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Results for “RUBIDIUM”

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At least 289 records · Page 16Linked to original sources
PubMed2004

Frequency-stabilized 1520-nm diode laser with rubidium 5S(1/2) --> 7S(1/2) two-photon absorption.

A 760-nm light source of >10 mW is obtained from a frequency-doubled external-cavity diode laser by use of using an erbium-doped fiber amplifier and a periodically poled lithium niobate waveguide. The 5S(1/2) --> 7S(1/2) two-photon transitions of rubidium are observed with such a light source. This laser frequency is locked to the Rb two-photon transitions with an instability of 10 kHz (1 s). Our experimental scheme provides a compact, high-performance frequency, standard in the S band (1480-1530 nm) for fiber-optic communication and sensing applications.

Journal Article↗
PubMed2004

Observation of rubidium 5S1/2 --> 7S1/2 two-photon transitions with a diode laser.

The 5S1/2 --> 7S1/2 two-photon transition of atomic rubidium, which is 100 times weaker than the 5S-5D transition, is observed with an extended-cavity diode laser and a vapor cell. Signals with a signal-to-noise ratio of 280 are obtained with a laser power of 10 mW, and the observed linewidth is 3 MHz. The laser wavelength is 760 nm and is locked on the transitions to a stability of 2 x 10(-11). For the first time to our knowledge, the isotope shift of this transition is measured to be 130(4) MHz in atomic frequency.

Journal Article↗
PubMed2006

Blue five-level frequency-upconversion system in rubidium.

We demonstrate production of continuous coherent blue laser light by using a five-level system in rubidium vapor. Two low-power lasers, at 780 and 776 nm, induce strong atomic coherence in the 5S-5P-5D states. The atoms decay to the 6P excited state, from which stimulated emission produces a coherent blue (420 nm) beam. We have coupled both ground-state hyperfine levels, effecting coherence between four levels. The coherent blue output is enhanced by several mechanisms, including stronger coupling to a larger fraction of the atomic population, operation at a detuning such that the vapor is nominally transparent to the 780 nm pump field, reduced losses owing to optical pumping, and optimal phase matching. We report experimental findings and compare them with results from a semiclassical Maxwell-Bloch model.

Journal Article↗
PubMed2007

Strong relative intensity squeezing by four-wave mixing in rubidium vapor.

We have measured -3.5 dB (-8.1 dB corrected for losses) relative intensity squeezing between probe and conjugate beams generated by stimulated, nondegenerate four-wave mixing in hot rubidium vapor. Unlike early observations of squeezing in atomic vapors based on saturation of a two-level system, our scheme uses a resonant nonlinearity based on ground-state coherences in a three-level system. Since this scheme produces narrowband, squeezed light near an atomic resonance, it is of interest for experiments involving cold atoms or atomic ensembles.

Journal Article↗
PubMed1993

Toxin sensitivity of the calcium-dependent rubidium efflux in Madin-Darby canine kidney cells.

86Rb+ efflux was measured on polarized Madin-Darby canine kidney cells under A23187 or ATP stimulation. This efflux, inhibited by barium, Leiurus quinquestriatus hebraeus venom and charybdotoxin was attributed to the stimulation of Ca(++)-activated maxi K+ channels. Snake venom from Dendroaspis polylepis did not alter the stimulation as well as did apamine. ATP was effective on both the apical and basolateral membranes and the Ca(++)-activated maxi K+ channels were predominantly found on the basolateral membrane. This study presents the physiological evidence that dendrotoxin is ineffective on the epithelial Ca(++)-activated maxi K+ channel present in MDCK cells.

Adenosine Triphosphate↗
PubMed1990

Interactions of methylmercury with rat primary astrocyte cultures: inhibition of rubidium and glutamate uptake and induction of swelling.

The ability of astrocytes to sequester MeHg may indicate an astrocyte-mediated role in MeHg's neurotoxicity. Hence, studies were undertaken to assess the effects of MeHg on metabolic functions in cultured astrocytes. MeHg (10(-5) M) significantly inhibited the initial rate (5 min) of uptake of 86RbCl, used as a tracer for K+. 86RbCl uptake was also sensitive to the omission of medium Na+. MeHg (10(-5) M) also markedly inhibited the initial rate of uptake (1 min) of the Na(+)-dependent uptake of [3H]L-glutamate. A second neurotoxin, MnCl2 (0-5 x 10(-4) M), did not alter [3H]glutamate or 86RbCl uptake. MeHg, but not MnCl2, also stimulated the release of intracellular 86Rb+ in a dose-dependent fashion. This effect could be prevented by the administration of MeHg as the glutathione conjugate. These observations support the hypothesis that the astrocyte plasma membrane is an important target for MeHg's toxic effect and specifically that small concentrations of this organometal inhibit the ability of astrocytes to maintain a transmembrane K+ gradient. This would be expected to compromise the ability of astrocytes to control extracellular K+ either by spatial buffering or active uptake, resulting in cellular swelling. We therefore studied volume changes in astrocytes using uptake of [14C]3-O-methyl-D-glucose, in attached cells in response to exposure to MeHg. Exposure to MeHg (0-5 x 10(-4) M) caused a marked increase in the cell volume that was proportional to concentrations of MeHg.

3-O-Methylglucose↗
PubMed1994

The role of sulfhydryl groups in D-aspartate and rubidium release from neonatal rat primary astrocyte cultures.

We have recently demonstrated that both methylmercury (MeHg) and mercuric chloride (MC) induce D-aspartate release from neonatal rat primary astrocyte cultures maintained in isotonic conditions. In the present study, we compare several other sulfhydryl-(-SH) selective alkylating reagents [methyl methanethiosulfonate (MMTS), N-ethylmaleimide (NEM), and iodoacetamide (IA)] in isotonic, as well as hypotonic conditions to discern the functional importance of -SH groups in [3H]D-aspartate and 86rubidium (86Rb) release from astrocytes. Treatment of astrocytes (5 min) in isotonic buffer with the hydrophobic reagent NEM (10 microM) caused a marked increase in 86Rb release but had no effect on [3H]D-aspartate release. Neither IA-, nor MMTS-treatment (both at 10 microM) induced increase in [3H]D-aspartate or 86Rb release in isotonic buffer. In hypotonic condition (-50 mM Na+), astrocytes were most sensitive to MC exposure (5 microM), exhibiting an increase in both [3H]D-aspartate and 86Rb efflux. The hydrophobic compounds MMTS and NEM, and the hydrophilic -SH modifying reagent, IA, attenuated the hypotonic-induced efflux of [3H]D-aspartate, in the absence of an effect on 86Rb release. These observations are consistent with a critical role for -SH groups both in basal (i.e. isotonic) and hypotonic-induced release of D-aspartate and Rb from astrocytes. Lack of uniformity of these effects may be attributed to site-specificity, related to the physicochemical properties of these -SH alkylating reagents.

Alkylating Agents↗
PubMed1991

Rubidium (86Rb+) influx into dorsal root ganglia and sciatic nerve endoneurium of control and streptozotocin-diabetic rats: comparison with enzymatic Na,K-ATPase activity.

Streptozotocin (STZ)-induced diabetes in the rat causes a significant reduction in ouabain-sensitive Na,K-ATPase pumping activity measured by 86Rb+ influx, in sciatic endoneurium (by 54%) and dorsal root ganglia (by 22%). For endoneurium, the change is similar to that of ouabain-sensitive enzymatic Na,K-ATPase activity (42%), but in dorsal root ganglia, the decrease in enzymatic Na,K-ATPase activity was much greater. 86Rb+ efflux from dorsal root ganglia showed no difference between diabetic and control animals, confirming that the abnormal 86Rb+ influx reflects Na,K-ATPase function and not abnormal membrane permeability. The significance of these findings to pathogenetic mechanisms in diabetic neuropathy is discussed.

Animals↗
PubMed1999

Manufacture of strontium-82/rubidium-82 generators and quality control of rubidium-82 chloride for myocardial perfusion imaging in patients using positron emission tomography.

We describe a protocol to manufacture 82Sr/82Rb generators and 82RbCl for myocardial imaging with PET. The generators are manufactured in 3 stages: (1) preparation of a tin oxide column, (2) leak test of the generator column and (3) loading of the generator with 82Sr. The generators produced sterile and non-pyrogenic 82RbCl for i.v. injection. No significant 82Sr/85Sr breakthroughs were observed after elution with 20 1 of saline. The automated system delivered human doses of 82RbCl accurately.

Chlorides↗