Search

We report an approximate energy distribution (coarse spectrum) over the range ~0.1 to > 10 keV for the X-ray output of an argon Z-pinch. The tests, conducted at ~15-MA peak current, utilized an 8-cm diameter double-shell nozzle. Sze et al. (2001) have previously described the performance of this Z-pinch with emphasis on the K-shell line emission at ~3 keV. Additional measurements that address the non-K-line output of the Z-pinches are presented here. On the one hand, > 4-keV photons due to the free-bound continuum constitute a significant fraction, almost 30%, of the nominal K-shell emission. On the other hand, the sub-3-keV L-shell lines and continuum show distinctive time histories and significant yields. These nonresonance-line emissions are important for a more complete understanding of the implosion physics, for proper analysis of diagnostic responses, and for their effects upon objects exposed to the Z-pinch's radiation. Index Terms--X-ray diagnostics, X-ray spectra, Z-pinches.

We have developed a 12-cm-diameter Ar gas Z-pinch load, which produces two annular gas shells and a center gas jet. The two-dimensional (2-D) gas density profiles of the load, in r-[theta]and r-z planes, were measured with submillimeter spatial resolutions using the planar-laser-induced fluorescence (PLIF) method, for conditions used in Z-pinch experiments. Due to interactions between the shells, the net gas density profile differs from the superposition of the individual shell profiles. Narrow density peaks are observed both at smaller and larger radii than the radius where the shells come in contact with each other. Two-dimensional flow velocity distributions are determined from the displacements between the fluorescence and later time phosphorescence images. The measured stream velocities of argon gas puffs are 650 [+ or -] 20 m/s, higher than the ideal gas velocity due to the formation of clusters in the supersonic gas flow. Indeed, clusters were observed in earlier Rayleigh scattering experiments. The gas measurements of the initial phase using the PLIF will be combined with other density measurements of the implosion and pinch phases to better understand the implosion dynamics and to provide initial conditions for simulation codes. Index Terms--Argon gas puff, laser-induced fluorescence, plasma radiation source, Z-pinch.

Mouse proximal tubular cells (BUMPT), when cultured in the absence of growth factors, activate a default apoptotic pathway. Although Wnt signaling antagonizes the effect of proapoptotic triggers, its role in regulating the default pathway of apoptosis is less well defined. The present study examines the hypothesis that lithium ([Li.sup.+]) and (2'Z,3'E)-6-bromoindirubin-3'-oxime (BIO), two glycogen synthase kinase-3[beta] (GSK3[beta]) inhibitors, promote survival of growth factor-deprived renal epithelial cells by activating the Wnt pathway. These studies demonstrate that [Li.sup.+] and BIO activate Wnt signaling as indicated by the following changes: phosphorylation (inhibition) of GSK3[beta]; decreased phosphorylation of [beta]-catenin (a GSK3[beta] substrate); nuclear translocation of [beta]-catenin; specific transcriptional activation of Tcf/catenin-responsive pTopflash constructs; and an increase in the expression of cyclin D1 (indicative of a promitogenic cell response). In addition, [Li.sup.+] or BIO significantly increases the phosphorylation (activation) of Akt, an anti-apoptotic protein, and inhibits apoptosis (decreases both annexin-V staining and caspase-3 activation), during serum deprivation. Inhibition of phosphatidylinositol 3-kinase (responsible for Akt activation) either by wortmanin or LY-294002 prevented [Li.sup.+]-or BIO-induced Akt phosphorylation and reduces cell survival without altering the phosphorylation state of GSK3[beta]. [Li.sup.+] or BIO also increases the expression of insulin-like growth factor-II (IGF-II), a potent proliferative signaling protein. [Li.sup.+] or BIO-free conditioned medium harvested from [Li.sup.+] or BIO-exposed cells also induced Akt phosphorylafion, mimicking the protective effect of the two GSK3[beta] inhibitors on serum-starved cells. Furthermore, the effect of conditioned medium on Akt phosphorylation could be inhibited by either LY-294002 or IGF-binding protein. BIO, a specific GSK3[beta] inhibitor, replicated the protective effect of [Li.sup.+] on cell viability, suggesting that GSK3[beta] activation is important for initiating the apoptotic pathway. Taken together, these data suggest that [Li.sup.+] or BIO promotes renal epithelial cell survival by inhibiting apoptosis through GSK3[beta]-dependent activation of the Wnt pathway and subsequent release of IGF-II. Extracellular IGF-II serves as an autocrine survival factor that is responsible, in part, for activating the anti-apoptotic phosphatidylinositol-3-kinase-Akt pathway during serum deprivation. serum deprivation; renal epithelial cells; insulin-like growth factors; [beta]-catenin; glycogen synthase kinase-3[beta]; apoptosis

The diagnosis, symptoms, and treatment of antiphospholipid syndrome are reviewed. This syndrome is characterized by the production of antibodies against phospholipids, which are a component of the cell membrane. Patients with the syndrome have abnormal blood clotting, which can occur in arteries and veins as well as in organs such as the heart, lungs, brain, and kidneys.

A model to account for the shortening of the relativistic magnetron microwave pulse length based on radial cathode plasma motion is put forth and corroborated with measurements. If the dense, conducting, cathode plasma (and not the cathode itself) sets the diode electrostatic and microwave boundary conditions, its motion changes the magnetron resonance condition. Time varying microwave power envelopes and frequencies are both expected and observed. based on the cathode plasma expansion rate, the main plasma ion constituent is inferred to be hydrogen. A magnetron experiment to defeat the pulse-shortening mechanism by heating the resonator successfully lengthened the pulse from 100 to 175 ns. Index Terms - Diode plasma motion, high power microwave, pulse shortening, low-Z contaminants, relativistic magnetron.

Primary cultures of proximal tubular cells from mice were used in the investigation of the effects of adenosine triphosphatase (ATP) depletion. Depleting ATP to at most 15% of normal levels induces cell death by necrosis while depletion to levels between 25% and 70% of normal induced cell death by apoptosis. The rate of cell demise is proportional to the degree of ATP depletion.

A study was conducted on the pleiotropic influences of lipophosphatidic acid. Lipophosphatidic acid, which was found to inhibit mouse renal proximal tubular cell apoptosis, is mediated by lipid kinase phosphatidylinositol 3-kinase. Proliferative and anti-apoptopic functions demonstrate the capacity of lipophosphatidic acid to act during tubular damage injury and recovery phases.

Apoptosis is an energy-requiring, highly regulated and genetically directed form of cell death characterized by a reduction in cytosolic volume and condensation of nuclear chromatin. Earlier studies have suggested that apoptosis contributes to the pathogenesis of acute and chronic forms of renal tubular cell injury after exposure to ischemic or toxic insult. Herein, evidence which support the role of apoptosis in the pathophysiology of renal failure are discussed.