50 research outputs found
Conformation of a Polyelectrolyte Complexed to a Like-Charged Colloid
We report results from a molecular dynamics (MD) simulation on the
conformations of a long flexible polyelectrolyte complexed to a charged sphere,
\textit{both negatively charged}, in the presence of neutralizing counterions
in the strong Coulomb coupling regime. The structure of this complex is very
sensitive to the charge density of the polyelectrolyte. For a fully charged
polyelectrolyte the polymer forms a dense two-dimensional "disk", whereas for a
partially charged polyelectrolyte the monomers are spread over the colloidal
surface. A mechanism involving the \textit{overcharging} of the polyelectrolyte
by counterions is proposed to explain the observed conformations.Comment: 4 pages, 4 figures (6 EPS files
Recommended from our members
Charge-transfer energy in iridates: A hard x-ray photoelectron spectroscopy study
We have investigated the electronic structure of iridates in the double perovskite crystal structure containing either Ir4+ or Ir5+ using hard x-ray photoelectron spectroscopy. The experimental valence band spectra can be well reproduced using tight-binding calculations including only the Ir 5d, O 2p, and O 2s orbitals with parameters based on the downfolding of the density-functional band structure results. We found that, regardless of the A and B cations, the A2BIrO6 iridates have essentially zero O 2p to Ir 5d charge-transfer energies. Hence double perovskite iridates turn out to be extremely covalent systems with the consequence being that the magnetic exchange interactions become very long ranged, thereby hampering the materialization of the long-sought Kitaev physics. Nevertheless, it still would be possible to realize a spin-liquid system using the iridates with a proper tuning of the various competing exchange interactions
Development and Validation of an Inflammatory Bowel Diseases Monitoring Index for Use With Mobile Health Technologies
Cellular mechanisms in basic and clinical gastroenterology and hepatolog
A Nationwide 2010-2012 Analysis of U.S. Health Care Utilization in Inflammatory Bowel Diseases
Cellular mechanisms in basic and clinical gastroenterology and hepatolog
Ischemic Tolerance Protects the Rat Retina from Glaucomatous Damage
Glaucoma is a leading cause of acquired blindness which may involve an ischemic-like insult to retinal ganglion cells and optic nerve head. We investigated the effect of a weekly application of brief ischemia pulses (ischemic conditioning) on the rat retinal damage induced by experimental glaucoma. Glaucoma was induced by weekly injections of chondroitin sulfate (CS) in the rat eye anterior chamber. Retinal ischemia was induced by increasing intraocular pressure to 120 mmHg for 5 min; this maneuver started after 6 weekly injections of vehicle or CS and was weekly repeated in one eye, while the contralateral eye was submitted to a sham procedure. Glaucoma was evaluated in terms of: i) intraocular pressure (IOP), ii) retinal function (electroretinogram (ERG)), iii) visual pathway function (visual evoked potentials, (VEPs)) iv) histology of the retina and optic nerve head. Retinal thiobarbituric acid substances levels were assessed as an index of lipid peroxidation. Ischemic conditioning significantly preserved ERG, VEPs, as well as retinal and optic nerve head structure from glaucomatous damage, without changes in IOP. Moreover, ischemia pulses abrogated the increase in lipid peroxidation induced by experimental glaucoma. These results indicate that induction of ischemic tolerance could constitute a fertile avenue for the development of new therapeutic strategies in glaucoma treatment
α2-Adrenergic blockade mimics the enhancing effect of chronic stress on breast cancer progression
Experimental studies in preclinical mouse models of breast cancer have shown that chronic restraint stress can enhance disease progression by increasing catecholamine levels and subsequent signaling of ÎČ-adrenergic receptors. Catecholamines also signal α-adrenergic receptors, and greater α-adrenergic signaling has been shown to promote breast cancer in vitro and in vivo. However, antagonism of α-adrenergic receptors can result in elevated catecholamine levels, which may increase ÎČ-adrenergic signaling, because pre-synaptic α2-adrenergic receptors mediate an autoinhibition of sympathetic transmission. Given these findings, we examined the effect of α-adrenergic blockade on breast cancer progression under non-stress and stress conditions (chronic restraint) in an orthotopic mouse model with MDA-MB-231HM cells. Chronic restraint increased primary tumor growth and metastasis to distant tissues as expected, and non-selective α-adrenergic blockade by phentolamine significantly inhibited those effects. However, under non-stress conditions, phentolamine increased primary tumor size and distant metastasis. Sympatho-neural gene expression for catecholamine biosynthesis enzymes was elevated by phentolamine under non-stress conditions, and the non-selective ÎČ-blocker propranolol inhibited the effect of phentolamine on breast cancer progression. Selective α2-adrenergic blockade by efaroxan also increased primary tumor size and distant metastasis under non-stress conditions, but selective α1-adrenergic blockade by prazosin did not. These results are consistent with the hypothesis that α2-adrenergic signaling can act through an autoreceptor mechanism to inhibit sympathetic catecholamine release and, thus, modulate established effects of ÎČ-adrenergic signaling on tumor progression-relevant biology