A low dropout (LDO) voltage regulator operated at 5 V power supply, along with a bandgap reference (BGR) voltage circuit with high power-supply rejection ratio (PSRR) is introduced. In the suggested LDO circuit, a low-pass filter for creating a common gate to transmit supply voltage to the power transistor gate is used. During deployment of the RC filter, an artificial resistor with a value of infinity is utilised, which in addition to reduce the chip occupied area, improves the performance of the low-pass filter at frequencies close to DC, and thus improves the PSRR at these frequencies. In addition, the high PSRR of the circuit is mediated by a low-voltage current mode regulator at the heart of the bandgap circuitry, which isolates the bandgap voltage from power supply variations and noise. The isolating current mirrors create an internal regulated voltage (V reg) for BGR core and op-amp rather than the V DD. These current mirrors reduce the impact of supply voltage variations. The circuit topology is discussed and simulation results are provided. The LDO is also stable without an output capacitor.

The loop‐handover (LHO) technique is proposed to overcome the problem of close‐loop performance in digitally controlled single‐inductor multiple‐output dc–dc boost converters during start‐up. The presented technique utilises an existing clock source and requires only a small number of blocks. It also occupies a smaller silicon area, thus consuming low power and increasing efficiency. The presented technique is validated with proposed on‐chip digital controller with multiple‐output boost converter architecture using segmented delay line digital pulse width modulation. Experimental results show a successful close loop with reduced transients by using the simpler LHO technique.

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the tumor size and DNT cell infiltration level were monitored. Result: The frequency of DNT cell was reduced in lung tumor when compared to the adjacent and non-tumoral tissues of the same patient. Like conventional CD4 and CD8 T cells, 36%-52% of DNT cells within tumor expressed elevated levels of PD1, suggesting that DNT cells function may be suppressed by PD-1 pathway in patients. Using xenograft mice, we show that treatment with DNT cell alone reduced tumor growth by 14%-38%. A greater reduction (30%-68%) was observed when DNT cell treatment was combined with PD1 blockade, where PD1 blockade alone had no significant effect. Compared to DNT cell transfer alone, DNT cells with PD1 blockade led to a greater infiltration of cells with higher expression of cytotoxicity markers NKG2D and IFN-y and reduced inhibitory markers TIM3 and LAG3. Conclusion: These studies indicate the potential of DNT cell for the treatment of established lung cancer and that combination of DNT cell with PD1 blockade may further enhance the treatment efficacy by increasing DNT cell infiltrating to solid tumor.

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