A Robust Low Power Static Random Access Memory Cell Design

Stability of a Static Random Access Memory (SRAM) cell is an important factor when considering an SRAM cell for any application. The Static Noise Margin (SNM) of a cell, which determines the stability, varies under different operating conditions. Based on the performance of three existing SRAM cell designs, 6T, 8T and 10T, a 10 Transistor SRAM cell is proposed which has good stability and has the advantage of reduced read power when compared to 6T and 8T SRAM cells. The proposed 10T SRAM cell has a single-ended read circuit which improves SNM over the 6T cell. The proposed 10T cell doesn\u27t require a pre-charge circuit and this in-turn improves read power and also reduces the read time since there is no need to pre-charge the bit-line before reading it. The Read SNM and Hold SNM of the proposed cell at a VDD of 1V and at 25°C is 254mV. The measured RSNM, HSNM and Write SNM at temperatures 0°C, 40°C, 80°C and 120°C and also at supply voltages 1V, 0.8V and 0.6V show the design is robust. The Write SNM of the proposed cell at a VDD of 1V and Pull-up Ratio of 1 is 275mV. Finally, a 32-byte memory array is built using the proposed 10T SRAM cell and the read, write times are 149ps and 21.6ps, respectively. The average power consumed by the 32-byte array over a 12ns period is 13.8uW. All the designs are done in the 32nm FinFET technology

A Robust Low Power Static Random Access Memory Cell Design

Stability of a Static Random Access Memory (SRAM) cell is an important factor when considering an SRAM cell for any application. The Static Noise Margin (SNM) of a cell, which determines the stability, varies under different operating conditions. Based on the performance of three existing SRAM cell designs, 6T, 8T and 10T, a 10 Transistor SRAM cell is proposed which has good stability and has the advantage of reduced read power when compared to 6T and 8T SRAM cells. The proposed 10T SRAM cell has a single-ended read circuit which improves SNM over the 6T cell. The proposed 10T cell doesn\u27t require a pre-charge circuit and this in-turn improves read power and also reduces the read time since there is no need to pre-charge the bit-line before reading it. The Read SNM and Hold SNM of the proposed cell at a VDD of 1V and at 25°C is 254mV. The measured RSNM, HSNM and Write SNM at temperatures 0°C, 40°C, 80°C and 120°C and also at supply voltages 1V, 0.8V and 0.6V show the design is robust. The Write SNM of the proposed cell at a VDD of 1V and Pull-up Ratio of 1 is 275mV. Finally, a 32-byte memory array is built using the proposed 10T SRAM cell and the read, write times are 149ps and 21.6ps, respectively. The average power consumed by the 32-byte array over a 12ns period is 13.8uW. All the designs are done in the 32nm FinFET technology

ATM promotes apoptosis and suppresses tumorigenesis in response to Myc

textPrecancerous lesions from a variety of human tissues display markers of DNA damage suggesting that genetic instability occurs early during the process of carcinogenesis. Consistent with this, several oncogenes can activate ATM and other components of the DNA damage response pathway when expressed in cultured cells. Here we demonstrate that preneoplastic epithelial tissues from four different transgenic mouse models expressing the oncogenes c-myc, SV40 T antigen, human papilloma virus (HPV) E7, or E2F3a display [gamma]-H2AX foci and other markers of DNA damage. Moreover, transgenic expression of these oncogenes leads to increased levels of damaged DNA as measured by the comet assay. In at least the Myc transgenic model, the formation of [gamma]-H2AX foci is dependent on functional ATM. Inactivation of Atm also impairs p53 activation and reduces the level of apoptosis observed in transgenic tissue overexpressing Myc. This correlates with accelerated tumor development in Myc transgenic mice lacking ATM. To understand the mechanism by which oncogenes induce DNA damage, we employed an adenoviral overexpression system. Under conditions in which Myc or E2F3a induced replication is inhibited, we see a reduction in the DNA damage induced by these oncogenes both by comet assay and levels of [gamma]-H2AX. Moreover, Myc and E2F3a induced increased levels of the Cdt1 protein, a replication origin- licensing factor implicated in aberrant DNA replication. Taken together, these findings suggest that deregulated oncogenes induce unscheduled DNA replication leading to DNA damage and activation of the ATM DNA damage response pathway, which is important for the activation of p53, induction of apoptosis and the suppression of tumorigenesis.Pharmac

Evolution over Time of Ventilatory Management and Outcome of Patients with Neurologic Disease∗

OBJECTIVES: To describe the changes in ventilator management over time in patients with neurologic disease at ICU admission and to estimate factors associated with 28-day hospital mortality. DESIGN: Secondary analysis of three prospective, observational, multicenter studies. SETTING: Cohort studies conducted in 2004, 2010, and 2016. PATIENTS: Adult patients who received mechanical ventilation for more than 12 hours. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Among the 20,929 patients enrolled, we included 4,152 (20%) mechanically ventilated patients due to different neurologic diseases. Hemorrhagic stroke and brain trauma were the most common pathologies associated with the need for mechanical ventilation. Although volume-cycled ventilation remained the preferred ventilation mode, there was a significant (p < 0.001) increment in the use of pressure support ventilation. The proportion of patients receiving a protective lung ventilation strategy was increased over time: 47% in 2004, 63% in 2010, and 65% in 2016 (p < 0.001), as well as the duration of protective ventilation strategies: 406 days per 1,000 mechanical ventilation days in 2004, 523 days per 1,000 mechanical ventilation days in 2010, and 585 days per 1,000 mechanical ventilation days in 2016 (p < 0.001). There were no differences in the length of stay in the ICU, mortality in the ICU, and mortality in hospital from 2004 to 2016. Independent risk factors for 28-day mortality were age greater than 75 years, Simplified Acute Physiology Score II greater than 50, the occurrence of organ dysfunction within first 48 hours after brain injury, and specific neurologic diseases such as hemorrhagic stroke, ischemic stroke, and brain trauma. CONCLUSIONS: More lung-protective ventilatory strategies have been implemented over years in neurologic patients with no effect on pulmonary complications or on survival. We found several prognostic factors on mortality such as advanced age, the severity of the disease, organ dysfunctions, and the etiology of neurologic disease