bluuebunny/crossref_metadata_2025_split huggingface dataset:
Goal-directed coagulation management of major trauma patients using thromboelastometry (ROTEM®)-guided administration of fibrinogen concentrate and prothrombin complex concentrate
Authors: Schöchl Herbert , Nienaber Ulrike , Hofer Georg , Voelckel Wolfgang , Jambor Csilla , Scharbert Gisela , Kozek-Langenecker Sibylle , Solomon Cristina 
Published: April 2010

Abstract
Introduction
The appropriate strategy for trauma-induced coagulopathy management is under debate. We report the treatment of major trauma using mainly coagulation factor concentrates.

Methods
This retrospective analysis included trauma patients who received ≥ 5 units of red blood cell concentrate within 24 hours. Coagulation management was guided by thromboelastometry (ROTEM®). Fibrinogen concentrate was given as first-line haemostatic therapy when maximum clot firmness (MCF) measured by FibTEM (fibrin-based test) was <10 mm. Prothrombin complex concentrate (PCC) was given in case of recent coumarin intake or clotting time measured by extrinsic activation test (EXTEM) >1.5 times normal. Lack of improvement in EXTEM MCF after fibrinogen concentrate administration was an indication for platelet concentrate. The observed mortality was compared with the mortality predicted by the trauma injury severity score (TRISS) and by the revised injury severity classification (RISC) score.

Results
Of 131 patients included, 128 received fibrinogen concentrate as first-line therapy, 98 additionally received PCC, while 3 patients with recent coumarin intake received only PCC. Twelve patients received FFP and 29 received platelet concentrate. The observed mortality was 24.4%, lower than the TRISS mortality of 33.7% (P = 0.032) and the RISC mortality of 28.7% (P > 0.05). After excluding 17 patients with traumatic brain injury, the difference in mortality was 14% observed versus 27.8% predicted by TRISS (P = 0.0018) and 24.3% predicted by RISC (P = 0.014).

Conclusions
ROTEM®-guided haemostatic therapy, with fibrinogen concentrate as first-line haemostatic therapy and additional PCC, was goal-directed and fast. A favourable survival rate was observed. Prospective, randomized trials to investigate this therapeutic alternative further appear warranted.
Characterization of transglutaminase type II role in dendritic cell differentiation and function
Authors: Matic Ivana , Sacchi Alessandra , Rinaldi Alessandra , Melino Gennaro , Khosla Chaitan , Falasca Laura , Piacentini Mauro 
Published: April 2010

Abstract
TG2 ablation affects DC maturation and functions leading to a decreased pro-inflammatory response upon endotoxic shock stimulation.
DCs play an essential role in the endotoxic shock, and their profound depletion occurs in septic patients and septic mice. TG2−/− mice are more resistant to the endotoxic shock induced by LPS. Here, we studied the cellular and molecular basis of this effect, analyzing the role of the enzyme in DC maturation and function. We show that TG2 is up-regulated drastically during the final, functional maturation of DCs consequent to LPS treatment. In keeping with this finding, the inhibition of the enzyme cross-linking activity determines the impairment of DC function highlighted by wide phenotypic changes associated with a reduced production of cytokines (IL-10, IL-12) after LPS treatment and a lower ability to induce IFN-γ production by naïve T cells. The in vivo analysis of DCs obtained from TG2−/− mice confirmed that the enzyme ablation leads to an impairment of DC maturation and their reduced responsiveness to LPS treatment. In fact, a marked decrease in DC death, TLR4 down-regulation, and impaired up-regulation of MHCII and CD86 were observed in TG2−/− mice. Taken together, these data suggest that TG2 plays an important role in regulating the response of DCs to LPS and could be a candidate target for treating endotoxin-induced sepsis.
CCL5 participates in early protection against Mycobacterium tuberculosis
Authors: Vesosky Bridget , Rottinghaus Erin K , Stromberg Paul , Turner Joanne , Beamer Gillian 
Published: April 2010

Abstract
CCL5-CCR5 interactions localize protective T cells to the lungs and contribute to pulmonary granuloma formation to control early infection with Mycobacterium tuberculosis.
Control of M.tb, the causative agent of TB, requires immune cell recruitment to form lung granulomas. The chemokines and chemokine receptors that promote cell migration for granuloma formation, however, are not defined completely. As immunity to M.tb manifests slowly in the lungs, a better understanding of specific roles for chemokines, in particular those that promote M.tb-protective TH1 responses, may identify targets that could accelerate granuloma formation. The chemokine CCL5 has been detected in patients with TB and implicated in control of M.tb infection. To define a role for CCL5 in vivo during M.tb infection, CCL5 KO mice were infected with a low dose of aerosolized M.tb. During early M.tb infection, CCL5 KO mice localized fewer APCs and chemokine receptor-positive T cells to the lungs and had microscopic evidence of altered cell trafficking to M.tb granulomas. Early acquired immunity and granuloma function were transiently impaired when CCL5 was absent, evident by delayed IFN-γ responses and poor control of M.tb growth. Lung cells from M.tb-infected CCL5 KO mice eventually reached or exceeded the levels of WT mice, likely as a result of partial compensation by the CCL5-related ligand, CCL4, and not because of CCL3. Finally, our results suggest that most T cells use CCR5 but not CCR1 to interact with these ligands. Overall, these results contribute to a model of M.tb granuloma formation dependent on temporal regulation of chemokines rather than on redundant or promiscuous interactions.
Un Chroniqueur Curieux de Paris Et de La Promenade: Edmond-Jean-François Barbier Et Son Journal (1718–1763)
Authors: Turcot Laurent 
Published: April 2010

Dans son journal de 1718 à 1763, Edmond-Jean-François Barbier raconte la ville de Paris et ses événements, ordinaires et extraordinaires. Le présent article se propose d'évaluer la manière dont l'avocat Barbier raconte la promenade et de montrer que son récit témoigne d'une transformation dans la manière de concevoir la promenade. Une pratique associée à la royauté et à la noblesse où prime la fonction de distinction sociale devient, au fil du journal de Barbier, une façon de découvrir et connaître sa ville afin de la raconter. Cette dimension permet de voir comment une source dite littéraire peut aider à comprendre la constitution des pratiques sociales, en l'occurrence la promenade et la transformation d'une ville.
The journal of Edmond-Jean-François Barbier, written from 1718 through 1763, can be considered both as a chronicle of Parisian everyday life and as a diary. This essay analyzes how Barbier narrates the promenade (stroll) and shows that his account illustrates a transformation in the way this pastime was conceived. Originally associated with the monarch and aristocracy, with civility and fashionable social ritual its dominant features, the promenade allowed practitioners to see and, most important, be seen. In his journal Barbier puts the promenade to a new purpose, using it to discover, become acquainted with, and narrate the city. In this light, the promenade creates a newly individualized and subjective relationship between the stroller and the city. This transformation of the stroller's appreciation for and perception of the city was made possible by the establishment of a new social role: the urban stroller. For Barbier, walking becomes an individual pursuit. Barbier's journal thus demonstrates how a literary source can be used to understand the transformation of social practice and of the urban landscape in eighteenth-century Paris.
Medaka as a model for human nonalcoholic steatohepatitis
Authors: Matsumoto Toshihiko , Terai Shuji , Oishi Toshiyuki , Kuwashiro Shinya , Fujisawa Koichi , Yamamoto Naoki , Fujita Yusuke , Hamamoto Yoshihiko , Furutani-Seiki Makoto , Nishina Hiroshi , Sakaida Isao 
Published: April 2010

SUMMARY
The global incidence of nonalcoholic steatohepatitis (NASH) is increasing and current mammalian models of NASH are imperfect. We have developed a NASH model in the ricefish medaka (Oryzias latipes), which is based on feeding the fish a high-fat diet (HFD). Medaka that are fed a HFD (HFD-medaka) exhibited hyperlipidemia and hyperglycemia, and histological examination of the liver revealed ballooning degeneration. The expression of lipogenic genes (SREBP-1c, FAS and ACC1) was increased, whereas the expression of lipolytic genes (PPARA and CPT1) was decreased. With respect to liver fatty acid composition, the concentrations of n-3 polyunsaturated fatty acids (PUFAs) and n-6 PUFAs had declined and the n-3:n-6 ratio was reduced. Treatment of HFD-medaka with the n-3 PUFA eicosapentaenoic acid (EPA) mitigated disease, as judged by the restoration of normal liver fatty acid composition and normal expression levels of lipogenic and lipolytic genes. Moreover, medaka that were fed a diet deficient in n-3 PUFAs developed NASH features. Thus, NASH can be induced in medaka by a HFD, and the proportion of n-3 PUFAs in the liver influences the progress of NASH pathology in these fish. Our model should prove helpful for the dissection of the causes of human NASH and for the design of new and effective therapies.
Increased vulnerability to psychosocial stress in heterozygous serotonin transporter knockout mice
Authors: Bartolomucci Alessandro , Carola Valeria , Pascucci Tiziana , Puglisi-Allegra Stefano , Cabib Simona , Lesch Klaus-Peter , Parmigiani Stefano , Palanza Paola , Gross Cornelius 
Published: April 2010

SUMMARYEpidemiological evidence links exposure to stressful life events with increased risk for mental illness. However, there is significant individual variability in vulnerability to environmental risk factors, and genetic variation is thought to play a major role in determining who will become ill. Several studies have shown, for example, that individuals carrying the S (short) allele of the serotonin transporter (5-HTT) gene-linked polymorphic region (5-HTTLPR) have an increased risk for major depression following exposure to stress in adulthood. Identifying the molecular mechanisms underlying this gene-by-environment risk factor could help our understanding of the individual differences in resilience to stress. Here, we present a mouse model of the 5-HTT-by-stress risk factor. Wild-type and heterozygous 5-HTT knockout male mice were subjected to three weeks of chronic psychosocial stress. The 5-HTT genotype did not affect the physiological consequences of stress as measured by changes in body temperature, body weight gain and plasma corticosterone. However, when compared with wild-type littermates, heterozygous 5-HTT knockout mice experiencing high levels of stressful life events showed significantly depressed locomotor activity and increased social avoidance toward an unfamiliar male in a novel environment. Heterozygous 5-HTT knockout mice exposed to high stress also showed significantly lower levels of serotonin turnover than wild-type littermates, selectively in the frontal cortex, which is a structure that is known to control fear and avoidance responses, and that is implicated in susceptibility to depression. These data may serve as a useful animal model for better understanding the increased vulnerability to stress reported in individuals carrying the 5-HTTLPR S allele, and suggest that social avoidance represents a behavioral endophenotype of the interaction between 5-HTT and stress.
Synthesis of a Kinetically Stabilized Homoditopic Nitrile N-Oxide Directed toward Catalyst-free Click Polymerization
Authors: Lee Young-Gi , Yonekawa Morio , Koyama Yasuhito , Takata Toshikazu 
Published: April 2010

Abstract
A kinetically stabilized homoditopic nitrile N-oxide was prepared for a catalyst-free click polymerization that efficiently proceeded via 1,3-dipolar cycloaddition with several bifunctional alkyne, alkene, and nitrile monomers. The polymerization afforded the corresponding polymers with high molecular weights and yields.
Brain tumor stem cells
Authors: Palm Thomas , Schwamborn Jens C. 
Published: April 2010

AbstractSince the end of the ‘no-new-neuron’ theory, emerging evidence from multiple studies has supported the existence of stem cells in neurogenic areas of the adult brain. Along with this discovery, neural stem cells became candidate cells being at the origin of brain tumors. In fact, it has been demonstrated that molecular mechanisms controlling self-renewal and differentiation are shared between brain tumor stem cells and neural stem cells and that corruption of genes implicated in these pathways can direct tumor growth. In this regard, future anticancer approaches could be inspired by uncovering such redundancies and setting up treatments leading to exhaustion of the cancer stem cell pool. However, deleterious effects on (normal) neural stem cells should be minimized. Such therapeutic models underline the importance to study the cellular mechanisms implicated in fate decisions of neural stem cells and the oncogenic derivation of adult brain cells. In this review, we discuss the putative origins of brain tumor stem cells and their possible implications on future therapies.
Multiple protective functions of catalase against intercellular apoptosis-inducing ROS signaling of human tumor cells
Authors: Heinzelmann Sonja , Bauer Georg 
Published: April 2010

Abstract
Tumor cells are protected against intercellular reactive oxygen species (ROS)-mediated apoptosis signaling mediated by the HOCl and/or the nitric oxide (NO)/peroxynitrite signaling pathway. We have recently shown that tumor cell resistance against HOCl signaling can be abrogated through inhibition of catalase. The protection of tumor cells against the NO/peroxynitrite signaling pathway has remained enigmatic so far. Here, we show that suboptimal inhibition of catalase by 3-aminotriazole or a monoclonal antibody against catalase, as well as partial knockdown of catalase by specific siRNA allows selective reactivation of the NO/peroxynitrite pathway in MKN 45 gastric carcinoma cells, followed by the HOCl pathway at higher inhibitor or siRNA concentrations. In SKN-MC Ewing sarcoma cells, catalase inhibition causes apoptosis induction solely based on the NO/peroxynitrite pathway. Protection against NO/peroxynitrite signaling is shown to be due to the potential of catalase to decompose peroxynitrite. The direct interaction of catalase with peroxynitrite is verified through the detection of compound I (CAT FeIV=O+·) after the interaction of peroxynitrite with catalase. In a complementary experiment, addition of catalase protects sensitive transformed cells against ROS-mediated apoptosis induction. Thus, the expression of membrane-associated catalase is sufficient to protect tumor cells against multiple intercellular ROS-mediated signaling pathways.
The mitochondria permeability transition pore complex in the brain with interacting proteins – promising targets for protection in neurodegenerative diseases
Authors: Azarashvili Tamara , Stricker Rolf , Reiser Georg 
Published: April 2010

AbstractMitochondria increasingly attract attention as control points within the mechanisms of neuronal death. Mitochondria play a central role in swinging the balance in favor of either survival or death of brain tissue. Cell death in vertebrates proceeds mostly via the mitochondrial pathway of apoptosis. Permeability transition pore (PTP) development in mitochondria is a decisive stage of apoptosis. Therefore, regulation of the permeability of both outer and inner mitochondrial membranes helps to induce neuroprotection. Through PTP control, mitochondria can to a large degree manage the intracellular calcium homeostasis, and thus control the potent death cascade initiated by excess calcium. Here we summarize the evidence for the role of mitochondria in brain cell death. We describe the involvement of the 18-kDa translocator protein (TSPO; previously called peripheral benzodiazepine receptor), and of two new mitochondrial proteins, that is, 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNP) and p42IP4(also designated centaurin α1; ADAP 1), in the control of the PTP. Furthermore, ligands of TSPO, as well as substrates of CNP, are possible modulators of PTP function. This scenario of control and regulation of PTP function might provide multiple important targets, which are suitable for developing protective strategies for neurons and non-neuronal brain cells in therapies of neurodegenerative diseases.
HLA-DR genotypes influence age at disease onset in children and juveniles with type 1 diabetes mellitus
Authors: Awa W L , Boehm B O , Kapellen T , Rami B , Rupprath P , Marg W , Becker M , Holl R W 
Published: April 2010

ObjectiveTo investigate HLA-DR genotype in association with chronological age or calendar year of disease onset and the time trend of genotype frequencies from 1969 to 2009. Additionally, to examine genotype frequency in relation to B-cell-, islet cell antibodies (ICA)-, autoantibodies to insulin-, insulinoma antigen 2 (IA2)-, glutamic acid decarboxylase-antibody positivity, thyroid antibody positivity, thyroid diseases or coeliac antibody positivity. Genotype associations with gender and ethnicity are also analyzed.Subjects and methodsHLA-typed children and juveniles (n=1445) aged ≤20 years at disease onset from the German/Austrian DPV-database were examined.χ2statistics and mixed hierarchical logistic regression models were used to compare genotype frequencies and establish associations with age at disease manifestation, autoimmune antibodies/diseases, ethnicity and time trend.ResultsSubjects aged <6 years predominantly carried the genotype HLA-DR3/4 (25.2%), whereas in subjects aged >12 years the most prevalent HLA-DR genotype was X/X (18.1%). IA2 positivity was associated with HLA-DR4/X and HLA-DR3/4 positivity (P=0.011), and hypothyroidism was linked to HLA-DR4/4 (P=0.0103). More females carried the HLA-DR4/4 genotype (18.2 vs 12.7%P=0.0048) or were thyroid antibody positive (24.5 vs 14.7%P=0.0001). Larger numbers of <6 year olds were coeliac antibody positive than >12 year olds (14.8 vs 9.1%P=0.0037). No associations between migration background and B-cell-, thyroid- or coeliac-antibody positivity, and no time trend were found.ConclusionHLA-DR genotype associated with age at disease onset, ICA positivity and hypothyroidism; female gender with thyroid antibody positivity and low age of diabetes onset with coeliac antibody positivity.
Acellular Dermal Matrix Seeded With Autologous Gingival Fibroblasts for the Treatment of Gingival Recession: A Proof‐of‐Concept Study
Authors: Jhaveri Hiral M. , Chavan Mahesh S. , Tomar Geetanjali B. , Deshmukh Vijay L. , Wani Mohan R. , Miller Preston D. 
Published: April 2010

Background: One of the most common esthetic concerns associated with periodontal tissues is gingival recession. There are multiple periodontal plastic surgery approaches documented in the literature for the treatment of such defects. With the tremendous advances being made in periodontal science and technology, tissue engineering could be considered among the latest exciting techniques for recession management.Methods: In this split‐mouth, controlled, double‐masked clinical case series, 20 sites from 10 patients with Miller Class I or II recessions affecting canines or premolars in the maxillary arch were selected. One tooth in each patient was randomized to receive either a subepithelial connective tissue graft (SCTG) (control group) or an acellular dermal matrix allograft (ADMA) seeded with autologous gingival fibroblasts (test group) under a coronally positioned flap. Clinical parameters, including recession depth, probing depth, clinical attachment level, width of keratinized tissue, attached gingiva, and plaque scores, were recorded by a calibrated examiner at baseline and 3 and 6 months. The inflammation of grafted sites was scored, and the healing time was calculated. The final esthetic outcome of treated sites was assessed by the root coverage esthetic score at the end of 6 months.Results: There were no significant differences between test and control sites for all measured clinical parameters. However, the test sites demonstrated less inflammation in the early postoperative period.Conclusion: Within the limits of this case series, the results indicate that an ADMA seeded with autologous gingival fibroblasts by tissue‐engineering technology may be explored as a substitute to an SCTG for the treatment of Miller Class I and II recession defects.
Clinical Evaluation of Single‐Stage Advanced Versus Rotated Flaps in the Treatment of Gingival Recessions
Authors: Santana Ronaldo B. , Furtado Maira B. , Mattos Carolina M.L. , de Mello Fonseca Edgard , Dibart Serge 
Published: April 2010

Background: Several procedures have been reported for the surgical correction of gingival recession (GR), including the laterally positioned flap (LPF) and the coronally advanced flap (CAF), performed as single‐ or two‐stage procedures without or with, respectively, the preceding placement and healing of a free gingival graft. The objective of the present report was to compare the efficacy of single‐stage LPF and CAF techniques in the treatment of localized maxillary GR defects.Methods: Thirty‐six patients, 10 men and 26 women, with average age of 34 ± 9 years with Miller Class I GR defects were randomly assigned to be treated by either a CAF (n = 18) or LPF (n = 18). Clinical parameters, including recession height, the width of keratinized tissue (WKT), probing depth, and vertical clinical attachment level were assessed at the mid‐buccal site. Visual plaque score and bleeding on probing were also assessed dichotomously. Clinical recordings were performed at baseline and 6 months later. Intermeasurements differences were analyzed with a chi‐square or a Wilcoxon test, with significance set at α<0.05.Results: Both flap designs were effective in treating recession defects resulting in similar improvements for percentage of root coverage, frequency of complete root coverage, and gain in clinical attachment level. The LPF resulted in significantly more gains in WKT than the CAF.Conclusion: The results obtained by CAF in the treatment of Miller Class I maxillary GR are clinically similar to the LPF albeit with more limited gains in WKT.
A Histomorphometric Study of Nanothickness and Plasma‐Sprayed Calcium–Phosphorous‐Coated Implant Surfaces in Rabbit Bone
Authors: Quaranta Alessandro , Iezzi Giovanna , Scarano Antonio , Coelho Paulo G. , Vozza Iole , Marincola Mauro , Piattelli Adriano 
Published: April 2010

Background: Novel implant surface treatments with a nanothickness bioactive ceramic deposition onto rough surfaces have been recently introduced. This study aims to evaluate histologically and histomorphometrically (bone‐to‐implant contact [BIC] and bone area fraction occupancy [BAFO]) the early bone response to plasma‐sprayed calcium–phosphate (PSCaP)‐coated versus a 300‐ to 500‐nm thickness bioactive ceramic nano‐coated plateau root form implants in a rabbit femur model.Methods: A total of 48 plateau root form implants were bilaterally placed in the distal aspect of the femur of 12 white New Zealand rabbits, remaining for 20, 30, and 60 days in vivo (n = 4 animals per time in vivo, n = 2 implants per surface per animal). After sacrifice, the implants in bone were non‐decalcified processed to slides of approximately 30 μm thickness, and were morphologically and morphometrically (BIC and BAFO) evaluated.Results: Higher degrees of bone structural organization were temporally observed for the PSCaP surface compared to the nano surface over time. BIC and BAFO was significantly higher (P <0.05) for PSCaP at all implantation times evaluated.Conclusions: Within the limits of this study it is possible to state that bioactive ceramic coatings of both thicknesses were biocompatible and osteoconductive. However, the early bone response was favored by the presence of the thicker PSCaP coating.