAC, score ≧ 101, N = 19). Multinomial logistic regression was used to study the association between TBS and CAC levels. RESULTS: CAC is present in 44.4% of the population. Mean TBS ± SD was 1.399 ± 0.090. Per 1 SD increase in TBS, the unadjusted odds ratio (2.393) of moderate CAC compared with no CAC was significantly increased (95% CI, 1.219-4.696, p = 0.011). However, there has been no association of TBS with high CAC (OR: 1.026, 95% CI: 0.586-1.797, p = 0.928). These relationships also existed when individually adjusted for age, sex, and multiple other covariates. CONCLUSIONS: Higher TBS was related to moderate CAC, but not high CAC; a possible explanation may be that bone microarchitecture remodeling becomes more active when early coronary artery calcification occurs. However, further researches are needed to clarify this pathophysiology.