The exhaust of excessively high heat and particle fluxes on the divertor target is crucial for EAST long-pulse operation. In the recent EAST experiments, stable partial energy detachment around the upper outer strike point with H 98,y2 ∼ 1 was achieved with either Ne or Ar seeding from the upper outer divetor target in the upper single null configuration with ITER-like tungsten divertor. With either Ar or Ne seeding, the electron temperature around the upper outer strike point (T et,UOSP) was maintained at around 5 eV, the peak temperature of divertor target surface around the upper outer strike point (T div,UO) decreased significantly, and material sputtering was well suppressed. It was observed that there was less Ar seeding needed for partial energy detachment onset than Ne seeding, which shows that Ar is more efficient in the cooling of T et on the upper outer divertor than Ne. However, there was no detachment on the upper inner divertor with T et around strike point (T et,UISP) remaining >10 eV with either Ar or Ne seeding from the upper outer divertor. Accompanied with the disappearance of double peak phenomenon of ion flux density on the upper inner divertor target (j s,UI), the peak T div,UI around the strike point increased to around 300 °C. Although the heat flux on the upper inner divertor target (q t,UI) is still in the acceptable level, either Ar or Ne seeding only from the upper outer divertor target is not enough to protect the upper inner divertor target from sputtering under current EAST conditions. On the other hand, Ar seeding always causes confinement degradation in the partial energy detachment state. It was observed that there is a slight confinement improvement (∼10%) with Ne seeding, which may be due to density peaking, dilution effects and stabilization of the ion temperature gradient mode.

Sphingosine kinase 1 (SPHK1) regulates cell proliferation and survival by converting sphingosine to the signaling mediator sphingosine 1-phosphate (S1P). SPHK1 is widely overexpressed in most cancers, promoting tumor progression and is associated with clinical prognosis. Numerous studies have explored SPHK1 as a promising target for cancer therapy. However, due to insufficient knowledge of SPHK1 oncogenic mechanisms, its inhibitors’ therapeutic potential in preventing and treating cancer still needs further investigation. In this review, we summarized the metabolic balance regulated by the SPHK1/S1P signaling pathway and highlighted the oncogenic mechanisms of SPHK1 via the upregulation of autophagy, proliferation, and survival, migration, angiogenesis and inflammation, and inhibition of apoptosis. Drug candidates targeting SPHK1 were also discussed at the end. This review provides new insights into the oncogenic effect of SPHK1 and sheds light on the future direction for targeting SPHK1 as cancer therapy.

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