The influence of dietary carbohydrate and fat on kidney calcification and the urinary excretion of N-acetyl-beta-glucosaminidase (EC 3.2.1.30).

1. Male Sprague-Dawley rats were fed on diets containing either sucrose or starch as the carbohydrate component. In one experiment, the diets also contained 200 g either butter or polyunsaturated margarine/kg; in a second experiment, the diets contained less fat in the form of 20 g maize oil/kg. 2. Over a period of 11 months assays were made in the urine of several ions and of the activity of the enzyme N-acetyl-β-glucosaminidase (β-2-acetamido-2-deoxy-β-D glucoside acetamidodeoxygluco-hydrolase; EC 3.2.1.30); at 13 months, examination was made of some of the abdominal viscera, especially of the kidneys. 3. In rats fed on the higher amount of fat, dietary sucrose produced a higher activity of the enzyme than did dietary starch, and a greater excretion of inorganic phosphate. 4. With both the higher and lower amounts of dietary fat, sucrose led to an increase in the weight of the liver and of the kidneys, and an increase in the concentration of calcium and of phosphate in kidney tissue. With the higher amount of fat, sucrose also produced an increase in the concentration of magnesium in the kidney. There was no difference in the concentration of any of the ions assayed in the plasma or, apart from inorganic phosphate, in the urine. 5. The kidneys of the sucrose-fed rats showed nephrocalcinosis, mostly in the cortico-medullary region, and basophilic deposits in the tubules. Attention is drawn to this unusual occurrence of nephrocalcinosis in male rats

Search for Kaluza-Klein Graviton Emission in ppˉp\bar{p} Collisions at s=1.8\sqrt{s}=1.8 TeV using the Missing Energy Signature

We report on a search for direct Kaluza-Klein graviton production in a data sample of 84 ${pb}^{-1}$ of \ppb collisions at $\sqrt{s}$ = 1.8 TeV, recorded by the Collider Detector at Fermilab. We investigate the final state of large missing transverse energy and one or two high energy jets. We compare the data with the predictions from a $3+1+n$-dimensional Kaluza-Klein scenario in which gravity becomes strong at the TeV scale. At 95% confidence level (C.L.) for $n$=2, 4, and 6 we exclude an effective Planck scale below 1.0, 0.77, and 0.71 TeV, respectively.Comment: Submitted to PRL, 7 pages 4 figures/Revision includes 5 figure

Measurement of the average time-integrated mixing probability of b-flavored hadrons produced at the Tevatron

We have measured the number of like-sign (LS) and opposite-sign (OS) lepton pairs arising from double semileptonic decays of $b$ and $\bar{b}$-hadrons, pair-produced at the Fermilab Tevatron collider. The data samples were collected with the Collider Detector at Fermilab (CDF) during the 1992-1995 collider run by triggering on the existence of $\mu \mu$ and $e \mu$ candidates in an event. The observed ratio of LS to OS dileptons leads to a measurement of the average time-integrated mixing probability of all produced $b$-flavored hadrons which decay weakly, $\bar{\chi} = 0.152 \pm 0.007$ (stat.) $\pm 0.011$ (syst.), that is significantly larger than the world average $\bar{\chi} = 0.118 \pm 0.005$.Comment: 47 pages, 10 figures, 15 tables Submitted to Phys. Rev.

Observation of the Decay B=> J/psi eta K and Search for X(3872)=> J/psi eta

We report the observation of the $B$ meson decay $B^\pm\to J/\psi \eta K^\pm$ and evidence for the decay $B^0\to J/\psi \eta K^0_S$, using {90} million $BBbar$ events collected at the \ensuremath{\Upsilon{(4S)}}\xspace resonance with the $BaBar$ detector at the PEP-II $e^+ e^-$ asymmetric-energy storage ring. We obtain branching fractions of $\cal{B}$$(B^\pm\to J/\psi \eta K^{\pm}$)=$(10.8\pm 2.3(\rm{stat.})\pm 2.4(\rm{syst.}))\times 10^{-5}$ and $\cal{B}$$(B^0\to J/\psi\eta K_{\rm{S}}^{0}$)=$(8.4\pm 2.6(\rm{stat.})\pm 2.7(\rm{syst.}))\times 10^{-5}$. We search for the new narrow mass state, the X(3872), recently reported by the Belle Collaboration, in the decay B^\pm\to X(3872)K^\pm, X(3872)\to \jpsi \eta and determine an upper limit of $\cal{B}$(B^\pm \to X(3872) K^\pm \to \jpsi \eta K^\pm) $<7.7\times 10^{-6}$ at 90% C.L.Comment: 7 pages and two figures, submitted to Phys. Rev. Lett

Measurement of time-dependent CP asymmetries in B-0 -> D-(*)+/-pi(-/+) decays and constraints on sin(2 beta+gamma)

We present a measurement of CP-violating asymmetries in fully reconstructed B-0-->D((*)+/-)pi(-/+) decays in approximately 88x10(6) Y(4S)-->B (B) over bar decays collected with the BABAR detector at the PEP-II asymmetric-energy B factory at SLAC. From a time-dependent maximum-likelihood fit we obtain the following for the CP-violating parameters: a=-0.022+/-0.038 (stat)+/-0.020 (syst), a(*)=-0.068+/-0.038 (stat)+/-0.020 (syst), c(lep)=+0.025+/-0.068 (stat)+/-0.033 (syst), and c(lep)(*)=+0.031+/-0.070 (stat)+/-0.033 (syst). Using other measurements and theoretical assumptions we interpret the results in terms of the angles of the Cabibbo-Kobayashi-Maskawa unitarity triangle, and find parallel tosin(2beta+gamma)parallel to>0.69 at 68% confidence level. We exclude the hypothesis of no CP violation [sin(2beta+gamma)=0] at 83% confidence level

Autosomal dominant hypercalciuria in a mouse model due to a mutation of the epithelial calcium channel, TRPV5

Contains fulltext : 118040.pdf (publisher's version ) (Open Access)Hypercalciuria is a major cause of nephrolithiasis, and is a common and complex disorder involving genetic and environmental factors. Identification of genetic factors for monogenic forms of hypercalciuria is hampered by the limited availability of large families, and to facilitate such studies, we screened for hypercalciuria in mice from an N-ethyl-N-nitrosourea mutagenesis programme. We identified a mouse with autosomal dominant hypercalciuria (HCALC1). Linkage studies mapped the Hcalc1 locus to a 11.94 Mb region on chromosome 6 containing the transient receptor potential cation channel, subfamily V, members 5 (Trpv5) and 6 (Trpv6) genes. DNA sequence analysis of coding regions, intron-exon boundaries and promoters of Trpv5 and Trpv6 identified a novel T to C transition in codon 682 of TRPV5, mutating a conserved serine to a proline (S682P). Compared to wild-type littermates, heterozygous (Trpv5(682P/+)) and homozygous (Trpv5(682P/682P)) mutant mice had hypercalciuria, polyuria, hyperphosphaturia and a more acidic urine, and approximately 10% of males developed tubulointerstitial nephritis. Trpv5(682P/682P) mice also had normal plasma parathyroid hormone but increased 1,25-dihydroxyvitamin D(3) concentrations without increased bone resorption, consistent with a renal defect for the hypercalciuria. Expression of the S682P mutation in human embryonic kidney cells revealed that TRPV5-S682P-expressing cells had a lower baseline intracellular calcium concentration than wild-type TRPV5-expressing cells, suggesting an altered calcium permeability. Immunohistological studies revealed a selective decrease in TRPV5-expression from the renal distal convoluted tubules of Trpv5(682P/+) and Trpv5(682P/682P) mice consistent with a trafficking defect. In addition, Trpv5(682P/682P) mice had a reduction in renal expression of the intracellular calcium-binding protein, calbindin-D(28K), consistent with a specific defect in TRPV5-mediated renal calcium reabsorption. Thus, our findings indicate that the TRPV5 S682P mutant is functionally significant and study of HCALC1, a novel model for autosomal dominant hypercalciuria, may help further our understanding of renal calcium reabsorption and hypercalciuria