Clock Phase Shifter Research Articles

A high-resolution clock phase shifter circuitry for ALTIROC

A high-resolution clock phase shifter is implemented to adjust the phase of multiple clocks at 40 MHz, 80 MHz, or 640 MHz in the ALTIROC chip. The phase shifter has a coarse-phase shifter and a fine-phase shifter to achieve a step size of 97.7 ps and an adjustable range of 25 ns. The fine delay unit is based on a Delay Locked Loop (DLL) operating at 640 MHz. The phase shifter is fabricated in a 130 nm CMOS process. The area of the phase shifter is 725 µm × 248 µm. The Differential Non-Linearity (DNL) and the Integral Non-Linearity (INL) are ±0.6 LSB and ±0.75 LSB, respectively. The jitter from −25 °C to 20 °C is less than 15.5 ps (RMS), including the contributions from the FPGA clock source and the PLL. The power consumption is 11.2 mW.

A light-induced small G-protein gem limits the circadian clock phase-shift magnitude by inhibiting voltage-dependent calcium channels.

Calcium signaling is pivotal to the circadian clockwork in the suprachiasmatic nucleus (SCN), particularly in rhythm entrainment to environmental light-dark cycles. Here, we show that a small G-protein Gem, an endogenous inhibitor of high-voltage-activated voltage-dependent calcium channels (VDCCs), is rapidly induced by light in SCN neurons via the calcium (Ca2+)-mediated CREB/CRE transcriptional pathway. Gem attenuates light-induced calcium signaling through its interaction with VDCCs. The phase-shift magnitude of locomotor activity rhythms by light, at night, increases in Gem-deficient (Gem-/-) mice. Similarly, in SCN slices from Gem-/- mice, depolarizing stimuli induce larger phase shifts of clock gene transcription rhythms that are normalized by the application of an L-type VDCC blocker, nifedipine. Voltage-clamp recordings from SCN neurons reveal that Ca2+ currents through L-type channels increase in Gem-/- mice. Our findings suggest that transcriptionally activated Gem feeds back to suppress excessive light-evoked L-type VDCC activation, adjusting the light-induced phase-shift magnitude to an appropriate level in mammals.

Rapid Jetlag Resetting of Behavioral, Physiological, and Molecular Rhythms in Proestrous Female Mice.

A gradual adaptation to a shifted light-dark (LD) cycle is a key element of the circadian clock system and believed to be controlled by the central circadian pacemaker, the suprachiasmatic nucleus (SCN). Endocrine factors have a strong influence on the regulation of the circadian clock network and alter acute photic responses of the SCN clock. In females, endocrine function depends on the stage of the ovarian cycle. So far, however, little is known about the effect of the estrous cycle on behavioral and molecular responses to shifts in the LD rhythm. Based on this, we investigated whether estrous state affects the kinetics of phase shift during jetlag in behavior, physiology, and molecular clock rhythms in the SCN and in peripheral tissues. Female mice exposed to an advanced LD phase at proestrous or metestrous showed different phase-shift kinetics, with proestrous females displaying accelerated adaptation in behavior and physiology. Constant darkness release experiments suggest that these fast phase shifts do not reflect resetting of the SCN pacemaker. Explant experiments on SCN, adrenal gland, and uterus confirmed this finding with proestrous females showing significantly faster clock phase shifts in peripheral tissues compared with the SCN. Together, these findings provide strong evidence for an accelerated adaptation of proestrous compared with metestrous females to new LD conditions that is accompanied by rapid behavioral, physiological, and molecular rhythm resetting. Not only do these findings open up a new avenue to understand the effect of estrous cycle on the clock network under changing environmental conditions but also imply a greater susceptibility in proestrous females.

180 Gbit/s 4:1 power multiplexer for NRZ‐OOK signals with high output voltage swing in SiGe BiCMOS technology

A 4:1 multiplexer (MUX) circuit in SiGe BiCMOS technology intended to directly drive a plasmonic Mach-Zehnder modulator for transmitter applications is presented. To achieve the highest data rates at a high output voltage swing, a power MUX concept is applied that maps the high-speed performance of the final clock signal onto the output data. In the clock tree a novel wideband 90° clock phase shifter circuit is utilised for timing adjustment and frequency doubling. Electrical measurements of the chip demonstrate open eye diagrams for non-return-to-zero on-off-keying (NRZ-OOK) signals up to 180 Gbit/s, which is record speed for Si-based technologies. A differential output voltage swing of 300 mV pp was measured that corresponds to an output voltage swing of more than 1 V pp without the bandwidth limit of the measurement equipment.

Irradiation setup at the U-120M cyclotron facility

This paper describes parameters of the proton beams provided by the U-120M cyclotron and the related irradiation setup at the open access irradiation facility at the Nuclear Physics Institute of the Czech Academy of Sciences. The facility is suitable for testing radiation hardness of various electronic components. The use of the setup is illustrated by a measurement of an error rate for errors caused by Single Event Transients in an SRAM-based Xilinx XC3S200 FPGA. This measurement provides an estimate of a possible occurrence of Single Event Transients. Data suggest that the variation of error rate of the Single Event Effects for different clock phase shifts is not significant enough to use clock phase alignment with the beam as a fault mitigation technique.

Urokinase-type plasminogen activator modulates mammalian circadian clock phase regulation in tissue-type plasminogen activator knockout mice.

Glutamate phase shifts the circadian clock in the mammalian suprachiasmatic nucleus (SCN) by activating NMDA receptors. Tissue-type plasminogen activator (tPA) gates phase shifts by activating plasmin to generate m(ature) BDNF, which binds TrkB receptors allowing clock phase shifts. Here, we investigate phase shifting in tPA knockout (tPA-/- ; B6.129S2-Plattm1Mlg /J) mice, and identify urokinase-type plasminogen activator (uPA) as an additional circadian clock regulator. Behavioral activity rhythms in tPA-/- mice entrain to a light-dark (LD) cycle and phase shift in response to nocturnal light pulses with no apparent loss in sensitivity. When the LD cycle is inverted, tPA-/- mice take significantly longer to entrain than C57BL/6J wild-type (WT) mice. SCN brain slices from tPA-/- mice exhibit entrained neuronal activity rhythms and phase shift in response to nocturnal glutamate with no change in dose-dependency. Pre-treating slices with the tPA/uPA inhibitor, plasminogen activator inhibitor-1 (PAI-1), inhibits glutamate-induced phase delays in tPA-/- slices. Selective inhibition of uPA with UK122 prevents glutamate-induced phase resetting in tPA-/- but not WT SCN slices. tPA expression is higher at night than the day in WT SCN, while uPA expression remains constant in WT and tPA-/- slices. Casein-plasminogen zymography reveals that neither tPA nor uPA total proteolytic activity is under circadian control in WT or tPA-/- SCN. Finally, tPA-/- SCN tissue has lower mBDNF levels than WT tissue, while UK122 does not affect mBDNF levels in either strain. Together, these results suggest that either tPA or uPA can support photic/glutamatergic phase shifts of the SCN circadian clock, possibly acting through distinct mechanisms.

A 28 nm Embedded Split-Gate MONOS (SG-MONOS) Flash Macro for Automotive Achieving 6.4 GB/s Read Throughput by 200 MHz No-Wait Read Operation and 2.0 MB/s Write Throughput at Tj of 170C

First-ever 28 nm embedded split-gate MONOS (SG-MONOS) flash macros have been developed to increase memory capacity embedded in micro controller units and to improve performance over wide junction temperature range from $-40^{\circ}{\hbox {C}}$ to 170 $^{\circ}{\hbox {C}}$ as demanded strongly in automotive uses. Much attention has been paid to the degradation of the reliability characteristics along with the process shrinkage. Temperature-adjusted word-line overdrive scheme improves random read access frequency by 15% and realizes both of 6.4 GB/s read throughput by 200 MHz no-wait random access of code flash macros and more than ten times longer TDDB lifetime of WL drivers. Temperature-adaptive step pulse erase control (TASPEC) improves the TDDB lifetime of dielectric films between metal interconnect layers by three times. TASPEC is particularly useful for a data flash macro with one million rewrite cycles. Source-side injection (SSI) program with negative back-bias voltage achieves 63% reduction of program pulse time and, consequently, realizes 2.0 MB/s write throughput of code flash macros. A spread spectrum clock generation and a clock phase shift technique are introduced for charge pump clock generation in order to suppress EMI noise due to high write throughput of code flash macros, and peak power of EMI noise is reduced by 19 dB.

Circadian rhythm phase shifts and endogenous free-running circadian period differ between African-Americans and European-Americans.

Successful adaptation to modern civilization requires the internal circadian clock to make large phase shifts in response to circumstances (e.g., jet travel and shift work) that were not encountered during most of our evolution. We found that the magnitude and direction of the circadian clock's phase shift after the light/dark and sleep/wake/meal schedule was phase-advanced (made earlier) by 9 hours differed in European-Americans compared to African-Americans. European-Americans had larger phase shifts, but were more likely to phase-delay after the 9-hour advance (to phase shift in the wrong direction). The magnitude and direction of the phase shift was related to the free-running circadian period, and European-Americans had a longer circadian period than African-Americans. Circadian period was related to the percent Sub-Saharan African and European ancestry from DNA samples. We speculate that a short circadian period was advantageous during our evolution in Africa and lengthened with northern migrations out of Africa. The differences in circadian rhythms remaining today are relevant for understanding and treating the modern circadian-rhythm-based disorders which are due to a misalignment between the internal circadian rhythms and the times for sleep, work, school and meals.

Rhythms in Energy Storage Control the Ability of the Cyanobacterial Circadian Clock to Reset

Circadian clocks are oscillatory systems that schedule daily rhythms of organismal behavior. The ability of the clock to reset its phase in response to external signals is critical for proper synchronization with the environment. In the model clock from cyanobacteria, the KaiABC proteins that comprise the core oscillator are directly sensitive to metabolites. Reduced ATP/ADP ratio and oxidized quinones cause clock phase shifts in vitro. However, it is unclear what determines the metabolic response of the cell to darkness and thus the magnitude of clock resetting. We show that the cyanobacterial circadian clock generates a rhythm in metabolism that causes cells to accumulate glycogen in anticipation of nightfall. Mutation of the histidine kinase CikA creates an insensitive clock-input phenotype by misregulating clock output genome wide, leading to overaccumulation of glycogen and subsequently high ATP in the dark. Conversely, we show that disruption of glycogen metabolism results in low ATP in the dark and makes the clock hypersensitive to dark pulses. The observed changes in cellular energy are sufficient to recapitulate phase-shifting phenotypes in an in vitro model of the clock. Our results show that clock-input phenotypes can arise from metabolic dysregulation and illustrate a framework for circadian biology where clock outputs feed back through metabolism to control input mechanisms.

Chronic subordination stress phase advances adrenal and anterior pituitary clock gene rhythms.

Circadian rhythms in glucocorticoids are the product of interactions between the hypothalamic-pituitary-adrenal (HPA) axis and the mammalian clock gene system. The adrenal clock can generate the glucocorticoid rhythm that in turn synchronizes other peripheral clocks to maintain homeostasis. Stress acutely activates and chronically upregulates the HPA axis, suggesting that the adrenal clock could be modulated by stress. However, there is no direct evidence that stress affects the adrenal clock rhythm. We tested the hypothesis that a model of chronic subordination stress (CSS) that has a major impact on HPA axis regulation, metabolism, and emotional behavior alters adrenal and pituitary clock gene rhythms. Clock gene rhythms were assessed using mPER2::Luciferase (PER2Luc) knockin mice in which in vitro bioluminescence rhythms reflect the Per2 clock gene expression. PER2Luc mice that experienced CSS for 2 wk showed positive energy balance reflected by increased body weight and food intake. Additionally, CSS phase advanced the adrenal (∼2 h) and the pituitary (∼1 h) PER2Luc rhythm compared with control mice. The activity rhythm was not affected. The adrenal clock phase shift was associated with increased feed conversion efficiency, suggesting that the metabolic phenotype in CSS mice may be related to altered adrenal clock rhythmicity. Interestingly, a single subordination experience followed by 8 h sensory housing also phase advanced the adrenal, but not the pituitary, PER2Luc rhythm. Overall, these data demonstrate a stress-induced phase shift in a peripheral clock gene rhythm and differential stress sensitivity of two peripheral clocks within the HPA axis, suggesting a link between clock desynchrony and individual vulnerability to stress.

Wide‐range (25 ns) and high‐resolution (48.8 ps) clock phase shifter

A wide-range (25 ns), high-resolution (48.8 ps) clock phase shifter developed and fabricated using a 0.13 µm CMOS technology is presented. To achieve both wide range and high resolution with good linearity while minimising area and power consumption, a coarse–fine two-step phase-shifting structure is proposed. A delay-locked loop with an unconventional clock input setup is used in the fine-shifting stage to ahieve the high resolution. Test results show that the standard deviations of the differential nonlinearity and integral nonlinearity are 4.7 ps and 4.3 ps, respectively.

Nocturnal Light and Nocturnal Rodents

Investigators typically study one function of the circadian visual system at a time, be it photoreception, transmission of photic information to the suprachiasmatic nucleus (SCN), light control of rhythm phase, locomotor activity, or gene expression. There are good reasons for such a focused approach, but sometimes it is advantageous to look at the broader picture, asking how all the parts and functions complete the whole. Here, several seemingly disparate functions of the circadian visual system are examined. They share common characteristics with respect to regulation by light and, to the extent known, share a common input neuroanatomy. The argument presented is that the 3 hypothalamically mediated effects of light for which there are the most data, circadian clock phase shifts, suppression of nocturnal locomotion ("negative masking"), and suppression of nocturnal pineal function, are regulated by a common photic input pathway terminating in the SCN. For each, light triggers a relatively fixed interval response that is irradiance-dependent, the effective stimulus can be very brief light exposure, and the response continues to completion in the absence of additional light. The presence of a triggered, fixed-length response interval is of particular importance to the understanding of the circuitry and mechanisms regulating circadian rhythm phase shifts because it implies that the SCN clock response to light is not instantaneous. It also may explain why certain stimuli (neuropeptide Y or novel wheel running) administered many minutes after light exposure are able to block light-induced phase shifts. The understanding of negative masking is complicated by the fact that it can be represented as a positive change, that is, light-induced sleep, not just as a reduction in locomotion. Acute nocturnal light exposure also induces adrenal hormone secretion and a rapid drop in body temperature, physiological responses that appear to be regulated similarly to the other light effects. The likelihood of a common regulatory basis for the several responses suggests that additional light-induced responses will be forthcoming and raises questions about the relationships between light, SCN cellular anatomy, the molecular clockworks of SCN neurons, and SCN throughput mechanisms for regulating disparate downstream activities.

An Over-1-Gb/s Transceiver Core for Integration Into Large System-on-Chips for Consumer Electronics

This paper describes an area-effective 1.5-Gb/s transceiver core with spread spectrum clocking (SSC) capability that is suitable for integration into large system-on-chips (SoCs) for consumer electronics applications such as audio and video stream data transmission. To achieve a good balance between SSC performance and the core area, a novel SSC scheme using a multi-level (hierarchical) phase-interpolator technique has been developed. This technique achieves a very fine clock phase shift of about 0.1 ps for precise and smooth frequency modulation. The SSC scheme is based on a digital feed-forward operation and leads to a small area and good noise robustness for SoC integration. This core also has digital clock data recovery (CDR) with jitter tolerance enhancement and a simple adaptive data equalizer (AEQ). These functions are also on a digital operation and controlled by digital codes, and the core presupposes a multiphase clock for the digital SSC, CDR, and AEQ with shared phase-locked loop (PLL) topology. A test chip including two of these cores was fabricated using shared PLL. The core showed significant peak power reduction (-19 dB to the non-SSC situation) and a small core area of 0.25 mm2 in 0.13-mum CMOS process. This core achieved a remarkable ratio of peak power reduction to area of 76 dB/mm2. Moreover, it achieved good jitter tolerance (flat 0.8 UI at >1 MHz) and stable data communication over an STP (shielded twist pair) cable ranging in length from 1 m to over 22 m.

Modeling the VPAC 2-Activated cAMP/PKA Signaling Pathway: From Receptor to Circadian Clock Gene Induction

Increasing evidence suggests an important role for VPAC 2-activated signal transduction pathways in maintaining a synchronized biological clock in the suprachiasmatic nucleus (SCN). Activation of the VPAC 2 signaling pathway induces per1 gene expression in the SCN and phase-shifts the circadian clock. Mice without the VPAC 2 receptor lack an overt, coherent circadian rhythm in clock gene expression, SCN neuron firing rate, and locomotor behavior. Using a systems approach, we have developed a kinetic model integrating VPAC 2 signaling mediated by the cyclic AMP (cAMP)/protein kinase A (PKA) pathway and leading to induced circadian clock gene expression. We fit the model to experimental data from the literature for cAMP accumulation, PKA activation, cAMP-response element binding protein phosphorylation, and per1 induction. By linking the VPAC 2 model to a published circadian clock model, we also simulated clock phase shifts induced by vasoactive intestinal polypeptide (VIP) and matched experimental data for the VIP response. The simulated phase response curve resembled the hamster response to a related neuropeptide, GRP 1–27, and light. Simulations using pulses of VIP revealed that the system response is extraordinarily robust to input signal duration, a result with physiologically relevant consequences. Lastly, simulations using varied receptor levels matched literature experimental data from animals overexpressing VPAC 2 receptors.

Chromatic dispersion monitoring technique using sideband optical filtering and clock phase-shift detection

We propose and demonstrate a novel technique for 40- and 10-Gb/s chromatic dispersion monitoring that uses an optical filter to select the upper and lower vestigial-sideband (VSB) signals in the transmitted optical data and determine the relative clock phase shift caused by dispersion. Without modification of transmitters, this technique provides low cost chromatic dispersion monitoring for WDM systems, <3 ps/nm dispersion resolution for 40-Gb/s data, and greatly reduced sensitivity to the influence of polarization mode dispersion.

Digital clock phase shifter without a phase locked loop

A digitally controlled clock phase shifter is described that avoids the use of conventional phase locked loops (PLLs) with their attendant stability problems. The hardware is suitable for implementation as part of an integrated circuit. Two implementations are discussed, one of which has low power consumption and is suitable for clocks of moderate speed and the second of which is suitable at higher frequencies. Simulation shows that the circuit is practically insensitive to component and timing tolerances. A prototype of the moderate speed version has been tested and has shown results comparable to simulation results. >