bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retrograde Intramedullary Nailing of Femoral Diaphyseal Fractures Caused by Low-velocity Gunshots
Authors: Cannada Lisa K. , Jones Thomas R. , Guerrero-Bejarano Maria , Viehe Thomas , Levy Michael , Farrell Eric D. , Ostrum Robert F. 
Published: April 2009

The purpose of this study was to evaluate the results of retrograde intramedullary nailing of femoral diaphyseal fractures caused by low-velocity gunshots. Seventy-three patients (68 men and 5 women) with 74 femoral diaphyseal fractures caused by gunshots were treated with reamed, retrograde, statically locked intramedullary nailing. The main outcome measures were fracture union, the need for additional operations, shortening, angular deformity, postoperative knee range of motion, and complication rate. Twenty-nine patients sustained additional injuries. During initial treatment, 18 patients underwent further orthopedic and nonorthopedic elective procedures. Three patients had fasciotomies for compartment syndrome. At follow-up, 3 patients had shortening >10 mm (range, 12–18 mm) and 1 had angulation >10° (13° recurvatum). Four patients underwent surgeries after discharge. Complications included 1 case of heterotopic bone formation, 1 hypertrophic nonunion that went on to union after dynamization, 2 postoperative positive blood cultures, and 1 wound dehiscence. There were no cases of septic arthritis.
Our data indicate that there is a low incidence of shortening, angular deformity, complication, and infection rates following treatment of femoral gunshot diaphyseal fractures with a retrograde nail. This study demonstrates that this is an acceptable alternative for the treatment of these injuries.
Femoral Artery Intimal Injury Following Open Reduction of an Acetabular Fracture
Authors: Gaheer Rajinder Singh , Rysavy Martin , Al Khayarin Mohammad M. , Kumar Krishna 
Published: April 2009

Vascular injury is a devastating complication of internal fixation of acetabular fractures. While lacerations of the large vessels may lead to massive bleeding, they are obvious and are addressed immediately during the surgery. We encountered a subtle case of intimal injury and thrombosis of the femoral artery.
A 20-year-old man presented with a fractured right acetabulum and right fourth, fifth, and sixth ribs with hemopneumothorax after a high-velocity motor vehicle accident. Twelve days after the injury, open reduction and internal fixation of the acetabular fracture from an ilioinguinal approach was performed. Postsurgically, examination showed no palpable femoral arterial pulse distal to the inguinal ligament. Exploration of the common femoral artery showed arterial thrombus, which was removed by a Fogarty catheter; however, the pulselessness persisted. Further exploration revealed intimal injury of the femoral artery. Replacement of the damaged segment by an inter-positional venous graft was performed and peripheral pulses were reestablished. The patient recovered uneventfully.
Extreme care should be taken to avoid vascular injury in pelvic fracture surgery. Meticulous surgical technique, particularly in the middle window, is vital to minimizing the risk of this complication. The insidious nature of the intimal arterial injury underlines the necessity of close intraoperative and postoperative monitoring of limb vascularity to detect such vascular lesions immediately and prevent this potentially disastrous complication.
Extraskeletal Myxoid Chondrosarcoma of the Perineum
Authors: Mavrogenis Andreas F. , Patapis Pavlos , Papaparaskeva Kleo Th. , Galanis Evanthia C. , Papagelopoulos Panayiotis J. 
Published: April 2009

Extraskeletal myxoid chondrosarcoma is an aggressive tumor with significant metastatic potential. A 40-year-old man presented with an asymptomatic mass at the left ischial fossa. Magnetic resonance imaging showed a 9x6-cm mass with variable signal intensity and cystic formations. A computed tomography scan of the chest showed multiple pulmonary nodules. A computed tomography–guided core needle biopsy was consistent with low-grade extraskeletal myxoid chondrosarcoma. Despite the presence of lung metastases, wide resection of the primary tumor was performed. Wide resection included the perineal mass and the adjacent ischiopubic ramus. Postoperative recovery was uneventful. One month postoperatively, thoracotomy was performed, and approximately 20 pulmonary nodules were excised. Histological analysis of the excised specimens was consistent with extraskeletal myxoid chondrosarcoma metastases. Two years postoperatively, the patient is alive without evidence of local recurrence or distant disease.
Extraskeletal myxoid chondrosarcoma is an unusual soft tissue sarcoma with ultrastructural and molecular features distinct from that of skeletal myxoid chondrosarcoma. The EWS-CHN gene fusion is highly specific to extraskeletal myxoid chondrosarcoma; the gene fusion is positive in ⩾75% of cases. Treatment should include wide excision for local tumor control. Resection of the lung metastases is feasible. Because of the prolonged survival of patients with extraskeletal myxoid chondrosarcoma, long-term follow-up is recommended for early detection of local recurrence or distant metastases.
Comparison of Hip and Knee Arthroplasty Outcomes at Early and Intermediate Follow-up
Authors: O'Brien Seamus , Bennett Damien , Doran Emer , Beverland David E. 
Published: April 2009

A common perception among clinicians and patients is that recovery is similar following total hip arthroplasty (THA) and total knee arthroplasty (TKA). Improvement in the outcomes of 337 THAs and 256 TKAs implanted by the same surgeon between April 2003 and November 2005 were compared. Improvement was measured using changes in Oxford hip and knee scores measured preoperatively, at first follow-up, and 1 year postoperatively for each patient.
Improvements between preoperative review and first follow-up and between preoperative review and 1-year postoperative follow-up were significantly greater for THA compared to TKA patients. Improvements between first postoperative follow-up and 1-year postoperative follow-up were not significantly different between THA and TKA patients. Although THA patients displayed a significantly worse score preoperatively, they displayed a significantly better score at both first follow-up and 1-year postoperative follow-up. While both procedures improve postoperative pain and physical function, as measured by the Oxford score, improvements measured relative to preoperative levels were significantly smaller for TKA compared to THA patients. Despite recent advances in knee arthroplasty surgery, a significant proportion of TKA patients achieve relatively poor outcome scores postoperatively.
This study shows that pain and function improve less and more slowly in the early and intermediate postoperative periods for knee compared to hip arthroplasty patients.
Postsurgical Chondrolysis of the Shoulder
Authors: Saltzman Matthew , Mercer Deana , Bertelsen Alexander , Warme Winston , Matsen Frederick 
Published: April 2009

There are multiple reports in the literature of chondrolysis following arthroscopic shoulder surgery. Although the etiology of these cases is not known for certain, there has been speculation that radiofrequency devices, young patient age, instability surgery, intra-articular pain pumps, and type of anesthetic may be precipitating factors.
This article describes a case of a 37-year-old law enforcement officer who injured both shoulders and ultimately underwent nearly identical bilateral procedures: arthroscopic superior labrum anteroposterior (SLAP) repair, Bankart repair, capsulorrhaphy, acromioplasty, and distal clavicle excision. Intra-articular pain catheters were placed following both procedures, but the right-sided catheter never functioned properly, as evidenced by continuous leakage outside of her body until it was removed. Subsequently she had an arthroscopic lysis of adhesions done for residual stiffness, in which the left humeral head and glenoid cavity were noted to be completely devoid of articular cartilage. Over the ensuing months, multiple cortisone injections, 5 viscosupplementation injections, physical therapy, and narcotics all failed to relieve her left shoulder pain. Radiographs showed significant left glenohumeral joint space narrowing and a normal-appearing joint space on the right. Our impression was postsurgical chondrolysis of the left shoulder. The patient has recently undergone humeral hemiarthroplasty with nonprosthetic glenoid arthroplasty.
This case differs from others reported in the literature in that nearly identical bilateral procedures were performed by the same surgeon, yet chondrolysis only developed on the side that had a functioning postoperative pain catheter.
C1–C2 Intra-articular Screw Fixation for Atlantoaxial Subluxation Due to Rheumatoid Arthritis
Authors: Tokuhashi Yasuaki , Ajiro Yasumitsu , Oshima Masashi , Umezawa Natsuki 
Published: April 2009

While various surgical procedures have been developed for the treatment of atlantoaxial subluxation due to rheumatoid arthritis, C1-C2 intra-articular screw fixation was developed to reduce intraoperative injuries to vertebral arteries.
The purpose of this study was to report the therapeutic outcome of this procedure, which was followed for >2 years. Preoperative symptoms were alleviated in all patients. Only 1 patient with subaxial canal stenosis underwent additional laminoplasty during follow-up. All patients with class IIIA or milder neural deficit according to Ranawat's classification showed improvement to class I or II. There were no surgery-related complications or incidents, including injuries to vertebral arteries. Bone union was observed in all patients. No change was observed in the reduced atlas-dens interval during follow-up. The atlantoaxial angle was −6° to 30° (average, 19.4°) at followup, and was ⩾30° after surgery (fusion in an overextended position) in only 1 patient. Although postoperative deterioration of cervical alignment was observed in 4 patients (18.2%), there was no additional surgery due to deterioration of cervical alignment.
With no surgery-related complications or incidents, this procedure could be a safe and acceptable option for atlantoaxial subluxation due to rheumatoid arthritis.
A Role for Bid in Eosinophil Apoptosis and in Allergic Airway Reaction
Authors: Maret Marielle , Ruffié Claude , Létuvé Séverine , Phelep Aurélie , Thibaudeau Olivier , Marchal Joëlle , Pretolani Marina , Druilhe Anne 
Published: April 2009

Abstract
Bid, a proapoptotic member of Bcl-2 family, is involved in Fas receptor signaling. Fas activation promotes human eosinophil cell death and is believed to accelerate the resolution of pulmonary Th2-driven allergic reaction in mice. We hypothesized that Bid would regulate eosinophil apoptosis and Ag-induced airway inflammation, particularly eosinophilia. C57BL/6 Bid−/− and wild-type mice were immunized and repeatedly challenged with OVA, and bronchoalveolar lavage (BAL) fluid, lung, and spleen were collected 4–240 h after the final challenge. Cultured BAL eosinophils from Bid-deficient mice showed resistance to Fas-mediated apoptotic DNA fragmentation, phosphatidylserine exposure, mitochondria depolarization, and caspase-3 activity. In addition, OVA-challenged Bid−/− mice had higher BAL eosinophilia and a lower proportion of BAL apoptotic eosinophils than Bid+/+ mice. This was accompanied by augmented BAL levels of the eosinophilotactic cytokine, IL-5, and of the eosinophil-associated mediators, TGF-β1 and fibronectin. Finally, cultured OVA-stimulated lung mononuclear cells and splenocytes from Bid-deficient mice showed increased release of the Th2-type cytokines, IL-4 and IL-5, but no change in cell number. We conclude that Bid modulates BAL eosinophilia by regulating both eosinophil apoptosis and Th2-type cytokine production.
Patterns of Receptor Revision in the Immunoglobulin Heavy Chains of a Teleost Fish
Authors: Lange Miles D. , Waldbieser Geoffrey C. , Lobb Craig J. 
Published: April 2009

Abstract
H chain cDNA libraries were constructed from the RNA derived from seven different organs and tissues from the same individual catfish. Sequence analysis of &gt;300 randomly selected clones identified clonal set members within the same or different tissues, and some of these represented mosaic or hybrid sequences. These hybrids expressed VH members of the same or different VH families within different regions of the same clone. Within some clonal sets multiple hybrids were identified, and some of these represented the products of sequential VH replacement events. Different experimental methods confirmed that hybrid clones identified in the cDNA library from one tissue could be reisolated in the cDNA pool or from the total RNA derived from the same or a different tissue, indicating that these hybrids likely represented the products of in vivo receptor revision events. Murine statistical recombination models were used to evaluate cryptic recombination signal sequences (cRSS), and significant cRSS pairs in the predicted VH donor and recipient were identified. These models supported the hypothesis that seamless revisions may have occurred via hybrid joint formation. The heptamers of the cRSS pairs were located at different locations within the coding region, and different events resulted in the replacement of one or both CDR as well as events that replaced the upstream untranslated region and the leader region. These studies provide phylogenetic evidence that receptor revision may occur in clonally expanded B cell lineages, which supports the hypothesis that additional levels of somatic H chain diversification may exist.
LTβR Signaling Induces Cytokine Expression and Up-Regulates Lymphangiogenic Factors in Lymph Node Anlagen
Authors: Vondenhoff Mark F. , Greuter Mascha , Goverse Gera , Elewaut Dirk , Dewint Pieter , Ware Carl F. , Hoorweg Kerim , Kraal Georg , Mebius Reina E. 
Published: April 2009

Abstract
The formation of lymph nodes is a complex process crucially controlled through triggering of LTβR on mesenchymal cells by LTα1β2 expressing lymphoid tissue inducer (LTi) cells. This leads to the induction of chemokines to attract more hematopoietic cells and adhesion molecules to retain them. In this study, we show that the extravasation of the first hematopoietic cells at future lymph node locations occurs independently of LTα and that these cells, expressing TNF-related activation-induced cytokine (TRANCE), are the earliest LTi cells. By paracrine signaling the first expression of LTα1β2 is induced. Subsequent LTβR triggering on mesenchymal cells leads to their differentiation to stromal organizers, which now also start to express TRANCE, IL-7, as well as VEGF-C, in addition to the induced adhesion molecules and chemokines. Both TRANCE and IL-7 will further induce the expression of LTα1β2 on newly arrived immature LTi cells, resulting in more LTβR triggering, generating a positive feedback loop. Thus, LTβR triggering by LTi cells during lymph node development creates a local environment to which hematopoietic precursors are attracted and where they locally differentiate into fully mature, LTα1β2 expressing, LTi cells. Furthermore, the same signals may regulate lymphangiogenesis to the lymph node through induction of VEGF-C.
A Proviral Role for CpG in Cytomegalovirus Infection
Authors: Iversen Ann-Charlotte , Steinkjer Bjørg , Nilsen Nadra , Bohnhorst Janne , Moen Siv Helen , Vik Randi , Stephens Phil , Thomas David W. , Benedict Chris A. , Espevik Terje 
Published: April 2009

Abstract
TLR9-dependent signaling in plasmacytoid dendritic cells is a key contributor to innate immune defense to mouse CMV infection. We aimed to study the expression and potential contribution of TLR9 signaling in human CMV (HCMV) infection of primary fibroblasts. HCMV infection strongly induced TLR9 expression in two of three fibroblast types tested. Furthermore, the TLR9 ligand CpG-B induced a strong proviral effect when added shortly after HCMV infection, enhancing virus production and cell viability. However, not all CpG classes displayed proviral activity, and this correlated with their IFN-β-inducing ability. The proviral effect of CpG-B correlated completely with concurrent viral up-regulation of TLR9 in fibroblasts. Importantly, the timing of CpG addition was a critical parameter; in striking contrast to the proviral effect, CpG addition at the time of infection blocked viral uptake and nearly abolished HCMV production. The contrasting and time-dependent effects of CpG on HCMV infectivity reveal a complex interplay between CpG, TLR9, and HCMV infection. Additionally, the data suggest a potentially harmful role for CpG in the promotion of HCMV infection.
Oncoprotein Signaling Mediates Tumor-Specific Inflammation and Enhances Tumor Progression
Authors: Pufnock Jeff S. , Rothstein Jay L. 
Published: April 2009

Abstract
The RET/PTC3 (RP3) fusion protein is an oncogene expressed during the development of thyroid cancer and in thyroid epithelial cells of patients with Hashimoto’s thyroiditis. RP3 has two immunological properties: 1) it encodes a chimeric protein including peptides that may be targets of antitumor immune responses and 2) it is a tyrosine kinase that can activate NF-κB transcriptional programs, induce secretion of proinflammatory mediators, and stimulate innate immunity. To distinguish the antigenic properties of the RP3 oncoprotein from its signaling function, a transplantable tumor system was developed. Tumors expressing the functional, but not mutant, form of RP3 show enhanced infiltration of CD8+ lymphocytes, myeloid-derived CD11b+Gr1+ cells, and enhanced growth in immunocompetent mice. In contrast, RP3 signaling mutant-expressing tumors maintained enhanced infiltration of CD8+ lymphocytes did not enhance recruitment of CD11b+Gr1+ cells and showed a decreased tumor incidence. These results implicate a role for RP3 function in enhancing a tumor-suppressive innate inflammatory response. These experiments support a mechanism whereby oncogenes can directly recruit and activate innate and adaptive immune cells, resulting in enhanced tumor progression.
PI3K p110β Positively Regulates Lipopolysaccharide-Induced IL-12 Production in Human Macrophages and Dendritic Cells and JNK1 Plays a Novel Role
Authors: Utsugi Mitsuyoshi , Dobashi Kunio , Ono Akihiro , Ishizuka Tamotsu , Matsuzaki Shin-ichi , Hisada Takeshi , Shimizu Yasuo , Kawata Tadayoshi , Aoki Haruka , Kamide Yosuke , Mori Masatomo 
Published: April 2009

Abstract
The PI3K family is thought to participate in TLR signaling, and it has been reported to be a negative regulator of TLR-mediated production of IL-12, a key inducer of Th1 responses. However, the role of individual PI3K subtypes in IL-12 production remains obscure. We defined the distinct regulation of LPS-mediated IL-12 production by p110α and p110β catalytic subunits of PI3K in human APCs. We observed that knockdown of PI3K p110β by small interfering RNA (siRNA) suppressed both LPS-induced IL-12 protein production and mRNA expression in monocyte-derived macrophages and dendritic cells (DCs). Knockdown of PI3K p110α by siRNA reduced LPS-induced IL-12 protein production in both cell types. Conversely, knockdown of PI3K p110α suppressed LPS-induced IL-12 mRNA expression in monocyte-derived macrophages but minimally affected monocyte-derived DCs. PI3K p110β siRNA inhibited JNK activation, but not p38 MAPK or ERK activation, stimulated by LPS, while PI3K p110α siRNA did not affect LPS-induced JNK, p38 MAPK, or ERK activation in both cell types. Transfection of siRNA against JNK1, JNK2, and both decreased LPS-induced IL-12 production. Furthermore, PI3K p110β siRNA attenuated LPS-induced JNK1 phosphorylation, while not affecting JNK2 phosphorylation. Our findings indicate that PI3K p110β positively controls LPS-induced IL-12 production through the JNK1-dependent pathway in human macrophages and DCs.
Luteinizing Hormone-Releasing Hormone Enhances T Cell Recovery following Allogeneic Bone Marrow Transplantation
Authors: Goldberg Gabrielle L. , King Christopher G. , Nejat Rebecca A. , Suh David Y. , Smith Odette M. , Bretz Jamison C. , Samstein Robert M. , Dudakov Jarrod A. , Chidgey Ann P. , Chen-Kiang Selina , Boyd Richard L. , van den Brink Marcel R. M. 
Published: April 2009

Abstract
Posttransplant immunodeficiency, specifically a lack of T cell reconstitution, is a major complication of allogeneic bone marrow transplantation. This immunosuppression results in an increase in morbidity and mortality from infections and very likely contributes to relapse. In this study, we demonstrate that sex steroid ablation using leuprolide acetate, a luteinizing hormone-releasing hormone agonist (LHRHa), increases the number of lymphoid and myeloid progenitor cells in the bone marrow and developing thymocytes in the thymus. Although few differences are observed in the peripheral myeloid compartments, the enhanced thymic reconstitution following LHRHa treatment and allogeneic bone marrow transplantation leads to enhanced peripheral T cell recovery, predominantly in the naive T cell compartment. This results in an increase in T cell function in vivo and in vitro. Graft-versus-host-disease is not exacerbated by LHRHa treatment and graft-versus-tumor activity is maintained. Because LHRHa allows for reversible (and temporary) sex steroid ablation, has a strong safety profile, and has been clinically approved for diseases such as prostate and breast cancer, this drug treatment represents a novel therapeutic approach to reversal of thymic atrophy and enhancement of immunity following immunosuppression.
Surface CD152 (CTLA-4) Expression and Signaling Dictates Longevity of CD28null T Cells
Authors: Hoff Holger , Knieke Karin , Cabail Zulema , Hirseland Heike , Vratsanos George , Burmester Gerd-Rüdiger , Jorch Gerhard , Nadler Steven G. , Bröker Barbara , Hebel Katrin , Brunner-Weinzierl Monika C. 
Published: April 2009

Abstract
CD28null T cells are a highly enriched subset of proinflammatory T cells in patients with autoimmune diseases that are oligoclonal and autoreactive. In this study, we analyzed the role of CD152 signaling on the longevity of human CD28null T cells. Using a sensitive staining method for CD152, we show that human CD4+CD28null and CD8+CD28null T cells rapidly express surface CD152. Serological inactivation of CD152 using specific Fab or blockade of CD152 ligands using CTLA-4Ig in CD4+CD28null and CD8+CD28null T cells enhances apoptosis in a Fas/FasL-dependent manner. CD152 cross-linking on activated CD28null cells prevents activation-induced cell death as a result of reduced caspase activity. Apoptosis protection conferred by CD152 is mediated by phosphatidylinositol 3′-kinase-dependent activation of the kinase Akt, resulting in enhanced phosphorylation and thereby inhibition of the proapoptotic molecule Bad. We show that signals triggered by CD152 act directly on activated CD28null T lymphocytes and, due to its exclusive expression as a receptor for CD80/CD86 on CD28null T cells, prevention of CD152-mediated signaling is likely a target mechanism taking place during therapy with CTLA-4Ig. Our data imply strongly that antagonistic approaches using CD152 signals for chronic immune responses might be beneficial.