358 research outputs found
Sous-groupes alg\'ebriques du groupe de Cremona
We give a complete classification of maximal algebraic subgroups of the
Cremona group of the plane and provide algebraic varieties that parametrize the
conjugacy classes.
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Nous donnons une classification compl\`ete des sous-groupes alg\'ebriques
maximaux du groupe de Cremona du plan et explicitons les vari\'et\'es qui
param\`etrent les classes de conjugaison.Comment: Text in French, Translated introduction, 35 pages, 1 figure, to
appear in Transform. Group
Interacting Preformed Cooper Pairs in Resonant Fermi Gases
We consider the normal phase of a strongly interacting Fermi gas, which can
have either an equal or an unequal number of atoms in its two accessible spin
states. Due to the unitarity-limited attractive interaction between particles
with different spin, noncondensed Cooper pairs are formed. The starting point
in treating preformed pairs is the Nozi\`{e}res-Schmitt-Rink (NSR) theory,
which approximates the pairs as being noninteracting. Here, we consider the
effects of the interactions between the Cooper pairs in a Wilsonian
renormalization-group scheme. Starting from the exact bosonic action for the
pairs, we calculate the Cooper-pair self-energy by combining the NSR formalism
with the Wilsonian approach. We compare our findings with the recent
experiments by Harikoshi {\it et al.} [Science {\bf 327}, 442 (2010)] and
Nascimb\`{e}ne {\it et al.} [Nature {\bf 463}, 1057 (2010)], and find very good
agreement. We also make predictions for the population-imbalanced case, that
can be tested in experiments.Comment: 10 pages, 6 figures, accepted version for PRA, discussion of the
imbalanced Fermi gas added, new figure and references adde
Action research within an elite rugby union coaching group to influence change in coach learning and pedagogic practice
The aim of this study was to investigate how I, a Welsh regional rugby academy head coach, could utilize practical collaborative action research (CAR) to influence collaboration, learning and pedagogic change within a coaching group. Action research (AR) aims to increase knowledge and improve practice in applied settings and utilises the experiences of the participants as researchers in the field. I acted as head coach and lead researcher with two other professional coaches and two sport science support staff over a three-month period. Data was collected through reflective logs, video observations of training sessions and team meetings. Whilst not without frustrations, difficulties and challenges, qualitative analysis revealed that the coaching team made significant strides in their collaboration, learning and pedagogic practice. Using CAR provided opportunities for the coaching team to develop their motivation, pedagogical knowledge, coaching practice and reflective abilities
The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation
The ability to ensure continuous availability of energy despite highly variable
supplies in the environment is a major determinant of the survival of all
species. In higher organisms, including mammals, the capacity to efficiently
store excess energy as triglycerides in adipocytes, from which stored energy
could be rapidly released for use at other sites, was developed. To orchestrate
the processes of energy storage and release, highly integrated systems operating
on several physiological levels have evolved. The adipocyte is no longer
considered a passive bystander, because fat cells actively secrete many members
of the cytokine family, such as leptin, tumor necrosis factor-alpha, and
interleukin-6, among other cytokine signals, which influence peripheral fuel
storage, mobilization, and combustion, as well as energy homeostasis. The
existence of a network of adipose tissue signaling pathways, arranged in a
hierarchical fashion, constitutes a metabolic repertoire that enables the
organism to adapt to a wide range of different metabolic challenges, such as
starvation, stress, infection, and short periods of gross energy excess
Finite Hilbert stability of (bi)canonical curves
We prove that a generic canonically or bicanonically embedded smooth curve
has semistable m-th Hilbert points for all m. We also prove that a generic
bicanonically embedded smooth curve has stable m-th Hilbert points for all m
\geq 3. In the canonical case, this is accomplished by proving finite Hilbert
semistability of special singular curves with G_m-action, namely the
canonically embedded balanced ribbon and the canonically embedded balanced
double A_{2k+1}-curve. In the bicanonical case, we prove finite Hilbert
stability of special hyperelliptic curves, namely Wiman curves. Finally, we
give examples of canonically embedded smooth curves whose m-th Hilbert points
are non-semistable for low values of m, but become semistable past a definite
threshold.
(This paper subsumes the previous submission and arXiv:1110.5960).Comment: To appear in Inventiones Mathematicae, 2012. The final publication is
available at http://www.springerlink.co
Cardiovascular Risk Associated with Interactions among Polymorphisms in Genes from the Renin-Angiotensin, Bradykinin, and Fibrinolytic Systems
Vascular fibrinolytic balance is maintained primarily by interplay of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1). Previous research has shown that polymorphisms in genes from the renin-angiotensin (RA), bradykinin, and fibrinolytic systems affect plasma concentrations of both t-PA and PAI-1 through a set of gene-gene interactions. In the present study, we extend this finding by exploring the effects of polymorphisms in genes from these systems on incident cardiovascular disease, explicitly examining two-way interactions in a large population-based study
WRAP53 Is Essential for Cajal Body Formation and for Targeting the Survival of Motor Neuron Complex to Cajal Bodies
The WRAP53 protein regulates the formation and maintenance of Cajal bodies (nuclear sub-organelles), as well as directs the recruitment of nuclear factors to Cajal bodies
Alterations of hemostatic parameters in the early development of allogeneic hematopoietic stem cell transplantation-related complications
Thrombotic events are common and potentially fatal complications in patients receiving hematopoietic stem cell transplantation (HSCT). Early diagnosis is crucial but remains controversial. In this study, we investigated the early alterations of hemostatic parameters in allogeneic HSCT recipients and determined their potential diagnostic values in transplantation-related thrombotic complications and other post-HSCT events. Results from 107 patients with allogeneic HSCT showed higher levels of plasma plasminogen activator inhibitor-1 (PAI-1), fibrinogen, and tissue-plasminogen activator (t-PA) and a lower level of plasma protein C after transplantation. No change was found for prothrombin time, antithrombin III, d-dimer, and activated partial thromboplastin time following HSCT. Transplantation-related complications (TRCs) in HSCT patients were defined as thrombotic (n = 8), acute graft-versus-host disease (aGVHD, n = 45), and infectious (n = 38). All patients with TRCs, especially the patients with thrombotic complications, presented significant increases in the mean and maximum levels of PAI-1 during the observation period. Similarly, a high maximum t-PA level was found in the thrombotic group. In contrast, apparent lower levels of mean and minimum protein C were observed in the TRC patients, especially in the aGVHD group. Therefore, the hemostatic imbalance in the early phase of HSCT, reflecting prothrombotic state and endothelial injury due to the conditioning therapy or TRCs, might be useful in the differential diagnosis of the thrombotic complication from other TRCs
Cytotoxic T lymphocytes that recognize decameric peptide sequences of retinoblastoma binding protein 1 (RBP-1) associated with human breast cancer
Retinoblastoma binding protein 1 (RBP-1) is a 143-kDa nuclear phosphoprotein that promotes cell growth by inhibiting the product of retinoblastoma tumour suppressor gene (pRB). We recently found that RBP-1 contains KASIFLK, a heptameric peptide (250–256) recognized by human antibodies and overexpressed by breast cancer cells. In the present study, we demonstrate that human T-cells stimulated with RBP-1 decameric peptides containing KASIFLK can kill human breast cancer cells. These decamers, GLQKASIFLK (247–256) and KASIFLKTRV (250–259), have anchor motifs for both HLA-A2 and HLA-A3. Peripheral blood lymphocytes from 41 normal donors were stimulated by these peptides in culture media containing 15 IU ml−1 interleukin-2, 25 IU ml−1 interleukin-7 and 500 IU ml−1 granulocyte–macrophage colony-stimulating factor. Cytotoxic activity of the T-cells was assessed against autologous B lymphoblastoid cells pulsed with each peptide. Stimulation by GLQKASIFLK generated specific cytotoxic T lymphocyte (CTL) lines from HLA-A2, A3 donors, HLA-A2 donors and HLA-A3 donors. Stimulation with KASIFLKTRV generated specific CTL lines from HLA-A2 donors. No HLA-A2−, A3− CTL line showed specific cytotoxicity against these target cells. These CTL lines were also cytotoxic against HLA-A2 and HLA-A3 breast cancer cells but not against normal fibroblastoid cell lines, normal epidermal cell lines, or a melanoma cell line. RBP-1 peptide antigens may be of clinical significance as a potential peptide vaccine against human breast cancer. © 1999 Cancer Research Campaig
Targeting of MCL-1 kills MYC-driven mouse and human lymphomas even when they bear mutations in p53
The transcriptional regulator c-MYC is abnormally overexpressed in many human cancers. Evasion from apoptosis is critical for cancer development, particularly c-MYC-driven cancers. We explored which anti-apoptotic BCL-2 family member (expressed under endogenous regulation) is essential to sustain c-MYC-driven lymphoma growth to reveal which should be targeted for cancer therapy. Remarkably, inducible Cre-mediated deletion of even a single Mcl-1 allele substantially impaired the growth of c-MYC-driven mouse lymphomas. Mutations in p53 could diminish but not obviate the dependency of c-MYC-driven mouse lymphomas on MCL-1. Importantly, targeting of MCL-1 killed c-MYC-driven human Burkitt lymphoma cells, even those bearing mutations in p53. Given that loss of one allele of Mcl-1 is well tolerated in healthy tissues, our results suggest that therapeutic targeting of MCL-1 would be an attractive therapeutic strategy for MYC-driven cancers
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