A Peripheral Blood Diagnostic Test for Acute Rejection in Renal Transplantation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/93759/1/j.1600-6143.2012.04253.x.pd

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

Effect of co-solutes on the physico-chemical properties of surfactant solutions

57-64Physico-chemical studies of some aqueous surfactant solutions were carried out by employing conductance, surface tension and spectrofluorometric techniques. From conductivity and surface tension measurements, critical micelle concentration (CMC), counter-ion association (α), equivalent conductance at infinite dilution (٨0), surface excess concentration (), minimum area per molecule (Amin), surface pressure at CMC ( CMC), thermodynamic properties of micellization (Gºmic, Hºmic, Sºmic) and adsorption (Gºads, Hºads and Sºads) have been obtained for an anionic [bis (2-ethylhexyl) sulphosuccinate sodium salt (AOT)], a cationic [cetyl trimethyl ammonium bromide (CTAB)] and a nonionic [polyethylene (23) lauryl ether (Brij-35)] surfactant solutions. Effect of mixing co-solutes (dioxane and glycerol) on the physico-chemical properties of surfactant systems at 298.15, 308.15 and 318.15 K has been investigated. Surfactants micellar characteristics and their interaction with co-solutes were also investigated by fluorescence measurements of solutions using pyrene as a fluorescence probe

Studies on quenching/antiquenching effect of some organic compounds on luminescence of CdS colloids

2746-2748Effect of some amines and phenol on luminescence intensity of CdS colloids has been studied. The additives with electron donors groups (-NH2 or -OH) bind to lower energy trap sites which are involved in non-radiative decay, causing enhanced fluorescence

Cystinosin-LKG rescues cystine accumulation and decreases apoptosis rate in cystinotic proximal tubular epithelial cells

Nephropathic cystinosis is a lysosomal storage disease that is caused by mutations in the CTNS gene encoding a cystine/proton symporter cystinosin and an isoform cystinosin-LKG which is generated by an alternative splicing of exon 12. We have investigated the physiological role of the cystinosin-LKG that is widely expressed in epithelial tissues

Cysteamine restores glutathione redox status in cultured cystinotic proximal tubular epithelial cells

Contains fulltext : 95780.pdf (publisher's version ) (Closed access)Recent evidence implies that impaired metabolism of glutathione has a role in the pathogenesis of nephropathic cystinosis. This recessive inherited disorder is characterized by lysosomal cystine accumulation and results in renal Fanconi syndrome progressing to end stage renal disease in the majority of patients. The most common treatment involves intracellular cystine depletion by cysteamine, delaying the development of end stage renal disease by a yet elusive mechanism. However, cystine depletion does not arrest the disease nor cures Fanconi syndrome in patients, indicating involvement of other yet unknown pathologic pathways. Using a newly developed proximal tubular epithelial cell model from cystinotic patients, we investigate the effect of cystine accumulation and cysteamine on both glutathione and ATP metabolism. In addition to the expected increase in cystine and defective sodium-dependent phosphate reabsorption, we observed less negative glutathione redox status and decreased intracellular ATP levels. No differences between control and cystinosis cell lines were observed with respect to protein turnover, albumin uptake, cytosolic and mitochondrial ATP production, total glutathione levels, protein oxidation and lipid peroxidation. Cysteamine treatment increased total glutathione in both control and cystinotic cells and normalized cystine levels and glutathione redox status in cystinotic cells. However, cysteamine did not improve decreased sodium-dependent phosphate uptake. Our data implicate that cysteamine increases total glutathione and restores glutathione redox status in cystinosis, which is a positive side-effect of this agent next to cystine depletion. This beneficial effect points to a potential role of cysteamine as anti-oxidant for other renal disorders associated with enhanced oxidative stress

The pathogenesis of cystinosis: mechanisms beyond cystine accumulation.

Contains fulltext : 87778.pdf (publisher's version ) (Closed access)Renal proximal tubules are highly sensitive to ischemic and toxic insults and are affected in diverse genetic disorders, of which nephropathic cystinosis is the most common. The disease is caused by mutations in the CTNS gene, encoding the lysosomal cystine transporter cystinosin, and is characterized by accumulation of cystine in the lysosomes throughout the body. In the majority of the patients, this leads to generalized proximal tubular dysfunction (also called DeToni-Debre-Fanconi syndrome) in the first year and progressive renal failure during the first decade. Extrarenal organs are affected by cystinosis as well, with clinical symptoms manifesting mostly after 10 yr of age. The cystine-depleting agent cysteamine significantly improves life expectancy of patients with cystinosis, but offers no cure, pointing to the complexity of the disease mechanism. In this review, current knowledge on the pathogenesis of cystinosis is described and placed in perspective of future research.1 november 201