bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stosunki Polski ze Stolicą Apostolską i kwestia konkordatu z 1993 roku (prezentacja książki)
Authors: Kowalczyk Józef 
Published: October 2014

The relations between Poland and the Holy See and the question of the concordat of 1993. A presentation of a book “The Concordat between the Holy See and the Republic of Poland 1993/1998”
During the course of John Paul II’s pontificate the moral authority of the Holy See considerably increased in the world, the consequence of which was the considerable development of diplomatic relations with the Vatican. In 1918 Poland began to regulate the relations with the Holy See through concordats. Unfortunately, soon after the Second World War there began a period of unfriendly and frequently hostile policy of the authorities toward the Church. With the passing of years the authorities of the People’s Republic of Poland arrived at a conclusion that the Catholic faith in Poland is a force to be reckoned with. Therefore the representatives of state authorities conducted talks with the Vatican, and the representatives of the Holy See made contacts with the authorities of the Polish Bishops’ Conference and the Office of Religious Denominations. The emergence of the social movement known as “Solidarność” [Solidarity] and a whole array of phenomena which took place in the 1980s brought about the change of the system in our Fatherland and facilitated the construction of a democratic state. This in turn brought about the establishment of diplomatic relations with the Holy See, the appointment of the ambassador of Poland at the Holy See and the appointment of the apostolic nuntio in Poland. On 3 April 1993 negotiations began about the elaboration and arrangement of the text of the concordat. The text that was agreed upon was accepted by the Council of Ministers and the Holy See, and it was signed on 28 July 1993. The ratification and the exchange of ratification documents took place in 1998. The principal aim of Archbishop Kowalczyk’s book is not to conduct an exegesis of the content of specific paragraphs of the concordat (this issue is treated in other publications), but to show the reader the way both entities of international law went through negotiations which lead them to the formulation of the specific paragraphs of this agreement.
Patient Report Improves Posthospital Discharge Event Capture in Total Joint
Replacement: A Novel Approach to Capturing All Posthospital Event Data
Authors: Harrold Leslie , Pascal Scott , Lewis Courtland , O'Keefe Regis , Pellegrini Vincent , Allison Jeroan , Ayers David , Franklin Patricia 
Published: October 2014

Introduction: Current approaches to quantifying total posthospital complications
and readmissions following surgical procedures are limited because the United States
does not have a single health care payer. Patients seek posthospital care in varied
locations, yet hospitals can only quantify those returning to the same facility. Seeking
information directly from patients about health care utilization following hospital
discharge holds promise to provide data that is missing for surgeons and health care
systems.Background: Because total joint replacement (TJR) is the most common and costly
elective surgical hospitalization, we examined the concordance between patients’
self-report of potential short-term complications and their readmissions and our review
of medical records in the initial hospital and surrounding facilities.Methods: Patients
undergoing primary total hip or knee replacement from July 1, 2011, through December 3,
2012, at a large site participating in a national cohort of TJR patients were
identified. Patients completed a six-month postoperative survey regarding emergency
department (ED), day surgery (DS), or inpatient care for possible medical or mechanical
post-TJR complications. We reviewed inpatient and outpatient medical records from all
regional facilities and examined the sensitivity, specificity, and positive- and
negative predictive values for patient self-report and medical records.Findings: There
were 413 patients who had 431 surgeries and completed the six-month questionnaire.
Patients reported 40 medical encounters (9 percent) including ED, DS or inpatient care,
of which 20 percent occurred at hospitals different from the initial surgery. Review of
medical records revealed 9 additional medical encounters that patients had not mentioned
including five hospitalizations following surgery and four ED visits. Overall patient
self-report of ED, DS, and inpatient care for possible complications was both sensitive
(82 percent) and specific (100 percent). The positive predictive value was 100 percent
and negative predictive value 98 percent.Discussion: Patient self-report of posthospital
events was accurate. Substantial numbers of patients required care at outlying hospitals
(not where the TJR occurred).Conclusion: Methods that directly engage patients can
augment current posthospital utilization surveillance to assure complete data.
Accounting for the turn towards secession in Catalonia
Authors: Dowling Andrew 
Published: October 2014

Abstract
Since the mid-2000s, the Catalan secessionist movement has become a key protagonist in the territory’s political landscape, moving from the margins to become the axis of political dispute. This article contextualizes this change and argues that its emergence can be accounted for by a series of structural changes, which include the evolution of Catalonia’s weight within Spain, identity shifts and comparative economic decline. The discrediting of once dominant political ideologies has intensified following the post-2008 economic crisis, which has resulted in a moderate pro-independence movement successfully subsuming a full range of grievances.
Insulin‐like growth factor‐1 stimulates regulatory T cells and suppresses autoimmune disease
Authors: Bilbao Daniel , Luciani Luisa , Johannesson Bjarki , Piszczek Agnieszka , Rosenthal Nadia 
Published: October 2014

AbstractThe recent precipitous rise in autoimmune diseases is placing an increasing clinical and economic burden on health systems worldwide. Current therapies are only moderately efficacious, often coupled with adverse side effects. Here, we show that recombinant human insulin‐like growth factor‐1 (rhIGF‐1) stimulates proliferation of both human and mouse regulatory T (Treg) cells in vitro and when delivered systemically via continuous minipump, it halts autoimmune disease progression in mouse models of type 1 diabetes (STZ and NOD) and multiple sclerosis (EAE) in vivo. rhIGF‐1 administration increased Treg cells in affected tissues, maintaining their suppressive properties. Genetically, ablation of the IGF‐1 receptor specifically on Treg cell populations abrogated the beneficial effects of rhIGF‐1 administration on the progression of multiple sclerotic symptoms in the EAE model, establishing a direct effect of IGF‐1 on Treg cell proliferation. These results establish systemically delivered rhIGF‐1 as a specific, effective stimulator of Treg cell action, underscoring the clinical feasibility of manipulating natural tolerance mechanisms to suppress autoimmune disease.
Neuronal Development in Caenorhabditis elegans Is Regulated by Inhibition of an MLK MAP Kinase Pathway
Authors: Baker Scott T , Turgeon Shane M , Tulgren Erik D , Wigant Jeanne , Rahimi Omeed , Opperman Karla J , Grill Brock 
Published: October 2014

Abstract
We show that loss-of-function mutations in kinases of the MLK-1 pathway (mlk-1, mek-1, and kgb-1/jnk) function cell-autonomously in neurons to suppress defects in synapse formation and axon termination caused by rpm-1 loss of function. Our genetic analysis also suggests that the phosphatase PPM-1, like RPM-1, is a potential inhibitor of kinases in the MLK-1 pathway.
Isolation of bacterial fish pathogen Aeromonas hydrophila and therapeutic effects of medicinal plants on its invasion
Authors: Tareq-Uz-Zaman Md. , Chowdhury Md. Bazlur Rashid , Dipu Md. Rasheduzzaman Khan 
Published: October 2014

Aeromonas hydrophila, a bacterial pathogen, was isolated form Pangasius hypophthalmus. For pathogenicity test, different doses were injected intramuscularly in Barbonymus gonionotus. Crude extracts were prepared from various parts Azadirachta indica, Curcuma longa, C. zedoaria, and Callotropis gigentia and applied to B. gonionotus for 7 days. Bath treatment was done up to their tolerance level and well ventilation was confirmed for aeration and 50% water was exchanged daily. Minimum inhibitory dose was detected as 7 mg/ml. High inhibitory effect was observed in case of A. indica and mixed extract of A. indica and C. gigentia. Both A. indica and C. gigentia showed the best result with 90-95% recovery of infected fish at a dose of 7 mg/l. C. zedoaria showed moderate to weak effect with 50-60% recovery at the same dose. The present study showed that medicinal plants would be an effective control measure against A. hydrophila.
Fracture of a BIOLOX Delta Ceramic Femoral Head Articulating Against a Polyethylene Liner
Authors: Heiner Anneliese D. , Mahoney Craig R. 
Published: October 2014

Case:
A forty-five-year-old woman underwent primary total hip arthroplasty with a 36-mm BIOLOX delta ceramic femoral head articulating against a polyethylene liner. She presented with hip pain at eighteen months postoperatively, two months after being in a bicycle accident; fracture of the femoral head was diagnosed.

Conclusion:
The possibility of a ceramic femoral head fracture should be decreased with use of the latest generation of ceramic material, a ceramic-on-polyethylene articulation rather than a ceramic-on-ceramic articulation, and a larger head size, all of which applied to this case. Taper-trunnion compatibility and correct intraoperative handling of the components are also essential.
Pitfalls in Single-Bundle Anterior Cruciate Ligament Reconstruction with the Flexible Reamer System
Authors: Lee Seung-Yup , Kim Jae-Gyoon , Jang Ki-Mo , Lim Hong-Chul 
Published: October 2014

Case:
We present two cases of anterior cruciate ligament reconstruction with use of the flexible reamer system. In both patients, the starting reamers were broken during femoral reaming. The location of the breaks was approximately 60 mm from the tip of the reamer, which is the transitional zone between the proximal and distal portions of the reamer.

Conclusion:
We believe that several conditions could have resulted in abnormal stress concentration on the flexible reamers, including engagement of the flexible reamer with a physeal scar or the posterior cortex, an inappropriate flexion angle of the knee, and acute bending of the flexible pin.
Osteomyelitis as a Late Complication of Percutaneous Pinning of a Supracondylar Fracture of the Distal Part of the Humerus
Authors: Pulos Nicholas , Carrigan Robert B. 
Published: October 2014

Case:
We report a case of an eleven-year-old boy who presented to our clinic with a draining wound from the left elbow. He had a history of a left closed supracondylar humeral fracture that had been treated with closed reduction and percutaneous pinning at five years of age, and he subsequently developed late-onset osteomyelitis. The patient was successfully treated with surgical irrigation and debridement, followed by intravenous and oral antibiotics.

Conclusion:
Dormant osteomyelitis should be considered in the differential diagnosis for any child who presents with elbow symptoms with a prior history of a supracondylar humeral fracture that has been treated with closed reduction and percutaneous pinning.
« Juste valeur » et « prix de modèle » : une comparaison internationale de la structure des portefeuilles de	trading et du ratio « rentabilité »
Authors: Clerc Laurent , Marteau Didier 
Published: October 2014

Mise en cause dès le déclenchement de la crise financière en 2007, en raison de sa dimension procyclique, la « juste valeur » reste, sept ans plus tard, le mode unique de valorisation comptable du portefeuille de négociation ( trading ) des banques. Cette situation soulève une question importante pour le régulateur dans la perspective de la prévention du risque systémique. Elle part de l’observation que l’évaluation comptable des portefeuilles de trading au « prix de marché » est en fait très marginale par rapport à l’évaluation au « prix de modèle ». Dans cet article, nous mesurons tout d’abord la répartition de la valorisation des portefeuilles de trading , entre le mark to market et le mark to model . Nous calculons ensuite une mesure du return on equity (ROE) des activités de trading, en rapportant le résultat brut au montant des fonds propres réglementaires assis sur la value at risk (VaR), et constatons que ce ROE est non seulement anormalement élevé mais également qu’il est resté stable depuis le déclenchement de la crise. En outre, nous établissons que la rentabilité des activités de trading des banques est positivement et significativement corrélée au poids du mark to model dans le total du portefeuille, et en particulier au poids des actifs de « niveau 3 ».	Classification JEL : G15, G21, G28, M48.
Programmed Death-1 Impairs Secondary Effector Lung CD8+ T Cells during Respiratory Virus Reinfection
Authors: Erickson John J. , Rogers Meredith C. , Hastings Andrew K. , Tollefson Sharon J. , Williams John V. 
Published: October 2014

Abstract
Reinfections with respiratory viruses are common and cause significant clinical illness, yet precise mechanisms governing this susceptibility are ill defined. Lung Ag-specific CD8+ T cells (TCD8) are impaired during acute viral lower respiratory infection by the inhibitory receptor programmed death-1 (PD-1). To determine whether PD-1 contributes to recurrent infection, we first established a model of reinfection by challenging B cell–deficient mice with human metapneumovirus (HMPV) several weeks after primary infection, and found that HMPV replicated to high titers in the lungs. A robust secondary effector lung TCD8 response was generated during reinfection, but these cells were more impaired and more highly expressed the inhibitory receptors PD-1, LAG-3, and 2B4 than primary TCD8. In vitro blockade demonstrated that PD-1 was the dominant inhibitory receptor early after reinfection. In vivo therapeutic PD-1 blockade during HMPV reinfection restored lung TCD8 effector functions (i.e., degranulation and cytokine production) and enhanced viral clearance. PD-1 also limited the protective efficacy of HMPV epitope–specific peptide vaccination and impaired lung TCD8 during heterotypic influenza virus challenge infection. Our results indicate that PD-1 signaling may contribute to respiratory virus reinfection and evasion of vaccine-elicited immune responses. These results have important implications for the design of effective vaccines against respiratory viruses.
Lyn Deficiency Leads to Increased Microbiota-Dependent Intestinal Inflammation and Susceptibility to Enteric Pathogens
Authors: Roberts Morgan E. , Bishop Jennifer L. , Fan Xueling , Beer Jennifer L. , Kum Winnie W. S. , Krebs Danielle L. , Huang Morris , Gill Navkiran , Priatel John J. , Finlay B. Brett , Harder Kenneth W. 
Published: October 2014

Abstract
The Lyn tyrosine kinase governs the development and function of various immune cells, and its dysregulation has been linked to malignancy and autoimmunity. Using models of chemically induced colitis and enteric infection, we show that Lyn plays a critical role in regulating the intestinal microbiota and inflammatory responses as well as protection from enteric pathogens. Lyn−/− mice were highly susceptible to dextran sulfate sodium (DSS) colitis, characterized by significant wasting, rectal bleeding, colonic pathology, and enhanced barrier permeability. Increased DSS susceptibility in Lyn−/− mice required the presence of T but not B cells and correlated with dysbiosis and increased IFN-γ+ and/or IL-17+ colonic T cells. This dysbiosis was characterized by an expansion of segmented filamentous bacteria, associated with altered intestinal production of IL-22 and IgA, and was transmissible to wild-type mice, resulting in increased susceptibility to DSS. Lyn deficiency also resulted in an inability to control infection by the enteric pathogens Salmonella enterica serovar Typhimurium and Citrobacter rodentium. Lyn−/− mice exhibited profound cecal inflammation, bacterial dissemination, and morbidity following S. Typhimurium challenge and greater colonic inflammation throughout the course of C. rodentium infection. These results identify Lyn as a key regulator of the mucosal immune system, governing pathophysiology in multiple models of intestinal disease.
Survival and Inflammation Promotion Effect of PTPRO in Fulminant Hepatitis Is Associated with NF-κB Activation
Authors: Jiang Runqiu , Chen Dianyu , Hou Jiajie , Tan Zhongming , Wang Youjing , Huang Xingxu , Wang Xuehao , Sun Beicheng 
Published: October 2014

Abstract
Previous investigations demonstrated that protein tyrosine phosphatase, receptor type, O (PTPRO) acts as a tumor suppressor in liver cancer; however, little is known about its role in liver inflammation. Thus, we investigated the role of PTPRO in fulminant hepatitis (FH) using a Con A–induced mouse model. Significantly more severe liver damage, but attenuated inflammation, was detected in PTPRO-knockout (KO) mice, and PTPRO deficiency could confer this phenotype to wild-type mice in bone marrow transplantation. Moreover, hepatocytes with PTPRO depletion were more sensitive to TNF-α–induced apoptosis, and secretion of cytokines was significantly decreased in both T and NK/NKT cells and led to marked impairment of NF-κB activation. Intriguingly, wild-type and PTPRO-KO cells responded equally to TNF-α in activation of IKK, but NF-κB activation was clearly decreased in PTPRO-KO cells. PTPRO associated with ErbB2, and loss of PTPRO potentiated activation of the ErbB2/Akt/GSK-3β/β-catenin cascade. Increased β-catenin formed a complex with NF-κB and attenuated its nuclear translocation and activation. Importantly, in humans, PTPRO was much decreased in FH, and this was associated with enhanced β-catenin accumulation but reduced IFN-γ secretion. Taken together, our study identified a novel PTPRO/ErbB2/Akt/GSK-3β/β-catenin/NF-κB axis in FH, which suggests that PTPRO may have therapeutic potential in this liver disease.
X-Chromosome Complement and Estrogen Receptor Signaling Independently Contribute to the Enhanced TLR7-Mediated IFN-α Production of Plasmacytoid Dendritic Cells from Women
Authors: Laffont Sophie , Rouquié Nelly , Azar Pascal , Seillet Cyril , Plumas Joël , Aspord Caroline , Guéry Jean-Charles 
Published: October 2014

Abstract
Human plasmacytoid dendritic cells (pDCs) play a major role in innate immunity through the production of type I IFNs after TLR engagement by pathogens. Sex-based differences in the innate function of human pDCs have been established, with pDCs from women exhibiting enhanced TLR7-mediated IFN-α production as compared with pDCs from males. In mice, we recently provided evidence for a role of estrogens as a positive regulator of pDC innate functions through cell-intrinsic estrogen receptor α signaling, but did not exclude a role for other X-linked factors, particularly in human pDCs. In this study, we investigated the respective contribution of X chromosome dosage and sex hormones using a humanized mouse model in which male or female NOD-SCID-β2m−/− were transplanted with human progenitor cells purified from either male or female cord blood cells. We showed that, in response to TLR7 ligands, the frequency of IFN-α– and TNF-α–producing pDCs from either sex was greater in female than in male host mice, suggesting a positive role for estrogens. Indeed, blockade of estrogen receptor signaling during pDC development in vitro inhibited TLR7-mediated IFN-α production by human pDCs, which expressed both ESR1 and ESR2 genes. Interestingly, we also found that X chromosome dosage contributed to this sex bias as female pDCs have an enhanced TLR7-mediated IFN-α response as compared with male ones, irrespective of the sex of the recipient mice. Together, these results indicate that female sex hormones, estrogens, and X chromosome complement independently contribute to the enhanced TLR7-mediated IFN-α response of pDCs in women.
Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway
Authors: Jiang Rongzhen , Cai Jingjing , Zhu Zhaowei , Chen Dandan , Wang Jiemei , Wang Qingde , Teng Yincheng , Huang Yajuan , Tao Minfang , Xia Aibin , Xue Min , Zhou Shenghua , Chen Alex F. 
Published: October 2014

Abstract
High mobility group box 1 (HMGB1) plays an important role in the pathologic processes of endothelial permeability under oxidative stress. Trophoblast oxidative stress has been implicated in the pathophysiology of preeclampsia (PE). HMGB1 serum levels are increased in PE. However, the potential roles of HMGB1 in endothelial permeability in PE remain unclear. We assessed the effects of the hypoxic trophoblast on the permeability of the endothelial monolayer. Our results showed that the hypoxic trophoblast displayed higher HMGB1 mRNA, intracellular HMGB1 protein, and HMGB1 in conditioned medium than those of the normoxic trophoblast did. The hypoxic trophoblast conditioned medium increased the endothelial monolayer permeability and increased TLR 4 and caveolin-1 (CAV-1) protein expression in endothelial cells, which was inhibited by glycyrrhizic acid and HMGB1 small interfering RNA transfection to trophoblasts before hypoxia. The increased endothelial permeability induced by hypoxic trophoblast conditioned medium could be inhibited with TLR4 or CAV-1 gene silencing in endothelial cells. Immunoprecipitation showed that CAV-1 and TLR4 are colocalized in HUVECs and C57BL/6 mouse kidney. TLR4 small interfering RNA suppressed CAV-1 protein expression in endothelial cells upon stimulation of hypoxic trophoblast conditioned medium or HMGB1. We conclude that hypoxic trophoblasts play an important role in the mechanism of general edema (including protein urine) in PE via increasing endothelial monolayer permeability through the HMGB1/TLR4/CAV-1 pathway.
Impaired B Cell Inhibition by Lupus Bone Marrow Mesenchymal Stem Cells Is Caused by Reduced CCL2 Expression
Authors: Che Nan , Li Xia , Zhang Lu , Liu Rui , Chen Haifeng , Gao Xiang , Shi Songtao , Chen Wanjun , Sun Lingyun 
Published: October 2014

Abstract
Mesenchymal stem cells (MSC) from healthy human and normal mice can inhibit normal B cell proliferation, differentiation, and Ab secretion in vitro. However, it remains unknown whether MSC from lupus-like mice and patients with systemic lupus erythematosus (SLE) exhibit the same immunoregulatory activity as normal MSC for B cell inhibition and, if not, what the underlying molecular mechanism would be. In this study, we showed that bone marrow–derived MSCs from lupus-like mice and SLE patients had an impairment in suppressing normal B cell proliferation and differentiation, which was caused by the reduction of CCL2 levels. Knockdown of CCL2 in normal MSC damaged their suppressive capacity for B cells. Conversely, overexpression of CCL2 in lupus MSCs restored their immunoregulatory ability for B cells in vitro and ameliorated the pathology of lupus nephritis and serological changes in MRL/lpr mice in vivo. Mechanistically, MSC-mediated B cell inhibition was dependent on matrix metalloproteinase proteolytic processing of CCL2. These findings reveal a novel function of CCL2 in B cell regulation by MSCs and suggest that CCL2 manipulation on MSCs may serve as a potential pathway for developing the more effective MSC-based therapy in autoimmune diseases associated with B cell activation, such as SLE.