Amplitude Sensing below the Zero-Point Fluctuations with a Two-Dimensional Trapped-Ion Mechanical Oscillator.

We present a technique to measure the amplitude of a center-of-mass (c.m.) motion of a two-dimensional ion crystal of ∼100 ions. By sensing motion at frequencies far from the c.m. resonance frequency, we experimentally determine the technique's measurement imprecision. We resolve amplitudes as small as 50 pm, 40 times smaller than the c.m. mode zero-point fluctuations. The technique employs a spin-dependent, optical-dipole force to couple the mechanical oscillation to the electron spins of the trapped ions, enabling a measurement of one quadrature of the c.m. motion through a readout of the spin state. We demonstrate sensitivity limits set by spin projection noise and spin decoherence due to off-resonant light scattering. When performed on resonance with the c.m. mode frequency, the technique demonstrated here can enable the detection of extremely weak forces (<1 yN) and electric fields (<1 nV/m), providing an opportunity to probe quantum sensing limits and search for physics beyond the standard model.

Arbitrary waveform generator for quantum information processing with trapped ions.

Atomic ions confined in multi-electrode traps have been proposed as a basis for scalable quantum information processing. This scheme involves transporting ions between spatially distinct locations by use of time-varying electric potentials combined with laser or microwave pulses for quantum logic in specific locations. We report the development of a fast multi-channel arbitrary waveform generator for applying the time-varying electric potentials used for transport and for shaping quantum logic pulses. The generator is based on a field-programmable gate array controlled ensemble of 16-bit digital-to-analog converters with an update frequency of 50 MHz and an output range of ±10 V. The update rate of the waveform generator is much faster than relevant motional frequencies of the confined ions in our experiments, allowing diabatic control of the ion motion. Numerous pre-loaded sets of time-varying voltages can be selected with 40 ns latency conditioned on real-time signals. Here we describe the device and demonstrate some of its uses in ion-based quantum information experiments, including speed-up of ion transport and the shaping of laser and microwave pulses.

The stimulatory effects of carbon tetrachloride on peroxidative reactions in rat liver fractions in vitro. Inhibitory effects of free-radical scavengers and other agents.

1. The effects of a number of free-radical scavengers and other agents on the stimulation of malonaldehyde production due to low concentrations of carbon tetrachloride have been studied in rat liver microsome suspensions. 2. Promethazine, propyl gallate and NN'-diphenyl-p-phenylenediamine were extremely active in inhibiting the stimulation of malonaldehyde production due to carbon tetrachloride; inhibitory effects were demonstrable with these agents at 0.1mum. 3. Low concentrations (1-100nm) of vitamin E-polyethylene glycol 1000-succinate increased the stimulation of malonaldehyde production due to carbon tetrachloride, but higher concentrations of the vitamin E preparation decreased both the stimulation due to carbon tetrachloride and the endogenous peroxidation that occurs in the absence of carbon tetrachloride. 4. Other agents tested that were effective in the range 1-20mum in decreasing the stimulation of malonaldehyde production due to carbon tetrachloride were inosine, desferrioxamine and EDTA. Agents tested that were not effective, except at very high concentrations (100mum or greater), were Nupercaine, Cetab and sodium phenobarbitone. 5. The results are discussed in terms of the mechanisms responsible for the observed inhibitions of malonaldehyde production, and of the relevance of the in vitro system to the liver damage produced by carbon tetrachloride in vivo.

The effects of carbon tetrachloride on rat liver microsomes during the first hour of poisoning in vivo, and the modifying actions of promethazine.

The effects of an oral administration of carbon tetrachloride on various liver microsomal and supernatant components were studied 1hr. and 2hr. after dosing. The modifications of such early changes resulting from a concomitant administration of promethazine together with the carbon tetrachloride were also investigated. The microsomal components studied were: cytochromes P-450 and b(5); inorganic pyrophosphatase; NADH- and NADPH-cytochrome c reductases; NADH- and NADPH-neotetrazolium reductases; a lipid-peroxidation system associated with the oxidation of NADPH and stimulated by ADP and Fe(2+). NAD- and NADP- DT-diaphorases were measured in the supernatant solution remaining after isolation of liver microsomes, and the distribution of RNA phosphorus between the microsomes and supernatant solution was also determined. Carbon tetrachloride produced a rapid fall in inorganic pyrophosphatase activity, a rather slower decrease in cytochrome P-450 content of the microsomes and small increases in the activities of NADH-cytochrome c reductase and neotetrazolium reductases. The activities of NADPH-cytochrome c reductase, the NADPH-ADP/Fe(2+)-linked lipid-peroxidation system, DT-diaphorases and the content of cytochrome b(5) in the microsomes were unchanged. There was also a loss of RNA phosphorus from the microsomes into the supernatant solution. The RNA phosphorus redistribution, the decrease in inorganic pyrophosphatase and the increases in neotetrazolium reductase activities were at least partially prevented by a concomitant dosing with promethazine. However, the decrease in cytochrome P-450 was not affected by promethazine treatment. These early changes are discussed in terms of the liver necrosis produced by carbon tetrachloride and which is greatly retarded in its onset by the administration of promethazine.

The stimulatory effects of carbon tetrachloride on peroxidative reactions in rat liver fractions in vitro. Interaction sites in the endoplasmic reticulum.

1. The actions of various inhibitors of the microsomal NADPH-cytochrome P-450 electron-transport chain have been studied on the stimulatory effect of carbon tetrachloride on malonaldehyde production. 2. Carbon monoxide, p-chloromercuribenzoate, beta-diethylaminoethyl-3,3'-diphenylpropyl acetate (SKF 525A) and nicotinamide did not decrease the stimulatory action of carbon tetrachloride on malonaldehyde production when present in concentrations shown to be capable of strongly inhibiting the demethylation of aminopyrine. 3. In contrast with the effects of the substances mentioned above, low concentrations of cytochrome c strongly depressed the stimulatory action of carbon tetrachloride on malonaldehyde production while increasing the endogenous rate of peroxidation. 4. Aging the microsomal suspensions at 0 degrees C caused a rapid decrease in aminopyrine demethylation activity and in lipid peroxidation catalysed by ADP and Fe(2+). The stimulation of malonaldehyde production by carbon tetrachloride was relatively unaffected, however, by aging the microsomes at 0 degrees C for 3 days; during this period cytochrome P-450 decreased by more than 30%. 5. The conclusion is reached that the interaction between carbon tetrachloride and the NADPH-cytochrome P-450 electron-transport chain necessary for the stimulation of malonaldehyde production involves a locus near to if not identical with the NADPH-cytochrome c reductase flavoprotein.

The stimulatory effects of carbon tetrachloride and other halogenoalkanes on peroxidative reactions in rat liver fractions in vitro. General features of the systems used.

1. The general features of the reaction by which carbon tetrachloride stimulates lipid peroxidation have been elucidated in rat liver microsomal suspensions and in mixtures of microsomes plus cell sap. The production of lipid peroxides has been correlated with malonaldehyde production in the systems used. 2. The stimulation of malonaldehyde production by carbon tetrachloride requires a source of reduced NADP(+) and is dependent on the extent of the endogenous peroxidation of the microsomal membranes: if extensive endogenous peroxidation occurs during incubation then no stimulation by carbon tetrachloride is apparent. 3. The stimulation of malonaldehyde production by carbon tetrachloride has been shown to be proportional to the square root of the carbon tetrachloride concentration in the incubation mixture. It is concluded that the stimulation of malonaldehyde production by carbon tetrachloride results from an initiation process that is itself dependent on the homolytic dissociation of carbon tetrachloride to free-radical products. 4. The increased production of malonaldehyde due to carbon tetrachloride is accompanied by a decreased activity of glucose 6-phosphatase in rat liver microsomal suspensions. 5. The relative activities of bromotrichloromethane, fluorotrichloromethane and chloroform have been evaluated in comparison with the effects of carbon tetrachloride in increasing malonaldehyde production and in decreasing glucose 6-phosphatase activity. Bromotrichloromethane was more effective, and fluorotrichloromethane and chloroform were less effective, than carbon tetrachloride in producing these two effects. It is concluded that homolytic bond fission of the halogenomethanes is a requisite for the occurrence of the two effects observed in the endoplasmic reticulum.

Liver nucleotides in acute experimental liver injury induced by dimethylnitrosamine and by thioacetamide.

1. The concentrations of the nicotinamide-adenine dinucleotides in rat liver have been determined at intervals during the period 1-24hr. after feeding adult female rats with dimethylnitrosamine or thioacetamide. 2. The administration of dimethylnitrosamine resulted in a rapid decrease in the sum of NAD+NADH(2). This sum was decreased by 40% 3hr. after dosing. 3. Dimethylnitrosamine administration also produced an overall decrease in the NADP+NADPH(2) but this decrease was not so early nor as marked as that found for NAD+NADH(2). 4. The changes produced by thioacetamide were quite different from those obtained with dimethylnitrosamine. Thioacetamide produced a temporary rise in the NAD+NADH(2) followed by a small fall. The NADP+NADPH(2) was little changed in the early hours after dosing with thioacetamide but had decreased by approx. 15% 18hr. after administration. 5. These changes are discussed in terms of the known hepatotoxic actions of dimethylnitrosamine and thioacetamide, and are compared with previously reported changes found after the administration of carbon tetrachloride.

Nicotinamide-adenine dinucleotides in acute liver injury induced by ethionine, and a comparison with the effects of salicylate.

1. The effects of single doses of ethionine or sodium salicylate on the nicotinamide-adenine dinucleotide content of rat liver have been studied. 2. There was no significant change in the sum of NAD+NADH(2) during the early period (0-2hr.) of the liver injury induced by ethionine but there was a decrease in this value of approx. 30% by 4hr. after administration. 3. Ethionine had no significant effect on the NADP+NADPH(2) during the first 2hr. period after administration. The sum then decreased to a value approx. 70% of the control by 3hr. after dosing but showed a partial recovery at the 4hr. period before decreasing again in later stages of the poisoning. 4. Salicylate produced a very rapid decrease in the NADP+NADPH(2) in the liver after intraperitoneal injection. After 1hr. the decrease was approx. 30% of the initial value; the sum slowly returned towards the normal range during the following 4hr. 5. A high parenteral dose of salicylate was found to cause only a small depression in the concentration of ATP in rat liver in contrast with the rapid depletion produced by ethionine. 6. These results are discussed in terms of the liver disturbances produced by ethionine and salicylate.