4,369 research outputs found
CP and charge asymmetries at CDF
We present CDF results on the branching fractions and time-integrated direct
CP asymmetries for B0 and B0s decay modes into pairs of charmless charged
hadrons (pions or kaons). We report also the first observation of B0s->DsK mode
and the measurement of its branching fraction.Comment: Proceedings of The 2007 Europhysics Conference on High Energy Physics
Manchester, England 19-25 July 2007. To be published electronically by IoP
Journals. FERMILAB-CONF-07-590-E. Nov 2007. 3p
Pair-wise decoherence in coupled spin qubit networks
Experiments involving phase coherent dynamics of networks of spins, such as
echo experiments, will only work if decoherence can be suppressed. We show
here, by analyzing the particular example of a crystalline network of Fe8
molecules, that most decoherence typically comes from pairwise interactions
(particularly dipolar interactions) between the spins, which cause `correlated
errors'. However at very low T these are strongly suppressed. These results
have important implications for the design of quantum information processing
systems using electronic spins.Comment: 4 pages, 4 figures. Final PRL versio
Hypoxia up-regulates SERPINB3 through HIF-2\u3b1 in human liver cancer cells.
SERPINB3 is a cysteine-proteases inhibitor up-regulated in a significant number of cirrhotic patients carrying hepatocellular carcinoma (HCC) and recently proposed as a prognostic marker for HCC early recurrence. SERPINB3 has been reported to stimulate proliferation, inhibit apoptosis and, similar to what reported for hypoxia, to trigger epithelial-to-mesenchymal transition (EMT) and increased invasiveness in liver cancer cells. This study has investigated whether SERPINB3 expression is regulated by hypoxia-related mechanisms in liver cancer cells. Exposure of HepG2 and Huh7 cells to hypoxia up-regulated SERPINB3 transcription, protein synthesis and release in the extracellular medium. Hypoxia-dependent SERPINB3 up-regulation was selective (no change detected for SERPINB4) and operated through hypoxia inducible factor (HIF)-2\u3b1 (not HIF-1\u3b1) binding to SERPINB3 promoter, as confirmed by chromatin immuno-precipitation assay and silencing experiments employing specific siRNAs. HIF-2\u3b1-mediated SERPINB3 up-regulation under hypoxic conditions required intracellular generation of ROS. Immuno-histochemistry (IHC) and transcript analysis, performed in human HCC specimens, revealed co-localization of the two proteins in liver cancer cells and the existence of a positive correlation between HIF-2\u3b1 and SERPINB3 transcript levels, respectively. Hypoxia, through HIF-2\u3b1-dependent and redox-sensitive mechanisms, up-regulates the transcription, synthesis and release of SERPINB3, a molecule with a high oncogenic potential
Medicinal Plants of Chile: Evaluation of their Anti-Trypanosoma cruzi Activity
San Martin, J (San Martin, Jose). Univ Talca, Inst Biol Vegetal & Biotecnol, Talca, ChileThe extracts of several plants of Central Chile exhibited anti-Trypanosoma cruzi trypomastigotes activity. Most active extracts were those obtained from Podanthus ovatifolius, Berberis microphylla, Kageneckia oblonga, and Drimys winteri. The active extract of Drimys winteri (IC50 51.2 mu g/mL) was purified and three drimane sesquiterpenes were obtained: polygodial, drimenol, and isodrimenin. Isodrimenin and drimenol were found to be active against the trypomastigote form of T cruzi with IC50 values of 27.9 and 25.1 mu M, respectivel
Vitamin D deficiency in myotonic dystrophy type 1
Myotonic dystrophy type 1 (DM1) is a multisystemic
disorder affecting, among others, the endocrine
system, with derangement of steroid hormones functions.
Vitamin D is a steroid recognized for its role in calcium
homeostasis. In addition, vitamin D influences muscle
metabolism by genomic and non-genomic actions,
including stimulation of the insulin-like-growth-factor 1
(IGF1), a major regulator of muscle trophism. To verify
the presence of vitamin D deficit in DM1 and its possible
consequences, serum 25-hydroxyvitamin D (25(OH)D),
calcium, parathormone (PTH), and IGF1 levels were
measured in 32 DM1 patients and in 32 age-matched
controls. Bone mineral density (BMD) and proximal
muscle strength were also measured by DXA and a
handheld dynamometer, respectively. In DM1 patients,
25(OH)D levels were reduced compared to controls, and a
significant decrease of IGF1 was also found. 25(OH)D
levels inversely correlated with CTG expansion size,
while IGF1 levels and muscle strength directly correlated
with levels of 25(OH)D lower than 20 and 10 ng/ml,
respectively. A significantly higher percentage of DM1
patients presented hyperparathyroidism as compared to
controls. Calcium levels and BMD were comparable
between the two groups. Oral administration of cholecalciferol
in 11 DM1 patients with severe vitamin D deficiency
induced a normal increase of circulating 25(OH)D,
ruling out defects in intestinal absorption or hepatic
hydroxylation. DM1 patients show a reduction of circulating
25(OH)D, which correlates with genotype and may
influence IGF1 levels and proximal muscle strength. Oral
supplementation with vitamin D should be considered in
DM1 and might mitigate muscle weakness
A case of PANDAS treated with tetrabenazine and tonsillectomy
PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) is a rare clinical syndrome characterized by the presence of tics, Tourette syndrome, obsessive-compulsive disorder, or chorea in the context of an imme- diately precedent streptococcal infection. In this report, we describe the case of an 11-year-old boy who developed PANDAS with severe choreic movements. The criteria for PANDAS diagnosis were met. Moreover, serum antibrain antibodies were present. The patient was initially treated with tetrabenazine 12.5 mg twice daily with remission of the neurological symptoms. Subsequently, the patient underwent tonsillectomy and has been asymptomatic since, with antistreptolysin O titer levels in range
The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis
The complement system is a major component of humoral innate immunity, acting as a first line of defense against microbes via opsonization and lysis of pathogens. However, novel roles of the complement system in inflammatory and immunological processes, including in cancer, are emerging. Endometriosis (EM), a benign disease characterized by ectopic endometrial implants, shows certain unique features of cancer, such as the capacity to invade surrounding tissues, and in severe cases, metastatic properties. A defective immune surveillance against autologous tissue deposited in the peritoneal cavity allows immune escape for endometriotic lesions. There is evidence that the glandular epithelial cells found in endometriotic implants produce and secrete the complement component C3. Here, we show, using immunofluorescence and RT-qPCR, the presence of locally synthesized C3 in the ectopic endometriotic tissue, but not in the eutopic tissue. We generated a murine model of EM via injection of minced uterine tissue from a donor mouse into the peritoneum of recipient mice. The wild type mice showed greater amount of cyst formation in the peritoneum compared to C3 knock-out mice. Peritoneal washings from the wild type mice with EM showed more degranulated mast cells compared to C3 knock-out mice, consistent with higher C3a levels in the peritoneal fluid of EM patients. We provide evidence that C3a participates in an auto-amplifying loop leading to mast cell infiltration and activation, which is pathogenic in EM. Thus, C3 can be considered a marker of EM and its local synthesis can promote the engraftment of the endometriotic cysts
Aperiodic dynamical decoupling sequences in presence of pulse errors
Dynamical decoupling (DD) is a promising tool for preserving the quantum
states of qubits. However, small imperfections in the control pulses can
seriously affect the fidelity of decoupling, and qualitatively change the
evolution of the controlled system at long times. Using both analytical and
numerical tools, we theoretically investigate the effect of the pulse errors
accumulation for two aperiodic DD sequences, the Uhrig's DD UDD) protocol [G.
S. Uhrig, Phys. Rev. Lett. {\bf 98}, 100504 (2007)], and the Quadratic DD (QDD)
protocol [J. R. West, B. H. Fong and D. A. Lidar, Phys. Rev. Lett {\bf 104},
130501 (2010)]. We consider the implementation of these sequences using the
electron spins of phosphorus donors in silicon, where DD sequences are applied
to suppress dephasing of the donor spins. The dependence of the decoupling
fidelity on different initial states of the spins is the focus of our study. We
investigate in detail the initial drop in the DD fidelity, and its long-term
saturation. We also demonstrate that by applying the control pulses along
different directions, the performance of QDD protocols can be noticeably
improved, and explain the reason of such an improvement. Our results can be
useful for future implementations of the aperiodic decoupling protocols, and
for better understanding of the impact of errors on quantum control of spins.Comment: updated reference
Generalized Connective Tissue Disease in Crtap-/- Mouse
Mutations in CRTAP (coding for cartilage-associated protein), LEPRE1 (coding for prolyl 3-hydroxylase 1 [P3H1]) or PPIB (coding for Cyclophilin B [CYPB]) cause recessive forms of osteogenesis imperfecta and loss or decrease of type I collagen prolyl 3-hydroxylation. A comprehensive analysis of the phenotype of the Crtap-/- mice revealed multiple abnormalities of connective tissue, including in the lungs, kidneys, and skin, consistent with systemic dysregulation of collagen homeostasis within the extracellular matrix. Both Crtap-/- lung and kidney glomeruli showed increased cellular proliferation. Histologically, the lungs showed increased alveolar spacing, while the kidneys showed evidence of segmental glomerulosclerosis, with abnormal collagen deposition. The Crtap-/- skin had decreased mechanical integrity. In addition to the expected loss of proline 986 3-hydroxylation in α1(I) and α1(II) chains, there was also loss of 3Hyp at proline 986 in α2(V) chains. In contrast, at two of the known 3Hyp sites in α1(IV) chains from Crtap-/- kidneys there were normal levels of 3-hydroxylation. On a cellular level, loss of CRTAP in human OI fibroblasts led to a secondary loss of P3H1, and vice versa. These data suggest that both CRTAP and P3H1 are required to maintain a stable complex that 3-hydroxylates canonical proline sites within clade A (types I, II, and V) collagen chains. Loss of this activity leads to a multi-systemic connective tissue disease that affects bone, cartilage, lung, kidney, and skin
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