bluuebunny/crossref_metadata_2025_split huggingface dataset:
Right Ventricular Ischemic Injury in Patients With Acute ST-Segment Elevation Myocardial Infarction
Authors: Masci Pier Giorgio , Francone Marco , Desmet Walter , Ganame Javier , Todiere Giancarlo , Donato Rocco , Siciliano Valeria , Carbone Iacopo , Mangia Matteo , Strata Elisabetta , Catalano Carlo , Lombardi Massimo , Agati Luciano , Janssens Stefan , Bogaert Jan 
Published: September 2010

Background—
Experimental data show that the right ventricle (RV) is more resistant to ischemia than the left ventricle. To date, limited data are available in humans because of the difficulty of discriminating reversible from irreversible ischemic damage. We sought to characterize RV ischemic injury in patients with reperfused myocardial infarction using cardiovascular magnetic resonance.

Methods and Results—

In 3 tertiary centers, 242 consecutive patients with reperfused acute ST-segment elevation myocardial infarction were studied with cardiovascular magnetic resonance at 1 week and 4 months after myocardial infarction. T2-weighted and postcontrast cardiovascular magnetic resonance scans were used to depict myocardial edema and late gadolinium enhancement, respectively. Early after infarction, RV edema was common (51% of patients), often associated with late gadolinium enhancement (31% of patients). Remarkably, RV edema and late gadolinium enhancement were found in 33% and 12% of anterior left ventricular infarcts, respectively. Baseline regional and global RV functions were inversely related to the presence and extent of RV edema and RV late gadolinium enhancement. At follow-up, a significant decrease in frequency (25/242 patients; 10%) and extent of RV late gadolinium enhancement was observed (
P
<0.001). With the use of multivariable analysis, the presence of RV edema was an independent predictor of RV global function improvement during follow-up (β-coefficient=0.221,
P=
0.003).

Conclusions—
Early postinfarction RV ischemic injury is common and is characterized by the presence of myocardial edema, late gadolinium enhancement, and functional abnormalities. RV injury is not limited to inferior infarcts but is commonly found in anterior infarcts as well. Cardiovascular magnetic resonance findings suggest reversibility of acute RV dysfunction with limited permanent myocardial damage at 4-month follow-up.
CD69 Limits the Severity of Cardiomyopathy After Autoimmune Myocarditis
Authors: Cruz-Adalia Aranzazu , Jiménez-Borreguero Luis Jesús , Ramírez-Huesca Marta , Chico-Calero Isabel , Barreiro Olga , López-Conesa Erica , Fresno Manuel , Sánchez-Madrid Francisco , Martín Pilar 
Published: September 2010

Background—
Experimental autoimmune myocarditis (EAM), a mouse model of post–infectious cardiomyopathy, reflects mechanisms of inflammatory cardiomyopathy in humans. EAM is characterized by an infiltration of inflammatory cells into the myocardium that can be followed by myocyte fibrosis, edema, and necrosis, leading to ventricular wall dysfunction and heart failure. Different data indicate that CD69 exerts an important immunoregulatory effect in vivo. However, the possible role of CD69 in autoimmune myocarditis has not been studied.

Methods and Results—

We have explored the role of the leukocyte regulatory molecule CD69 in the inflammation that leads to cardiac dysfunction after myocardial injury in EAM. We have found that after induction of EAM, the draining lymph nodes from CD69-deficient mice developed an exacerbated Th17 inflammatory response, resulting in increases in the numbers of infiltrating leukocytes in the myocardium. In the chronic phase of EAM, transthoracic echocardiography revealed a significantly reduced left ventricular fractional shortening and a decreased ejection fraction in CD69-deficient mice, indicative of an impaired cardiac contractility. This condition was accompanied by a greater extent of myocardial fibrosis, an elevated number of sinus pauses on ECG, and an enhanced ratio of heart weight to body weight in CD69
−/−
mice. Moreover, both bone marrow transplantation and adoptive transfer of Th17 cells isolated from immunized CD69
−/−
mice with EAM into naive wild-type recipients reproduced the severity of the disease, demonstrating that CD69 exerts its function within the lymphocyte compartment.

Conclusion—
Our findings indicate that CD69 negatively regulates heart-specific Th17 responses, cardiac inflammation, and heart failure progression in EAM.
Rediscovery of the 'Reality' of Magic: The Revival of Magic in Post-Socialist Russia
Authors: Fujiwara Junko 
Published: September 2010

AbstractThis paper focuses on the revival of magic in post-socialist Russia. In socialist times, atheistic propaganda that insisted religions and magic are unworthy of belief was widespread and scientific knowledge was widely promoted. Therefore a majority of people came to consider magic only a 'superstition'. However, after the collapse of the Soviet Union, a movement to revive magic began. During fieldwork in the years 2002–2006, the author heard from some people such narratives as, 'Before, because I was a member of the communist organisation, I never believed in magic at all. I believe in it now, though'. In this paper I discuss what kinds of discourse about the 'reality' of magic exist in contemporary Russian society and how they are tied to the memory of the atheistic policy.
Can the Subalterns Not Speak? On the Regime of Oral History in Socialist China
Authors: Bulag Uradyn 
Published: September 2010

AbstractRescuing the voice of 'the people' is arguably the most important mission of oral history, and it is now promoted in post-socialist or late socialist states such as China as an effective measure to rewrite history. This article argues, however, that socialist China was and remains in effect an oral-history regime, in which the people in whose name the Communist Party legitimises itself must speak up and narrate their life histories. Oral history in China is a manifestation of 'the people' making history, but it is also an instrument to process them from raw materials into products useful to the Party. This paper brings together issues on the ideologies of orality with the political power of history-making, as well as reflection on the terminological nuance needed to understand the language of 'oral history'.
Socialist Modernisation in Mongolia as Narrated after Socialism
Authors: Konagaya Yuki 
Published: September 2010

AbstractIn this article I introduce our collection of oral histories composed of life histories recorded between 2001 and 2006. First, I discuss some devices implemented in the process of collecting life histories, which was to make oral histories 'polyphonic'. I then suggest that oral history always has a 'dual' tense, in that people talk about 'the past' from the view point of 'the present'. This is illustrated by six cases of statesmen narrating their views about socialist modernisation. Finally, using one of the cases, I demonstrate the co-existence of non-official or private opinions along with official opinions about the socialist period in life-history narratives in the post-socialist period. I call this 'ex-post value'.
Aura attacks from acute convexity subarachnoid haemorrhage not due to cerebral amyloid angiopathy
Authors: Field DK , Kleinig TJ 
Published: September 2010

Background and purpose: Convexity subarachnoid haemorrhage (cSAH) has recently been recognised as a cause of recurrent aura-like symptoms, mimicking transient ischaemic attacks (TIAs). Subarachnoid haemorrhage and recurrent aura-like episodes can occur in patients with cerebral amyloid angiopathy (CAA), which has been the presumed cause in the majority of reported cases. However, this syndrome can occur following cSAH secondary to other conditions, and it is important for clinicians to investigate and manage such patients appropriately. Method: Case series. Results: We describe two patients who presented with recurrent stereotyped transient neurological symptoms in the setting of acute cSAH identified on MRI. In one patient, SAH occurred secondary to cerebral venous sinus thrombosis. In the other, SAH was due to extension of a traumatic subdural haematoma. Conclusions: Conditions other than CAA can cause the clinicoradiological syndrome of cSAH with recurrent TIA-like events. Gradient echo or susceptibility-weighted imaging should be included in the diagnostic work-up of patients presenting with such events. When cSAH is detected, the full differential diagnosis for this should be considered. Aetiologies other than CAA can cause this syndrome and management can vary greatly depending on the underlying cause.
Delay of 2 or 6 Weeks Adversely Affects the Functional Outcome of Augmented Primary Repair of the Porcine Anterior Cruciate Ligament
Authors: Magarian Elise M. , Fleming Braden C. , Harrison Sophia L. , Mastrangelo Ashley N. , Badger Gary J. , Murray Martha M. 
Published: September 2010

Background Enhanced primary anterior cruciate ligament repair, in which suture repair is performed in conjunction with a collagen-platelet composite to stimulate healing, is a potential new treatment option for anterior cruciate ligament injuries. Previous studies have evaluated this approach at the time of anterior cruciate ligament disruption. Hypothesis Delaying surgery by 2 or 6 weeks would have a significant effect on the functional outcome of the repair. Study Design Controlled laboratory study. Methods Sixteen female Yorkshire pigs underwent staged, bilateral surgical anterior cruciate ligament transections. Anterior cruciate ligament transection was initially performed on 1 knee and the knee closed. Two or 6 weeks later, enhanced primary repair was performed in that knee while the contralateral knee had an anterior cruciate ligament transection and immediate repair. Biomechanical parameters were measured after 15 weeks in vivo to determine the effect of delay time relative to immediate repair on the healing response. Results Yield load of the repairs at 15 weeks was decreased by 40% and 60% in the groups where repair was delayed for 2 and 6 weeks, respectively ( P = .01). Maximum load showed similar results (55% and 60% decrease in the 2- and 6-week delay groups, respectively; P = .011). Linear stiffness also was adversely affected by delay (50% decrease compared with immediate repair after either a 2- or 6-week delay, P = .011). Anterior-posterior laxity after 15 weeks of healing was 40% higher in knees repaired after a 2-week delay and 10% higher in those repaired after a 6-week delay ( P = .012) when tested at 30° of flexion, but was not significantly affected by delay when tested at 60° or 90° ( P = .21). Conclusion A delay between anterior cruciate ligament injury and enhanced primary repair has a significant negative effect on the functional performance of the repair. Clinical Relevance As future investigations assess new techniques of anterior cruciate ligament repair, the timing of the repair should be considered in the design and the interpretation of experimental studies.
Effects of Supplemental Intra-articular Lubricin and Hyaluronic Acid on the Progression of Posttraumatic Arthritis in the Anterior Cruciate Ligament–Deficient Rat Knee
Authors: Teeple Erin , Elsaid Khaled A. , Jay Gregory D. , Zhang Ling , Badger Gary J. , Akelman Matthew , Bliss Thomas F. , Fleming Braden C. 
Published: September 2010

Background: Lubricin and hyaluronic acid lubricate articular cartilage and prevent wear. Because lubricin loss occurs after anterior cruciate ligament injury, intra-articular lubricin injections may reduce cartilage damage in the anterior cruciate ligament–deficient knee. Purpose: This study was conducted to determine if lubricin and/or hyaluronic acid supplementation will reduce cartilage damage in the anterior cruciate ligament–deficient knee. Study Design: Controlled laboratory study. Methods: Thirty-six male rats, 3 months old, underwent unilateral anterior cruciate ligament transection. They were randomized to 4 treatments: (1) saline (phosphate-buffered saline [PBS]), (2) hyaluronic acid (HA), (3) purified human lubricin (LUB), and (4) LUB and HA (LUB+HA). Intra-articular injections were given twice weekly for 4 weeks starting 1 week after surgery. Knees were harvested 1 week after the final injection. Radiographs of each limb and synovial fluid lavages were obtained at harvest. Histologic analysis was performed to assess cartilage damage using safranin O/fast green staining. Radiographs were scored for the severity of joint degeneration using the modified Kellgren-Lawrence scale. Synovial fluid levels of sulfated glycosaminoglycan, collagen II breakdown, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and lubricin were measured using enzyme-linked immunosorbent assay (ELISA). Results: Treatment with LUB or LUB+HA significantly decreased radiographic and histologic scores of cartilage damage ( P = .039 and P = .015, respectively) when compared with the PBS and HA conditions. There was no evidence of an effect of HA nor was the LUB effect HA-dependent, suggesting that the addition of HA did not further reduce damage. The synovial fluid of knees treated with LUB had significantly more lubricin in the synovial fluid at euthanasia, although there were no differences in the other cartilage metabolism biomarkers. Conclusion: Supplemental intra-articular LUB reduced cartilage damage in the anterior cruciate ligament–transected rat knee 6 weeks after injury, while treatment with HA did not. Clinical Relevance: Although longer term studies are needed, intra-articular supplementation (tribosupplementation) with lubricin after anterior cruciate ligament injury may protect the articular cartilage in the anterior cruciate ligament–injured knee.
Shockwave Therapy for the Treatment of Chronic Proximal Hamstring Tendinopathy in Professional Athletes
Authors: Cacchio Angelo , Rompe Jan D. , Furia John P. , Susi Piero , Santilli Valter , De Paulis Fosco 
Published: September 2010

Background: Chronic proximal hamstring tendinopathy is an overuse syndrome that is usually managed by nonoperative methods. Shockwave therapy has proved to be effective in many tendinopathies. Hypothesis: Shockwave therapy may be more effective than other nonoperative treatments for chronic proximal hamstring tendinopathy. Study Design: Randomized controlled clinical study; Level of evidence, 1. Methods: Forty professional athletes with chronic proximal hamstring tendinopathy were enrolled between February 1, 2004, and September 30, 2006. Patients were randomly assigned to receive either shockwave therapy, consisting of 2500 impulses per session at a 0.18 mJ/mm2 energy flux density without anesthesia, for 4 weeks (SWT group, n = 20), or traditional conservative treatment consisting of nonsteroidal anti-inflammatory drugs, physiotherapy, and an exercise program for hamstring muscles (TCT group, n = 20). Patients were evaluated before treatment, and 1 week and 3, 6, and 12 months after the end of treatment. The visual analog scale (VAS) score for pain and Nirschl phase rating scale (NPRS) were used as primary outcome measures. Results: The patients were observed for a mean of 10.7 months (range, 1-12 months). Six patients were lost to follow-up because they underwent a surgical intervention: 3 (all in TCT group) were lost at 3 months; 2 (1 in each group), at 6 months; and 1 (in the TCT group), at 12 months. Primary follow-up was at 3 months after the beginning of treatment. The VAS scores in the SWT and TCT groups were 7 points before treatment ( P = .84), and 2 points and 5 points, respectively, 3 months after treatment ( P < .001). The NPRS scores in the SWT and TCT groups were 5 points in either group before treatment ( P = .48), and 2 points and 6 points, respectively, 3 months after treatment ( P < .001). At 3 months after treatment, 17 of the 20 patients (85%) in the SWT group and 2 of the 20 patients (10%) in the TCT group achieved a reduction of at least 50% in pain ( P < .001). There were no serious complications in the SWT group. Conclusion: Shockwave therapy is a safe and effective treatment for patients with chronic proximal hamstring tendinopathy.
Characterization of immune cell subsets during the active phase of multiple sclerosis reveals disease and c-Jun N-terminal kinase pathway biomarkers
Authors: Ferrandi Chiara , Richard Fabien , Tavano Patrizia , Hauben Ehud , Barbié Valerie , Gotteland Jean-Pierre , Greco Beatrice , Fortunato Mara , Mariani Maurizio F , Furlan Roberto , Comi Giancarlo , Martino Gianvito , Zaratin Paola F 
Published: September 2010

Background:Autoimmune activation and deregulated apoptosis of T lymphocytes are involved in multiple sclerosis (MS). c-Jun N-terminal kinase (JNK) plays a role in T-cell survival and apoptosis. Objectives:The aim of this work was to investigate the role of the JNK-dependent apoptosis pathway in relapsing–remitting MS (RRMS). Methods:The immunomodulatory effect of AS602801, a JNK inhibitor, was firstly evaluated on activated peripheral blood mononuclear cells (PBMCs) from healthy volunteers (HVs) and secondly in unstimulated purified CD4+, CD8+ and CD11b+ cells from RRMS patients and HVs. Moreover JNK/inflammation/apoptosis related genes were investigated in RRMS and HV samples. Results:In activated PBMCs from HVs, we showed that AS602801 blocked T-lymphocyte proliferation and induced apoptosis. In RRMS CD4+ and CD8+ cells, AS602801 induced apoptosis genes and expression of surface markers, while in RRMS CD11b+ cells it induced expression of innate immunity receptors and co-stimulatory molecules. Untreated cells from RRMS active-phase patients significantly released interleukin-23 (IL-23) and interferon-gamma (IFN-γ) and expressed less apoptosis markers compared to the cells of HVs. Moreover, gene expression was significantly different in cells from RRMS active-phase patients vs. HVs. By comparing RRMS PBMCs in the active and stable phases, a specific genomic signature for RRMS was indentified. Additionally, CASP8AP2, CD36, ITGAL, NUMB, OLR1, PIAS-1, RNASEL, RTN4RL2 and THBS1 were identified for the first time as being associated to the active phase of RRMS. Conclusions:The analysis of the JNK-dependent apoptosis pathway can provide biomarkers for activated lymphocytes in the active phase of RRMS and a gene expression signature for disease status. The reported results might be useful to stratify patients, thereby supporting the development of novel therapies.
The relationship between meniscal tears and meniscal position
Authors: Allen Deborah M. , Ling Li  , Crema Michel D. , Marra Monica D. , Guermazi Ali , Wyman Brad T. , Hellio Le Graverand Marie-Pierre , Englund Martin , Brandt Kenneth D. , Hunter David J. 
Published: September 2010

Objective: To investigate how different types of meniscal tears predispose to different patterns of meniscal position in subjects with and without symptomatic knee osteoarthritis (OA). Methods: A cross-sectional analysis of 161 women participating in an observational study to evaluate knee OA progression was performed using baseline MRI data. Meniscal morphologic features were scored in three separate locations. Meniscal position measures were determined for extrusion and proportion of coverage. Analysis was performed using multiple linear regression models treating each tear type as an individual variable with a binary response. Results: Complex tears, cysts and maceration of the medial meniscus were associated with more medial ( p = 0.0004, p = 0.004, p < 0.0001, respectively) and anterior extrusion ( p = 0.03, p = 0.03, p < 0.0001, respectively) than normal menisci. Horizontal tears of the lateral meniscus had more lateral ( p = 0.005) and anterior extrusion ( p < 0.0001) than normal menisci. Anterior and body tears of the medial meniscus were associated with more anterior extrusion ( p = 0.0006, p = 0.01, respectively), whereas meniscal body tears alone had more medial extrusion than normal menisci ( p = 0.0002). Meniscal body tears of the lateral meniscus had more lateral extrusion than normal menisci ( p = 0.01). Conclusion: Anterior horn and meniscal body tears and the more severe macerated and complex tear types predisposed to more medial meniscal extrusion. Laterally, only meniscal body and horizontal tears significantly affected extrusion, potentially reflecting a lower overall prevalence of lateral meniscal tears. These results may have important implications in identifying tear types associated with more meniscal dysfunction, with the ultimate goal of identifying those at greatest risk for knee OA progression.
Diminished contact-dependent reinforcement of Syk activation underlies impaired thrombus growth in mice lacking Semaphorin 4D
Authors: Wannemacher Kenneth M. , Zhu Li , Jiang Hong , Fong Karen P. , Stalker Timothy J. , Lee Dooyoung , Tran Anh N. , Neeves Keith B. , Maloney Sean , Kumanogoh Atsushi , Kikutani Hitoshi , Hammer Daniel A. , Diamond Scott L. , Brass Lawrence F. 
Published: September 2010

AbstractWe recently reported that Semaphorin 4D (Sema4D) and its receptors are expressed on the platelet surface and showed that Sema4D(−/−) mice have a selective defect in collagen-induced platelet aggregation and an impaired vascular injury response. Here we investigated the mechanisms involved, tested the role of platelet-platelet contacts in Sema4D-mediated events, and examined the relationship between Sema4D-dependent signaling and integrin αIIbβ3 outside-in signaling. The results show that spleen tyrosine kinase (Syk) activation, an early step in collagen signaling via the glycoprotein VI (GPVI)/FcRγ complex, is greatly reduced in Sema4D(−/−) platelets and can be restored by adding soluble Sema4D. Earlier events, including FcRγ phosphorylation, occur normally; later events are impaired. In contrast, when engagement of αIIbβ3 was blocked, Sema4D(−/−) and control platelets were indistinguishable in assays of Syk activation, adhesion, spreading on collagen, and activation of αIIbβ3. Finally, we found that, unlike the Sema4D knockout, αIIbβ3 blockade inhibited FcRγ phosphorylation and that stimulating aggregation with Mn2+ failed to normalize Syk activation in the absence of Sema4D. Collectively, these results show that αIIbβ3 and Sema4D jointly promote collagen responses by amplifying Syk activation, partly by forming integrin-mediated contacts that enable the binding of Sema4D to its receptors and partly through integrin outside-in signaling. These 2 processes are interdependent, but distinguishable.
Beyond the enhanceosome: cluster of novel κB sites downstream of the human IFN-β gene is essential for lipopolysaccharide-induced gene activation
Authors: Goh Fui G. , Thomson Scott J. P. , Krausgruber Thomas , Lanfrancotti Alessandra , Copley Richard R. , Udalova Irina A. 
Published: September 2010

Abstract
The expression of interferon-β (IFN-β) in virus-infected HeLa cells established a paradigm of multifactorial gene regulation, in which cooperative assembly of transcription factors (TFs) at the composite DNA element (enhanceosome), is central for amplification of weak activating signals provided by individual TFs. However, whether the same TFs and the same DNA element are essential for IFN-β induction in response to bacterial stimuli are less well understood. Here we report that rapid and transient transcription of IFN-β in response to TLR4 stimulation with bacterial lipopolysaccharide (LPS) follows nuclear factor-κB (NF-κB) RelA activation and recruitment to the IFN-β genomic locus at multiple spatially separated regulatory regions. We demonstrate that the IFN-β enhanceosome region is not sufficient for maximal gene induction in response to LPS and identify an essential cluster of homotypic κB sites in the 3′ downstream of the gene. The cluster is characterized by elevated levels of histone 3 lysine 4 mono-methylation, a chromatin signature of enhancers, and efficiently binds RelA-containing NF-κB complexes in vitro and in vivo. These findings demonstrate that IFN-β gene activation via multifactorial enhanceosome assembly is potentiated in LPS-stimulated cells by NF-κB interactions with all functional κB sites in the locus.