In photoemission spectra of strongly correlated systems one usually observes a satellite structure below the main peak. Description of such satellite structures in the commonly used GW approximation has been found to be insufficient. To account for these satellite structures that originate from shortrange correlations, we have developed a T -matrix formalism for performing ab initio calculations on real systems. The method is applied to Ni and we obtain a satellite structure below the Fermi level as well as a reduced exchange splitting. We also found a new interesting satellite structure above the Fermi level, which can be ascribed to particle-particle scattering. [S0031-9007(98)05337-X]
Key pointsr The synaptic organization of paravertebral sympathetic ganglia enables them to relay activity from the spinal cord to the periphery and thereby control autonomic functions, including blood pressure and body temperature.r The present experiments were done to reconcile conflicting observations in tissue culture, intact isolated ganglia and living animals. By recording intracellularly from dissociated neurons and intact ganglia, we found that when electrode damage makes cells leaky it could profoundly distort cellular excitability and the integration of synaptic potentials.r The experiments relied on the dynamic clamp method, which allows the creation of virtual ion channels by injecting current into a cell based upon a mathematical model and using rapid feedback between the model and cell.r The results support the hypothesis that sympathetic ganglia can produce a 2.4-fold amplification of presynaptic activity. This could aid understanding of the neural hyperactivity that is believed to drive high blood pressure in some patients. AbstractThe excitability of rat sympathetic neurons and integration of nicotinic EPSPs were compared in primary cell culture and in the acutely isolated intact superior cervical ganglion using whole cell patch electrode recordings. When repetitive firing was classified by Hodgkin's criteria in cultured cells, 18% displayed tonic class 1 excitability, 36% displayed adapting class 2 excitability and 46% displayed phasic class 3 excitability. In the intact ganglion, 71% of cells were class 1 and 29% were class 2. This diverges from microelectrode reports that nearly 100% of superior cervical ganglion neurons show phasic class 3 firing. The hypothesis that the disparity between patch and microelectrode data arises from a shunt conductance was tested using the dynamic clamp in cell culture. Non-depolarizing shunts of 3-10 nS converted cells from classes 1 and 2 to class 3 dynamics with current-voltage relations that replicated microelectrode data. Primary and secondary EPSPs recorded from the intact superior cervical ganglion were modelled as virtual synapses in cell culture using the dynamic clamp. Stimulating sympathetic neurons with virtual synaptic activity, designed to replicate in vivo recordings of EPSPs in muscle vasoconstrictor neurons, produced a 2.4-fold amplification of presynaptic activity. This gain in postsynaptic output did not differ between neurons displaying the three classes of excitability. Mimicry of microelectrode damage by virtual leak channels reduced and eventually obliterated synaptic gain by inhibiting summation of subthreshold EPSPs. These results provide a framework for interpreting sympathetic activity recorded from intact animals and support the hypothesis that paravertebral ganglia function as activity-dependent amplifiers of spinal output from preganglionic circuitry.
Plexiform neurofibroma, a benign peripheral nerve tumor, is associated with the biallelic loss of function of the NF1 tumor suppressor in Schwann cells. Here, we show that FLLL32, a small molecule inhibitor of JAK/STAT3 signaling, reduces neurofibroma growth in mice with conditional, biallelic deletion of Nf1 in the Schwann cell lineage. FLLL32 treatment or Stat3 deletion in tumor cells reduced inflammatory cytokine expression and tumor macrophage numbers in neurofibroma. Although STAT3 inhibition down-regulated the chemokines CCL2 and CCL12, which can signal through CCR2 to recruit macrophages to peripheral nerves, deletion of Ccr2 did not improve survival or reduce macrophage numbers in neurofibroma-bearing mice. Interestingly, macrophages accounted for ~20-40% of proliferating cells in untreated tumors. FLLL32 suppressed this proliferation, as well as Schwann cell proliferation, implicating STAT3-dependent, local proliferation in neurofibroma macrophage accumulation. The functions of STAT3 signaling in neurofibroma Schwann cells and macrophages, and its relevance as a therapeutic target in neurofibroma, merit further investigation.
The phosphorescence excitation (PE) spectrum of 4H-pyran-4-one (4PN) vapor at 40-50 degrees C was recorded near 366 nm. The most intense vibronic feature in this region of the spectrum is the T(1)(n,pi*)<--S(0) origin band. The value of nu(0) for the 0(0)(0) transition was determined to be 27 291.5 cm(-1) by comparing the observed spectrum to a simulation in the T(1)<--S(0) origin-band region. Attached to the origin band in the PE spectrum are several Deltav=0 sequence bands involving low-frequency ring modes. From the positions of these bands, together with the known ground-state combination differences, fundamental frequencies for nu(18') (ring bending), nu(13') (ring twisting), and nu(10') (in-plane ring deformation) in the T(1)(n,pi*) excited state were determined to be 126, 269, and 288 cm(-1), respectively. These values represent drops of 15%, 32%, and 43%, compared to the respective fundamental frequencies in the S(0) state. The changes in these ring frequencies indicate that the effects of T(1)(n,pi*)<--S(0) excitation extend beyond the nominal carbonyl chromophore and involve the conjugated ring atoms as well. The delocalization may be more extensive for T(1)(n,pi*) than for S(1)(n,pi*) excitation.
Apoptosis-enabling neuronal potassium efflux is mediated by an enhancement of K+ currents. In cortical neurons, increased currents are triggered by dual phosphorylation of Kv2.1 by Src and p38 at channel residues Y124 and S800. It was recently shown that a K+ current surge is also present in hepatocytes undergoing apoptosis, and that the hepatitis C virus (HCV) nonstructural protein 5A (NS5A) could inhibit Kv2.1-mediated currents and block cell death. Here, we show that NS5A1b (from HCV genotype 1b) expression in rat neurons depresses delayed rectifier potassium currents, limits the magnitude of the K+ current surge following exposure to activated microglia, and is neuroprotective. In a non-neuronal recombinant expression system, cells expressing Kv2.1 mutated at residue Y124, but not S800 mutants, are insensitive to NS5A1b-mediated current inhibition. Accordingly, NS5A1b co-expression prevents phosphorylation of wild-type Kv2.1 by Src at Y124, but is unable to inhibit p38 phosphorylation of the channel at S800. The actions of the viral protein are genotype-selective, as NS5A1a does not depress neuronal potassium currents nor inhibit Src phosphorylation of Kv2.1. Our results indicate that NS5A1b limits K+ currents following injury, leading to increased neuronal viability. NS5A1b may thus serve as a model for a new generation of neuroprotective agents.
Maintenance of a stable, properly folded, and catalytically active proteome is a major challenge to organisms in the face of multiple internal and external stresses which damage proteins and lead to protein misfolding. Here we show that internal metabolic stress produced by reactive intermediates resulting from tyrosine degradation triggers the expression of the aip-1 gene, which is critical in responses to the environmental toxin arsenic and the clearance of unstable polyglutamine and A proteins. aip-1 acts via binding to the proteosome and enhancing proteosomal function. We find that full induction of aip-1 depends on the oxidative-stressresponsive skn-1 transcription factor but significant induction still occurs without skn-1. Importantly, activation of skn-1 with wdr-23(RNAi), which dramatically induces the expression of other skn-1 target genes, produces a minimal increase in aip-1 expression. This suggests that the previously demonstrated specificity in aip-1/AIRAP induction could reflect the actions of multiple synergistic activators, such as the heat shock factor homolog hsf-1, which we also find is required for full induction. These may be triggered by proteosome dysfunction, as we find that this event links the multiple inducers of aip-1. Together, our results show that cell stress triggers aip-1 expression by both skn-1-dependent and -independent pathways.
In the present work we perform a straightforward gradient expansion of the exchange energy of a perturbed electron gas. Studied perturbations range from very weak to those that produce, e.g., a siliconlike band structure with a band gap. The expansions involve density gradients up to fourth degree and we include all terms originating in linear-and second-order response theory. The expansion reproduces our exactly calculated exchange energies with an accuracy of the order of a few mRy per electron for metallic systems. For systems with a bandgap the accuracy is reduced by an order of magnitude. When the coefficient of the fourth-degree gradient originating in second-order response theory is used as a variable parameter, we find a best fit to calculated exchange energies when the coefficient agrees with that obtained in previous work on second-order response theory. Thus, the present results corroborate our previous analytical work. We emphasize the possibility of obtaining very accurate exchange energies for s-p bonded solids and we discuss the possibility of also including correlation energies within the same simple scheme. ͓S0163-1829͑96͒01547-0͔
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