B cells secrete antibodies and mediate the humoral immune response, making them extremely important in protective immunity against SARS-CoV-2, which caused the coronavirus disease 2019 (COVID-19) pandemic. In this review, we summarize the positive function and pathological response of B cells in SARS-CoV-2 infection and re-infection. Then, we structure the immunity responses that B cells mediated in peripheral tissues. Furthermore, we discuss the role of B cells during vaccination including the effectiveness of antibodies and memory B cells, viral evolution mechanisms, and future vaccine development. This review might help medical workers and researchers to have a better understanding of the interaction between B cells and SARS-CoV-2 and broaden their vision for future investigations.

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A photoredox 1,1‐dichloromethylation of alkenes with the readily available bulk chemical chloroform was described, furnishing a variety of 1,1‐dichloroalkane products selectively. Furthermore, this transformation could proceed smoothly on gram‐scale, and the obtained products could transform into diverse γ‐lactam derivatives with simple treatment. Mechanistically, the single electron transfer (SET) with excited photocatalyst and subsequent deprotonation of triethylamine generates the key α‐aminoradical intermediate, which enables selective Cl‐atom transfer of chloroform. The specific selectivity, broad substrate scope, as well as the mild reaction conditions make this strategy especially attractive.

Background Cancer-associated fibroblasts (CAFs), an important component of the tumor microenvironment (TME), play crucial roles in tumor stemness. It has been shown in various cancer studies that stanniocalcin-1 (STC1) is secreted by CAFs, however, its function in HCC is still not clear. Methods The serum concentration and intracellular expression level of STC1 were quantified by ELISA and western blotting, respectively. The role of CAF-derived STC1 in HCC stemness was investigated by sphere formation, sorafenib resistance, colony formation, and transwell migration and invasion assays in vitro and in an orthotopic liver xenograft model in vivo. An HCC tissue microarray containing 72 samples was used to evaluate the expression of STC1 and Notch1 in HCC tissues. Coimmunoprecipitation (CoIP) and dual-luciferase reporter assays were performed to further explore the underlying mechanisms. ELISAs were used to measure the serum concentration of STC1 in HCC patients. Results We demonstrated that CAFs were the main source of STC1 in HCC and that CAF-derived STC1 promoted HCC stemness through activation of the Notch signaling pathway. In HCC patients, the expression of STC1 was positively correlated with Notch1 expression and poor prognosis. The co-IP assay showed that STC1 directly bound to Notch1 receptors to activate the Notch signaling pathway, thereby promoting the stemness of HCC cells. Our data further demonstrated that STC1 was a direct transcriptional target of CSL in HCC cells. Furthermore, ELISA revealed that the serum STC1 concentration was higher in patients with advanced liver cancer than in patients with early liver cancer. Conclusions CAF-derived STC1 promoted HCC stemness via the Notch1 signaling pathway. STC1 might serve as a potential biomarker for the prognostic assessment of HCC, and the stromal-tumor amplifying STC1-Notch1 feedforward signal could constitute an effective therapeutic target for HCC patients.

Background Cancer associated fibroblasts (CAFs), an important component of the tumor microenvironment (TME), play crucial roles in tumor stemness. Stanniocalcin-1 (STC1) was found secreted by CAFs in various cancers, but its main source and its role in hepatocellular carcinoma (HCC) was still unclear. Methods The serum and intracellular expression levels of STC1 were detected by ELISA and western blot. The role of CAFs-derived STC1 in HCC stemness was probed by sphere formation, sorafenib resistance, colony formation, and transwell migration and invasion assays in vitro and orthotopic liver xenograft tumor model in vivo. An HCC tissue microarray containing 72 samples was used to identify the STC1 and the Notch1 in HCC tissues. Co-immunoprecipitation (CoIP) and dual-luciferase reporter assay were performed to further explore the underlying mechanisms. ELISA assays were used to detect the serum concentration of STC1 in HCC patients. Results We demonstrated that CAFs were the main source of STC1 in HCC and that CAFs-derived STC1 promoted HCC stemness through the activation of the Notch signaling pathway. In HCC patients, the expression of STC1 was positively correlated with poor prognosis and the Nocth1 expression. Co-IP assay showed that STC1 directly bound to Notch1 receptors to activate the Notch signaling pathway, thereby promoting the stemness of HCC. Our data further demonstrated that STC1 was a direct transcriptional target of CSL in HCC cells. Furthermore, ELISA revealed that the serum STC1 concentration was higher in patients with advanced liver cancer than patients with early liver cancer. Conclusions CAFs-derived STC1 promoted HCC stemness via the Notch signaling pathway. STC1 might serve as a potential biomarker for the prognostic assessment of HCC, and the stromal-tumor amplifying STC1-Notch1 feedforward signal could provide an effective therapeutic target for HCC patients.

Concurrent exposure to cadmium (Cd) and lead (Pb) is prevalent in the environment, but information on the long-term impacts of complex Cd–Pb exposure on herbivorous insects, especially at low doses, is scant. We studied the effects of complex Cd–Pb exposure (4.06 mg/kg Cd and 12.5 mg/kg Pb) on the growth and food utilization of the herbivorous insect Spodoptera litura for 10 continuous generations. Cd or Pb ingestion, excretion and accumulation by insect at the different developmental stages was determined for ten generations. The weighted scores calculated by the analytic hierarchy process (AHP) on the basis of the parameters of survival, growth and food utilization indicated that complex Cd–Pb exposure had positive impacts on the insects, regardless of generations. Compared with Cd (4.06 mg/kg Cd) and Pb (12.5 mg/kg Pb) alone, complex Cd–Pb exposure showed antagonistic interactions. After exposure to complex Cd–Pb, although larvae significantly increased heavy metal uptake along with the elevated ECD and ECI, insects enhanced heavy metal excretion via the feces and puparium; consequently, heavy metal accumulation in the insect body significantly decreased. With increasing generations, the positive impacts of complex Cd–Pb stress on insects became increasingly obvious, and the uptake of Cd or Pb decreased while the excretion of Cd or Pb increased, which demonstrated that insect tolerance to Cd–Pb exposure at low concentrations increased over generations.

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