Lab-on-a-chip optical biosensor platform: a micro-ring resonator integrated with a near-infrared Fourier transform spectrometer.

In this paper, we demonstrated the design and experimental results of the near-infrared lab-on-a-chip optical biosensor platform that monolithically integrates the MRR and the on-chip spectrometer on the silicon-on-insulator (SOI) wafer, which can eliminate the external optical spectrum analyzer for scanning the wavelength spectrum. The symmetric add-drop MRR biosensor is designed to have a free spectral range (FSR) of ∼19 nm and a bulk sensitivity of ∼73 nm/RIU; then the drop-port output resonance peaks are reconstructed from the integrated spatial-heterodyne Fourier transform spectrometer (SHFTS) with the spectral resolution of ∼3.1 nm and the bandwidth of ∼50 nm, which results in the limit of detection of 0.042 RIU.

A point-of-care biosensor for rapid detection and differentiation of COVID-19 virus (SARS-CoV-2) and influenza virus using subwavelength grating micro-ring resonator.

In the context of continued spread of coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 and the emergence of new variants, the demand for rapid, accurate, and frequent detection is increasing. Moreover, the new predominant strain, Omicron variant, manifests more similar clinical features to those of other common respiratory infections. The concurrent detection of multiple potential pathogens helps distinguish SARS-CoV-2 infection from other diseases with overlapping symptoms, which is significant for providing tailored treatment to patients and containing the outbreak. Here, we report a lab-on-a-chip biosensing platform for SARS-CoV-2 detection based on the subwavelength grating micro-ring resonator. The sensing surface is functionalized by specific antibody against SARS-CoV-2 spike protein, which could produce redshifts of resonant peaks by antigen-antibody combination, thus achieving quantitative detection. Additionally, the sensor chip is integrated with a microfluidic chip featuring an anti-backflow Y-shaped structure that enables the concurrent detection of two analytes. In this study, we realized the detection and differentiation of COVID-19 and influenza A H1N1. Experimental results indicate that the limit of detection of our device reaches 100 fg/ml (1.31 fM) within 15 min detecting time, and cross-reactivity tests manifest the specificity of the optical diagnostic assay. Furthermore, the integrated packaging and streamlined workflow facilitate its use for clinical applications. Thus, the biosensing platform presents a promising approach for attaining highly sensitive, selective, multiplexed, and quantitative point-of-care diagnosis and distinction between COVID-19 and influenza.

A microfluidic chip with a serpentine channel enabling high-throughput cell separation using surface acoustic waves.

As an acute inflammatory response, sepsis may cause septic shock and multiple organ failure. Rapid and reliable detection of pathogens from blood samples can promote early diagnosis and treatment of sepsis. However, traditional pathogen detection methods rely on bacterial blood culture, which is complex and time-consuming. Although pre-separation of bacteria from blood can help with the identification of pathogens for diagnosis, the required low-velocity fluid environment of most separation techniques greatly limits the processing capacity for blood samples. Here, we present an acoustofluidic device for high-throughput bacterial separation from human blood cells. Our device utilizes a serpentine microfluidic design and standing surface acoustic waves (SSAWs), and separates bacteria from blood cells effectively based on their size difference. The serpentine microstructure allows the operating distance of the acoustic field to be multiplied in a limited chip size via the "spatial multiplexing" and "pressure node matching" of SSAW field. Microscopic observation and flow cytometry analysis shows that the device is helpful in improving the flow rate (2.6 µL min-1 for blood samples; the corresponding velocity is ∼3 cm s-1) without losing separation purity or cell recovery. The serpentine microfluidic design provides a compatible solution for high-throughput separation, which can synergize with other functional designs to improve device performance. Further, its advantages such as low cost, high biocompatibility, label-free separation and ability to integrate with on-chip biosensors are promising for clinical utility in point-of-care diagnostic platforms.

COX-2 regulates Snail expression in gastric cancer via the Notch1 signaling pathway.

The conversion of arachidonic acid into prostaglandins by cyclooxygenase (COX)-2 contributes to the biological properties of malignant tumours. During the initiation and development of various tumours, the Notch family plays a key role. However, the association between COX­2 and the Notch family in gastric cancer (GC) remains unclear. The present study aimed to clarify the mechanisms through which COX­2 participates in the pathogenesis of GC. Quantitative PCR and western blot analysis were used to detect the expression of Notch family members and COX­2 in human GC and paracancerous tissues, GES­1 cells and GC cell lines (AGS, SGC­7901, BGC­823, and MGC­803) treated with or without celecoxib, prostaglandin E2 and small interfering RNA (siRNA). A CCK­8 assay was performed to detect the proliferation of GC cells transfected with siRNA against COX­2 (si­COX­2). A high mRNA expression of Notch1 and a decreased expression of Notch-1 intracellular active domain (N1IC) in GC were found to be related to the depth of invasion and TNM staging. The mRNA levels of Notch2, Notch3, Jagged1 and N2IC were found to be high in GC. A High expression of COX­2 was associated with poorly differentiated and deeply invasive GC. COX­2 and Notch1 exhibited an inverse expression pattern in the GES­1 cells and different GC cell lines; the inhibition of COX­2 increased Notch1 expression and activated the GC cells, whereas Notch1 downregulation had the opposite effect. Notch1 exhibited varying effects on Snail in the GC cell lines. The downregulation of COX­2 expression significantly inhibited the proliferation of GC cells. On the whole, the expression of Notch signalling molecules differed in GC. COX­2 inversely regulated Notch1 in GC and partially depended on the Notch1 signalling pathway in altering the expression of Snail.