331) d ex vivo expansion of tumor-primed CD4+T cells could induce effective tumor specifi |
332) Invariant natural killer T (iNKT) cells differentiate in the thymus into NKT |
333) Innate-like T cells differentiate into mature functional |
334) rotocol for immature naïve mouse CD4+ T cells, including details for splenocyte is |
335) Innate-like T cells, including invariant NKT cells, muco |
336) ent of fluid, ions, molecules, and immune cells into and out of the brain parenchyma |
337) cytes and effective infiltration of the T cells into tumor tissue. |
338) Loss of GPR171 in T cells leads to hyperactivity to antigen st |
339) differentiation program of skeletal stem cells leads to indecorous skeletogenesis. |
340) the chemosensitivity of colorectal cancer cells regardless of the microsatellite sta |
341) d enhance the chemosensitivity of tumoral cells regardless of the microsatellite sta |
342) lucose and glutamine by immune and cancer cells, respectively. |
343) or the upper route, subpolar, and abyssal cells, respectively. |
344) g 3D/2D Rb+-incorporated perovskite solar cells show a peak PCE of >20%, which is |
345) isease is transplantable and mutCALR stem cells show proliferative advantage when co |
346) dual allelic mutants in CRACR2A-deleted T cells showed that the CRACR2AE278D mutant |
347) By contrast, cancer cells showed the highest uptake of glutami |
348) nd basal mitochondrial oxidation of CD4+T cells, suggesting a role of high salt in e |
349) to alter migration and function of immune cells, suggesting the potential for electr |
350) ate and range of locomotion of interphase cells, supporting an impact of FQI1-induce |
351) n of DNA repair genes DDB2 and XPC in Ctr cells, supporting the idea that hyperoxia |
352) oxidative stress induces dual injury in T cells via crosstalk between telomeres and |
353) potent anticancer effect against SGC-7901 cells via mitochondrial apoptotic pathway |
354) y genetic information present in the germ cells will be inherited by future generati |
355) is that overexpression of NQO1 in BEAS-2B cells will mitigate cell injury and oxidat |
356) a monolayer of human bronchial epithelial cells (16HBE) before exposure to the viral |
357) r divided into subpolar (20%) and abyssal cells (48%). |
358) easuring the number of Antibody Secreting Cells (ASCs) using an ELISpot assay. |
359) e studied protection of brain endothelial cells (BECs) by selective and nonselective |
360) ration and chemoresistance of cancer stem cells (CSCs). |
361) different quantities of circulating tumor cells (CTCs) and cell-free DNA (cfDNA) int |
362) roxia decreased cell viability in control cells (Ctr), but this effect was different |
363) collectively in both vascular endothelial cells (EC) and SMCs in IH ex vivo model. |
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