bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hurwitz Equivalence in the Braid Group B3
Authors: Ben-Itzhak T. , Teicher M. 
Published: August 2003

In this paper we prove certain Hurwitz equivalence properties of Bn. In particular we prove that for n = 3 every two Artin factorizations of [Formula: see text] of the form Hi1 ⋯ Hi6, Fj1 ⋯ Fj6 (with ik, jk ∈ {1, 2}) where {H1, H2}, {F1, F2} are frames, are Hurwitz equivalent. The proof provided here is geometric, based on a newly defined frame type. The results will be applied to the classification of algebraic surfaces up to deformation. It is already known that there exist surfaces that are diffeomorphic to each other but are not deformations of each other (Manetti's example). We construct a new invariant based on Hurwitz equivalence of factorizations, to distinguish among diffeomorphic surfaces which are not deformation of each other. The main result of this paper will help us to compute the new invariant.
Lyndon's Group is Conjugately Residually Free
Authors: Lioutikova Ekaterina 
Published: August 2003

Lyndon's group FZ[x] is the free exponential group over the ring of integral polynomials Z[x]. This group, introduced by Lyndon in the 1960s, continues to be of interest to group theorists due to its importance in the study of first-order properties of free groups, in particular, equations over free groups. One of the crucial results of Lyndon's study was that the group FZ[x] is fully residually F; i.e. for any finite collection of nontrivial elements in FZ[x] there exists a homomorphism φ : FZ[x] → F which is the identity on F and maps the given elements of FZ[x] into nontrivial elements of F. The importance of FZ[x] was further emphasized when Kharlampovich and Myasnikov proved in [3] that a finitely generated group is fully residually free if and only if it is embeddable into FZ[x]. Lyndon's group and its subgroups play a vital role in the technique employed by O. Kharlampovich and A. Myasnikov in their solution of the famous Tarski problem on the decidability of the elementary theory of a free group (see [4, 5]). In this paper, we show that Lyndon's group is conjugately residually free, i.e. it is possible to map FZ[x] to the free group F preserving the nonconjugacy of two elements. This result is a further step towards the understanding of the properties of FZ[x]; moreover, it is closely related to the problem of "lifting solutions" of equations from F to FZ[x], since our result implies that the solutions can indeed be "lifted" from F to FZ[x] for equations of the type x-1 c1 x = c2. The structure of Lyndon's group, described by A. Myasnikov and V. Remeslennikov in [8], involves an infinite sequence of free constructions of a specific type, called free extensions of centralizers. For more results on residual properties of certain types of free constructions, see also the works of Ribes, Segal and Zalesskii (for example [9]).
Logical Distinction Between Diagrammatic and Cohen–Lyndon Asphericity
Authors: Biskup Igor 
Published: August 2003

We resolve the status of the implication CLA ⇒ DA in the negative by showing that the two-dimensional model of the group presentation (a, b : a, b-1 aba-1 b-1) is DA but not CLA. This settles a question that has been addressed in [2, 7, 10, 11]. In 1941, Whitehead posed the question whether asphericity is a hereditary property for two-dimensional CW complexes. This question remains unanswered. Out of its study developed the formulation of several combinatorial properties for group presentations that are sufficient (but not necessary) for asphericity of the associated two-dimensional model. The logical relationships between these flavors of asphericity are just partially understood. In this article we show that two of these flavors of asphericity are in fact distinct. As a consequence, all of the known flavors are distinct. An argument of Lyndon and Schupp [5, III Property 10.6] shows that if a two-dimensional CW complex K is Cohen–Lyndon aspherical (CLA), then K is also diagrammatically aspherical (DA). The status of the reverse implication had been open prior to this writing. We will present an alternative proof for the implication CLA ⇒ DA and demonstrate that every spherical picture over the presentation (a, b : a, b-2 aba-1) can be reduced without insertions of dipoles, thus concluding that the presentation is DA. A straightforward argument shows that the presentation cannot be CLA. Our main tool is the theory of spherical pictures and picture moves of which we will give a short survey.
Implications of Muscle Relative Position as a Co-Determinant of Isometric Muscle Force
Authors: Maas Huub , Yucesoy Can A. , Baan Guus C. , Huijing Peter A. 
Published: August 2003

Force is transmitted from muscle fiber to bone via several pathways: (1) via the tendons (i.e. myotendinous force transmission), (2) via intermuscular connective tissue to adjacent muscles (i.e. intermuscular myofascial force transmission), (3) via structures other than muscles (i.e. extramuscular myofascial force transmission). In vivo, the position of a muscle relative to adjacent muscles changes due to differences in moment arm between synergists as well as due to the fact that some muscles span only one joint and other muscles more than one joint. The position of a muscle relative to non-muscular structures within a compartment is altered with each change of the length of the muscle.The aim of this article is to describe recent experimental results, as well as some new experimental data, that have elucidated the role of muscle relative position on force transmission from muscle. Furthermore, relevant literature is discussed, taking into consideration these new insights of muscle functioning. It is concluded that the position of a muscle relative to surrounding tissues is a major co-determinant of isometric muscle force. For muscles operating within their in vivo context of connective tissue, such position effects should be taken into account.
Randomized Clinical Trial of Therapeutic Exercise in Subacute Stroke
Authors: Duncan Pamela , Studenski Stephanie , Richards Lorie , Gollub Steven , Lai Sue Min , Reker Dean , Perera Subashan , Yates Joni , Koch Victoria , Rigler Sally , Johnson Dallas 
Published: August 2003

Background and Purpose—Rehabilitation care after stroke is highly variable and increasingly shorter in duration. The effect of therapeutic exercise on impairments and functional limitations after stroke is not clear. The objective of this study was to determine whether a structured, progressive, physiologically based exercise program for subacute stroke produces gains greater than those attributable to spontaneous recovery and usual care.Methods—This randomized, controlled, single-blind clinical trial was conducted in a metropolitan area and 17 participating healthcare institutions. We included persons with stroke who were living in the community. One hundred patients (mean age, 70 years; mean Orpington score, 3.4) consented and were randomized from a screened sample of 582. Ninety-two subjects completed the trial. Intervention was a structured, progressive, physiologically based, therapist-supervised, in-home program of thirty-six 90-minute sessions over 12 weeks targeting flexibility, strength, balance, endurance, and upper-extremity function. Main outcome measures were postintervention strength (ankle and knee isometric peak torque, grip strength), upper- and lower-extremity motor control (Fugl Meyer), balance (Berg and functional reach), endurance (peak aerobic capacity and exercise duration), upper-extremity function (Wolf Motor Function Test), and mobility (timed 10-m walk and 6-minute walk distance).Results—In the intention-to-treat multivariate analysis of variance testing the overall effect, the intervention produced greater gains than usual care (Wilk’s λ=0.64,P=0.0056). Both intervention and usual care groups improved in strength, balance, upper- and lower-extremity motor control, upper-extremity function, and gait velocity. Gains for the intervention group exceeded those in the usual care group in balance, endurance, peak aerobic capacity, and mobility. Upper-extremity gains exceeded those in the usual care group only in patients with higher baseline function.Conclusions—This structured, progressive program of therapeutic exercise in persons who had completed acute rehabilitation services produced gains in endurance, balance, and mobility beyond those attributable to spontaneous recovery and usual care.
Systematic Review of the Risks of Carotid Endarterectomy in Relation to the Clinical Indication for and Timing of Surgery
Authors: Bond R. , Rerkasem K. , Rothwell P.M. 
Published: August 2003

Background and Purpose—Reliable data on the risk of carotid endarterectomy (CEA) in relation to clinical indication and timing of surgery are necessary to target CEA more effectively, to inform patients, to adjust risks for case mix, and to understand the mechanisms of operative stroke.Methods—We performed a systematic review of all studies published from 1980 to 2000 inclusive that reported the risk of stroke and death resulting from CEA. Pooled estimates of risk by type of presenting ischemic event and time since the last event were obtained by Mantel-Haenszel meta-analysis.Results—Of 383 published studies, only 103 stratified risk by indication. Although the operative risk for symptomatic stenosis overall was higher than for asymptomatic stenosis (odds ratio [OR], 1.62; 95% confidence interval [CI], 1.45 to 1.81;P<0.00001; 59 studies), risk in patients with ocular events only tended to be lower than for asymptomatic stenosis (OR, 0.75, 95% CI, 0.50 to 1.14; 15 studies). Operative risk was the same for stroke and cerebral transient ischemic attack (OR, 1.16; 95% CI, 0.99 to 1.35;P=0.08; 23 studies) but higher for cerebral transient ischemic attack than for ocular events only (OR, 2.31; 95% CI, 1.72 to 3.12;P<0.00001; 19 studies) and for CEA for restenosis than primary surgery (OR, 1.95; 95% CI, 1.21 to 3.16;P=0.018; 6 studies). Urgent CEA for evolving symptoms had a much higher risk (19.2%, 95% CI, 10.7 to 27.8) than CEA for stable symptoms (OR, 3.9; 95% CI, 2.7 to 5.7;P<0.001; 13 studies), but there was no difference between early (<3 to 6 weeks) and late (>3 to 6 weeks) CEA for stroke in stable patients (OR, 1.13; 95% CI, 0.79 to 1.62;P=0.62; 11 studies). All observations were highly consistent across studies.Conclusions—Risk of stroke and death resulting from CEA is highly dependent on the clinical indication. Audits of risk should be stratified accordingly, and patients should be informed of the risk that relates to their presenting event.
The New Politics, History and History of Religions: The World After 11 September 2001
Authors: Antes Peter 
Published: August 2003

Many people say that the world changed after 9/11 and that nothing is as it was. What does indeed appear true is that international politics has to change and come up with a new concept with new tasks and principles appropriate to the requirements of the situation.This brief contribution aims to suggest an outline by tackling the transformation of the old concept of politics into a new politics, a politics adapted to the challenge thrown down by the events of 11 September 2001 that so shocked the world. A first draft of the tasks required will define the new principles on which these tasks are based, and will conclude with a short observation on the future political analysis of the university disciplines involved.
Religious Pluralism and Crises of Identity
Authors: Filoramo Giovanni 
Published: August 2003

At the dawn of the new millennium religion is going through some radical changes: the first of these is related to the fact that the processes of secularization have had an influence on traditional religions, are doing so today and will continue to do so, starting with Christianity in its different forms, but they have not precipitated the decline of religion as an institutional and public factor and still less the decline of faith as a private phenomenon.What we are experiencing is rather a huge process of transformation and adaptation of the religious as a private dimension and religion as an institutional factor, resulting in a profound metamorphosis of the socio-cultural situation (see Lyon, 2000). The two main elements of the change are as follows: the triumph of the mass media and consumer society and the processes of globalization (Kurz, 1995) are radically changing the very face of religion: groups and movements with a clear religious identity are involved in a relentless process that is at the same time a process of adaptation and resistance to these changes. The outcome of this process is uncertain, but there is no doubt that it is only where religions prove they are capable of using and adapting their messages of salvation to the new mass media system that they will be able to survive and maybe even spread.
The Emancipation of Thought: On the Work of Michel De Certeau
Authors: Cravetto Maria Letizia 
Published: August 2003

Today it seems to be an urgent and necessary task to return to the texts by Michel de Certeau (1925-86). Not because Michel Foucault said of him that he was ‘the best, the brightest of [his] generation’, but for reasons to do with our present thinking.Indeed, when we consider the social and political disarray of the moment, we are forced to recognize how hard it is, in periods of crisis, to clarify the changes taking place. That implies the emancipation of thought, a process that consists of an inventive interrogation of knowledge and a rigorous elaboration of understanding. This process is one that would not be subject to the dominant ideological models. In addition, thinking of the way clarification and emancipation are intertwined in the most successful intellectual constructions, some of us remember Certeau's work, whose central aim is to clarify the fundamental but stealthy transformations that abruptly emerge into the light of day and undermine the most tenacious assumptions.
Fas ligation induces IL-1β-dependent maturation and IL-1β-independent survival of dendritic cells: different roles of ERK and NF-κB signaling pathways
Authors: Guo Zhenhong , Zhang Minghui , An Huazhang , Chen Weilin , Liu Shuxun , Guo Jun , Yu Yizhi , Cao Xuetao 
Published: August 2003

AbstractThe mechanisms that underpin the intriguing capacity of Fas ligation on dendritic cells (DCs) to induce maturation and activation, rather than apoptosis, remain unclear. In the present study we confirm that Fas signaling induces both phenotypic and functional maturation of murine DCs, and we demonstrate that phenotypic maturation is associated with phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, activation of caspase-1, and secretion of interleukin-β (IL-1β). Specific inhibition of ERK1/2 diminished Fas ligation-induced caspase-1 activation, IL-1β secretion, and ensuing up-regulation of developmental markers, whereas treatment with neutralizing anti-IL-1β antibody abrogated phenotypic and functional maturation, indicating that IL-1β mediates Fas ligation-induced DC maturation in an autocrine manner. NF-κB activation was responsible for maintaining DC viability after Fas ligation. Inhibiting NF-κB did not affect either IL-1β secretion or phenotypic maturation but rather sensitized DCs to Fas-mediated apoptosis. In conclusion, positive signals originating from Fas are transduced through at least 2 different intracellular pathways in DCs, promoting not only survival but also an increase in maturation that correlates with increased antigen-presentation capability. (Blood. 2003;102:4441-4447)
Desmopressin antagonizes the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors and aspirin
Authors: Reiter Rosemarie A. , Mayr Florian , Blazicek Hannes , Galehr Elisabeth , Jilma-Stohlawetz Petra , Domanovits Hans , Jilma Bernd 
Published: August 2003

AbstractWhereas bleeding is the most frequent adverse event encountered in patients receiving glycoprotein (GP) IIb/IIIa inhibitors, there are currently no recommendations for how to treat such patients. The present study tested the hypothesis that infusion of desmopressin (DDAVP) reverses the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors (+l-aspirin). Study group 1 (10 healthy volunteers) received a DDAVP infusion to establish dose-response curves for the in vitro inhibition of platelet function by eptifibatide, abciximab, and tirofiban together with l-aspirin before and after DDAVP. In a randomized, double-blind, placebo-controlled, crossover study (group 2) volunteers received l-aspirin and a standard eptifibatide infusion. Thereafter, DDAVP or a physiologic saline infusion was given over 30 minutes. In group 1, all GPIIb/IIIa inhibitors prolonged collagen-epinephrine (CEPI) and collagen-adenosine diphosphate (CADP) closure times (CTs), measured with the platelet function analyzer 100 (PFA-100). DDAVP caused a shift in the concentration response curves to the right of all 3 GPIIb/IIIa inhibitors. In group 2, DDAVP accelerated the normalization of CADP-CT and CEPI-CT after the stop of eptifibatide infusion with a maximum effect at 1.5 hours to 2 hours. In contrast, CEPI-CT remained above normal in the placebo group for more than 4 hours. In conclusion, DDAVP accelerates normalization of the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors (+l-aspirin). (Blood. 2003;102:4594-4599)
Resistance to different classes of drugs is associated with impaired apoptosis in childhood acute lymphoblastic leukemia
Authors: Holleman Amy , Boer Monique L. den , Kazemier Karin M. , Janka-Schaub Gritta E. , Pieters Rob 
Published: August 2003

AbstractResistance of leukemic cells to chemotherapeutic agents is associated with an unfavorable outcome in pediatric acute lymphoblastic leukemia (ALL). To investigate the underlying mechanisms of cellular drug resistance, the activation of various apoptotic parameters in leukemic cells from 50 children with ALL was studied after in vitro exposure with 4 important drugs in ALL therapy (prednisolone, vincristine, l-asparaginase, and daunorubicin). Exposure to each drug resulted in early induction of phosphatidylserine (PS) externalization and mitochondrial transmembrane (Δψm) depolarization followed by caspase-3 activation and poly(ADP-ribose) polymerase (PARP) inactivation in the majority of patients. For all 4 drugs, a significant inverse correlation was found between cellular drug resistance and (1) the percentage of cells with PS externalization (&lt; .001 &lt; P &lt; .008) and (2) the percentage of cells with Δψm depolarization (.002 &lt; P &lt; .02). However, the percentage of cells with caspase-3 activation and the percentage of cells with PARP inactivation showed a significant inverse correlation with cellular resistance for prednisolone (P = .001; P = .001) and l-asparaginase (P = .01; P = .001) only. This suggests that caspase-3 activation and PARP inactivation are not essential for vincristine- and daunorubicin-induced apoptosis. In conclusion, resistance to 4 unrelated drugs is associated with defect(s) upstream or at the level of PS externalization and Δψm depolarization. This leads to decreased activation of apoptotic parameters in resistant cases of pediatric ALL. (Blood. 2003;102:4541-4546)
Monocyte-expressed urokinase inhibits vascular smooth muscle cell growth by activating Stat1
Authors: Kunigal Sateesh , Kusch Angelika , Tkachuk Natalia , Tkachuk Sergey , Jerke Uwe , Haller Hermann , Dumler Inna 
Published: August 2003

AbstractAfter vascular injury, a remodeling process occurs that features leukocyte migration and infiltration. Loss of endothelial integrity allows the leukocytes to interact with vascular smooth muscle cells (VSMCs) and to elicit “marching orders”; however, the signaling processes are poorly understood. We found that human monocytes inhibit VSMC proliferation and induce a migratory potential. The monocytes signal the VSMCs through the urokinase-type plasminogen activator (uPA). The VSMC uPA receptor (uPAR) receives the signal and activates the transcription factor Stat1 that, in turn, mediates the antiproliferative effects. These results provide the first evidence that monocytes signal VSMCs by mechanisms involving the fibrinolytic system, and they imply an important link between the uPA/uPAR-related signaling machinery and human vascular disease. (Blood. 2003;102: 4377-4383)
Induction of human γ globin gene expression by histone deacetylase inhibitors
Authors: Cao Hua , Stamatoyannopoulos George , Jung Manfred 
Published: August 2003

AbstractWe investigated the induction of human γ globin gene activity by 3 classes of histone deacetylase inhibitors: amide analogues of trichostatin A, hydroxamic acid analogues of trapoxin, and scriptaid and its analogues. The screening consisted of measuring the effects of these compounds on γ and β human gene promoter activity by using cultures of GM979 cells stably transfected with a construct containing a γ promoter linked to firefly luciferase and a β promoter linked to renilla luciferase. Compounds belonging to all 3 classes induced γ gene promoter activity in the screening assay in low micromolar concentrations. Histone deacetylase (HDAC) inhibitors increased acetylation of histone H4 and induced the expression of endogenous murine embryonic genes. They also increased the levels of γ mRNA and the frequency of fetal hemoglobin-containing erythroblasts in erythroid burst-forming unit (BFUe) cultures from healthy adult individuals. Compounds that displayed very similar degrees of inhibition of the HDAC activity in an HDAC enzymatic assay differed strikingly on their effects on γ gene promoter activity, raising the possibility of selectivity of HDACs that interact with the γ globin gene chromatin.
Involvement of reactive oxygen species in adaphostin-induced cytotoxicity in human leukemia cells
Authors: Chandra Joya , Hackbarth Jennifer , Le Son , Loegering David , Bone Nancy , Bruzek Laura M. , Narayanan Ven L. , Adjei Alex A. , Kay Neil E. , Tefferi Ayalew , Karp Judith E. , Sausville Edward A. , Kaufmann Scott H. 
Published: August 2003

Abstract
Adaphostin (NSC 680410), an analog of the tyrphostin AG957, was previously shown to induce Bcr/abl down-regulation followed by loss of clonogenic survival in chronic myelogenous leukemia (CML) cell lines and clinical samples. Adaphostin demonstrated selectivity for CML myeloid progenitors in vitro and remained active in K562 cells selected for imatinib mesylate resistance. In the present study, the mechanism of action of adaphostin was investigated in greater detail in vitro. Initial studies demonstrated that adaphostin induced apoptosis in a variety of Bcr/abl- cells, including acute myelogenous leukemia (AML) blasts and cell lines as well as chronic lymphocytic leukemia (CLL) samples. Further study demonstrated that adaphostin caused intracellular peroxide production followed by DNA strand breaks and, in cells containing wild-type p53, a typical DNA damage response consisting of p53 phosphorylation and up-regulation. Importantly, the antioxidant N-acetylcysteine (NAC) blunted these events, whereas glutathione depletion with buthionine sulfoximine (BSO) augmented them. Collectively, these results not only outline a mechanism by which adaphostin can damage both myeloid and lymphoid leukemia cells, but also indicate that this novel agent might have a broader spectrum of activity than originally envisioned. (Blood. 2003;102:4512-4519)