bluuebunny/crossref_metadata_2025_split huggingface dataset:
Biomechanical Analysis of a Knotless Transtendon Interimplant Mattress Repair for Partial-Thickness Articular-Sided Rotator Cuff Tears
Authors: Park Maxwell C. , Jun Bong J. , Park Chong J. , Oh Joo H. , Lee Thay Q. 
Published: November 2009

Background A transtendon interimplant mattress repair along the medial row for partial-thickness rotator cuff repairs has been described with clinical success. However, the biomechanical characteristics for such a repair have not been elucidated. Hypothesis A knotless interimplant mattress repair may show improved or equivalent load and strain characteristics, compared with a repair using isolated mattress repairs over each of 2 anchors. Study Design Controlled laboratory study. Methods Seven matched pairs of human cadaveric shoulders were dissected. Articular-sided tears were created involving 50% of the supraspinatus footprint. In 7 shoulders, repairs were performed with mattress configurations isolated over each of 2 anchor sites (control group). In 7 contralateral shoulders, a knotless interimplant mattress suture configuration was employed creating bridging sutures between implants. For all specimens, a materials-testing machine was used to cyclically load each repair from 10 to 180 N for 30 cycles; each repair was then loaded to failure. A deformation rate of 1 mm per second was employed for all tests. A video-digitizing system was employed to quantitatively measure the gap formation and strain on the footprint area of the repair. For detecting gap formation, 7 matched pairs were necessary for achieving a power of at least 90%. Results During cyclic loading, gap formation at the anterior tendon was significantly lower in the control group ( P < .05) but did not exceed 0.5 mm. There were no significant differences for linear stiffness, hysteresis, and strain between the 2 constructs. During tensile load-to-failure testing, there were no significant differences at yield load between the control and knotless techniques (293.90 ± 132.72 N and 320.38 ± 237.01 N, respectively; P > .05). There were no differences for stiffness, ultimate load, and energy absorbed to failure between the 2 repairs ( P > .05). Gap formation in 3 regions was not significantly different between groups at yield and ultimate loads ( P > .05). The anterior regions of the repair were the first to fail in all constructs. Conclusion A transtendon interimplant mattress rotator cuff repair for partial articular-sided tendon tears involving 50% of the footprint has biomechanical characteristics similar to those of a repair employing 2 isolated mattress configurations. An interim-plant mattress repair can protect tendon strain; it also exhibits yield loads that exceed those typically experienced in the early postoperative period. Clinical Relevance A medial-row interimplant mattress repair configuration that is knotless may facilitate repair without compromising biomechanical characteristics.
Anatomy of Normal Human Anterior Cruciate Ligament Attachments Evaluated by Divided Small Bundles
Authors: Hara Kenji , Mochizuki Tomoyuki , Sekiya Ichiro , Yamaguchi Kumiko , Akita Keiichi , Muneta Takeshi 
Published: November 2009

Background Double-bundle anterior cruciate ligament (ACL) reconstruction has several potential advantages over single-bundle reconstruction with hamstring tendons. However, there are still controversies regarding tunnel placement in tibial and femoral attachments. Hypothesis The macroscopically normal ACL consists of small bundles about 1 mm in diameter. Detailed observation of the divided smaller bundles will achieve better understanding of the tunnel placement in anatomic ACL reconstruction. Study Design Descriptive laboratory study. Methods This study used 20 cadaveric knees. The ACL was divided into anteromedial and posterolateral bundles, then separated into 10 small bundles of 2-mm diameters, with preservation of their attachment sites marked with color markers. The positional relationship between the femoral and tibial attachments of each small bundle was investigated. Results A layered positional correlation of small bundles was found between the tibial and femoral attachments. Small bundles aligned in the anterior-posterior direction in the tibia corresponded to the bundles aligned in a high-low direction in the femur in flexion. The femoral attachment pattern was relatively similar in each specimen; however, the tibial attachment showed 2 patterns: an oblique type (12 of 20) and a transverse type (8 of 20). The posterior portion of the posterolateral bundle was separately attached to the medial and lateral portions of the tibial attachment. There was no fibrous insertion in the center of the posterior portion of the ACL tibial attachment in any specimen. In this bare area, there was fat tissue and vascular bundles. Conclusion Small bundles constituting the ACL showed a relatively layered arrangement between 2 attachments. The tibial attachment showed 2 patterns of oblique and transverse types, and the vascular bundles were located in the center of the posterolateral bundle. Clinical Relevance The results of this study of the normal ACL will provide insights for surgeons when placing grafts during anatomic ACL reconstruction.
Anterior Cruciate Ligament Deficiency Causes Brain Plasticity
Authors: Kapreli Eleni , Athanasopoulos Spyros , Gliatis John , Papathanasiou Matilda , Peeters Ronald , Strimpakos Nikolaos , Van Hecke Paul , Gouliamos Athanasios , Sunaert Stefan 
Published: November 2009

Background The mechanoreceptors located in anterior cruciate ligament (ACL) constitute an afferent source of information toward the central nervous system. It has been proposed that ACL deficiency causes a disturbance in neuromuscular control, affects central programs and consequently the motor response resulting in serious dysfunction of the injured limb. Purpose The objective of this study was to investigate whether chronic anterior cruciate ligament injury causes plastic changes in brain activation patterns. Study Design Case control study; Level of evidence, 3. Methods Seventeen right leg–dominant male participants with chronic anterior cruciate ligament deficiency and 18 matched healthy male participants with no special sport or habitual physical activity participated in this study. Patient selection criteria comprised a complete right unilateral anterior cruciate ligament rupture ≥6 months before testing. Brain activation was examined by using functional magnetic resonance imaging technique (1.5-T scanner). Results Results show that patients with anterior cruciate ligament deficiency had diminished activation in several sensorimotor cortical areas and increased activation in 3 areas compared with controls: presupplementary motor area, posterior secondary somatosensory area, and posterior inferior temporal gyrus. Conclusion The current study reveals that anterior cruciate ligament deficiency can cause reorganization of the central nervous system, suggesting that such an injury might be regarded as a neurophysiologic dysfunction, not a simple peripheral musculoskeletal injury. This evidence could explain clinical symptoms that accompany this type of injury and lead to severe dysfunction. Understanding the pattern of brain activation after a peripheral joint injury such as anterior cruciate ligament injury lead to new standards in rehabilitation and motor control learning with a wide application in a number of clinical and research areas (eg, surgical procedures, patient re-education, athletic training, etc).
Outcomes after Arthroscopic Revision Rotator Cuff Repair
Authors: Piasecki Dana P. , Verma Nikhil N. , Nho Shane J. , Bhatia Sanjeev , Boniquit Nicole , Cole Brian J. , Nicholson Gregory P. , Romeo Anthony A. 
Published: November 2009

Background Although a number of reports have documented outcomes after open revision rotator cuff repair, there are few studies reporting results after arthroscopic revision. Hypothesis Arthroscopic repair of failed rotator cuff results in significant improvement in shoulder functional outcome and pain relief. Study Design Case series; Level of evidence, 4. Methods Multiple variables including demographic data, the number of prior ipsilateral shoulder surgeries, and tear size were recorded from chart review. An independent examiner then measured shoulder strength, range of motion, and shoulder functional outcome scores including American Shoulder and Elbow Surgeons score, Simple Shoulder Test, and visual analog pain scale. Paired t tests were performed to compare preoperative and postoperative measures. Additionally, contingency table analysis was performed to identify prognostic factors for failure of repair requiring further surgery and American Shoulder and Elbow Surgeons score less than 50. Results Fifty-four patients (88.5%) were available for follow-up evaluation with a mean age of 54.9 ± 10.1 years (range, 22.7-82.5 years) and a mean follow-up of 31.1 ± 11.9 months. American Shoulder and Elbow Surgeons scores improved from 43.8 ± 5.7 (mean ± 95% confidence interval) before revision to 68.1 ± 7.2 at final follow-up (P = .0039). The Simple Shoulder Test improved significantly from 3.56 ± 0.8 before surgery to 7.5 ± 1.1 at most recent follow-up (P < .0001). Visual analog pain scale scores improved from 5.17 ± 0.8 to 2.75 ± 0.8 (P = .03), and forward elevation increased from 121.0° ± 12.3° to 136° ± 11.8° postoperatively (P = .025). Greater than 1 prior shoulder surgery was associated with cases that required additional surgery (P = .031). Female gender (P = .007) and preoperative abduction less than 90° (P = .009) were associated with American Shoulder and Elbow Surgeons scores less than 50. Conclusion Arthroscopic revision rotator cuff repair may be a reasonable treatment option even after prior open repairs and provides both improved pain relief and shoulder function. Nonetheless, results are not completely optimal. Female patients and those who have undergone more than 1 ipsilateral shoulder surgery are at increased risk for poorer results.
Simultaneous 3D Assessment of Glenohumeral Shape, Humeral Head Centering, and Scapular Positioning in Atraumatic Shoulder Instability
Authors: von Eisenhart-Rothe Rüdiger , Mayr Hermann Otto , Hinterwimmer Stefan , Graichen Heiko 
Published: November 2009

Background Success rates in the treatment of atraumatic shoulder instability differ, and in vivo identification of the individual insufficient stabilizers is difficult. Hypothesis Atraumatic shoulder instability is an inhomogeneous entity with varying alterations of the active and passive stabilizers. This might be a reason for inferior treatment results. Study Design Case control study; Level of evidence, 3. Methods Shoulders of 28 healthy volunteers and both shoulders of 14 patients with atraumatic instability and multidirectional laxity were examined in different arm positions using open magnetic resonance imaging. Three-dimensional postprocessing techniques were applied to determine 3D glenoid size and retroversion, radius of the humeral head, and curvature of the glenoid. The results of static stabilizers were compared with those of glenohumeral and scapular positioning in the same patients for identification of the individual insufficient stabilizers. Results The atraumatic unstable shoulders showed an increased mean retroversion on both sides, the difference being significant on the affected side (9.4° ± 4.8° vs healthy 3.9° ± 1.3°; P < .05) with a range of 2.6° to 16.6°. The curvature analysis demonstrated a pronounced flatness of the glenoid with a significantly increased mean radius (103.8 mm vs healthy 41.7 mm). The extent of these changes varied widely among patients. Comparison of the static stabilizers with glenohumeral and scapular positioning revealed that isolated changes of the active stabilizers exist in some patients, whereas no isolated changes of passive stabilizers were found. Conclusion All active and passive stabilizers need to be analyzed in patients with atraumatic instability because the magnitude of alteration varied widely among individuals. Different combinations of alterations of the stabilizers were found. The presented technique allows for in vivo identification of the specific alterations. This is necessary for a better understanding of individual pathomechanics and for initiating a specific causal treatment.
Rap1 controls lymphocyte adhesion cascade and interstitial migration within lymph nodes in RAPL-dependent and -independent manners
Authors: Ebisuno Yukihiko , Katagiri Koko , Katakai Tomoya , Ueda Yoshihiro , Nemoto Tomomi , Inada Hiroyuki , Nabekura Junichi , Okada Takaharu , Kannagi Reiji , Tanaka Toshiyuki , Miyasaka Masayuki , Hogg Nancy , Kinashi Tatsuo 
Published: November 2009

AbstractThe small GTPase Rap1 and its effector RAPL regulate lymphocyte adhesion and motility. However, their precise regulatory roles in the adhesion cascade preceding entry into lymph nodes and during interstitial migration are unclear. Here, we show that Rap1 is indispensably required for the chemokine-triggered initial arrest step of rolling lymphocytes through LFA-1, whereas RAPL is not involved in rapid arrest. RAPL and talin play a critical role in stabilizing lymphocyte arrest to the endothelium of blood vessels under flow or to the high endothelial venules of peripheral lymph nodes in vivo. Further, mutagenesis and peptide studies suggest that release of a trans-acting restraint from the β2 cytoplasmic region of LFA-1 is critical for Rap1-dependent initial arrest. Rap1 or RAPL deficiency severely impaired lymphocyte motility over lymph node stromal cells in vitro, and RAPL deficiency impaired high-velocity directional movement within lymph nodes. These findings reveal the several critical steps of Rap1, which are RAPL-dependent and -independent, in lymphocyte trafficking.
DNA methylation for subtype classification and prediction of treatment outcome in patients with childhood acute lymphoblastic leukemia
Authors: Milani Lili , Lundmark Anders , Kiialainen Anna , Nordlund Jessica , Flaegstad Trond , Forestier Erik , Heyman Mats , Jonmundsson Gudmundur , Kanerva Jukka , Schmiegelow Kjeld , Söderhäll Stefan , Gustafsson Mats G. , Lönnerholm Gudmar , Syvänen Ann-Christine 
Published: November 2009

Abstract
Despite improvements in the prognosis of childhood acute lymphoblastic leukemia (ALL), subgroups of patients would benefit from alternative treatment approaches. Our aim was to identify genes with DNA methylation profiles that could identify such groups. We determined the methylation levels of 1320 CpG sites in regulatory regions of 416 genes in cells from 401 children diagnosed with ALL. Hierarchical clustering of 300 CpG sites distinguished between T-lineage ALL and B-cell precursor (BCP) ALL and between the main cytogenetic subtypes of BCP ALL. It also stratified patients with high hyperdiploidy and t(12;21) ALL into 2 subgroups with different probability of relapse. By using supervised learning, we constructed multivariate classifiers by external cross-validation procedures. We identified 40 genes that consistently contributed to accurate discrimination between the main subtypes of BCP ALL and gene sets that discriminated between subtypes of ALL and between ALL and controls in pairwise classification analyses. We also identified 20 individual genes with DNA methylation levels that predicted relapse of leukemia. Thus, methylation analysis should be explored as a method to improve stratification of ALL patients. The genes highlighted in our study are not enriched to specific pathways, but the gene expression levels are inversely correlated to the methylation levels.
Tumor necrosis factor–related apoptosis-inducing ligand 1 (TRAIL1) enhances the transition of red blood cells from the larval to adult type during metamorphosis in Xenopus
Authors: Tamura Kei , Mawaribuchi Shuuji , Yoshimoto Shin , Shiba Tadayoshi , Takamatsu Nobuhiko , Ito Michihiko 
Published: November 2009

AbstractThe transition of red blood cells (RBCs) from primitive to definitive erythropoiesis is conserved across vertebrates. In anuran amphibians, the larval RBCs from primitive erythropoiesis are replaced by adult RBCs from definitive erythropoiesis during metamorphosis. The molecular mechanisms by which the primitive (larval) blood cells are specifically removed from circulation are not yet understood. In this study, we identified Xenopus tumor necrosis factor–related apoptosis-inducing ligand 1 (xTRAIL1) and xTRAIL2 as ligands of Xenopus death receptor-Ms (xDR-Ms) and investigated whether TRAIL signaling could be involved in this transition. The Trail and xDR-M genes were highly expressed in the liver and RBCs, respectively, during metamorphosis. Interestingly, xTRAIL1 enhanced the transition of the RBCs, and a dominant-negative form of the xTRAIL1 receptor attenuated it, when injected into tadpoles. Moreover, xTRAIL1 induced apoptosis in larval RBCs, but had little effect on adult RBCs in vitro. We also found that adult RBCs treated with staurosporine, a protein kinase C (PKC) inhibitor, were sensitized to xTRAIL1. The mRNAs for PKC isoforms were up-regulated in RBCs during metamorphosis. These results suggest that xTRAIL1 can cause apoptosis, probably mediated through xDR-Ms, in larval RBCs, but may not kill adult RBCs, presumably owing to PKC activation, as part of the mechanism for RBC switching.
Immunomodulatory derivatives induce PU.1 down-regulation, myeloid maturation arrest, and neutropenia
Authors: Pal Rekha , Monaghan Sara A. , Hassett Andrea Cortese , Mapara Markus Y. , Schafer Peter , Roodman G. David , Ragni Margaret V. , Moscinski Lynn , List Alan , Lentzsch Suzanne 
Published: November 2009

AbstractThe immunomodulatory drugs (IMiDs) lenalidomide and pomalidomide yield high response rates in patients with multiple myeloma, but the use of IMiDs in multiple myeloma is associated with neutropenia and increased risk for venous thromboembolism (VTE) by mechanisms that are unknown. We show that IMiDs down-regulate PU.1, a key transcription factor involved in granulocyte differentiation in vitro and in patients treated with lenalidomide. Loss of PU.1 results in transient maturation arrest with medullary accumulation of immature myeloid precursors and subsequent neutropenia. Accumulation of promyelocytes leads to high levels of the platelet aggregation agonist, cathepsin G stored in the azurophilic granules of promyelocytes. High levels of cathepsin G subsequently may increase the risk of VTE. To our knowledge, this is the first report investigating the underlying mechanism of IMiD-induced neutropenia and increased risk of VTE in multiple myeloma.
The t(14;18)(q32;q21)/IGH-MALT1 translocation in MALT lymphomas contains templated nucleotide insertions and a major breakpoint region similar to follicular and mantle cell lymphoma
Authors: Murga Penas Eva Maria , Callet-Bauchu Evelyne , Ye Hongtao , Gazzo Sophie , Berger Françoise , Schilling Georgia , Albert-Konetzny Nadine , Vettorazzi Eik , Salles Gilles , Wlodarska Iwona , Du Ming-Qing , Bokemeyer Carsten , Dierlamm Judith 
Published: November 2009

Abstract
The t(14;18)(q32;q21) involving the immunoglobulin heavy chain locus (IGH) and the MALT1 gene is a recurrent abnormality in mucosa-associated lymphoid tissue (MALT) lymphomas. However, the nucleotide sequence of only one t(14;18)–positive MALT lymphoma has been reported so far. We here report the molecular characterization of the IGH-MALT1 fusion products in 5 new cases of t(14;18)–positive MALT lymphomas. Similar to the IGH-associated translocations in follicular and mantle cell lymphomas, the IGH-MALT1 junctions in MALT lymphoma showed all features of a recombination signal sequence–guided V(D)J-mediated translocation at the IGH locus. Furthermore, analogous to follicular and mantle cell lymphoma, templated nucleotides (T-nucleotides) were identified at the t(14;18)/IGH-MALT1 breakpoint junctions. On chromosome 18, we identified a novel major breakpoint region in MALT1 upstream of its coding region. Moreover, the presence of duplications of MALT1 nucleotides in one case suggests an underlying staggered DNA-break process not consistent with V(D)J-mediated recombination. The molecular characteristics of the t(14;18)/IGH-MALT1 resemble those found in the t(14;18)/IGH-BCL2 in follicular lymphoma and t(11;14)/CCND1-IGH in mantle cell lymphoma, suggesting that these translocations could be generated by common pathomechanisms involving illegitimate V(D)J-mediated recombination on IGH as well as new synthesis of T-nucleotides and nonhomologous end joining (NHEJ) or alternative NHEJ repair pathways on the IGH-translocation partner.
Posttranslational stability of the heme biosynthetic enzyme ferrochelatase is dependent on iron availability and intact iron-sulfur cluster assembly machinery
Authors: Crooks Daniel R. , Ghosh Manik C. , Haller Ronald G. , Tong Wing-Hang , Rouault Tracey A. 
Published: November 2009

AbstractMammalian ferrochelatase, the terminal enzyme in the heme biosynthetic pathway, possesses an iron-sulfur [2Fe-2S] cluster that does not participate in catalysis. We investigated ferrochelatase expression in iron-deficient erythropoietic tissues of mice lacking iron regulatory protein 2, in iron-deficient murine erythroleukemia cells, and in human patients with ISCU myopathy. Ferrochelatase activity and protein levels were dramatically decreased in Irp2−/− spleens, whereas ferrochelatase mRNA levels were increased, demonstrating posttranscriptional regulation of ferrochelatase in vivo. Translation of ferrochelatase mRNA was unchanged in iron-depleted murine erythroleukemia cells, and the stability of mature ferrochelatase protein was also unaffected. However, the stability of newly formed ferrochelatase protein was dramatically decreased during iron deficiency. Ferrochelatase was also severely depleted in muscle biopsies and cultured myoblasts from patients with ISCU myopathy, a disease caused by deficiency of a scaffold protein required for Fe-S cluster assembly. Together, these data suggest that decreased Fe-S cluster availability because of cellular iron depletion or impaired Fe-S cluster assembly causes reduced maturation and stabilization of apo-ferrochelatase, providing a direct link between Fe-S biogenesis and completion of heme biosynthesis. We propose that decreased heme biosynthesis resulting from impaired Fe-S cluster assembly can contribute to the pathogenesis of diseases caused by defective Fe-S cluster biogenesis.
Thrombotic risk assessment in the antiphospholipid syndrome requires more than the quantification of lupus anticoagulants
Authors: Devreese Katrien , Peerlinck Kathelijne , Hoylaerts Marc F. 
Published: November 2009

Abstract
Lupus anticoagulants (LACs) are associated with thromboembolic complications (TECs). LACs can be detected by their anticoagulant properties in thrombin generation assays, by the peak height (PH) and lag time (LT). To assess the thrombotic risk in LAC-positive patients, we have expressed the LAC activity quantitatively by PH/LT calibration curves, constructed for mixtures of monoclonal antibodies against β2-glycoprotein I (β2GPI) and prothrombin, spiked in normal plasma. PH/LT was determined in LAC patients, with (n = 38) and without (n = 21) TECs and converted into arbitrary LAC units. LAC titers ranged from 0 to 200 AU/mL, with 5 of 59 patients being negative. In the positive LAC titer population (54 of 59), LAC and anti-β2GPI immunoglobulin G (IgG) titers correlated with TECs, with odds ratios of 3.54 (95% CI, 1.0-1.7) and 10.0 (95% CI, 1.98-50.6), respectively. In patients with single or combined low titers, useful predictions on thrombosis could be made only after additional measurements of soluble P-selectin and factor VII. This layered strategy yielded positive and negative predictive values, sensitivity, and specificity values approximately 90% in this subgroup. Hence, LAC and anti-β2GPI IgG titers, when combined with selected markers of the hypercoagulable state, allow a relevant thrombotic risk assessment in nearly all patients with LACs.