Biomedical subjects

D Chen

Publications and source records attributed to D Chen.

At least 289 records · Page 16Linked to original sources

PubMed1999

Smad1 interacts with homeobox DNA-binding proteins in bone morphogenetic protein signaling.

Bone morphogenetic proteins (BMP) transduce their signals into the cell through a family of mediator proteins known as Smads. Upon phosphorylation by the BMP receptors, Smad1 interacts with Smad4 and translocates into the nucleus where the complex recruits DNA-binding protein(s) to activate specific gene transcription. However, the DNA-binding protein(s) involved in BMP signaling has not been identified. Using a yeast two-hybrid approach, we found that Smad1 interacts with Hoxc-8, a homeodomain transcription factor. The interaction between Smad1 and Hoxc-8 was confirmed by a "pull-down" assay and a co-immunoprecipitation experiment in COS-1 cells. Interestingly, purified Smad1 inhibited Hoxc-8 binding to the osteopontin Hoxc-8 site in a concentration-dependent manner. Transient transfection studies showed that native osteopontin promoter activity was elevated upon BMP stimulation. Consistent with the gel shift assay, overexpression of Hoxc-8 abolished the BMP stimulation. When a wild type or mutant Hoxc-8 binding element was linked to an SV40 promoter-driven reporter gene, the wild type but not the mutant Hoxc-8 binding site responded to BMP stimulation. Again, overexpression of Hoxc-8 suppressed the BMP-induced activity of the wild type reporter construct. Our findings suggest that Smad1 interaction with Hoxc-8 dislodges Hoxc-8 from its DNA binding element, resulting in the induction of gene expression.

Animals↗

PubMed1999

Microstructure and Viscosity of Aggregating Colloids under Strong Shearing Force.

Disaggregation under strong shearing force is simulated for an aggregating colloid based on a sticky particle model which can describe the disaggregating and aggregating kinetics, the deformation, and the rupture of clusters with a minimum number of parameters. For a 2-dimensional system, the viscosity and coordination number of the model colloid are calculated at each time step, and the changes of microstructure with shear flow are observed directly by displaying the configuration of particles onto a monitor. The viscosity depends on both area fraction and shear rate, but coordination number depends only on shear rate. Furthermore, the viscosity and coordination number at steady state are independent of the initial state of particles, which indicates that the disaggregation and aggregation are mutually reversible. Copyright 1999 Academic Press.

Journal Article↗

PubMed1999

Specific interaction of Tat with the human but not rodent P-TEFb complex mediates the species-specific Tat activation of HIV-1 transcription.

Tat stimulation of HIV-1 transcriptional elongation is species-specific and is believed to require a specific cellular cofactor present in many human and primate cells but not in nonpermissive rodent cells. Human P-TEFb, composed of Cdk9 and cyclin T1, is a general transcription elongation factor that phosphorylates the C-terminal domain of RNA polymerase II. Previous studies have also implicated P-TEFb as a Tat-specific cellular cofactor and, in particular, human cyclin T1 as responsible for the species-specific Tat activation. To obtain functional evidence in support of these hypotheses, we generated and examined the activities of human-rodent "hybrid" P-TEFb complexes. We found that P-TEFb complexes containing human cyclin T1 complexed with either human or rodent Cdk9 supported Tat transactivation and interacted with the Tat activation domain and the HIV-1 TAR RNA element to form TAR loop-dependent ribonucleoprotein complexes. Although a stable complex containing rodent cyclin T1 and human Cdk9 was capable of phosphorylating CTD and mediating basal HIV-1 elongation, it failed to interact with Tat and to mediate Tat transactivation, indicating that the abilities of P-TEFb to support basal elongation and Tat activation can be separated. Together, our data indicated that the specific interaction of human P-TEFb with Tat/TAR, mostly through cyclin T1, is crucial for P-TEFb to mediate a Tat-specific and species-restricted activation of HIV-1 transcription. Amino acid residues unique to human Cdk9 also contributed partially to the formation of the P-TEFb-Tat-TAR complex. Moreover, the cyclin box of cyclin T1 and its immediate flanking region are largely responsible for the specific P-TEFb-Tat interaction.

Animals↗

PubMed1999

Bone marrow and peripheral blood dendritic cells from patients with multiple myeloma are phenotypically and functionally normal despite the detection of Kaposi's sarcoma herpesvirus gene sequences.

Multiple myeloma (MM) cells express idiotypic proteins and other tumor-associated antigens which make them ideal targets for novel immunotherapeutic approaches. However, recent reports show the presence of Kaposi's sarcoma herpesvirus (KSHV) gene sequences in bone marrow dendritic cells (BMDCs) in MM, raising concerns regarding their antigen-presenting cell (APC) function. In the present study, we sought to identify the ideal source of DCs from MM patients for use in vaccination approaches. We compared the relative frequency, phenotype, and function of BMDCs or peripheral blood dendritic cells (PBDCs) from MM patients versus normal donors. DCs were derived by culture of mononuclear cells in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4. The yield as well as the pattern and intensity of Ag (HLA-DR, CD40, CD54, CD80, and CD86) expression were equivalent on DCs from BM or PB of MM patients versus normal donors. Comparison of PBDCs versus BMDCs showed higher surface expression of HLA-DR (P =.01), CD86 (P =. 0003), and CD14 (P =.04) on PBDCs. APC function, assessed using an allogeneic mixed lymphocyte reaction (MLR), demonstrated equivalent T-cell proliferation triggered by MM versus normal DCs. Moreover, no differences in APC function were noted in BMDCs compared with PBDCs. Polymerase chain reaction (PCR) analysis of genomic DNA from both MM patient and normal donor DCs for the 233-bp KSHV gene sequence (KS330233) was negative, but nested PCR to yield a final product of 186 bp internal to KS330233 was positive in 16 of 18 (88.8%) MM BMDCs, 3 of 8 (37.5%) normal BMDCs, 1 of 5 (20%) MM PBDCs, and 2 of 6 (33.3%) normal donor PBDCs. Sequencing of 4 MM patient PCR products showed 96% to 98% homology to the published KSHV gene sequence, with patient specific mutations ruling out PCR artifacts or contamination. In addition, KHSV-specific viral cyclin D (open reading frame [ORF] 72) was amplified in 2 of 5 MM BMDCs, with sequencing of the ORF 72 amplicon revealing 91% and 92% homology to the KSHV viral cyclin D sequence. These sequences again demonstrated patient specific mutations, ruling out contamination. Therefore, our studies show that PB appears to be the preferred source of DCs for use in vaccination strategies due to the ready accessibility and phenotypic profile of PBDCs, as well as the comparable APC function and lower detection rate of KSHV gene sequences compared with BMDCs. Whether active KSHV infection is present and important in the pathophysiology of MM remains unclear; however, our study shows that MMDCs remain functional despite the detection of KSHV gene sequences.

Adult↗

PubMed1999

Intracellular localization of SNAP-23 to endosomal compartments.

We have reexamined the intracellular localization of the ubiquitously expressed target membrane SNAP receptor (t-SNARE), SNAP-23. While SNAP-23 appears on the plasma membrane, in the cell types examined there is a significant pool associated with endosomal compartments. Immuno-staining and expression of green fluorescent protein-tagged SNAP-23, show that it has a punctate, perinuclear localization in HepG2 and HT4 cells. This distribution overlaps significantly with transferrin receptor and slightly with the late endosome/lysosomal protein LAMP-1. The localization of SNAP-23 changes as HepG2 cells polarize. Initially it is concentrated at sites of cell-cell contact and then almost exclusively to the apical (or bile canalicular) domain of the cell. These data are consistent with a role for SNAP-23 in both endosome-plasma membrane trafficking as well as endosome-endosome transport.

Animals↗

PubMed1999

The effect of locking fixation screws on the stability of anterior cervical plating.

STUDY DESIGN: Current anterior cervical plate systems were tested with locked and unlocked fixation screws and with unicortical and bicortical fixation screws to determine fixation rigidity and pull-off strengths. OBJECTIVES: To evaluate the effects of screw-plate locking and screw length on fixation strength and stability of anterior cervical plates. SUMMARY OF BACKGROUND DATA: New plate systems provide for rigid locking of the screw-plate interface, theoretically increasing construct rigidity, allowing unicortical fixation, and preventing screw back-out. There are few data on the effects of locking screws on the stability of anterior cervical plating. METHODS: Eighty fresh lamb vertebrae (C3-T1) were used. Test systems included: Cervical Spine Locking Plate (CSLP; Synthes, Paoli, PA, Orion plate (Sofamor-Danek, Memphis, TN), and Acroplate (AcroMed, Cleveland, OH). The CSLP and Orion plates were tested with fixation screws, locked and unlocked, and the AcroMed plate with unicortical and bicortical screw purchase. Biomechanical testing of the screw-plate constructs was performed to determine the initial bone-plate rigidity and pull-off strength. A 2.5-Nm cyclic bending moment was then applied to additional constructs for 10(5) cycles, and these constructs retested. RESULTS: Locked CSLP and Orion constructs were more rigid than all unlocked unicortical systems initially and after cyclic loading (P < 0.05). After cycling, the rigidity of all unlocked unicortical constructs decreased significantly (P < 0.05). There was no significant difference in pull-off strengths between the CSLP, the Orion, and the unicortical AcroMed plate. However, all had significantly less pull-off strength than the AcroMed plate with bicortical screws. A negative correlation was observed between initial pull-off strength and sagittal vertebral body diameter. CONCLUSIONS: Locking screws significantly increased the rigidity of the tested screw-plate systems initially and after cyclic loading. Because pull-off strength was affected by the vertebral body diameter, use of longer unicortical screws may be clinically beneficial in the patient with larger cervical vertebrae.

Animals↗

PubMed1999

Inhibition of tissue factor-dependent and -independent coagulation by cell surface expression of novel anticoagulant fusion proteins.

BACKGROUND: Thrombotic vascular occlusion occurs in disorders of diverse etiology, including atherosclerosis, vasculitis, and disseminated intravascular coagulation. The same process results in hyperacute rejection of renal allografts transplanted into sensitized patients and remains a major problem in experimental xenotransplantation. METHODS: We have previously described the design and expression of several genetic constructs encoding novel fusion proteins with anticoagulant properties. They are based on two naturally occurring soluble anticoagulant proteins, human tissue factor pathway inhibitor (hTFPI) and the leech protein hirudin, which act early and late in the clotting cascade, respectively. We report the expression of human hTFPI-CD4 on the surface of immortalized porcine endothelial cells (IPEC), and show that it functions across the species divide as evidenced by the binding of membrane-expressed porcine tissue factor (pTF)-human factor VIIa complexes. RESULTS: Using a human plasma recalcification clotting assay, we distinguished between pTF-dependent and pTF-independent fibrin generation, and we have demonstrated that expression of hTFPI-CD4 on IPEC effectively prevented pTF-dependent clotting. Moreover, we show that when hTFPI-CD4 was co-expressed with the hirudin construct, the procoagulant properties of in vitro cultured, activated IPEC were almost completely abolished. CONCLUSIONS: These results suggest that these novel anticoagulant molecules may prove useful therapeutic agents for gene therapy or for transgenic expression in animals whose organs may be used for cliniCal xenotransplantation.

Animals↗

PubMed1999

Molecular cloning of mouse Lrp7(Lr3) cDNA and chromosomal mapping of orthologous genes in mouse and human.

LRP7 (the HGMW-approved gene symbol for LR3) is a novel member of the low-density lipoprotein receptor (LDLR) family. The unique modular features in both its extracellular and its intracellular regions and functional analysis suggest it to be a multifunctional protein with mitogenic activity and potential ligand-induced signal transduction capability. We describe here the cloning of Lrp7, the orthologue of the human LRP7 gene, from a mouse liver cDNA library and its expression profile in mouse tissues and developmental stages. Lrp7 is highly homologous to the human sequence, with 95% identity at the amino acid level and a perfect conservation of all the recognizable functional domains. A 6-kb mRNA transcript could be detected in all the tissues examined, with the highest expression levels in liver, heart, and lung and the lowest levels in brain and spleen. A similar expression level of a smaller transcript (4.5 kb) was seen at the four embryonic stages examined. We mapped the Lrp 7 gene to mouse chromosome 19B and the LRP7 gene to human chromosome 11q13.4. The LRP7 gene was also localized by radiation hybrid mapping between markers D11S24270 and D11S1975.

3T3 Cells↗

PubMed1999

Differential reactivity of the rat S100A4(p9Ka) gene to sodium bisulfite is associated with differential levels of the S100A4 (p9Ka) mRNA in rat mammary epithelial cells.

Elevated intracellular levels of S100A4, an S100-related calcium-binding protein, induce metastatic capability in benign mammary tumor-derived epithelial cells and in transgenic mice bearing oncogene-induced benign mammary tumors. The S100A4(p9Ka) gene in rat mammary epithelial cells expressing low levels of S100A4 yields a reduced number of fragments upon digestion with the methylation-sensitive restriction enzyme, HpaII, compared with the gene from high S100A4-expressing cells. Genomic sequencing of two potential regulatory elements in the S100A4 gene, an intronic enhancer and TATA box region, revealed that in low S100A4-expressing cells, most cytosine bases exhibited high levels of resistance to conversion to thymine by sodium bisulfite. In derivative cell lines, which express high levels of S100A4, only a small number of cytosine bases were resistant to treatment with sodium bisulfite. In contrast, cytosine bases in the DNA surrounding an upstream regulatory region, which binds inhibitory GC factor in the low-expressing cell lines, are sensitive to conversion to thymine by sodium bisulfite in both low- and high-expressing cell lines. The results suggest that the rat S100A4 gene is maintained in a different state in the low-expressing cell lines and that this state might be a consequence of the pattern of methylation in this regulated gene that does not contain a CpG island.

Animals↗

PubMed1999

Transcription-induced hypersupercoiling of plasmid DNA.

Transcription can induce high levels of negative supercoiling into plasmid DNA under some circumstances. This is especially true when the plasmid carries a functional tetracycline-resistance gene tetA, and is borne in a topA strain of Escherichia coli or Salmonella typhimurium. An important mechanism in transcription-induced supercoiling is believed to be the twin supercoiled-domain effect resulting from hindered rotation of the transcriptional complex, and this is very much more efficient where there is coupled transcription, translation and membrane insertion of the gene product. However, we have noted that strong promoters inserted into tetA-carrying plasmids can greatly increase the fraction of hypersupercoiled DNA. We show here that this effect is clearly present when the inserted promoter transcribes a very short segment of DNA (down to transcript lengths of approximately 45 nt), and where there is no possibility of translation of the RNA transcript. We suggest that the repeated helical opening due to transcriptional initiation is a significant contributor to the induction of high levels of supercoiling.

Base Sequence↗

PubMed1999

Analysis of internal (n-1)mer deletion sequences in synthetic oligodeoxyribonucleotides by hybridization to an immobilized probe array.

The purity of a drug substance can influence its toxicity and potency, so impurities must be specifically determined. In the case of synthetic oligodeoxyribonucleotide drugs, however, product complexity makes complete impurity speciation difficult. The goal of the present work was to develop a new analytical method for speciation of individual internal (n-1)mer impurities arising from formal nucleotide deletion in synthetic oligodeoxyribonucleotides. A complete series of oligodeoxyribonucleotide probes were designed, each complementary to an (n-1)mer deletion sequence of the drug in question. Glass plates were used as a solid support for individually immobilizing the entire probe array. The total mixture of internal (n-1) length impurities was isolated from a synthetic oligodeoxyribonucleotide by PAGE and labeled with 35S. Under stringently optimized conditions, only the perfectly sequence-matched oligodeoxyribonucleotide hybridized to each probe, while all other deletion sequences were removed by washing with buffer. The 35S signal intensity of the bound oligodeoxyribonucleotide was proportional to the concentration of each (n-1)mer deletion sequence in the analyte solution. This method has been applied to a number of synthetic phosphorothioate oligodeoxy-ribonucleotide lots and shown to be reliable for speciation and relative quantitation of the internal (n -1)mer deletion sequences present.

Base Pair Mismatch↗

PubMed1999

Gastrectomy induces impaired insulin and glucagon secretion: evidence for a gastro-insular axis in mice.

1. Mice were subjected to gastrectomy (GX) or food deprivation (24 h). The release of insulin and glucagon in response to different secretagogues was monitored in vivo and in isolated islets 3-4 weeks after surgery. 2. GX animals responded to glucose with an impaired glucose tolerance and a poor increase in plasma insulin. Islets from GX or food-deprived mice displayed impaired insulin release to high glucose and enhanced glucagon release at low glucose. 3. After GX the insulinogenic index, Delta insulin (microU ml-1)/Delta glucose (mg ml-1), was suppressed by 65% after oral glucose and by 59% after i.v. glucose. The integrated insulin response after oral glucose was reduced by 90% in GX mice. After i.v. glucose the reduction was 67%. 4. Carbachol-induced insulin release in vivo was reduced after food deprivation and exaggerated after GX. Carbachol-stimulated glucagon secretion was suppressed after GX and after food deprivation. A similar pattern was found in vitro. 5. Cyclic AMP activation (by the phosphodiesterase inhibitor isobutylmethylxanthine or the adenylate cyclase stimulator forskolin) induced a greater insulin response in GX or food-deprived mice than in sham-operated, fed mice. A similar pattern was found in vitro. The glucagon response was enhanced in vitro but not in vivo. 6. Crude extracts of rat oxyntic mucosa enhanced basal as well as glucose-induced insulin release from isolated islets, whereas glucagon release was markedly inhibited. The effects were dose dependent, the inhibition of glucagon release being achieved at lower concentrations than the potentiation of glucose-induced insulin release. The active principle was inactivated by incubation with trypsin or leucine aminopeptidase. 7. The data suggest that a circulating agent, probably a peptide, from gastric oxyntic mucosa stimulates glucose-induced insulin secretion. It also suppresses glucagon secretion. The GX-evoked impairment of the insulin (and glucagon) response to glucose is partly compensated for by an enhanced insulin response to cholinergic and/or cyclic AMP activation.

1-Methyl-3-isobutylxanthine↗

PubMed1999

Vitiligo antibodies are not directed to tyrosinase.

BACKGROUND: Patients with vitiligo have a markedly increased incidence of antibodies to melanocytes, referred to as vitiligo antibodies. Antibodies to tyrosinase have been reported in some patients with vitiligo, suggesting that vitiligo antibodies may be directed to this enzyme. However, there is considerable controversy as to the frequency with which these antibodies occur, and, hence, about their relevance to the pathogenesis of vitiligo. The frequency with which antityrosinase antibodies occur in vitiligo is critical to evaluate their potential role in the pathogenesis of this disease. OBJECTIVE: To examine the prevalence of antibodies to tyrosinase in a large group of patients with vitiligo. DESIGN: We examined the incidence of antibodies to enzymatically and immunologically active tyrosinase in patients with and without vitiligo. SETTING: Outpatient clinic in referral center. PATIENTS: The study was conducted on serum samples obtained from 54 patients with active (n = 40) and inactive (n = 14) uncomplicated vitiligo and from 52 age- and sex-matched individuals without vitiligo. MAIN OUTCOME MEASURE: Presence in the serum of antibodies to enzymatically and/or immunologically active tyrosinase. RESULTS: By immunoblotting, 20 patients (50%) with active vitiligo, 9 of those (64.3%) with inactive vitiligo, and 29 control individuals (55.8%) had antibodies to an antigen that comigrated with tyrosinase. However, by immunoprecipitation DOPA stain and by sandwich enzyme-linked immunosorbent assay, none of the vitiligo or control individuals had antibodies to tyrosinase, even though both assays easily detected control antityrosinase antibodies. CONCLUSION: These results indicate that while antibodies to an antigen(s) that comigrates with tyrosinase are common in patients with or without vitiligo, vitiligo antibodies are not directed to tyrosinase.

Adolescent↗

PubMed1999

Study on the bioavailability of baicalin-phospholipid complex by using HPLC.

A complex of baicalin with soy phospholipid was prepared to improve the bioabsorption of baicalin. A simple and sensitive HPLC method was developed for baicalin determination in rat plasma. It was shown that its plasma concentration reached a peak of 0.42 microgram/mL 5.3 h after oral administration, 600 mg/kg. However, after intake of its phospholipid complex, a peak of 0.90-microgram/mL occurred at a later time, 6.1 h. The elimination of the complex tended to be slower than that of the free drug. There was a significant difference in the mean area under the concentration-time curves (AUC) between the free drug and the complex (p < 0.01).

Animals↗

PubMed1999

Lineage-specific differences among CD8+ T cells in their dependence of NF-kappa B/Rel signaling.

Whereas most CD8+ T cells in lymph nodes and spleen express the CD8alpha beta heterodimer and depend absolutely on thymic competence for their development, a substantial population of T cells expressing CD8alpha alpha matures extrathymically. Although the existence of these CD8 sublineages is well established, relatively little is known about differences that might exist among CD8 cells in their requirement for particular transcriptional pathways during the development and maintenance of normal populations. Transgenic mice whose T lineage expresses an IkappaBalpha mutant exhibited decreased NF-kappaB signaling and a diminution in mature CD8 T cells. We now have determined that although TCR-dependent CD69 induction by CD8alpha alpha and CD8alpha beta T cells was unaffected by inhibition of NF-kappaB, TCRalpha beta CD8alpha beta T cells were preferentially reduced compared to their TCRalpha beta CD8alpha alpha or TCRgamma delta counterparts. This finding was most prominent in spleen, but was also apparent in Peyer's patches of transgenic mice. In addition, diminished antiviral cytotoxic responses of CD8alpha beta intraepithelial lymphocytes were observed after enteric reovirus infection. Taken together, these results indicate that NF-kappaB signaling is more important for the thymus-dependent TCRalpha beta CD8alpha beta population than for other CD8 lineages, and thus regulates the number, function, and normal balance of CD8 subsets in the periphery.

Animals↗

PubMed1999

Determination of free calcium in guinea-pig cochlea perilymph by capillary electrophoresis with direct injection.

At present, the tinnitus mechanism is still not clear. Our experiments demonstrated that the concentration of free calcium in cochlea perilymph of tinnitus model guinea-pigs is lower than that in normal guinea-pigs. However, the volume of cochlea perilymph is so small that only 5-10 microL of sample can be obtained from each animal. We describe the application of CE to the detection of free calcium in guinea-pig cochlea perilymph. Direct injection was employed in this study. The separation was carried out at 10 kV. The capillary temperature was maintained at 20 degrees C, and indirect UV detection at 214 nm was employed. The samples were vacuum injected for 3 s. The run buffer was 0.005 mol/L imidazole with a pH of 4.30-4.50. The concentration of free calcium in the normal group was found to be in accordance with the reference data. The method has been applied to research on the tinnitus mechanism and for medical treatment.

Animals↗

PubMed1999

Intracameral muramyl dipeptide-induced paracellular permeability associated with decreased glutamate transporter and gamma -glutamyltranspeptidase activities.

Muramyl dipeptide (MDP) (N -acetylmuramyl- L -alanyl- D - isoglutamine) was injected intracamerally to test if MDP applied to the aqueous side of the blood-aqueous barrier would increase paracellular permeability in association with diminished uptake of glutamate. The symptoms of anterior uveitis, i.e., increase in vascular dilatation, could be detected as early as 30 min post MDP injection while aqueous protein concentration did not increase at this time suggesting an initial dissociation between the circulatory and epithelial barrier responses. However, at 45 min, the aqueous protein concentration increased 10-fold (201+/-174 to 2094+/-1835 micrograms ml-1;P<0.001) rising progressively to 20-fold above the control eye at 60 min post injection (254+/-194 vs. 5038+/-2514 micrograms ml-1;P<0.001). Epithelial cell barrier paracellular permeability increased at 45 min as evidenced by the enhanced efflux of radiolabelled L -glucose out of the aqueous (8% and 13% faster than control at 45 and 60 min post MDP injection, respectively), coinciding with the accelerated protein influx. A near 50% reduction in efflux of both radiolabelled glutamate and D -aspartate was consistent with reduced glutamate uptake by the transport system X-AG. In addition, a 24% decline in aqueous glutamate, but not aspartate, was detected in the aqueous of the MDP-treated eyes in association with a 54% decrease in iris/ciliary body gamma-glutamyltranspeptidase activity consistent with reduced de novo glutamate formation from glutamine. The aqueous of MDP injected eyes also had 6-fold and 34-fold higher prostaglandin E2and F2alphaconcentrations, respectively (P</=0.03) as well as reduced AH bicarbonate concentration. These results suggest that increased paracellular permeability is associated with diminished gamma-glutamyltranspepidase-mediated glutamate production, X-AGtransport activity, and cellular acidosis in the MDP-induced prostaglandin-mediated inflammation.

ATP-Binding Cassette Transporters↗

PubMed1999

The 6svarsigma, 6dvarsigma, and 7dvarsigma Rydberg (1)Sigma(+)(g) States and Two Doubly Excited (1)Sigma(+)(g) States of Na(2).

Five highly excited (1)Sigma(+)(g) states of Na(2) were observed for the first time by pulsed optical-optical double resonance (OODR) fluorescence excitation spectroscopy. Three of the five states are assigned to the 6svarsigma (1)Sigma(+)(g), 6dvarsigma (1)Sigma(+)(g), and 7dvarsigma (1)Sigma(+)(g) Rydberg states. The other two states are assigned to doubly excited (1)Sigma(+)(g) states. Copyright 1999 Academic Press.

Journal Article↗