bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chondral Resurfacing and High Tibial Osteotomy in the Varus Knee
Authors: Sterett William I. , Steadman J. Richard 
Published: May 2004

Background Treatment of patients with degenerative knees and varus malalignment presents a difficult clinical problem. Hypothesis Combining a medial opening wedge high tibial osteotomy with the microfracture chondral resurfacing procedure is a viable treatment option. Study Design Retrospective review of prospectively collected data. Methods A group of 38 consecutive patients (mean age, 51.3 years; range, 34 to 72 years; 29 men and 10 women) with varus malalignment and chondral lesions who were treated with chondral resurfacing (an abrasion and microfracture technique) combined with a medial opening wedge high tibial osteotomy. All patients had >5° of varus malalignment. Patients were evaluated preoperatively with the Lysholm and Western Ontario & McMasters Universities Osteoarthritis Index scoring systems and at a minimum of 2 years follow-up. Results Thirty-three of 38 patients (87%) were available for 2-year follow-up (average, 45 months; range, 24 to 80 months). Lysholm scores improved from a preoperative score of 43.5 to 78.0 at follow-up; Western Ontario & McMasters Universities Osteoarthritis Index scores improved from 45.8 to 16.2. The average Tegner score was 5.0. Conclusions Combining a medial opening wedge high tibial osteotomy with the microfracture chondral resurfacing procedure in the varus knee is an effective method of decreasing pain and increasing function at a minimum of 2 years follow-up.
Semitendinosus Regrowth
Authors: Gill Sanjitpal S. , Turner Maria A. , Battaglia Todd C. , Leis Henry T. , Balian Gary , Miller Mark D. 
Published: May 2004

Background Previous studies have suggested that hamstring tendons can regenerate following harvesting for anterior cruciate ligament reconstruction. Hypothesis This “neo-tendon” is a true, functional tendon, not scar tissue. Study Design Controlled laboratory study. Methods Semitendinosus tendons were harvested from 35 New Zealand white rabbits using a standard tendon stripper. The rabbits were sacrificed 9 to 12 months following the index procedure and thoroughly evaluated. Results Thirty-one rabbits were available at the time of sacrifice. The neo-tendon was present in 26 rabbits but was highly variable in size and location of its tibial insertion. Histologic and immunohistochemical staining confirmed that the regenerate tissue was indeed tendon with normal cellularity, organization, and immunolocalization of type I collagen. Electron microscopy showed regeneration of organized collagen tissue that simulated native tendon but with a smaller cross-sectional diameter. Functionally, the neo-tendon was able to transmit force across the musculotendinous junction but at a significantly slower rate than the opposite, control leg. Biomechanical properties of the neo-tendon were significantly less than the control side. Biochemical analysis revealed that the neo-tendons contained glycosaminoglycans and collagen, but levels were significantly lower than normal tendons. Conclusions Semitendinosus tendons regenerate with biologically reactive tendinous tissues in an animal model. This tissue has many of the characteristics of a normal tendon but appears to be inferior to the original musculotendinous unit at 9- to 12-month evaluation. Further characterization of the “lizard tail phenomenon” is still needed. Clinical Relevance Hamstring tendon regrowth may have a dramatic impact on postoperative function of patients who undergo anterior cruciate ligament reconstruction with these tendons. Further modulation of this regeneration may further reduce graft harvesting morbidity.
Catastrophic Injuries in High School and College Baseball Players
Authors: Boden Barry P. , Tacchetti Robin , Mueller Fred O. 
Published: May 2004

Background There are few epidemiologic studies of catastrophic baseball injuries. Purpose To develop a profile of catastrophic injuries in baseball players and to describe relevant risk factors. Study Design Retrospective cohort study. Methods The authors reviewed 41 incidents of baseball injuries reported to the National Center for Catastrophic Sports Injury Research from 1982 until 2002. Results There were an estimated 1.95 direct catastrophic injuries per year, or 0.43 injuries per 100,000 participants. The most common mechanisms of injury were a collision of fielders (9) or of a base runner and a fielder (8), a pitcher hit by a batted ball (14), and an athlete hit by a thrown ball (4). Catastrophic injuries included 23 severe head injuries, 8 cervical injuries, 3 cases of commotio cordis, and 2 cases each of a collapsed trachea and facial fractures. Three athletes sustained a severe head injury and facial fractures. Ten of the 41 injuries were fatalities. Conclusions Suggestions for reducing catastrophic injuries in baseball include teaching proper techniques to avoid fielding and base running collisions, protecting the pitcher via a combination of screens and/or helmets with faceguards, continued surveillance and modifications of the bat and ball, eliminating headfirst slides, and continued analysis of chest protectors and automatic external defibrillators for commotio cordis.
Excessive Humeral External Rotation Results in Increased Shoulder Laxity
Authors: Mihata Teruhisa , Lee YeonSoo , McGarry Michelle H. , Abe Muneaki , Lee Thay Q. 
Published: May 2004

Background The quantitative relationship between increased anterior shoulder laxity and increased humeral external rotation observed in throwers remains unclear. Hypothesis An elongated anterior capsule, especially the anterior band of the inferior glenohumeral ligament, produced by excessive humeral external rotation will result in increased anterior shoulder laxity and increased humeral external rotation. Study Design Controlled laboratory study. Methods Seven cadaveric shoulders were tested to measure the humeral rotational range of motion, glenohumeral translations, and length of the anterior band of the inferior glenohumeral ligament. Data were collected for the intact shoulders and after nondestructive stretching of 10%, 20%, and 30% beyond maximum humeral external rotation. Results Nondestructive excessive external rotational stretching resulted in a significant increase in superior (30%, 3.3 mm) and inferior (30%, 2.3 mm) length of the anterior band of the inferior glenohumeral ligament, external rotation (30%, 35°), and anterior (30%, 2.4 mm), inferior (30%, 2.2 mm), and anterior-posterior (30%, 5.1 mm) translations. There were significant positive linear correlations between the length of the anterior band of the inferior glenohumeral ligament, external rotation, and anterior translation. Conclusions Excessive humeral external rotation results in an elongation of the anterior band of the inferior glenohumeral ligament and an increase in anterior and inferior glenohumeral translations and humeral external rotation. Clinical Relevance Repetitive excessive humeral external rotation observed in throwers may be one of the biomechanical causes for increased shoulder laxity and increased humeral external rotation.
Shoulder Outcome Measures
Authors: Placzek Jeff D. , Lukens Steven C. , Badalanmenti Sabrina , Roubal Paul J. , Freeman D. Carl , Walleman Kim M. , Parrot Amy , Wiater J. Michael 
Published: May 2004

Background Several shoulder function scores are used in research, with no universally adopted standard. This study compares 6 shoulder outcome scales. Hypothesis Correlations exist between shoulder outcome scales, allowing conversion between scales. Shoulder scales are correlated with age. Study Design Regression and correlation study. Methods Seventy subjects with shoulder pain completed 6 shoulder outcome scales. Pearson correlations were calculated between the total scores of the 6 instruments, between the components of the scales, and with age. Regression equations were calculated between scales. Results The range of r values for total scores was 0.495 [.lessequal] r [.lessequal] 0.770, P [.lessequal] .01. In general, a scale's components were themselves highly correlated and added little new information to the scale (0.260 [.lessequal] r [.lessequal] 0.705, P [.lessequal] .05). Most of the scale scores were highly correlated with age (0.291 [.lessequal] r [.lessequal] 0.582, P [.lessequal] .05). Constant's reported corrections for age reduced (from r = -0.582 to r = -0.250, P < .05) but did not eliminate age as a confounding variable. Conclusions Correlations exist between shoulder outcome scales, but existing shoulder scales are not equivalent in their assessments of function; they contain redundant information and, in some cases, may reflect a patient's age better than his/her shoulder function. The utility of conversion equations is minimized as a result of low to moderate correlations between scales.
Effect of Increased Excursion of the Ankle on the Severity of Acute Eccentric Contraction-Induced Strain Injury in the Gastrocnemius
Authors: Song Hongsun , Nakazato Koichi , Nakajima Hiroyuki 
Published: May 2004

Background Although muscle strain injury models are frequently employed, highly invasive procedures, including surgical intervention, are typically used to produce these models. In this study, a minimally invasive model of acute strain injury was produced with a single eccentric contraction. Hypothesis The authors tested whether the severity of strain injury in the in vivo gastrocnemius depends on the excursion of the ankle. Study Design Controlled laboratory study. Methods Animals were randomly assigned to 2 groups: a small range of motion group (90°-105°, n = 10) and a large range of motion group (90°-125°, n = 10). Tetanically activated gastrocnemius muscles with percutaneous electrical stimulation were simultaneously elongated by forced dorsiflexion of the ankle joint. Results Isometric tetanic force of the large range of motion group was significantly lower than the pretreatment control 1, 2, and 3 days after treatment. Such reduction was not observed in the small range of motion group. Apparent pathologic damage was observed in the large range of motion group throughout the study period of 10 days. Conclusions A larger range of motion causes more damage in eccentric contraction by using the in vivo model. Clinical Relevance This in vivo model is useful to elucidate mechanisms of prevention and recovery of strain injury.
Immediate Effects of a Knee Brace with a Constraint to Knee Extension on Knee Kinematics and Ground Reaction Forces in a Stop-Jump Task
Authors: Yu Bing , Herman Daniel , Preston Jennifer , Lu William , Kirkendall Donald T. , Garrett William E. 
Published: May 2004

Background A small knee flexion angle in landing tasks was identified as a possible risk factor for noncontact anterior cruciate ligament injuries that are common in sports. Hypothesis A specially designed knee brace with a constraint to knee extension would significantly increase the knee flexion angle at the landing of athletic tasks preceded with horizontal movement components, such as stop-jump tasks. Study Design Repeated measure design for brace effects. Methods Three-dimensional videographic and force plate data were collected for 10 male and 10 female recreational athletes performing a stop-jump task with and without the specially designed brace. Knee flexion angle at landing, maximum knee flexion angle, and peak ground reaction forces during the stance phase of the stop-jump task were determined for each subject with and without the knee brace. Results The knee brace decreased the knee flexion angle at the landing by 5° for both genders but did not significantly affect the peak ground reaction forces during the landing. Conclusions The specially designed knee brace may be a useful device in the prevention and rehabilitation of noncontact anterior cruciate ligament injuries in sports.
Differences in the Ultimate Strength of the Biceps Anchor and the Generation of Type II Superior Labral Anterior Posterior Lesions in a Cadaveric Model
Authors: Shepard Michael F. , Dugas Jeff R. , Zeng Nigel , Andrews James R. 
Published: May 2004

Background The pathogenesis of superior labral anterior posterior lesions remains controversial. Hypothesis The biceps anchor is more vulnerable to loading with a posterior vector as opposed to an in-line pull. Study Design Controlled laboratory study. Methods Eight pairs of cadaveric shoulders were dissected, and the biceps tendon was loaded to failure in 1 of 2 loading patterns. Loading pattern A was meant to simulate the eccentric load of the biceps in the deceleration phase of throwing; loading pattern B was meant to simulate the posterior biceps load of the late cocking phase. Results The biceps anchor demonstrated significantly increased ultimate strength with in-line loading (group A, 508 N) as opposed to posterior loading (group B, 262 N, P < .001). All group B specimens failed at the biceps anchor, resulting in a type II superior labral anterior posterior lesion. Specimens in group A did not create a superior labral anterior posterior lesion. Conclusions Direction of biceps loading resulted in significant differences in the ultimate strength of the biceps anchor and the generation of superior labral anterior posterior lesions. The biceps anchor was significantly weaker when loaded with a posterior vector. Relevance The superior labrum may be most vulnerable to injury in late cocking. The reproducible generation of type II superior labral anterior posteriorlesions may have applications as a biomechanical model.
Treatment of myelodysplastic syndromes with valproic acid alone or in combination with all-trans retinoic acid
Authors: Kuendgen Andrea , Strupp Corinna , Aivado Manuel , Bernhardt Alf , Hildebrandt Barbara , Haas Rainer , Germing Ulrich , Gattermann Norbert 
Published: May 2004

Abstract
Valproic acid (VPA) has been shown to inhibit histone deacetylase activity and to synergize with all-trans retinoic acid (ATRA) in the differentiation induction of acute myelogenous leukemia (AML) blasts in vitro. We treated 18 patients with myelodysplastic syndromes (MDS) and AML secondary to MDS (sAML/MDS) with VPA monotherapy (serum concentrations 346-693 μM [50-100 μg/mL]). Five patients received VPA and ATRA (80 mg/m2/d, days 1-7, every other week). Response according to international working group (IWG) criteria was observed in 8 patients (44%) on VPA monotherapy, including 1 partial remission. Median response duration was 4 months (range, 3-9 months). Four of 5 patients relapsing were treated with VPA + ATRA, 2 of them responding again. Among 5 patients receiving VPA + ATRA from the start, none responded according to IWG criteria, but 1 patient with sAML/MDS achieved a marked reduction in peripheral and marrow blasts. Thus, VPA is of therapeutic benefit for patients with MDS, and ATRA may be effective when added later.
Chromosomal localization, hematologic characterization, and iron metabolism of the hereditary erythroblastic anemia (hea) mutant mouse
Authors: White Robert A. , McNulty Steven G. , Roman Shelly , Garg Uttam , Wirtz Eric , Kohlbrecher Deanna , Nsumu Ndona N. , Pinson David , Gaedigk Roger , Blackmore Krista , Copple Angela , Rasul Sidrah , Watanabe Masayo , Shimizu Koji 
Published: May 2004

AbstractUnderstanding iron metabolism has been enhanced by identification of genes for iron deficiency mouse mutants. We characterized the genetics and iron metabolism of the severe anemia mutant hea (hereditary erythroblastic anemia), which is lethal at 5 to 7 days. The hea mutation results in reduced red blood cell number, hematocrit, and hemoglobin. The hea mice also have elevated Zn protoporphyrin and serum iron. Blood smears from hea mice are abnormal with elevated numbers of smudge cells. Aspects of the hea anemia can be transferred by hematopoietic stem cell transplantation. Neonatal hea mice show a similar hematologic phenotype to the flaky skin (fsn) mutant. We mapped the hea gene near the fsn locus on mouse chromosome 17 and show that the mutants are allelic. Both tissue iron overloading and elevated serum iron are also found in hea and fsn neonates. There is a shift from iron overloading to iron deficiency as fsn mice age. The fsn anemia is cured by an iron-supplemented diet, suggesting an iron utilization defect. When this diet is removed there is reversion to anemia with concomitant loss of overloaded iron stores. We speculate that the hea/fsn gene is required for iron uptake into erythropoietic cells and for kidney iron reabsorption.
Recipient CD4+ T cells that survive irradiation regulate chronic graft-versus-host disease
Authors: Anderson Britt E. , McNiff Jennifer M. , Matte Catherine , Athanasiadis Ionna , Shlomchik Warren D. , Shlomchik Mark J. 
Published: May 2004

AbstractChronic graft-versus-host disease (cGVHD) is an increasingly common cause of morbidity and mortality in allogeneic stem cell transplantation (alloSCT). Relative to acute GVHD (aGVHD), much less is understood about cGVHD. Using the B10.D2 → BALB/c murine cGVHD model, which shares critical pathologic features with human cGVHD, we find that radiation-resistant host T cells regulate cGVHD. We initially observed that recipients lacking all lymphocytes developed accelerated and more severe cGVHD. Using genetically deficient recipients, we determined that αβ+CD4+ T cells were required to regulate cGVHD. Increased cGVHD severity was not due to the absence of T cells per se. Rather, the potency of regulation was proportional to host T-cell receptor (TCR) diversity. Only CD4+CD25+, and not CD4+CD25-, host T cells ameliorated cGVHD when added back, indicating that host T cells acted not via host-versus-graft activity or by reducing homeostatic proliferation but by an undefined regulatory mechanism. Thus, preparative regimens that spare host CD4+CD25+ T cells may reduce cGVHD. Donor CD4+CD25+ T cells also reduced cGVHD. Depletion of CD4+CD25+ cells from the inoculum exacerbated disease, whereas transplantation of additional CD4+CD25+ cells protected against severe cGVHD. Additional CD4+CD25+ cells also promoted healing of established lesions, suggesting that their effects persist during the evolution of cGVHD.
Labile plasma iron (LPI) as an indicator of chelatable plasma redox activity in iron-overloaded β-thalassemia/HbE patients treated with an oral chelator
Authors: Pootrakul Pensri , Breuer William , Sametband Matias , Sirankapracha Pornpan , Hershko Chaim , Cabantchik Z. Ioav 
Published: May 2004

AbstractPersistent levels of plasma nontransferrin bound iron (NTBI) have been associated with tissue iron overload and toxicity. We characterized NTBI's susceptibility to deferoxamine (directly chelatable iron [DCI]) and redox activity (labile plasma iron [LPI]) during the course of long-term, continuous L1 (deferiprone) treatment of patients with hemoglobin E disease and β-thalassemia (n = 17). In 97% of serum samples (n = 267), the LPI levels were more than 0.4 μM (mean ± SEM, 3.1 ± 0.2 μM) and the percent transferrin (Tf) saturation more than 85 (111 ± 6), whereas only in 4% of sera were the LPI levels more than 0.4 μM for Tf saturation less than 85%. Daily administration of L1 (50 mg/kg) for 13 to 17 months caused both LPI and DCI to decrease from respective initial 5.1 ± 0.5 and 5.4 ± 0.6 μM to steady mean levels of 2.18 ± 0.24 and 2.81 ± 0.14 μM. The steady lowest levels of LPI and DCI were attained after 6 to 8 months, with a half time (t1/2) of 2 to 3 months. Serum ferritin and red cell membrane–associated iron followed a similar course but attained steady basal levels only after 10 to 12 months of continuous treatment, with a t1/2 of 5 to 7 months. These studies indicate that LPI and DCI can serve as early indicators of iron overload and as measures for the effectiveness of iron chelation in reducing potentially toxic iron in the plasma.
Molecular and cellular mechanisms underlying iron transport deficiency in microcytic anemia
Authors: Touret Nicolas , Martin-Orozco Natalia , Paroutis Paul , Furuya Wendy , Lam-Yuk-Tseung Steven , Forbes John , Gros Philippe , Grinstein Sergio 
Published: May 2004

AbstractA mutation of the iron transporter Nramp2 (DMT1, Slc11a2) causes microcytic anemia in mk mice and in Belgrade rats by impairing iron absorption in the duodenum and in erythroid cells, causing severe iron deficiency. Both mk and Belgrade animals display a glycine-to-arginine substitution at position 185 (G185R) in the fourth predicted transmembrane domain of Nramp2. To study the molecular basis for the loss of function of Nramp2G185R, we established cell lines stably expressing extracellularly tagged versions of wild-type (WT) or mutated transporters. Like WT Nramp2, the G185R mutant was able to reach the plasmalemma and endosomal compartments, but with reduced efficiency. Instead, a large fraction of Nramp2G185R was detected in the endoplasmic reticulum, where it was unstable and was rapidly degraded by a proteasome-dependent mechanism. Moreover, the stability of the mutant protein that reached the plasma membrane was greatly reduced, further diminishing its surface density at steady state. Last, the specific metal transport activity of plasmalemmal Nramp2G185R was found to be significantly depressed, compared with its WT counterpart. Thus, a singlepoint mutation results in multiple biosynthetic and functional defects that combine to produce the impaired iron deficiency that results in microcytic anemia.
Novel di-2-pyridyl–derived iron chelators with marked and selective antitumor activity: in vitro and in vivo assessment
Authors: Yuan Jun , Lovejoy David B. , Richardson Des R. 
Published: May 2004

AbstractAroylhydrazone and thiosemicarbazone iron (Fe) chelators have potent antitumor activity. The aim of the current study was to examine the antitumor effects and mechanisms of action of a novel series of Fe chelators, the di-2-pyridyl thiosemicarbazones. Of 7 new chelators synthesized, 4 showed pronounced antiproliferative effects. The most active chelator was Dp44mT, which had marked and selective antitumor activity—for example, an IC50 of 0.03 μM in neuroepithelioma cells compared with more than 25 μM in mortal fibroblasts. Indeed, this antiproliferative activity was the greatest yet observed for an Fe chelator. Efficacy was greater than it was for the cytotoxic ligand 311 and comparable to that of the antitumor agent doxorubicin. Strikingly, Dp44mT significantly (P &lt; .01) decreased tumor weight in mice to 47% of the weight in the control after only 5 days, whereas there was no marked change in animal weight or hematologic indices. Terminal deoxyribonucleotidyl transferase (TdT)–mediated dUTP nick end-labeling (TUNEL) staining demonstrated apoptosis in tumors taken from mice treated with Dp44mT. This chelator caused a marked increase of caspase-3 activity in murine Madison-109 (M109) cells. Caspase activation was at least partially mediated by the release of mitochondrial holo-cytochrome c (h-cytc) after incubation with Dp44mT. In conclusion, Dp44mT is a novel, highly effective antitumor agent in vitro and in vivo that induces apoptosis.