Digital enhancement techniques for data converters in scaled CMOS technologies

This thesis presents digital enhancement techniques for data converters in advanced technology nodes. With technology scaling, traditional voltage-domain (VD) analog-to-digital converters (ADCs) face two major challenges: (1) reduction of dynamic range due to supply voltage scaling, and (2) decrease in intrinsic gain of transistors which makes high gain amplifier design tough. To address these challenges, a two-stage ADC architecture is presented which uses time-domain quantization to exploit the advantages of technology scaling. The architecture, consisting of a first stage successive approximation register (SAR) and a second stage ring oscillator, is highly digital and scaling friendly. Two prototypes have been developed to validate the proposed architecture. The 40nm CMOS prototype achieves 75.7 dB dynamic range at an excellent Schreier figure-of-merit of 172.2 dB. The proposed architecture has been extended to a capacitance-to-digital converter and a prototype has been developed in 40nm CMOS. The prototype can sense capacitances with a resolution of 1.3fF and has a Walden figure-of-merit of 60 fJ/step which is more than two times better than the current state-of-the-art. This thesis also presents digital techniques to improve performance of continuous-time(CT), delta-sigma digital-to-analog converters (DACs). Recently, CT delta-sigma DACs have received more attention than their discrete, switched-capacitor counterpart mainly because of low power and/or higher speed of operation. However, a critical disadvantage of CT, delta-sigma DACs is their greatly increased sensitivity to inter-symbol interference (ISI) error. To address this shortcoming of CT DACs, this thesis presents several algorithms that can mitigate ISI error simultaneously with static mismatch error. Further, the proposed algorithms are fully digital in nature and as such, are best poised to take maximum advantage of technology scaling. Thus, the techniques presented in this thesis will be important enabling factors in raising the envelope of performance of CT delta-sigma DACs in advanced technology nodes.Electrical and Computer Engineerin

Charged Higgs induced 5 and 6 lepton signatures from heavy neutrinos at the LHC

We propose an anomaly free gauged U$(1)$ extension of the SM where three right handed heavy neutrinos, being charged under the general U$(1)$ gauge group, are introduced to explain the origin of the tiny neutrino mass through the seesaw mechanism after the general U$(1)$ symmetry is broken. Due to the breaking of the general U$(1)$ symmetry a neutral beyond the standard model gauge boson $Z^\prime$ acquires mass. There are two Higgs doublets in this model where one interacts with the SM fermions and the other one interacts with the right handed heavy neutrinos and charged leptons. The charged multiplet of the second Higgs can completely decay into the heavy neutrinos and charged lepton in the neutrinophilic limit of the model parameters. The charged Higgs pair production can be influenced due to presence of the $Z^\prime$ boson at the High Luminosity LHC (HL-LHC) in addition to the neutral SM gauge bosons. The pair produced charged Higgs bosons decay into SM charged leptons and heavy neutrinos. Following the leading decay modes of the heavy neutrinos into charged leptons and $W$ boson we study the 5 and 6 lepton final states after the leptonic and hadronic decay of the $W$ bosons considering solely muons and electrons in the final state. Combining the electron and muon final states we estimate the significance of the 5 and 6 charged lepton processes in the $m_{H^\pm}-m_N$ plane for different benchmark points of $m_{Z^\prime}$. It is found that the 5 (6) charged lepton processes could be probed at the High Luminosity LHC (HL-LHC) with at least 5 (3) $\sigma$ significance and there are parameter regions where the significance could be larger.Comment: Published version in European Journal of Physics

Temporal-Coded Deep Spiking Neural Network with Easy Training and Robust Performance

Spiking neural network (SNN) is interesting both theoretically and practically because of its strong bio-inspiration nature and potentially outstanding energy efficiency. Unfortunately, its development has fallen far behind the conventional deep neural network (DNN), mainly because of difficult training and lack of widely accepted hardware experiment platforms. In this paper, we show that a deep temporal-coded SNN can be trained easily and directly over the benchmark datasets CIFAR10 and ImageNet, with testing accuracy within 1% of the DNN of equivalent size and architecture. Training becomes similar to DNN thanks to the closed-form solution to the spiking waveform dynamics. Considering that SNNs should be implemented in practical neuromorphic hardwares, we train the deep SNN with weights quantized to 8, 4, 2 bits and with weights perturbed by random noise to demonstrate its robustness in practical applications. In addition, we develop a phase-domain signal processing circuit schematic to implement our spiking neuron with 90% gain of energy efficiency over existing work. This paper demonstrates that the temporal-coded deep SNN is feasible for applications with high performance and high energy efficient

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

BACKGROUND: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. METHODS: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). FINDINGS: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29-146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0- 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25-1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39-1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65-1·60]; p=0·92). INTERPRETATION: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention. FUNDING: British Heart Foundation