bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation of Coracoid Thickness and Glenoid Width
Authors: Bueno Rogerio Serpone , Ikemoto Roberto Yukio , Nascimento Luis Gustavo Prata , Almeida Luiz Henrique de Oliveira , Strose Eric , Murachovsky Joel 
Published: May 2012

Background: The coracoid has been widely used as a graft to reconstruct anterior glenoid bone defects, as described by the Latarjet and Bristow procedures, with successful results. Nevertheless, at the present, there are no studies correlating the size of the coracoid graft and its relation to the glenoid. Purpose: To assess the mediolateral (M-L) and anteroposterior (A-P) thickness of the coracoid process as well as the widest anterior-to-posterior glenoid distance (glenoid width) and to analyze the correlation between these measurements, while comparing these with the A-P coracoid process thickness. Study Design: Descriptive laboratory study. Methods: Sixty-one unpaired, adult human cadaveric scapulae were evaluated. Three examiners performed 3 independent measurements of the largest M-L thickness of the coracoid process and also the widest anterior-to-posterior distance of the glenoid. The A-P coracoid process thickness was also measured to compare for correlations with M-L coracoid thickness. Results: The glenoid width was 26.38 ± 2.69 mm (range, 20.03-32.35 mm), and the M-L coracoid thickness was 14.51 ± 1.90 mm (range, 9.60-19.31 mm). Calculating the ratio between the M-L thickness of the coracoid and glenoid width, we observed that the coracoid represented 43% to 70% of the glenoid width (54% on average). The A-P coracoid process thickness was 8.37 ± 0.93 mm (range, 6.61-9.76 mm), representing 31% of the glenoid width on average. Conclusion: A strong positive and statistically significant relationship between the coracoid process M-L thickness and the anterior-to-posterior glenoid width exists; the coracoid represents, on average, 54% of the glenoid width. Clinical Relevance: Most cases of glenoid bone loss in recurrent shoulder dislocation can be reconstructed with the coracoid process to re-establish its anatomy.
Incidence and Outcome After Revision Anterior Cruciate Ligament Reconstruction
Authors: Lind Martin , Menhert Frank , Pedersen Alma B. 
Published: May 2012

Background: Revision anterior cruciate ligament (ACL) reconstruction is poorly described because of its rare incidence and mainly small case series presented in the literature. The Danish ACL reconstruction registry has monitored the development in revision ACL reconstruction since 2005. Hypothesis: We hypothesized that younger patients had a higher risk of revision ACL reconstruction than older patients and that subjective clinical outcome was worse after revision ACL reconstruction than after primary ACL reconstruction. Study Design: Cohort study; Level of evidence, 2. Methods: All clinics performing ACL reconstructions in Denmark report to the national ACL reconstruction registry. The revision rate after primary ACL reconstruction (n = 12,193 procedures) and re-revision rate after revision ACL reconstruction (n = 1099 procedures) were calculated for the period of 2005 to 2010. Outcome at 1-year follow-up for the revision cohort was reported using the Knee Injury and Osteoarthritis Outcome Score (KOOS), Tegner function score, and objective knee stability measurement. Results: The rate of revision ACL reconstruction was 4.1% after 5 years. Revision occurred most frequently after 1 to 2 years. Patients below 20 years of age at the time of primary ACL reconstruction had a higher risk of revision (8.7%) than did patients older than 20 years of age (2.8%) (adjusted relative risk, 2.58; 95% confidence interval, 2.02-3.30). The KOOS scores 1 year after revision ACL reconstruction (mean ± standard deviation) were 73 ± 18 for symptoms, 78 ± 17 for pain, 84 ± 16 for activities of daily living, 52 ± 28 for sports, and 48 ± 21 for quality of life. All these scores were significantly lower than for primary ACL reconstruction: 77 ± 17 for symptoms, 84 ± 15 for pain, 89 ± 13 for activities of daily living, 62 ± 25 for sports, and 59 ± 21 for quality of life. Side-to-side difference in knee laxity improved from 5.8 mm before revision ACL reconstruction to 1.9 mm 1 year after revision ACL surgery. The use of allograft tissue for the revision procedure resulted in a higher risk of re-revision than did autograft tissue (relative risk, 2.05; 95% confidence interval, 1.5-2.4) ( P < .01). The rate of re-revision after 5 years was 5.4%. Conclusion: In this observational population-based study, the 5-year revision ACL reconstruction rate was 4.1%. Despite achieving acceptable knee stability after revision ACL reconstruction, subjective outcome is less favorable than after primary ACL reconstruction.
Intrauterine environment and multiple sclerosis: a population- based case-control study
Authors: Mueller Beth A , Nelson J Lee , Newcomb Polly A 
Published: May 2012

Background: Associations of several autoimmune disorders with intrauterine and early life exposures have been reported. Objective: We used population-based linked hospital discharge-birth records data to explore maternal, prenatal, and infant characteristics in relation to MS-related hospitalization among Washington State residents. Methods: 272 cases hospitalized for MS during 1988–2008 and 2720 birth record controls were identified from linked hospital discharge-birth certificate data. Exposure information from their birth records were compared in a population-based case-control study to estimate adjusted odds ratios (ORs) and 95% confidence intervals (95%CIs) for associations with MS hospitalization. Results: Most factors examined were not associated with MS. Having a mother with 3+ prior live births (OR 0.54, 95%CI 0.31–0.95) or having 3+ older siblings (OR 0.49, 95%CI 0.28–0.85) were negatively associated. Maternal prenatal smoking (OR 3.09, 95%CI 1.22–7.84) was positively associated. Conclusion: Transplacental exposure to smoke constituents including chemicals affecting myelin may help explain any association with maternal prenatal smoking; however, we were unable to assess childhood or adult smoke exposures which may also account at least partly for this effect. The negative associations observed with greater maternal parity and number of siblings are consistent with some other studies. Reasons for these associations may involve various pathways.
Estimation of risk and interaction of single nucleotide polymorphisms at angiotensinogen locus causing susceptibility to essential hypertension: a case control study
Authors: Charita Bh , Padma G , Sushma P , Deepak P , Padma T 
Published: May 2012

Introduction: The risk conferred by the variants and haplotypes of single nucleotide polymorphisms (SNPs) at human angiotensinogen (AGT) gene to essential hypertension (EHT) have been described in several populations with variations in the results attributed to their ethnicity. We attempted to evaluate the risk of -217G>A, -152G>A, -20A>C, -6G>A, T174M, M235T and 15241A>G polymorphisms at AGT locus along with the analyses of haplotype and epistatic interactions in causing susceptibility to EHT. Method: Two-hundred and forty-nine hypertensives and 248 controls were genotyped for the selected markers. Results: Study of demographic parameters revealed significant association of obesity, positive family history and non-vegetarian diet habit, suggesting elevated risk of the condition when associated with these parameters. Significantly high risk for males with AA genotype of -217G>A polymorphism was observed for developing EHT ( p = .07). Males with -217A ( p = .01) showed a two-fold higher risk for EHT. Markers -217G>A and -6G>A were in strong linkage disequilibrium in patients as compared to controls. Strong epistatic interactions were found between -6G>A, M235T and -217G>A markers, supporting the synergistic effect between them leading to EHT. Conclusion: Our findings suggest that -217A variant is significantly associated with the risk for EHT in males. Further studies on the functional role of the marker -217 are recommended for understanding the cause of association with EHT.
Long-Term Evaluation of Autologous Chondrocyte Implantation
Authors: Corpus Keith T. , Bajaj Sarvottam , Daley Erika L. , Lee Andrew , Kercher James S. , Salata Michael J. , Verma Nikhil N. , Cole Brian J. 
Published: May 2012

Purpose: The purpose of this study was to report the clinical outcomes of autologous chondrocyte implantation (ACI) procedures performed by a single orthopedic surgeon at a minimum of 7 years follow-up. Methods: A retrospective review of prospectively collected data was performed on 29 patients who underwent ACI of the knee between the years of 1998 and 2003. Prospective data were collected to assess changes in standardized outcome measures preoperatively and 2, 4, and 7 years postoperatively. All patients enrolled in the study were also recruited to undergo physical examination when possible. Results: The final cohort consisted of 29 patients with a mean final follow-up time of 8.40 years (range = 7.14-10.88 years). Comparing preoperative scores to 7-year postoperative values, the mean International Knee Documentation Committee (IKDC) score improved from 39.80 to 59.24 ( P < 0.001), mean Tegner-Lysholm score increased from 48.07 to 74.17 ( P < 0.001), SF-12 physical score improved from 40.38 to 48.66 ( P < 0.001), and SF-12 mental score improved from 44.14 to 48.98 ( P < 0.05). Significant improvement occurred in Knee Injury and Osteoarthritis Outcome Score (KOOS) pain (56.03 to 80.36), symptoms (54.19 to 74.75), activities of daily living (72.01 to 85.90), sports (23.34 to 55.34), and quality of life (24.56 to 56.03) ( P < 0.001). In addition, 7-year postoperative scores were at or near levels seen at 2 years (mean = 2.16; range = 0.94-4.03 years) and 4 years (mean = 4.43; range = 2.16-5.88 years) postoperatively, reflecting durable improvement. Subjectively, on a scale of 1 to 10 (10 being completely satisfied), the mean postoperative satisfaction rate was 8.14. Additionally, 88.9% of the patients would elect to have this surgery again if the same problem was to occur in the contralateral joint. Conclusions: The results of ACI in patients who present with symptomatic, full-thickness chondral defects remain durable at a minimum of 7-year follow-up with persistent, high levels of patient satisfaction. Level of Evidence: Case series; Level of evidence, IV.
The Augmentation of a Collagen/Glycosaminoglycan Biphasic Osteochondral Scaffold with Platelet-Rich Plasma and Concentrated Bone Marrow Aspirate for Osteochondral Defect Repair in Sheep
Authors: Getgood Alan , Henson Frances , Skelton Carrie , Herrera Emilio , Brooks Roger , Fortier Lisa A. , Rushton Neil 
Published: May 2012

Objective: This study investigates the combination of platelet-rich plasma (PRP) or concentrated bone marrow aspirate (CBMA) with a biphasic collagen/glycosaminoglycan (GAG) osteochondral scaffold for the treatment of osteochondral defects in sheep. Design: Acute osteochondral defects were created in the medial femoral condyle (MFC) and the lateral trochlea sulcus (LTS) of 24 sheep ( n = 6). Defects were left empty or filled with a 6 × 6-mm scaffold, either on its own or in combination with PRP or CBMA. Outcome measures at 6 months included mechanical testing, International Cartilage Repair Society (ICRS) repair score, modified O’Driscoll histology score, qualitative histology, and immunohistochemistry for type I, II, and VI collagen. Results: No differences in mechanical properties, ICRS repair score, or modified O’Driscoll score were detected between the 4 groups. However, qualitative assessments of the histological architecture, Safranin O content, and collagen immunohistochemistry indicated that in the PRP/scaffold groups, there was a more hyaline cartilage–like tissue repair. In addition, the addition of CBMA and PRP to the scaffold reduced cyst formation in the subchondral bone of healed lesions. Conclusion: There was more hyaline cartilage–like tissue formed in the PRP/scaffold group and less subchondral cystic lesion formation in the CBMA and PRP/scaffold groups, although there were no quantitative differences in the repair tissue formed.
Red blood cell alloimmunization in sickle cell disease: pathophysiology, risk factors, and transfusion management
Authors: Yazdanbakhsh Karina , Ware Russell E. , Noizat-Pirenne France 
Published: May 2012

AbstractRed blood cell transfusions have reduced morbidity and mortality for patients with sickle cell disease. Transfusions can lead to erythrocyte alloimmunization, however, with serious complications for the patient including life-threatening delayed hemolytic transfusion reactions and difficulty in finding compatible units, which can cause transfusion delays. In this review, we discuss the risk factors associated with alloimmunization with emphasis on possible mechanisms that can trigger delayed hemolytic transfusion reactions in sickle cell disease, and we describe the challenges in transfusion management of these patients, including opportunities and emerging approaches for minimizing this life-threatening complication.
Hemostatic effect of a monoclonal antibody mAb 2021 blocking the interaction between FXa and TFPI in a rabbit hemophilia model
Authors: Hilden Ida , Lauritzen Brian , Sørensen Brit Binow , Clausen Jes Thorn , Jespersgaard Christina , Krogh Berit Olsen , Bowler Andrew Neil , Breinholt Jens , Gruhler Albrecht , Svensson L. Anders , Petersen Helle Heibroch , Petersen Lars Christian , Balling Kristoffer W. , Hansen Lene , Hermit Mette Brunsgaard , Egebjerg Thomas , Friederichsen Birgitte , Ezban Mirella , Bjørn Søren Erik 
Published: May 2012

AbstractHemophilia is treated by IV replacement therapy with Factor VIII (FVIII) or Factor IX (FIX), either on demand to resolve bleeding, or as prophylaxis. Improved treatment may be provided by drugs designed for subcutaneous and less frequent administration with a reduced risk of inhibitor formation. Tissue factor pathway inhibitor (TFPI) down-regulates the initiation of coagulation by inhibition of Factor VIIa (FVIIa)/tissue factor/Factor Xa (FVIIa/TF/FXa). Blockage of TFPI inhibition may facilitate thrombin generation in a hemophilic setting. A high-affinity (KD = 25pM) mAb, mAb 2021, against TFPI was investigated. Binding of mAb 2021 to TFPI effectively prevented inhibition of FVIIa/TF/FXa and improved clot formation in hemophilia blood and plasma. The binding epitope on the Kunitz-type protease inhibitor domain 2 of TFPI was mapped by crystallography, and showed an extensive overlap with the FXa contact region highlighting a structural basis for its mechanism of action. In a rabbit hemophilia model, an intravenous or subcutaneous dose significantly reduced cuticle bleeding. mAb 2021 showed an effect comparable with that of rFVIIa. Cuticle bleeding in the model was reduced for at least 7 days by a single intravenous dose of mAb 2021. This study suggests that neutralization of TFPI by mAb 2021 may constitute a novel treatment option in hemophilia.
Plasminogen is a key proinflammatory regulator that accelerates the healing of acute and diabetic wounds
Authors: Shen Yue , Guo Yongzhi , Mikus Peter , Sulniute Rima , Wilczynska Malgorzata , Ny Tor , Li Jinan 
Published: May 2012

Abstract
Despite decades of research on wound healing, effective biologic agents for the treatment of chronic wounds, especially diabetic wounds, are still lacking. In the present study, we report that the inert plasma protein plasminogen (plg) acts as a key regulatory molecule that potentiates wound healing in mice. Early in the healing process, plg bound to inflammatory cells is transported to the wound area, where the level of plg is increased locally, leading to the induction of cytokines and intracellular signaling events and to a potentiation of the early inflammatory response. Systemic administration of additional plg not only accelerates the healing of acute burn wounds in wild-type mice, but also improves the healing of chronic diabetic wounds in a mouse model of diabetes. Our results suggest that the administration of plg may be a novel therapeutic strategy to treat many different types of wounds, especially chronic wounds such as those caused by diabetes.
Coinhibitory molecules in hematologic malignancies: targets for therapeutic intervention
Authors: Norde Wieger J. , Hobo Willemijn , van der Voort Robbert , Dolstra Harry 
Published: May 2012

AbstractThe adaptive immune system can be a potent defense mechanism against cancer; however, it is often hampered by immune suppressive mechanisms in the tumor microenvironment. Coinhibitory molecules expressed by tumor cells, immune cells, and stromal cells in the tumor milieu can dominantly attenuate T-cell responses against cancer cells. Today, a variety of coinhibitory molecules, including cytotoxic T lymphocyte–associated antigen-4, programmed death-1, B and T lymphocyte attenuator, LAG3, T-cell immunoglobulin and mucin domain 3, and CD200 receptor, have been implicated in immune escape of cancer cells. Sustained signaling via these coinhibitory molecules results in functional exhaustion of T cells, during which the ability to proliferate, secrete cytokines, and mediate lysis of tumor cells is sequentially lost. In this review, we discuss the influence of coinhibitory pathways in suppressing autologous and allogeneic T cell–mediated immunity against hematologic malignancies. In addition, promising preclinical and clinical data of immunotherapeutic approaches interfering with negative cosignaling, either as monotherapy or in conjunction with vaccination strategies, are reviewed. Numerous studies indicate that coinhibitory signaling hampers the clinical benefit of current immunotherapies. Therefore, manipulation of coinhibitory networks is an attractive adjuvant immunotherapeutic intervention for hematologic cancers after standard treatment with chemotherapy and hematopoietic stem cell transplantation.
Genomic characterization of the conditionally dispensable chromosome in Alternaria arborescens provides evidence for horizontal gene transfer
Authors: Hu Jinnan , Chen Chenxi , Peever Tobin , Dang Ha , Lawrence Christopher , Mitchell Thomas 
Published: May 2012

Abstract

Background
Fungal plant pathogens cause serious agricultural losses worldwide. Alternaria arborescens is a major pathogen of tomato, with its virulence determined by the presence of a conditionally dispensable chromosome (CDC) carrying host-specific toxin genes. Genes encoding these toxins are well-studied, however the genomic content and organization of the CDC is not known.

Results
To gain a richer understanding of the molecular determinants of virulence and the evolution of pathogenicity, we performed whole genome sequencing of A. arborescens. Here we present the de-novo assembly of the CDC and its predicted gene content. Also presented is hybridization data validating the CDC assembly. Predicted genes were functionally annotated through BLAST. Gene ontology terms were assigned, and conserved domains were identified. Differences in nucleotide usage were found between CDC genes and those on the essential chromosome (EC), including GC3-content, codon usage bias, and repeat region load. Genes carrying PKS and NRPS domains were identified in clusters on the CDC and evidence supporting the origin of the CDC through horizontal transfer from an unrelated fungus was found.

Conclusions
We provide evidence supporting the hypothesis that the CDC in A. arborescens was acquired through horizontal transfer, likely from an unrelated fungus. We also identified several predicted CDC genes under positive selection that may serve as candidate virulence factors.
Expansion of CORE-SINEs in the genome of the Tasmanian devil
Authors: Nilsson Maria A , Janke Axel , Murchison Elizabeth P , Ning Zemin , Hallström Björn M 
Published: May 2012

AbstractBackgroundThe genome of the carnivorous marsupial, the Tasmanian devil (Sarcophilus harrisii, Order: Dasyuromorphia), was sequenced in the hopes of finding a cure for or gaining a better understanding of the contagious devil facial tumor disease that is threatening the species’ survival. To better understand the Tasmanian devil genome, we screened it for transposable elements and investigated the dynamics of short interspersedelement (SINE) retroposons.ResultsThe temporal history of Tasmanian devil SINEs, elucidated using a transposition in transposition analysis, indicates that WSINE1, a CORE-SINE present in around 200,000 copies, is the most recently active element. Moreover, we discovered a new subtype of WSINE1 (WSINE1b) that comprises at least 90% of all Tasmanian devil WSINE1s. The frequencies of WSINE1 subtypes differ in the genomes of two of the other Australian marsupial orders. A co-segregation analysis indicated that at least 66 subfamilies of WSINE1 evolved during the evolution of Dasyuromorphia. Using a substitution rate derived from WSINE1 insertions, the ages of the subfamilies were estimated and correlated with a newly established phylogeny of Dasyuromorphia. Phylogenetic analyses and divergence time estimates of mitochondrial genome data indicate a rapid radiation of the Tasmanian devil and the closest relative the quolls (Dasyurus) around 14 million years ago.ConclusionsThe radiation and abundance of CORE-SINEs in marsupial genomes indicates that they may be a major player in the evolution of marsupials. It is evident that the early phases of evolution of the carnivorous marsupial order Dasyuromorphia was characterized by a burst of SINE activity. A correlation between a speciation event and a major burst of retroposon activity is for the first time shown in a marsupial genome.
Genome-wide expression profiling shows transcriptional reprogramming in Fusarium graminearum by Fusarium graminearum virus 1-DK21 infection
Authors: Cho Won Kyong , Yu Jisuk , Lee Kyung-Mi , Son Moonil , Min Kyunghun , Lee Yin-Won , Kim Kook-Hyung 
Published: May 2012

AbstractBackgroundFusarium graminearum virus 1 strain-DK21 (FgV1-DK21) is a mycovirus that confers hypovirulence toF. graminearum, which is the primary phytopathogenic fungus that causes Fusarium head blight (FHB) disease in many cereals. Understanding the interaction between mycoviruses and plant pathogenic fungi is necessary for preventing damage caused byF. graminearum. Therefore, we investigated important cellular regulatory processes in a host containing FgV1-DK21 as compared to an uninfected parent using a transcriptional approach.ResultsUsing a 3′-tiling microarray covering all knownF. graminearumgenes, we carried out genome-wide expression analyses ofF. graminearumat two different time points. At the early point of growth of an infected strain as compared to an uninfected strain, genes associated with protein synthesis, including ribosome assembly, nucleolus, and ribosomal RNA processing, were significantly up-regulated. In addition, genes required for transcription and signal transduction, including fungal-specific transcription factors and cAMP signaling, respectively, were actively up-regulated. In contrast, genes involved in various metabolic pathways, particularly in producing carboxylic acids, aromatic amino acids, nitrogen compounds, and polyamines, showed dramatic down-regulation at the early time point. Moreover, genes associated with transport systems localizing to transmembranes were down-regulated at both time points.ConclusionThis is the first report of global change in the prominent cellular pathways in theFusariumhost containing FgV1-DK21. The significant increase in transcripts for transcription and translation machinery in fungal host cells seems to be related to virus replication. In addition, significant down-regulation of genes required for metabolism and transporting systems in a fungal host containing the virus appears to be related to the host defense mechanism and fungal virulence. Taken together, our data aid in the understanding of how FgV1-DK21 regulates the transcriptional reprogramming ofF. graminearum.