bluuebunny/crossref_metadata_2025_split huggingface dataset:
‘The Open Church’ and ‘the Closed Church’ and the discourse on Jews in Poland between 1989 and 2000
Authors: Michlic Joanna 
Published: November 2004

This paper analyzes the attitudes of the Roman Catholic Church in Poland towards the Jews and anti-Semitism during the first decade since the political transformation of 1989–1990. After discussing briefly the main patterns of the development of the Roman Catholic Church in Poland in the modern era I examine two opposing positions within the institutionalized Roman Catholic Church—the ‘Open Church’ and the ‘Closed Church’—dthat emerged in the aftermath of Poland’s regaining full sovereignty in 1989. The ‘Open Church’ and the ‘Closed Church’ represent opposite views on the role of the church in society and on the dialogue with Jews and Judaism and on anti-Semitism.
The ‘Open Church’ is a relatively recent phenomenon that originated in the circles of the layman progressive Catholic intelligentsia in the post-1945 period. It is the first visible formation within Roman Catholic Church in Poland, which advocates dialogue with Jews and Judaism and is engaged in the eradication of anti-Semitic attitudes. The ‘Closed Church,’ which represents the formation of the ‘besieged fortress’ was historically strongly intertwined with the exclusivist ethno-nationalistic political movement of the National Democracy. The remnants of this fusion were still visible in the statements of high rank clergy in the 1990s and early 2000. This formation ignores the concept of the dialogue with Jews and Judaism advocated by Pope John Paul II and among its supporters there are still many holders of anti-Semitic views. The paper provides various examples of anti-Semitic occurrences and pronouncements of the 1990s and it discusses various initiatives aimed at the facilitating dialogue between Christians and Jews introduced by the members of the ‘Open Church’ in the 1990s. It assess the importance of the ‘Open Church’ in the eradication of anti-Semitic views and the extent of the influence of the ‘Closed Church’ on both the clergy and Catholic community at large.
Pathogen survival in the external environment and the evolution of virulence
Authors: Walther Bruno A. , Ewald Paul W. 
Published: November 2004

ABSTRACTRecent studies have provided evolutionary explanations for much of the variation in mortality among human infectious diseases. One gap in this knowledge concerns respiratory tract pathogens transmitted from person to person by direct contact or through environmental contamination. The sit‐and‐wait hypothesis predicts that virulence should be positively correlated with durability in the external environment because high durability reduces the dependence of transmission on host mobility. Reviewing the epidemiological and medical literature, we confirm this prediction for respiratory tract pathogens of humans. Our results clearly distinguish a high‐virulence high‐survival group of variola (smallpox) virus, Mycobacterium tuberculosis, Corynebacterium diphtheriae, Bordetella pertussis, Streptococcus pneumoniae, and influenza virus (where all pathogens have a mean percent mortality 0.01% and mean survival time >10 days) from a low‐virulence low‐survival group containing ten other pathogens. The correlation between virulence and durability explains three to four times of magnitude of difference in mean percent mortality and mean survival time, using both across‐species and phylogenetically controlled analyses. Our findings bear on several areas of active research and public health policy: (1) many pathogens used in the biological control of insects are potential sit‐and‐wait pathogens as they combine three attributes that are advantageous for pest control: high virulence, long durability after application, and host specificity; (2) emerging pathogens such as the‘hospital superbug’methicillin‐resistant Staphylococcus aureus (MRSA) and potential bioweapons pathogens such as smallpox virus and anthrax that are particularly dangerous can be discerned by quantifying their durability; (3) hospital settings and the AIDS pandemic may provide footholds for emerging sit‐and‐wait pathogens; and (4) studies on food‐borne and insect pathogens point to future research considering the potential evolutionary trade‐offs and genetic linkages between virulence and durability.
Classification using partial least squares with penalized logistic regression
Authors: Fort Gersende , Lambert-Lacroix Sophie 
Published: November 2004

Abstract
Motivation: One important aspect of data-mining of microarray data is to discover the molecular variation among cancers. In microarray studies, the number n of samples is relatively small compared to the number p of genes per sample (usually in thousands). It is known that standard statistical methods in classification are efficient (i.e. in the present case, yield successful classifiers) particularly when n is (far) larger than p. This naturally calls for the use of a dimension reduction procedure together with the classification one.
Results: In this paper, the question of classification in such a high-dimensional setting is addressed. We view the classification problem as a regression one with few observations and many predictor variables. We propose a new method combining partial least squares (PLS) and Ridge penalized logistic regression. We review the existing methods based on PLS and/or penalized likelihood techniques, outline their interest in some cases and theoretically explain their sometimes poor behavior. Our procedure is compared with these other classifiers. The predictive performance of the resulting classification rule is illustrated on three data sets: Leukemia, Colon and Prostate.
Availability: Software that implements the procedures and data source on which this paper focuses are freely available at http://www-lmc.imag.fr/SMS/membres/Gersende_Fort,Sophie_Lambert.html
Contact: sophie.lambert@imag.fr
INTERACTION OF NEURONAL POPULATIONS WITH DELAY: EFFECT OF FREQUENCY MISMATCH AND FEEDBACK GAIN
Authors: MENON V. 
Published: November 2004

The effect of frequency mismatch, signal transduction delay and inter-population feedback gain on the interaction of neuronal populations, mediated by long-range excitation, is investigated using physiologically realistic system parameters. Self-consistent solutions for the frequency, amplitude, and relative phase of the component signals are derived for limit cycle oscillations. These solutions predict important qualitative features including discontinuous changes in frequency of oscillation and phase reversal between symmetric and anti-symmetric limit cycles. A singularity in the solutions is used to predict parameter regions in which limit cycles do not exist. If limit cycles exist at zero delay, it is shown that limit cycles and quasi-periodic attractors alternate as a function of delay. The implications of these results for estimating physiologically meaningful delays from observed phase shifts in EEG time series are discussed. Spectral peaks for the quasi-periodic attractor occur at mν1±nν2, where the difference ν1−ν2 is approximately equal to the intrinsic population frequency mismatch δν. The cross-correlation function is amplitude modulated with a frequency equal to δν/2, indicating that the two populations slip in and out of phase with a mean correlation duration equal to 1/δν. These findings underpin the dynamical basis of delay induced “desynchronization” of oscillations reported in computer simulations. Bifurcation diagrams indicate that quasi-periodic attractors exist for a wide range of parameters in the presence of delay in long-range excitation and non-zero frequency mismatch. If the frequency mismatch is sufficiently large and the feedback gain is sufficiently small, quasi-periodic attractors exist for all delays. Delays of a few milliseconds, much smaller than the system time scale, can destabilize limit cycle oscillations. The role of synaptic change in inducing bifurcations of limit cycles to quasi-periodic attractors and vice versa is discussed. The implication of these findings for the generation of chaos in distributed neural systems is discussed.
NONLINEAR GATED EXPERTS FOR TIME SERIES: DISCOVERING REGIMES AND AVOIDING OVERFITTING
Authors: WEIGEND ANDREAS S. , MANGEAS MORGAN , SRIVASTAVA ASHOK N. 
Published: November 2004

In the analysis and prediction of real-world systems, two of the key problems are nonstationarity (often in the form of switching between regimes), and overfitting (particularly serious for noisy processes). This article addresses these problems using gated experts, consisting of a (nonlinear) gating network, and several (also nonlinear) competing experts. Each expert learns to predict the conditional mean, and each expert adapts its width to match the noise level in its regime. The gating network learns to predict the probability of each expert, given the input. This article focuses on the case where the gating network bases its decision on information from the inputs. This can be contrasted to hidden Markov models where the decision is based on the previous state(s) (i.e. on the output of the gating network at the previous time step), as well as to averaging over several predictors. In contrast, gated experts soft-partition the input space, only learning to model their region. This article discusses the underlying statistical assumptions, derives the weight update rules, and compares the performance of gated experts to standard methods on three time series: (1) a computer-generated series, obtained by randomly switching between two nonlinear processes; (2) a time series from the Santa Fe Time Series Competition (the light intensity of a laser in chaotic state); and (3) the daily electricity demand of France, a real-world multivariate problem with structure on several time scales. The main results are: (1) the gating network correctly discovers the different regimes of the process; (2) the widths associated with each expert are important for the segmentation task (and they can be used to characterize the sub-processes); and (3) there is less overfitting compared to single networks (homogeneous multilayer perceptrons), since the experts learn to match their variances to the (local) noise levels. This can be viewed as matching the local complexity of the model to the local complexity of the data.
α-Adrenergic-mediated activation of human reconstituted fibrinogen receptor (integrin αIIbβ3) in Chinese hamster ovary cells
Authors: Butta Nora , Larrucea Susana , Gonzalez-Manchon Consuelo , Alonso Sonia , Parrilla Roberto 
Published: November 2004

SummaryThis work reports the functional studies of CHO cells coexpressing α-adrenergic (αAR) and human fibrinogen (Fg) receptors (integrin αIIbβ3). Stimulation of these cells with α-agonists produced a transient rise in the free cytosolic calcium (Ca++) accompanied by enhanced binding to soluble Fg, and these effects were prevented by specific αAR antagonists. The αadrenergic-induced activation of αIIbβ3 in CHO-αIIbβ3-αAR increased the rate of adhesion and extension of cells onto Fg coated plates, and also induced a soluble Fgand αIIbβ3-dependent formation of cell aggregates, whereas no effects were observed by the stimulation of CHO-αIIbβ3 cells. α-Adrenergic antagonists, the ligand mimetic peptide RGDS, pertussis toxin (PTX), or EDTA, they all prevented the α-adrenergic stimulation of adhesion and aggregation. However, inhibition of PKC prevented the α-adrenergic stimulation of cell adherence, whereas blocking the intracellular Ca++ mobilization impeded the stimulation of cell aggregation. The α-adrenergic activation was associated with phosphorylation of a protein of ∼100 kDa and proteins of the MAPK family. The former was selectively phosphorylated by α-adrenergic stimulation whereas the latter were phosphorylated by the binding of cells to Fg and markedly intensified by α-adrenergic stimulation.
Platelet deposition on stainless steel, spiral, and braided polylactide stents
Authors: Maasilta Paula , Juuti Hanne , Nuutinen Juha-Pekka , Harjula Ari , Salminen Ulla-Stina , Lassila Riitta , Hietala Eeva-Maija 
Published: November 2004

SummaryPlatelets play a key role in (sub)acute thrombotic occlusion after stenting. We examined the possible differences between biodegradable polylactide (PLA) and stainless steel (SS) stents in platelet attachment and morphology after whole blood perfusion. PLA stents of different configurations (spiral/braided) and polycaprolactone-polylactide (PCL-PLA)-coatings, or SS stents were implanted into a PVC tube (Ø 3.2 mm), with or without precoating of the tube with type-I collagen. PPACK (30 µM)-anticoagulated blood with 3H-serotonin prelabeled platelets was perfused (flow rate: 30 ml/min, 90 s) over the stents. Platelet deposition was assessed by scintillation counting and morphology by scanning electron microscopy (SEM). To examine coagulation activation, plasma prothrombin fragments (F1+2) were measured before and after the perfusion. Protein deposition on PLA/SS stents was assessed at augmented shear forces mimicking coronary flow (rate: 60 ml/min, 60 s) under minimal anticoagulation (PPACK 1 µM). More platelets deposited on PLA stents than on SS stents under all study conditions (p <0.03). Under anticoagulation (PPACK 30 µM) the generation of F1+2 remained unaltered. Under higher flow rate and limited anticoagulation SS stents accumulated 3.27 ± 0.75 µg and PLA stents 5.25 ± 1.74 µg of protein (Mean ± SD, p <0.95). Among all biodegradable stents, the braided PLA stent coated with PCL-PLA-heparin accumulated the fewest platelets (p <0.02). In SEM, signs of platelet activation on braided heparin-coated PLA stents, when compared with uncoated braided PLA/SS stents, appeared modest. In conclusion, PCL-PLAheparin coating of biodegradable stents may enhance their hemocompatibility, expressed by less platelet deposition. Nevertheless, materials, design, and coating techniques of biodegradable stents must be further developed.
Inhibition of the endothelial cell activation by antithrombin in vitro
Authors: Uchiba Mitsuhiro , Kaun Christoph , Wojta Johann , Binder Bernd , Okajima Kenji 
Published: November 2004

SummaryWe examined whether antithrombin (AT) inhibits tumor necrosis factor (TNF)-α-induced endothelial cell activation to elucidate molecular mechanism(s) of the anti-inflammatory activity of AT. AT inhibited the increase in E-selectin expression in cultured human umbilical vein endothelial cells (HUVECs) stimulated with TNF-α. In contrast, chemically modified AT that lacks affinity for heparin did not. AT inhibited the TNF-αinduced interaction of NF-κB p65 with p300, a homologue of cAMP-responsive element binding protein (CREB)-binding protein (CBP). AT increased both intracellular levels of cAMP and binding of phosphorylated-CREB to DNA in HUVECs. Forskolin showed the inhibitory effect similar to that of AT and pretreatment of HUVECs with KT-5720, an inhibitor of protein kinase A, reversed the inhibitory effect of AT. These observations suggested that AT inhibited the TNF-α-induced increase in E-selectin expression in HUVECs by inhibiting the interaction of NF-κB with CBP/p300 through cAMP-dependent protein kinase A-induced CREB activation. This inhibitory activity of AT might depend on its binding to heparin-like substances on the endothelial cell. Such an inhibitory effect of AT on TNF-α-induced endothelial cell activation might at least partly contribute to its anti-inflammatory activity.
The indazole derivative YD-3 inhibits thrombin-induced vascular smooth muscle cell proliferation and attenuates intimal thickening after balloon injury
Authors: Guh Jih-Hwa , Liu Yi-Nan , Chang Ya-Ling , Kuo Sheng-Chu , Lee Fang-Yu , Peng Chieh-Yu , Pan Shiow-Lin , Teng Che-Ming 
Published: November 2004

SummaryProliferation of vascular smooth muscle cells (VSMCs) is postulated to be one of the key events in the pathogenesis of atherosclerosis and restenosis. We investigated whether YD-3, a lowmolecular weight, non-peptide compound, could modulate proliferation of VSMCs in vitro and restenosis after balloon angioplasty in vivo. We examined the effect of YD-3 on thrombininduced VSMC proliferation by [3H]thymidine incorporation assay. The data demonstrated that YD-3 inhibited VSMC proliferation in a concentration-dependent manner. To define the mechanisms of YD-3 action, we found that YD-3 showed a profound inhibition on thrombin-induced Ras and ERK1/2 activities by using Western blotting analysis. Furthermore, oral administration of YD-3 exhibited a marked reduction in neointimal thickness using the carotid injury model in rats. Using immunochemical detection, our experiments also revealed that YD-3 significantly suppressed expression of the PAR-1 receptor, and markedly inhibited PAR-1-activating peptide (SFLLRN)-induced VSMC proliferation in a concentration-dependent manner. These results suggest that YD-3 inhibits thrombin-induced VSMC growth via the Rasand ERK1/2-mediated signaling pathway. Moreover, YD-3 also shows a developmental potential in the treatment of atherosclerosis and restenosis after vascular injury.
Gradually glycosylated protein C mutants (Arg178Gln and Cys331Arg) are degraded by proteasome after mannose trimming
Authors: Nakahara Masako , Nakazawa Fumie , Nishio Miwako , Shibamiya Aya , Hirosawa Shinsaku , Koyama Takatoshi 
Published: November 2004

SummaryProteins that fail to attain their correct three-dimensional structure are retained in the endoplasmic reticulum (ER) and eventually degraded within the cells. We investigated the degradation of mutant proteins, using naturally occurring protein C (PC) mutants (Arg178Gln and Cys331Arg) which lead to congenital deficiencies. Chinese hamster ovary (CHO) cells were transfected with normal or mutant expression vectors. The introduction of mutation at Asn329 of an unusual sequence Asn-X-Cys for N-linked glycosylation revealed that the mutation at Cys331, which may preclude a formation of disulfide bond with Cys345, resulted in no addition of N-linked oligosaccharides at Asn329. PC mutants with 4 glycosylation sites were gradually glycosylated in the ER, and the fourth glycosylation site is less accessible for glycosylation as reported for PC in plasma.The half lives of PC178 and PC331 mutants were about 5 and 4 h, respectively. PC mutants were degraded, but the degradation was inhibited by inhibitors for proteasome. Mannose trimming of N-linked oligosaccharides after glucose removal targeted PC mutants for degradation by proteasomes. And also the inhibition of glucose trimming immediately led to mannose trimming, resulting in the accelerated degradation of PC mutants. These degradations were inhibited by mannosidase I inhibitor, kifunensine. These results indicate that the initiation of mannose trimming by mannosidase I leads to the proteasomemediated degradation of glucose-trimmed or untrimmed PC mutants.
Itch and skin rash from chocolate during fluoxetine and sertraline treatment: Case report
Authors: Cederberg Jonas , Knight Stefan , Svenson Svante , Melhus Håkan 
Published: November 2004

Abstract
Background
The skin contains a system for producing serotonin as well as serotonin receptors. Serotonin can also cause pruritus when injected into the skin. SSRI-drugs increase serotonin concentrations and are known to have pruritus and other dermal side effects.

Case presentation
A 46-year-old man consulted his doctor due to symptoms of depression. He did not suffer from any allergy but drinking red wine caused vasomotor rhinitis. Antidepressive treatment with fluoxetine 20 mg daily was initiated which was successful. After three weeks of treatment an itching rash appeared. An adverse drug reaction (ADR) induced by fluoxetine was suspected and fluoxetine treatment was discontinued. The symptoms disappeared with clemastine and betametasone treatment. Since the depressive symptoms returned sertraline medication was initiated. After approximately two weeks of sertraline treatment he noted an intense itching sensation in his scalp after eating a piece of chocolate cake. The itch spread to the arms, abdomen and legs and the patient treated himself with clemastine and the itch disappeared. He now realised that he had eaten a chocolate cake before this episode and remembered that before the first episode he had had a chocolate mousse dessert. He had never had any reaction from eating chocolate before and therefore reported this observation to his doctor.

Conclusions
This case report suggests that there may be individuals that are very sensitive to increases in serotonin concentrations. Dermal side reactions to SSRI-drugs in these patients may be due to high activity in the serotonergic system at the dermal and epidermo-dermal junctional area rather than a hypersensitivity to the drug molecule itself.
Allergic conditions and risk of hematological malignancies in adults: a cohort study
Authors: Söderberg Karin C , Hagmar Lars , Schwartzbaum Judith , Feychting Maria 
Published: November 2004

Abstract
Background
Two contradictory hypotheses have been proposed to explain the relationship between allergic conditions and malignancies, the immune surveillance hypothesis and the antigenic stimulation hypothesis. The former advocates that allergic conditions may be protective against development of cancer, whereas the latter proposes an increased risk. This relationship has been studied in several case-control studies, but only in a few cohort studies.

Methods
The association between allergic conditions and risk of developing leukemia, Hodgkin's disease, non-Hodgkin's lymphoma and myeloma was investigated in a cohort of 16,539 Swedish twins born 1886–1925. Prospectively collected, self-reported information about allergic conditions such as asthma, hay fever or eczema was obtained through questionnaires administered in 1967. The cohort was followed 1969–99 and cancer incidence was ascertained from the Swedish Cancer Registry.

Results
Hives and asthma tended to increase the risk of leukemia (relative risk [RR] = 2.1, 95% Confidence Interval [CI] 1.0–4.5 and RR = 1.6, 95% CI 0.8–3.5, respectively). There was also an indication of an increased risk of non-Hodgkin's lymphoma associated with eczema during childhood (RR = 2.3, 95% CI 1.0–5.3).

Conclusion
In contrast to most previous studies, our results do not indicate a protective effect of allergic conditions on the risk of developing hematological malignancies. Rather, they suggest that allergic conditions might increase the risk of some hematological malignancies.
Alteration of T cell immunity by lentiviral transduction of human monocyte-derived dendritic cells
Authors: Chen Xiaochuan , He Jin , Chang Lung-Ji 
Published: November 2004

Abstract
Background
Dendritic cells (DCs) are professional antigen-presenting cells that play important roles during human immunodeficiency virus type 1 (HIV-1) infection. HIV-1 derived lentiviral vectors (LVs) transduce DCs at high efficiency but their effects on DC functions have not been carefully studied. Modification of DCs using LVs may lead to important applications in transplantation, treatment of cancer, autoimmune and infectious diseases.

Results
Using DCs prepared from multiple blood donors, we report that LV transduction of DCs resulted in altered DC phenotypes and functions. Lentiviral transduction of DCs resulted in down-regulation of cell surface molecules including CD1a, co-stimulatory molecules CD80, CD86, ICAM-1, and DC-SIGN. DCs transduced with LVs displayed a diminished capacity to polarize naive T cells to differentiate into Th1 effectors. This impaired Th1 response could be fully corrected by co-transduction of DCs with LVs encoding interleukin-12 (IL-12), interferon-gamma (IFN-γ), or small interfering RNA (siRNA) targeting IL-10.

Conclusions
DCs transduced with LVs in vitro displayed diminished Th1 functions due to altered DC phenotypes. Our study addresses an important issue concerning lentiviral infection and modification of DC functions, and provides a rational approach using LVs for immunotherapy.