Anomalous Behavior Of The Complex Conductivity Of Y_{1-x}Pr_xBa_2Cu_3O_7 Observed With THz Spectroscopy

We have measured the electrodynamic properties of Y_{1-x}Pr_xBa_2Cu_3O_7 single crystal thin films as a function of temperature using coherent THz-time-domain spectroscopy. We obtain directly the complex conductivity $\sigma=\sigma_1+i\sigma_2$, the London penetration depth $\lambda_L$, the plasma frequency $\omega_p$, and the quasiparticle scattering rate $1/\tau$. We find that $1/\tau$ drops exponentially rapidly with $T$ below the critical temperature in {\em all} the superconducting samples, implying that this behavior is a {\em signature} of high-$T_c$ superconductivity. The plasma frequency decreases with increasing Pr content, providing evidence that Pr depletes carriers, leaving the CuO planes {\em underdoped}. Both the conductivity in the THz region and the dc resistivity yield evidence for the opening of a spin gap {\em above} $T_c$.Comment: 9 pages, REVTEX 3.

Anisotropic Vacuum Induced Interference in Decay Channels

We demonstrate how the anisotropy of the vacuum of the electromagnetic field can lead to quantum interferences among the decay channels of close lying states. Our key result is that interferences are given by the {\em scalar} formed from the antinormally ordered electric field correlation tensor for the anisotropic vacuum and the dipole matirx elements for the two transitions. We present results for emission between two conducting plates as well as for a two photon process involving fluorescence produced under coherent cw excitationComment: 6 pages with 2 figures, to appear in Phys. Rev. Lett. (tentative june 2000

Estrogen protects neuronal cells from amyloid beta-induced apoptosis via regulation of mitochondrial proteins and function

BACKGROUND: Neurodegeneration in Alzheimer's disease is associated with increased apoptosis and parallels increased levels of amyloid beta, which can induce neuronal apoptosis. Estrogen exposure prior to neurotoxic insult of hippocampal neurons promotes neuronal defence and survival against neurodegenerative insults including amyloid beta. Although all underlying molecular mechanisms of amyloid beta neurotoxicity remain undetermined, mitochondrial dysfunction, including altered calcium homeostasis and Bcl-2 expression, are involved in neurodegenerative vulnerability. RESULTS: In this study, we investigated the mechanism of 17β-estradiol-induced prevention of amyloid beta-induced apoptosis of rat hippocampal neuronal cultures. Estradiol treatment prior to amyloid beta exposure significantly reduced the number of apoptotic neurons and the associated rise in resting intracellular calcium levels. Amyloid beta exposure provoked down regulation of a key antiapoptotic protein, Bcl-2, and resulted in mitochondrial translocation of Bax, a protein known to promote cell death, and subsequent release of cytochrome c. E(2 )pretreatment inhibited the amyloid beta-induced decrease in Bcl-2 expression, translocation of Bax to the mitochondria and subsequent release of cytochrome c. Further implicating the mitochondria as a target of estradiol action, in vivo estradiol treatment enhanced the respiratory function of whole brain mitochondria. In addition, estradiol pretreatment protected isolated mitochondria against calcium-induced loss of respiratory function. CONCLUSION: Therefore, we propose that estradiol pretreatment protects against amyloid beta neurotoxicity by limiting mitochondrial dysfunction via activation of antiapoptotic mechanisms

Destruction of spirochete Borrelia burgdorferi round-body propagules (RBs) by the antibiotic Tigecycline

Persistence of tissue spirochetes of Borrelia burgdorferi as helices and round bodies (RBs) explains many erythema-Lyme disease symptoms. Spirochete RBs (reproductive propagules also called coccoid bodies, globular bodies, spherical bodies, granules, cysts, L-forms, sphaeroplasts, or vesicles) are induced by environmental conditions unfavorable for growth. Viable, they grow, move and reversibly convert into motile helices. Reversible pleiomorphy was recorded in at least six spirochete genera (>12 species). Penicillin solution is one unfavorable condition that induces RBs. This antibiotic that inhibits bacterial cell wall synthesis cures neither the second “Great Imitator” (Lyme borreliosis) nor the first: syphilis. Molecular-microscopic techniques, in principle, can detect in animals (insects, ticks, and mammals, including patients) helices and RBs of live spirochetes. Genome sequences of B. burgdorferi and Treponema pallidum spirochetes show absence of >75% of genes in comparison with their free-living relatives. Irreversible integration of spirochetes at behavioral, metabolic, gene product and genetic levels into animal tissue has been documented. Irreversible integration of spirochetes may severely impair immunological response such that they persist undetected in tissue. We report in vitro inhibition and destruction of B. burgdorferi (helices, RBs = “cysts”) by the antibiotic Tigecycline (TG; Wyeth), a glycylcycline protein-synthesis inhibitor (of both 30S and 70S ribosome subunits). Studies of the pleiomorphic life history stages in response to TG of both B. burgdorferi and Treponema pallidum in vivo and in vitro are strongly encouraged