Mobilizing phospholipids on tumor plasma membrane implicates phosphatidylserine externalization blockade for cancer immunotherapy.

In "healthy" tumor cells, phosphatidylserine (PS) is predominately localized in the inner plasma membrane leaflet. During apoptosis, PS relocates to the outer leaflet. Herein, we established PS tumor models with tumor cells lacking PS flippase component CDC50A, constantly exposing PS but alive.

Sensing plasma membrane pore formation induces chemokine production in survivors of regulated necrosis.

Although overwhelming plasma membrane integrity loss leads to cell lysis and necrosis, cells can tolerate a limited level of plasma membrane damage, undergo ESCRT-III-mediated repair, and survive. Here, we find that cells which undergo limited plasma membrane damage from the pore-forming actions of MLKL, GSDMD, perforin, or detergents experience local activation of PKCs through Ca influx at the damage sites. S660-phosphorylated PKCs subsequently activate the TAK1/IKKs axis and RelA/Cux1 complex to trigger chemokine expressions.

Typhoid fever survey in two localities in Vietnam.

As a part of multipurpose health survey of the population in Vietnam the antibodies against S. typhi were determined by the micromethod using haemagglutination test (O-antigen 9, 12) and agglutination test using standard H-diagnostic antigen (d). Totally 292 sera were examined, 139 from Duyen Thai village and 154 from Mai Chau.