Detection of SARS-CoV-2 Neutralizing Antibodies in Vaccinated Pregnant Women and Neonates by Using a Lateral Flow Immunoassay Coupled with a Spectrum-Based Reader.

The focus of this study was to investigate the detection of neutralizing antibodies (Nabs) in maternal serum and cord blood as the targeted samples by employing a lateral flow immunoassay combined with a spectrum reader (LFI-SR) and the correlation of Nab protection against different types of SARS-CoV-2. We enrolled 20 pregnant women who were vaccinated with the Moderna (mRNA-1273) vaccine during pregnancy and collected 40 samples during delivery. We used an LFI-SR for the level of spike protein receptor binding domain antibody (SRBD IgG) as Nabs and examined the correlation of the SRBD IgG concentration and Nab inhibition rates (NabIR) via enzyme-linked immunosorbent assays (ELISA). The LFI-SR had high confidence for the SRBD IgG level (p < 0.0001). Better NabIR were found in wild-type SARS-CoV-2 (WT) compared to Delta-type (DT) and Omicron-type (OT). Women with two-dose vaccinations demonstrated greater NabIR than those with a single dose. The cut-off value of the SRBD IgG level by the LFI-SR for NabIR to DT (≥30%; ≥70%) was 60.15 and 150.21 ng/mL for mothers (both p = 0.005), and 156.31 (p = 0.011) and 230.20 ng/mL (p = 0.006) for babies, respectively. An additional vaccine booster may be considered for those mothers with SRBD IgG levels < 60.15 ng/mL, and close protection should be given for those neonates with SRBD IgG levels < 150.21 ng/mL, since there is no available vaccine for them.

Sulforaphane Induces Cell Death Through G2/M Phase Arrest and Triggers Apoptosis in HCT 116 Human Colon Cancer Cells.

Sulforaphane (SFN), an isothiocyanate, exists exclusively in cruciferous vegetables, and has been shown to possess potent antitumor and chemopreventive activity. However, there is no available information that shows SFN affecting human colon cancer HCT 116 cells. In the present study, we found that SFN induced cell morphological changes, which were photographed by contrast-phase microscopy, and decreased viability. SFN also induced G2/M phase arrest and cell apoptosis in HCT 116 cells, which were measured with flow cytometric assays. Western blotting indicated that SFN increased Cyclin A, cdk 2, Cyclin B and WEE1, but decreased Cdc 25C, cdk1 protein expressions that led to G2/M phase arrest. Apoptotic cell death was also confirmed by Annexin V/PI and DAPI staining and DNA gel electrophoresis in HCT 116 cells after exposure to SFN. The flow cytometric assay also showed that SFN induced the generation of reactive oxygen species (ROS) and Ca[Formula: see text] and decreased mitochondria membrane potential and increased caspase-8, -9 and -3 activities in HCT 116 cell. Western blotting also showed that SFN induced the release of cytochrome c, and AIF, which was confirmed by confocal microscopy examination. SFN induced ER stress-associated protein expression. Based on those observations, we suggest that SFN may be used as a novel anticancer agent for the treatment of human colon cancer in the future.

Cantharidin induces DNA damage and inhibits DNA repair-associated protein expressions in TSGH8301 human bladder cancer cell.

Cantharidin is an active component of mylabris, which has been used as a traditional Chinese medicine. Cantharidin has been shown to have antitumor activity against several types of human cancers in vitro and in animal models in vivo. We investigated whether cantharidin induces DNA damage and affects DNA damage repair-associated protein levels in TSGH8301 human bladder cancer cells. Using flow cytometry to measure viable cells, cantharidin was found to reduce the number of viable cells in a dose-dependent manner. Comet assay, 4',6-diamidino-2-phenylindole (DAPI) staining and DNA gel electrophoresis were used to measure DNA damage and condensation; the results indicated that cantharidin induced DNA damage (comet tail), DNA condensation (white DAPI staining) and DNA damage (DNA smear). Results from western blotting showed that cantharidin inhibited the expression of DNA-dependent serine/threonine protein kinase, poly-ADP ribose polymerase, phosphate-ataxia-telangiectasia and RAD3-related, O-6-methylguanine-DNA methyltransferase, breast cancer susceptibility protein 1, mediator of DNA damage checkpoint protein 1, phospho-histone H2A.X, but increased that of phosphorylated p53 following 6 and 24 h treatment. Confocal laser microscopy was used to examine the protein translocation; cantharidin suppressed the levels of p-H2A.X and MDC1 but increased the levels of p-p53 in TSGH8301 cells. In conclusion, we found that cantharidin-induced cell death may occur through the induction of DNA damage and suppression of DNA repair-associated protein expression in TSGH8301 cells.