47,342 research outputs found
Quantification Of Continuous Variable Entanglement With Only Two Types Of Simple Measurements
No full textHere we propose an experimental set-up in which it is possible to obtain the entanglement of a two-mode Gaussian state, be it pure or mixed, using only simple linear optical measurement devices. After a proper unitary manipulation of the two-mode Gaussian state only number and purity measurements of just one of the modes suffice to give us a complete and exact knowledge of the state's entanglement. © 2008 Elsevier Inc. All rights reserved.323921722182Bennett, C.H., DiVincenzo, D.P., (2000) Nature (London), 404, p. 247Braunstein, S.L., van Loock, P., (2005) Rev. Mod. Phys., 77, p. 513Adesso, G., Illuminati, F., (2007) J. Phys. A Math. Theor., 40, p. 7821Eisert, J., Plenio, M.B., (2003) Int. J. Quant. Inf., 1, p. 479Ekert, A.K., (1991) Phys. Rev. Lett., 67, p. 661Cohen, O., (1997) Helv. Phys. Acta, 70, p. 710Pereira, S.F., Ou, Z.Y., Kimble, H.J., (2000) Phys. Rev. A, 62, p. 042311Bennett, C.H., Wiesner, S.J., (1992) Phys. Rev. Lett., 69, p. 2881Ban, M., (1999) J. Opt. B Quantum Semiclass. Opt., 1, pp. L9Braunstein, S.L., Kimble, H.J., (2000) Phys. Rev. A, 61, p. 042302Bennett, C.H., (1993) Phys. Rev. Lett., 70, p. 1895Vaidman, L., (1994) Phys. Rev. A, 49, p. 1473Braunstein, S.L., Kimble, H.J., (1998) Phys. Rev. Lett., 80, p. 869Mintert, F., Kuś, M., Buchleitner, A., (2005) Phys. Rev. Lett., 95, p. 260502Walborn, S.P., Souto Ribeiro, P.H., Davidovich, L., Mintert, F., Buchleitner, A., (2006) Nature (London), 440, p. 1022Adesso, G., Serafini, A., Illuminati, F., (2004) Phys. Rev. Lett., 92, p. 087901Adesso, G., Serafini, A., Illuminati, F., (2004) Phys. Rev. A, 70, p. 022318Fiurášek, J., Cerf, N.J., (2004) Phys. Rev. Lett., 93, p. 063601Josse, V., Dantan, A., Bramati, A., Pinard, M., Giacobino, E., (2004) Phys. Rev. Lett., 92, p. 123601Vidal, G., Werner, R.F., (2002) Phys. Rev. A, 65, p. 032314Giedke, G., Wolf, M.M., Krüger, O., Werner, R.F., Cirac, J.I., (2003) Phys. Rev. Lett., 91, p. 107901Simon, R., (2000) Phys. Rev. Lett., 84, p. 2726noteRigolin, G., Escobar, C.O., (2004) Phys. Rev. A, 69, p. 012307notede Oliveira, M.C., (2005) Phys. Rev. A, 72, p. 012317notenoteD'Auria, V., Porzio, A., Solimeno, S., Olivares, S., Paris, M.G.A., (2005) J. Opt. B Quantum Semiclass. Opt., 7, pp. S750Banaszek, K., Wódkiewicz, K., (1996) Phys. Rev. Lett., 76, p. 4344Banaszek, K., Radzewicz, C., Wódkiewicz, K., Krasinski, J.S., (1999) Phys. Rev. A, 60, p. 674Wenger, J., Fiurášek, J., Tualle-Brouri, R., Cerf, N.J., Grangier, P., (2004) Phys. Rev. A, 70, p. 053812Ourjoumtsev, A., Tualle-Brouri, R., Grangier, P., (2006) Phys. Rev. Lett., 96, p. 213601Zambra, G., (2005) Phys. Rev. Lett., 95, p. 063602Nemoto, K., Braunstein, S.L., (2002) Phys. Rev. A, 66, p. 032306Slusher, R.E., Grangier, P., LaPorta, A., Yurke, B., Potasek, M.J., (1987) Phys. Rev. Lett., 59, p. 2566Leibfried, D., (1996) Phys. Rev. Lett., 77, p. 4281da Cunha, B.R., de Oliveira, M.C., (2007) Phys. Rev. A, 75, p. 063615Haruna, L.F., de Oliveira, M.C., Rigolin, G., (2007) Phys. Rev. Lett., 98, p. 150501Haruna, L.F., de Oliveira, M.C., Rigolin, G., (2007) Phys. Rev. Lett., 99, pp. 059902ESimon, R., Mukunda, N., Dutta, B., (1994) Phys. Rev. A, 49, p. 1567de Oliveira, M.C., (2004) Phys. Rev. A, 70, p. 03430
RESPONSE TO IBRUTINIB OF AN AGGRESSIVE IG-A LYMPHOPLASMACYTIC LYMPHOMA CARRYING THE MYD88 L265P GENE MUTATION
No full textLymphoplasmacytic lymphoma (LPL) is characterized by the prolif-
eration of B lymphocytes with varying degrees of plasmacytic differ-
entiation involving bone marrow (BM), lymph nodes or spleen.
Waldenstrom macroglobulinemia (WM) is a subset of LPL in which the
malignant clone produces an IgM paraprotein. LPL patients with
IgA/IgG paraprotein account for less than 5% of LPLs. MYD88 muta-
tion triggers survival through BTK activation in WM, a disease respond-
ing to ibrutinib, whereas non-IgM LPL has not been extensively
investigated at the molecular level. In 2014 a 66 year-old woman pre-
sented with symptomatic anemia (Hb 9 g/dl), with IgAk monoclonal
spike (1.6 g/dl) (Figure 1) and an otherwise unremarkable serum chem-
istry profile. A BM biopsy showed an 80% infiltrate by lymphocytes and lym-
phoplasmacytoid cells. A CT scan documented neither adenopathy nor
splenomegaly. Diagnosis of IgA-secreting LPL was made. The patient
was treated with RCD with minor response (Figure 1). Eighteen months
later she presented with progressive disease (Hb 8 g/dl, IgAk mono-
clonal spike 1.9 g/dl). After 5 cycles of bendamustine, the BM aspirate
showed 90% lymphoid cells. Adenopathies, splenomegaly and ascitis
were noted on a CT scan. After CHOP (3 cycles) our patient developed
thrombocytopenia (30x109/L), transfusion-dependent anemia (Hb 7.7
g/dl) and clinical deterioration (Figure 1). We performed genetic studies
with a targeted NGS approach detecting mutations in 20 genes fre-
quently mutated in CLL (ATM, BIRC3, BRAF, CDKN2A, PTEN, CDH2,
DDX3X, FBXW7, KIT, KLHL6, KRAS, MYD88, NOTCH1, NRAS,
PIK3CA, POT1, SF3B1, TP53, XPO1, ZMYM3). The MYD88 L265P mu-
tation was identified. Given the identification of MYD88 L265P in the
peripheral blood, ibrutinib appeared a reasonable option. In February
2018 our patient started ibrutinib 420 mg/die (Figure 1). Hb and PLT
improved from day +35 (Hb 10-12 g/dl, PLT > 100x109/L). In July 2018
no ascitis and 50% reduction of adenopathies and spleen were shown
on a CT scan. In April 2019 the patient is still on full dose ibrutinib with
transfusion independence and good performance status. To the best of
our knowledge this is the first case of response to ibrutinib in an ag-
gressive IgA LPL with MYD88 mutation
Operational classification and quantification of multipartite entangled states
No full textWe formalize and extend an operational multipartite entanglement measure introduced by T. R. Oliveira, G. Rigolin, and M. C. de Oliveira, Phys. Rev. A 73, 010305(R) (2006), through the generalization of global entanglement (GE) [D. A. Meyer and N. R. Wallach, J. Math. Phys. 43, 4273 (2002)]. Contrarily to GE the main feature of this measure lies in the fact that we study the mean linear entropy of all possible partitions of a multipartite system. This allows the construction of an operational multipartite entanglement measure which is able to distinguish among different multipartite entangled states that GE failed to discriminate. Furthermore, it is also maximum at the critical point of the Ising chain in a transverse magnetic field, being thus able to detect a quantum phase transition.74
Flow cytometry evaluation of urokinase-type plasminogen activator receptor (UPA-R) in acute myeloid leukemia cells.
No full textThe aim of this study was to investigate by flow cytometry the expression of the UPA-R (Urokinase type plasminogen activator receptor-CD87) on the blastic population of AML and ALL patients in order to evaluate whether the presence of this molecule could be associated with peculiar clinical and biologic features of leukemic cells. Five different monoclonal antibodies (MoAbs) (clones: 3B10#; VIM5*; 109#; 68#; 100#) were used in order to detect the distinct forms of this cellular receptor. Cell reactivity varied significantly from case to case, also depending on the MoAb used for the flow cytometry analysis. In brief, 3B10# and VIM5* MoAbs were found to be positive in more than 90% of monocytes and neutrophils from healthy subjects, while the number of positive cells was decreased (60%) using the 109# MoAb. However, either 68# and 100# MoAbs recognised only a low number of blood monocytes and neutrophils (8-20%), while lymphocytes were unreactive with all the five UPA-R MoAbs. ALL cells were found to be CD87 negative in all cases. Blasts from AML showed a heterogeneous pattern of expression for the UPA-R MoAbs, being the reactivity strictly dependent on the MoAb used, and, to a higher extent, on the degree and type of maturation of the blastic cells. The number of blasts recognising 3B10# and VIM5* MoAbs was significantly higher than that reacting with the remaining MoAbs irrespective of the FAB subtype. Since proteolytic enzymes, like UPA, play a key role in the dissolution of the extracellular matrix, and in facilitating the cell egress from the bone marrow, it is conceivable that the expression of the UPA-R could contribute to the invasive properties and, possibly, metastatic potential of leukemic cells
Optimal Management of Chronic Lymphocytic Leukemia and Economic Constraints
No full textIn this article, we carry out an overview on the management options available for chronic lymphocytic leukemia (CLL) patients and discuss possible treatment decisions, taking into account the issue of sustainability and availability. Targeted agents have shown to be superior compared with chemoimmunotherapy (CIT) in terms of progression-free survival in high-risk CLL. In the majority of studies, however, continuous treatment was compared with fixed-duration CIT and no overall survival or progression-free survival-2 (time from randomization to second progression or death) advantage could be documented. Meanwhile, a substantial financial burden on both patients and payers has raised issues about affordability and adherence to treatment. Therefore, value-based pricing of new drugs has been used to set up price negotiation policies in several countries, and fixed-duration therapy has shown to be less costly than continuous treatment. Thus, CIT continues to have a role in the treatment of CLL patients with a favorable genetic profile, that is, with a mutated IGHV gene profile and a wild-type TP53. Targeted treatment represents the preferred choice in patients with an unmutated IGHV gene configuration and/or a TP53 disruption, provided that adherence to treatment is guaranteed and bearing in mind that should costly drugs not be available for frontline treatment, new agents can be very effective as first salvage treatment
G. M. Hopkins
No full text[sound recording] / Brendan O'Grady. G. B. Shaw by Fran Frazer.; 1 sound cassette (60 minutes); Broadcast on CFCY Radio, Charlottetown, March 07 & 11, 1974.; G. B. ShawSource type: Electronic(1
OBINUTUZUMAB PLUS CHLORAMBUCIL VERSUS IBRUTINIB IN PREVIOUSLY UNTREATED PATIENTS WITH CHRONIC LYM- PHOCYTIC LEUKEMIA WITHOUT TP53 DISRUPTIONS. A CAMPUS CLL STUDY
No full textIntroduction:Although, Ibrutinib (IB) and obinutuzumab (G) have sig-
nificantly improved the treatment landscape of chronic lymphocytic
leukemia (CLL), no head-to-head comparison has been reported for IB
vsG-chlorambucil (G-CHL) in CLL patients.
Aim:The aim of this study was to compare the clinical efficacy of G-
CHL and IB in a real-life retrospective study within the Italian CLL Cam-
pus network.
Methods: Patients received ibrutinib 420 mg daily until progression
or unacceptable toxicity, while G was administrated at 100 mg on day 1,
900 mg on day 2 and 1000 mg on days 8 and 15 of the 1st cycle, then at
1000 mg for cycles 2-6. An IGHV gene sequence homology >98% was
considered as unmutated (U-IGHV), as opposed to mutated (M-IGHV).
Progression-free survival (PFS), time-to-next treatment (TTNT) and
overall survival (OS) were compared with the log-rank test. Minimal
residual disease (MRD), assessed by flow cytometry, was considered un-
detectable when <10-4(uMRD4). A propensity score matching analysis
1:1 was also done, caliper 0.2. The study was approved by the Ethic
Committee.
Results:This study included patients without TP53 disruption who re-
ceived IB (102 patients) or G-CHL at 16 hematologic centers till De-
cember 2020. Clinical features of enrolled patients are summarized in
Table 1. Patients in treated with G-CHL had a higher CIRS score
(p=0.0015), lower creatinine clearance (p=0.0041) and were enriched in
M-IGHV cases (p=0.0004). The best overall response rates in the G-CHL
and IB arms were 87%vs77%, including 25%vs6% complete remis-
sions (CR, p=0.0029). After a median follow-up of 30 months, the PFS,
TTNT and OS was 70%vs93% (p=0.0061), 88%vs97% (p=0.0043) and
91%vs96% (p=0.6642) for the G-CHL and IB arms, respectively. In the
G-CHL arm the depth of response in terms of iwCLL responses (No re-
sponsevspartial remissionvsCR: 30-month PFS, 38%, 68% and 79%;
p<0.0001) and responses with uMRD in the PB influenced PFS (data on
87 patients: 30-month PFS, 78%vs 53% for uMRD4vs MRD+,
p=0.0203). PFS and TTNT were better with IB than G-CHL in U-IGHV
(p=0.0190 and 0.0137, Figure 1A and 1C), while they were superimpos-
able for M-IGHV patients (p=0.1900 and 0.1380, Figure 1B and 1D).
Similar results were found after patients matching analysis.
Conclusions:Although continuous ibrutinib provides a better disease
control in CLL, M-IGHV patients and those achieving an uMRD4 show
a marked clinical benefit from a fixed-duration obinutuzumab-based
therapy
In patients with myelodysplastic syndromes response to rHuEPO and G-CSF treatment is related to an increase of cytogenetically normal CD34 cells.
No full textAbstract: The in vivo effect of recombinant human erythropoietin (rHuEpo) and granulocyte colony-stimulating factor (G-CSF) combined treatment on CD34(+) cells was evaluated by fluorescence in situ hybridization (FISH) in 13 myelodysplastic syndrome (MDS) patients with known cytogenetic abnormalities. After treatment, responsive patients presented a significantly lower proportion of FISH abnormal CD34(+) cells than before treatment (P = 0.003), and in comparison with unresponsive cases (P = 0.007). Response to treatment was associated with a reduced degree of apoptosis in CD34(+) cells (P = 0.021): however, no difference in telomere length was observed in responsive patients after growth factor administration. Although the number of patients analysed was relatively small, the present data suggest that, in MDS patients, response to rHuEpo and G-CSF may be related to the proliferation of karyotypically normal but potentially defective CD34(+) progenitor cell
Erratum to: Effect of moderate red wine intake on cardiac prognosis after recent acute myocardial infarction of subjects with Type 2 diabetes mellitus (Diabetic Medicine, (2006), 23, 9, (974-981), 10.1111/j.1464-5491.2006.01886.x)
No full textIn an article by Marfella et al, the author name C. Saron is incorrect and should be listed as C. Sardu. Therefore the correct author list is: R. Marfella, F. Cacciapuoti, M. Siniscalchi, F. C. Sasso, F. Marchese, F. Cinone, E. Musacchio, M. A. Marfella, L. Ruggiero, G. Chiorazzo, D. Liberti, G. Chiorazzo, G. F. Nicoletti, C. Sardu, F. D'Andrea, C. Ammendola, M. Verza and L. Coppola.In an article by Marfella et al, the author name C. Saron is incorrect and should be listed as C. Sardu. Therefore the correct author list is: R. Marfella, F. Cacciapuoti, M. Siniscalchi, F. C. Sasso, F. Marchese, F. Cinone, E. Musacchio, M. A. Marfella, L. Ruggiero, G. Chiorazzo, D. Liberti, G. Chiorazzo, G. F. Nicoletti, C. Sardu, F. D'Andrea, C. Ammendola, M. Verza and L. Coppola
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