bluuebunny/crossref_metadata_2025_split huggingface dataset:
The end-Frasnian mass extinction in the Eifel Mountains, Germany: new insights from organic matter composition and preservation
Authors: Hartkopf-Fröder C. , Kloppisch M. , Mann U. , Neumann-Mahlkau P. , Schaefer R. G. , Wilkes H. 
Published: November 2007

Abstract
The Büdesheimer Bach borehole in the Prüm Syncline, Eifel Mountains, Germany encountered upper Frasnian and lowermost Famennian sediments including the Upper Kellwasser Horizon (UKW) and a limestone-dominated sequence (‘LKW’) which can be correlated with the Lower Kellwasser Horizon in other sections. The palynofacies is characterized by a high abundance of amorphous organic matter (AOM), prasinophytes, miospores and acritarchs indicative of a fully marine, rather distal and oxygen-deficient environment. AOM and a low sterane/hopane ratio suggest that cyanobacteria were important primary producers and that bacterial reworking and oxidation influenced the organic matter composition resulting in reduced total organic carbon (TOC) contents and lower hydrogen index (HI) values. The ‘LKW’ and the UKW can be distinguished from the adjacent units by the abundant prasinophytes and some geochemical parameters (e.g. higher HI, lower pristane/phytane ratio, lower aryl isoprenoid ratio) but these differences are not highly significant. However, the sediments between these two horizons show an increased input of bacteria and terrestrial plant material as a result of the regression that follows after the deposition of the Lower Kellwasser Horizon. Aryl isoprenoids originating from diagenetic transformation of the carotenoid isorenieratene, which are markers for anoxygenic photosynthetic green sulphur bacteria, have been detected in all samples but are more abundant in the ‘LKW’ and UKW. Hence, photic zone anoxia seems to have been more pronounced during deposition of these horizons, supporting the view that widespread anoxia was an important trigger of the massive end-Frasnian biotic decline.
Hypercoagulability after partial liver resection
Authors: Denninger Marie Hélène , Dondero Federica , Saada Véronique , Venisse Laurence , Huisse Marie Geneviève , Belghiti Jacques , Guillin Marie Claude , Bezeaud Annie 
Published: November 2007

SummaryOne concern of living donor liver transplantation remains the risk of morbidity and/or mortality for the donors, including the risk of postoperative thrombosis. We studied the coagulation changes after partial liver resection in l2 living donors and eight patients with non-malignant hepatic tumors (controls) and searched for potential predictive markers of thrombotic complications. Thrombosis (pulmonary embolism and portal vein thrombosis) developed in two donors and two controls. In donors and controls, we observed an early postoperative decrease in coagulation inhibitors protein C and antithrombin together with an increase in factor VIII and von Willebrand factor, which both persisted when prothrombin time had returned to normal. Dysregulation in the haemostatic system was confirmed by increased prothrombotic markers, with a 10- to 30-fold increase in thrombin-antithrombin complexes and moderate increase( 1.5- to 2.0-fold) in sP-Selectin. No difference between donors and controls was observed and the data were pooled for comparison of patients with (n=4) versus without (n=16) thrombosis. Thrombin-antithrombin complexes were significantly higher in the thrombosis group, on day 1 (28.8 vs. 13.5 μg/l, p = 0.027) and day 2 (52.3 vs. 9.3 μg/l, p = 0.013). sPselectin was also significantly higher in the thrombosis group on day 2 (103 vs. 53 ng/ml, p= 0.044) and day 4 (116 vs. 58 ng/ml, p= 0.026) after surgery. Our study indicates that improvement of thromboprophylaxis in partial liver resection is needed. It also suggests that thrombin-antithrombin complexes and sP-selectin could serve as early biological predictors of thrombotic complications in the post-operative period.
Role of haemorheological factors in patients with retinal vein occlusion
Authors: Mannini Lucia , Marcucci Rossella , Bolli Paola , Sodi Andrea , Giambene Barbara , Menchini Ugo , Gensini Gian Franco , Abbate Rosanna , Prisco Domenico , Sofi Francesco 
Published: November 2007

SummaryRetinal vein occlusion (RVO) is an important cause of permanent visual loss. Hyperviscosity, due to alterations of blood cells and plasma components, may play a role in the pathogenesis of RVO. Aim of this case-control study was to evaluate the possible association between haemorheology and RVO. In 180 RVO patients and in 180 healthy subjects comparable for age and gender we analysed the whole haemorheological profile: [whole blood viscosity (WBV), erythrocyte deformability index (DI), plasma viscosity (PLV), and fibrinogen]. WBV and PLV were measured using a rotational viscosimeter, whereas DI was measured by a microcomputer-assisted filtrometer. WBV at 0.512 sec-1 and 94.5 sec-1 shear rates as well as DI, but not PLV, were found to be significantly different in patients as compared to healthy subjects. At the logistic univariate analysis,a significant association between the highest tertiles of WBV at 94.5 sec-1 shear rate (OR:4.91,95%CI 2.95–8.17;p<0.0001),WBV at 0.512 sec-1 shear rate (OR: 2.31, 95%CI 1.42–3.77; p<0.0001), and the lowest tertile of DI (OR: 0.18, 95%CI 0.10–0.32; p<0.0001) and RVO was found. After adjustment for potential confounders,the highest tertiles of WBV at 0.512 sec-1 shear rate (OR: 3.23, 95%CI 1.39–7.48; p=0.006),WBV at 94.5 sec-1 shear rate (OR: 6.74, 95%CI 3.06–14.86; p<0.0001) and the lowest tertile of DI (OR:0.20,95%CI 0.09–0.44,p<0.0001) remained significantly associated with the disease. In conclusion,our data indicate that an alteration of haemorheological parameters may modulate the susceptibility to the RVO, by possibly helping to identify patients who may benefit from haemodilution.
The influence of established genetic variation in the haemostatic system on clinical restenosis after percutaneous coronary interventions
Authors: Pons Douwe , Monraats Pascalle , de Maat Moniek , Pires Nuno , Quax Paul , van Vlijmen Bart , Rosendaal Frits , Zwinderman Aeilko , Doevendans Pieter , Waltenberger Johannes , de Winter Robbert , Tio René , Frants Rune , van der Laarse Arnoud , Vander Wall Ernst , Jukema Wouter 
Published: November 2007

SummarySince activation of the haemostatic system is an important feature of the wound healing response triggered by arterial injury, variations in genes involved in thrombus formation may play a role in restenosis after percutaneous coronary interventions (PCI). Therefore, our aim was to examine the relationship between polymorphisms that are known to play a role in the haemostatic system and the risk of clinical restenosis in the GENetic DEterminants of Restenosis (GENDER) study,a multicenter prospective study design that enrolled 3,104 consecutive patients after successful PCI. Target vessel revascularization (TVR) was the primary endpoint. All patients were genotyped for six polymorphisms in the Factor II, Factor V, Factor VII and PAI-1 genes. The PAI-1 4G variant was associated with an increased risk ofTVR. When compared to 5G/5G homozygotes, heterozygous patients were at higher risk for TVR (HR: 1.46, 95%CI: 1.05–2.03), whereas patients with the 4G/4G genotype had an even further increased risk (HR: 1.69, 95%CI: 1.19–2.41). In contrast, the factor V 506Gln (factor V Leiden) amino acid substitution was associated with a decreased risk of TVR (HR: 0.41, 95%CI: 0.19–0.86). Our findings indicate that polymorphisms in the factorV and PAI-1 genes may play a role in the process of restenosis.
Alternative splicing of platelet cyclooxygenase-2 mRNA in patients after coronary artery bypass grafting
Authors: Censarek Petra , Steger Gerhard , Paolini Carla , Hohlfeld Thomas , Grosser Tilo , Zimmermann Norbert , Fleckenstein Diana , Schrör Karsten , Weber Artur-Aron 
Published: November 2007

SummaryRecently, we cloned from platelet mRNA a novel cyclooxygenase (COX)-2 splice variant, designated COX-2a, which is characterized by a partial deletion of exon 5. Preliminary studies of mRNA distribution of COX-2 isoforms in platelets from coronary artery bypass grafting (CABG) patients showed a variable increase in COX-2a mRNA expression after cardiac surgery. Thus, we assessed whether this variant may play a functional role in these patients. We report a marked (about 20346-fold) increase in the expression of COX-2a mRNA after CABG. Evidence is presented that ribosomal frame-shifting may correct the coding sequence resulting in the expression of a full-length COX-2a pro-tein. In addition, a reading frame-corrected COX-2a mutant (COX-2aΔG) was generated by site-directed mutagenesis and expressed in COS-7 cells using an adenoviral expression system. However, COX-2a protein was not active in terms of prostaglandin formation. Thus, alternative mRNA splicing might represent an intriguing posttranscriptional mechanism to oppose a transcriptional activation of the COX-2 gene. Evolutionary, this mechanism may prevent COX-2-dependent thromboxane synthesis in the platelet, which would potentiate the likelihood of thrombosis; pharmacologically, this mechanism would prevent an aspirin-insensitive pathway of thromboxane formation.
Localization of the low-density lipoprotein receptor-related protein regions involved in binding to the A2 domain of coagulation factor VIII
Authors: Makogonenko Evgeny , Andersen Olav , Mikhailenko Irina , Ananyeva Natalya , Khrenov Alexey , Shima Midori , Strickland Dudley , Saenko Evgueni , Sarafanov Andrey 
Published: November 2007

SummaryCatabolism of coagulation factorVIII (FVIII) is mediated by lowdensity lipoprotein receptor-related protein (LRP). The ligandbinding sites of LRP are formed by complement-type repeats (CR), and CR clusters II and IV bind most of LRP ligands. FVIII contains two major LRP-binding sites located in the A2 and A3 domains. This study was aimed to identify specific complementtype repeats of LRP involved in interaction with the A2 site and to probe their functional importance in A2 catabolism. We generated individual LRP clusters II, III and IV, along with nine overlapping CR triplets encompassing clusters II and IV in a baculovirus expression system and studied their interaction with isolated A2. In surface plasmon resonance (SPR) assay, A2 bound to clusters II and IV with KDs 22 and 39 nM, respectively, and to the majority of CR triplets with affinities in the range of KDs 25–90 nM. Similar affinities were determined for A2 interaction with a panel of CR doublets overlapping cluster II (CR 3–4, 4–5, 5–6 6–7 and 7–8). These LRP fragments inhibited the binding of 125I-A2 to LRP in solid-phase assay,LRP-mediated internalization of 125I-A2 in cell culture and 125I-A2 clearance from the mouse circulation. Point mutations of critical A2 residues of the LRPbinding site resulted in differential reduction or abolishment of its binding to LRP fragments. We conclude that A2 interacts with LRP via multiple binding sites spanning CR 3–8 in cluster II and CR 23–29 in cluster IV, and the minimal A2-binding unit of LRP is formed by two adjacent CR.
Determinants of platelet conjugate formation with polymorphonuclear leukocytes or monocytes in whole blood
Authors: Costanzo Simona , Vohnout Branislav , Iacoviello Licia , Gaetano Giovanni de , Izzi Benedetta , Pampuch Agnieszka , Cerletti Chiara 
Published: November 2007

SummaryFollowing preliminary in-vitro experiments, platelet-leukocyte conjugates and their determinants were evaluated in citrated whole blood from 349 subjects (209 women, age 16–92 years) randomly recruited from the general population. Platelet activation by ADP/collagen but not leukocyte stimulation by fMLP or LTB4 resulted in formation of platelet conjugates with PMN or monocytes. In the population study, mixed cell conjugates, platelet P-selectin and leukocyte CD11b were measured by flow cytometry both at baseline and after in-vitro stimulation with ADP/collagen. The latter significantly increased platelet conjugates with either PMN or monocytes, platelet P-selectin and leukocyte CD11b expression. Platelet count significantly correlated with platelet-PMN, platelet-monocyte conjugates and P-selectin both at baseline and upon stimulation. In all conditions, both conjugate levels correlated with each other, when adjusted for gender, age and platelet count. Age correlated with platelet-PMN conjugate numbers in basal and stimulated conditions and with basal P-selectin. ADP/collagen stimulation resulted in higher P-selectin and conjugates values in women. Among risk factors, a significant correlation was found between conjugate and glucose levels. In conclusion, the presence and formation in whole blood from a large population of plateletleukocyte conjugates reflects primary platelet – but not leukocyte – activation and varies with gender, age, platelet count and blood glucose.
Interleukin 6 plasma levels predict with high sensitivity and specificity coronary stenosis detected by coronary angiography
Authors: Cefalù Angelo Baldassare , Vadalà Anna , Barbagallo Carlo Maria , Rizzo Manfredi , Pernice Vincenzo , Minà Mariangela , Fayer Francesca , Cerasola Giovanni , Notarbartolo Alberto , Noto Davide , Cottone Santina , Averna Maurizio Rocco 
Published: November 2007

SummaryIn recent years new biomarkers able to measure the coronary atherosclerotic burden have been investigated. The aim of the present study was: i) to measure plasma levels of four biomarkers: C reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), interleukin 6 (IL-6), 8-isosprostane (8-ISO),in a series of patients undergoing coronary angiography; ii) to assess the power of the biomarkers to predict critical coronary stenosis detected by angiography. The study population consisted of a group of 438 subjects undergoing coronary angiography; 160 patients with 0, 1, 2, or 3 critical vessels were selected, and biomarkers plasma levels were measured in plasma samples obtained before the procedure. The most predictive biomarker was then assayed in 120 patients with critical stenosis and 120 unmatched patients without stenosis. CRP, sICAM-1, IL-6 and 8-ISO plasma levels increased with the number of diseased vessels. All biomarkers were good predictors of critical stenosis (receiver-operator-curve [ROC] areas; CRP=0.880, IL-6=0.936, sICAM-1=0.907, 8-ISO=0.873). IL-6 was confirmed in an expanded sample of 240 subjects to be the best predictor with a ROC area=0.959.With a threshold of 3.6 ng/l,a 100% sensitivity (120/120) and a 90% specificity (108/120) was observed. In conclusion, IL-6, sICAM-1, CRP and 8-ISO are predictive of CAD. IL-6 predicts critical coronary stenosis with the highest sensitivity and specificity.
Plasma cholesteryl ester transfer protein and blood coagulability
Authors: Deguchi Hiroshi , Fernndez José , Griffin John 
Published: November 2007

SummaryDyslipoproteinemia involving low levels of high density lipoprotein (HDL) is linked to venous thrombosis in young male adults and to recurrence of venous thrombosis in patients who have experienced a previous unprovoked venous thrombosis episode. Plasma cholesteryl ester transfer protein (CETP) modulates HDL metabolism and some lipoproteins can affect blood coagulation reactions with either procoagulant or anticoagulant effects. Hence, we evaluated relationships between the mass of CETP and blood coagulability in plasma samples from 39 normal healthy adults. For clotting initiated by dilute tissue factor or factor XIa,clotting times significantly correlated with CETP antigen levels. Thus,coagulation initiated by either the extrinsic or intrinsic coagulation pathway is positively correlated with CETP plasma levels. When added to plasma, a recombinant CETP preparation dose-dependently shortened factor Xa-1-stage clotting times, showing that it augmented procoagulant activity in plasma. In reaction mixtures containing purified factors Xa and Va and prothrombin, the recombinant CETP preparation dose-dependently increased prothrombin activation, suggesting it specifically enhances prothrombinase activity. Thus, our data highlight a previously unknown positive relationship between CETP plasma levels and blood coagulability that might relate to risks for thrombotic events.
Situating Texas School Finance Policy in a CRT Framework: How “Substantially Equal” Yields Racial Inequity
Authors: Alemán Enrique 
Published: November 2007

Purpose: The purpose of this article is to conduct a critical race policy analysis of Texas school finance policy. This empirical article examines three chapters of the Texas education code (TEC) and identifies the racial effects that the school funding system has on seven majority-Mexican American school districts. Methodology: Critical Race Theory (CRT) and Latina/o Critical (LatCrit) theoretical frameworks are employed in this article in which race and property are highlighted as concepts central to the analysis. The methodology allows for a critical perspective on history and the racial effects of policy to be outlined. First, a historical analysis of race and racism, schooling, and politics in Texas contextualizes the debate over school finance equity. Second, an analysis of the effects that the school finance system has on communities of color is completed. Analysis and Findings: An examination of primarily 2002—2003 school finance data, Texas Supreme Court opinions, and TEC indicates that majority-Mexican American school districts are disadvantaged by Texas school finance policy. Whether it is operational, maintenance, or facilities funding, the school finance system institutes inequity.
Camouflaging Power and Privilege: A Critical Race Analysis of University Diversity Policies
Authors: Iverson Susan VanDeventer 
Published: November 2007

Background: Universities continue to undertake a range of initiatives to combat inequities and build diverse, inclusive campuses. Diversity action plans are a primary means by which U.S. postsecondary institutions articulate their professed commitment to an inclusive and equitable climate for all members of the university and advance strategies to meet the challenges of an increasingly diverse society. Purpose: To examine, using critical race theory, how discourses of diversity, circulating in educational policies, reflect and produce particular realities for people of color on university campuses. Data Collection and Analysis: Data were collected from 20 U.S. land-grant universities. Line-by-line analysis, employing inductive and deductive coding strategies, was conducted to identify images of diversity and the problems and solutions related to diversity as represented in 21 diversity action plans generated throughout a 5-year period (1999-2004). Findings: Analysis reveals four predominant discourses shaping images of people of color: access, disadvantage, marketplace, and democracy. These discourses construct images of people of color as outsiders, at-risk victims, commodities, and change agents. These discourses coalesce to produce realities that situate people of color as outsiders to the institution, at risk before and during participation in education, and dependent on the university for success in higher education. Using critical race theory as an analytic framework, this article aims to enhance understanding about how racial inequality is reproduced through educational policies. Conclusions: The findings suggest that well-intentioned attempts to create a more inclusive campus may unwittingly reinforce practices that support exclusion and inequity.
Protein kinase C–associated kinase is required for NF-κB signaling and survival in diffuse large B-cell lymphoma cells
Authors: Kim Sang-Woo , Oleksyn David W. , Rossi Randall M. , Jordan Craig T. , Sanz Ignacio , Chen Luojing , Zhao Jiyong 
Published: November 2007

AbstractDiffuse large B-cell lymphoma (DLBCL) is an aggressive and the most common type of non-Hodgkin lymphoma. Despite recent advances in treatment, less than 50% of the patients are cured with current multiagent chemotherapy. Abnormal NF-κB activity not only contributes to tumor development but also renders cancer cells resistant to chemotherapeutic agents. Identifying and targeting signaling molecules that control NF-κB activation in cancer cells may thus yield more effective therapy for DLBCL. Here, we show that while overexpression of protein kinase C–associated kinase (PKK) activates NF-κB signaling in DLBCL cells, suppression of PKK expression inhibits NF-κB activity in these cells. In addition, we show that NF-κB activation induced by B cell–activating factor of tumor necrosis factor family (BAFF) in DLBCL cells requires PKK. Importantly, we show that knockdown of PKK impairs the survival of DLBCL cells in vitro and inhibits tumor growth of xenografted DLBCL cells in mice. Suppression of PKK expression also sensitizes DLBCL cells to treatment with chemotherapeutic agents. Together, these results indicate that PKK plays a pivotal role in the survival of human DLBCL cells and represents a potential target for DLBCL therapy.
Regulation of tight junction assembly and epithelial morphogenesis by the heat shock protein Apg-2
Authors: Aijaz Saima , Sanchez-Heras Elena , Balda Maria S , Matter Karl 
Published: November 2007

Abstract

Background
Tight junctions are required for epithelial barrier formation and participate in the regulation of signalling mechanisms that control proliferation and differentiation. ZO-1 is a tight junction-associated adaptor protein that regulates gene expression, junction assembly and epithelial morphogenesis. We have previously demonstrated that the heat shock protein Apg-2 binds ZO-1 and thereby regulates its role in cell proliferation. Here, we addressed the question whether Apg-2 is also important for junction formation and epithelial morphogenesis.

Results
We demonstrate that depletion of Apg-2 by RNAi in MDCK cells did not prevent formation of functional tight junctions. Similar to ZO-1, however, reduced expression of Apg-2 retarded de novo junction assembly if analysed in a Ca-switch model. Formation of functional junctions, as monitored by measuring transepithelial electrical resistance, and recruitment of tight and adherens junction markers were retarded. If cultured in three dimensional extracellular matrix gels, Apg-2 depleted cells, as previously shown for ZO-1 depleted cells, did not form hollow polarised cysts but poorly organised, irregular structures.

Conclusion
Our data indicate that Apg-2 regulates junction assembly and is required for normal epithelial morphogenesis in a three-dimensional culture system, suggesting that Apg-2 is an important regulator of epithelial differentiation. As the observed phenotypes are similar to those previously described for ZO-1 depleted cells and depletion of Apg-2 retards junctional recruitment of ZO-1, regulation of ZO-1 is likely to be an important functional role for Apg-2 during epithelial differentiation.