148 research outputs found
Gene Expression and Distribution of Key Bone Turnover Markers in the Callus of Estrogen-Deficient, Vitamin D-Depleted Rats
An experimental rat model was used to test the hypothesis that in osteoporosis (OP) the molecular composition of the extracellular matrix in the fracture callus is disturbed. OP was induced at 10 weeks of age by ovariectomy and a vitamin D3-deficient diet, and sham-operated animals fed normal diet served as controls. Three months later a closed tibial fracture was made and stabilized with an intramedullary nail. After 3 and 6 weeks of healing, the animals were killed and the fracture calluses examined with global gene expression, in situ mRNA expression, and ultrastructural protein distribution of four bone turnover markers: osteopontin, bone sialoprotein, tartrate-resistant acid phosphatase, and cathepsin K. Global gene expression showed a relatively small number of differently regulated genes, mostly upregulated and at 3 weeks. The four chosen markers were not differently regulated, and only minor differences in the in situ mRNA expression and ultrastructural protein distribution were detected. Gene expression and composition of fracture calluses are not generally disturbed in experimental OP
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
, the London penetration depth , the
plasma frequency , and the quasiparticle scattering rate . We
find that drops exponentially rapidly with below the critical
temperature in {\em all} the superconducting samples, implying that this
behavior is a {\em signature} of high- 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} .Comment: 9 pages, REVTEX 3.
Kinetic Inductance and Penetration Depth of Thin Superconducting Films Measured by THz Pulse Spectroscopy
We measure the transmission of THz pulses through thin films of YBCO at
temperatures between 10K and 300K. The pulses possess a useable bandwidth
extending from 0.1 -- 1.5 THz (3.3 cm^-1 -- 50 cm^-1). Below T_c we observe
pulse reshaping caused by the kinetic inductance of the superconducting charge
carriers. From transmission data, we extract values of the London penetration
depth as a function of temperature, and find that it agrees well with a
functional form (\lambda(0)/\lambda(T))^2 = 1 - (T/T_c)^{\alpha}, where
\lambda(0) = 148 nm, and \alpha = 2. *****Figures available upon request*****Comment: 7 Pages, LaTe
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
Borrelia burgdorferi Requires the Alternative Sigma Factor RpoS for Dissemination within the Vector during Tick-to-Mammal Transmission
While the roles of rpoSBb and RpoS-dependent genes have been studied extensively within the mammal, the contribution of the RpoS regulon to the tick-phase of the Borrelia burgdorferi enzootic cycle has not been examined. Herein, we demonstrate that RpoS-dependent gene expression is prerequisite for the transmission of spirochetes by feeding nymphs. RpoS-deficient organisms are confined to the midgut lumen where they transform into an unusual morphotype (round bodies) during the later stages of the blood meal. We show that round body formation is rapidly reversible, and in vitro appears to be attributable, in part, to reduced levels of Coenzyme A disulfide reductase, which among other functions, provides NAD+ for glycolysis. Our data suggest that spirochetes default to an RpoS-independent program for round body formation upon sensing that the energetics for transmission are unfavorable
The impact of surgeon and patient treatment preferences in an orthopaedic trauma surgery trial
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
Meta-analysis of locking plate versus intramedullary nail for treatment of proximal humeral fractures
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