bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrastructure of the mature spermatozoon of Eubothrium rugosum (Batsch, 1786) with a re-assessment of the spermatozoon ultrastructure of Eubothrium crassum (Bloch, 1779) (Cestoda: Bothriocephalidea)
Authors: Bruňanská M. , Fagerholm H.-P. , Nebesářová J. , Kostič B. 
Published: December 2010

Abstract
The ultrastructure of the mature spermatozoon of the bothriocephalidean tapeworm Eubothrium rugosum, a parasite of the burbot, Lota lota (L.), was studied by transmission electron microscopy for the first time. In addition, spermatozoon ultrastructure of Eubothrium crassum has been re-assessed. New is the finding, that the mature spermatozoa of both species of the genus Eubothrium exhibit essentially the same general morphology. They are filiform cells tapering at both extremities, and they possess the two axonemes with 9+“1” pattern of Trepaxonemata, attachment zones, a nucleus, cortical microtubules (CMs), electron-dense granules, and a single crested body. Structural polymorphism of the CBs has been found within the two Eubothrium species for the first time. The anterior ring of electron-dense tubular structures surrounding a single axoneme marks the border between the two defined regions, region I and region II of the spermatozoon. This unique feature has only been observed in the Bothriocephalidea. The anuclear axoneme region II of Eubothrium spermatozoa fluently verges into a nuclear region III. The posterior part of the spermatozoon contains one-axoneme, few CMs and a posterior extremity of the nucleus that subsequently disappears. The posterior extremity of the male gametes of the genus Eubothrium exhibits elements of a disorganized axoneme which characterize also spermatozoa of the family Triaenophoridae. Discussed are interspecific similarities and differences between the spermatozoa of the two Eubothrium species as well as between these and other Eucestoda.
The notes on the occurrence of Longidorus poessneckensis Altherr, 1974 (Nematoda: Dorylaimida) in the Slovak Republic
Authors: Lišková M. , Kumari S. 
Published: December 2010

Abstract
The record of occurrence of Longidorus poessneckensis Altherr, 1974 in forest soils with Betuleto-Carpineto-Quercetum in geographically specific conditions of a hilltop contributes to the broadening of ecological knowledge about this species. To date, the species was considered to prefer the habitats along river banks — narrow or large valleys and plains. The ecological, morphometrical and molecular characteristics of recorded L. poessneckensis are presented here.
The Role of Benzodiazepines in the Treatment of Anxiety Disorders: A Clinical Review
Authors: Macaluso Matthew , Kalia Rachna , Ali Faryal , Khan Ahsan Y. 
Published: December 2010

CME Educational Objectives

1.
Identify which benzodiazepines are FDA approved for specific anxiety disorders.

2.
Describe common adverse effects and safety issues relative to benzodiazepines.

3.
Describe the evidence supporting the off-label use of benzodiazepines to treat particular anxiety disorders.
Removed But Not Out of Reach: Seniors with Depression in Smaller Center, Rural, and Remote Communities
Authors: Welch Twilla , Welch Mark , Baer John , Dias Jeff , Gurney Corinne , Van Dale Bev , Lockie Marianne , Millar Kathy , Noon Joe , Psiurski Sandy 
Published: December 2010

CME Educational Objectives

1.
Identify key differences in the presentation of depression in older adults compared with a younger population.

2.
Review the challenges of initiating cognitive behavioral therapy (CBT) in a group setting with older adults in a rural setting.

3.
Name two validated assessment scales for anxiety and depression in older adults.
Efficacy of Percutaneous Kyphoplasty in Treating Osteoporotic Multithoracolumbar Vertebral Compression Fractures
Authors: Tang Hai , Zhao Jin-Dong , Li Yuan , Chen Hao , Jia Pu , Chan Kai-Ming , Li Gang 
Published: December 2010

Percutaneous kyphoplasty is a minimally invasive technique that has become an effective and routine alternative for managing osteoporotic vertebral compression fractures. This article reports the clinical outcome of a series of 54 cases of osteoporotic thoracolumbar vertebrae compression fractures treated by percutaneous kyphoplasty. Fifty-four patients with confirmed osteoporosis and at least 1 level of thoracolumbar vertebrae compression fracture were retrospectively selected. Pre- and postoperative and last follow-up clinical evaluation and radiological data were analyzed, including change of visual analog scale (VAS), reduced use of painkillers, locomotor activity, Cobb’s angle, and average vertebral body height.
Mean follow-up was 20.4 months (range, 6–36 months). In all cases, percutaneous kyphoplasty treatment was successful, significantly increasing vertebral body height, diminishing kyphosis in the fractured vertebrae, and decreasing painkiller use. In all patients, percutaneous kyphoplasty partially or completely relieved back pain. No new deformity was found within the follow-up period, nor were any other complications. The cement leakage rate was 3.86% (8 of 207 vertebrae) with percutaneous kyphoplasty, but no neurological or other complaints were received.
Percutaneous kyphoplasty is a simple and safe procedure in managing osteoporotic vertebrae compression fractures. It relieves pain quickly, restores vertebral height, prevents further fracture, and improves patient quality of life.
Clinical Benefits of Intra-Articular Anakinra for Arthrofibrosis
Authors: Brown Christopher A. , Toth Alison P. , Magnussen Bob 
Published: December 2010

Postoperative inflammation and stiffness, as well as the struggle to achieve full range of motion (ROM), following knee surgery is a significant clinical challenge. Interleukin-1 is a crucial mediator of the inflammatory response and development of pathological conditions leading to chronic inflammation. We hypothesized that intra-articular injection of intra-articular anakinra, an IL-1 antagonist, would result in sustained improvements of chronic refractory arthrofibrosis and limited arthrofibrosis of the knee joint.
We retrospectively reviewed 8 patients who underwent injection of intra-articular anakinra, 200 mg. Four patients (3 women, 1 man) had intra-articular anakinra for treatment of chronic refractory arthrofibrosis, and 4 patients (4 women) had intra-articular anakinra for limited arthrofibrosis. All 4 of the refractory arthrofibrosis patients had failed conservative treatment with intensive physical therapy, corticosteroid injections, and anti-inflammatory medication. Three of the 4 patients had failed a prior manipulation under anesthesia with lysis of adhesions. All 4 reported improvement in ROM (10°–45°) and swelling, with 75% reporting improvement in pain. Seventy-five percent of these patients returned to prior activity level. All 4 of the limited arthrofibrosis also failed similar attempts at conservative treatment, and 2 of the 4 had failed a prior manipulation under anesthesia with lysis of adhesions. After intra-articular anakinra, all 4 reported improvement in ROM (20°–45°) and swelling, with 80% reporting improvement in pain. Seventy-five percent of these patients were able to return to prior activity level.
We found intra-articular anakinra to be effective in this small cohort of patients with refractory arthrofibrosis and limited arthrofibrosis.
Two-Stage Flexor Tendon Reconstruction in Zone II Using Hunter’s Technique
Authors: Sun Siguo , Ding Yong , Ma Baoan , Zhou Yong 
Published: December 2010

Tendon injuries in the digital flexor sheath area (zone II) are the most difficult to treat and remain a focus of both clinical attention and basic investigations. Although some new techniques have been developed, the clinical results are still not satisfying, especially in old injuries. This retrospective study was designed to investigate the results of delayed zone II flexor tendon repair using Hunter rods.
Between July 1974 and June 1998, 81 patients at our institution underwent 2-stage reconstruction using Hunter’s technique. Sixty-one patients with 106 fingers were included in this study. Digital flexor tendon resection and Hunter rod implantation were performed in the first-stage operation. Combined digital nerve injuries and damaged pulleys were repaired or reconstructed at the same time. Plaster was used to immobilize the hand for 3 weeks. During the second-stage operation, performed 2 to 6 months later, palmaris longus or plantaris were grafted into the pseudosheath formed surrounding the Hunter rods. The proximal end of the transplanted tendon was fixated with flexor digitorum profundus tendon using the Pulvertaft method, and the distal end was fixated to the distal phalanx using Bunnell’s pullout wire method. Early controlled motion was performed in all cases. Evaluation based on total active motion was good to excellent in 84%, fair in 12%, and poor in 4% of patients.
Flexor tendon reconstruction using Hunter technique is an effective way to restore digital function in delayed zone II flexor tendon injuries.
Interface Fluid Syndrome After Bioptics
Authors: Bardet Emilie , Touboul David , Kerautret Julien , Léger François , Binder Perry S. , Colin Joseph 
Published: December 2010

Purpose:
To report an unusual case of interface fluid syndrome after refractive surgery.

Methods:
A 37-year-old man with high myopia underwent a planned bioptics procedure including creation of a corneal flap using a mechanical microkeratome and concurrent anterior chamber phakic intraocular lens implantation; excimer laser ablation was not performed at this time.

Results:
Postoperatively, the patient developed corneal edema and was referred to our department. Interface fluid syndrome was confirmed using optical coherence tomography; the mechanism was due to endothelial cell pump dysfunction.

Conclusions:
This is the first report to document interface fluid syndrome following a planned bioptics procedure.
A Mouse Model of Airway Disease: Oncostatin M-Induced Pulmonary Eosinophilia, Goblet Cell Hyperplasia, and Airway Hyperresponsiveness Are STAT6 Dependent, and Interstitial Pulmonary Fibrosis Is STAT6 Independent
Authors: Fritz Dominik K. , Kerr Christine , Fattouh Ramzi , Llop-Guevara Alba , Khan Waliul I. , Jordana Manel , Richards Carl D. 
Published: December 2010

AbstractOncostatin M (OSM), a pleiotropic cytokine of the gp130 cytokine family, has been implicated in chronic allergic inflammatory and fibrotic disease states associated with tissue eosinophilia. Mouse (m)OSM induces airway eosinophilic inflammation and interstitial pulmonary fibrosis in vivo and regulates STAT6 activation in vitro. To determine the requirement of STAT6 in OSM-induced effects in vivo, we examined wild-type (WT) and STAT6-knockout (STAT6−/−) C57BL/6 mouse lung responses to transient ectopic overexpression of mOSM using an adenoviral vector (AdmOSM). Intratracheal AdmOSM elicited persistent eosinophilic lung inflammation that was abolished in STAT6−/− mice. AdmOSM also induced pronounced pulmonary remodeling characterized by goblet cell hyperplasia and parenchymal interstitial fibrosis. Goblet cell hyperplasia was STAT6 dependent; however, parenchymal interstitial fibrosis was not. OSM also induced airway hyperresponsiveness in WT mice that was abolished in STAT6−/− mice. OSM stimulated an inflammatory signature in the lungs of WT mice that demonstrated STAT6-dependent regulation of Th2 cytokines (IL-4, IL-13), chemokines (eotaxin-1/2, MCP-1, keratinocyte chemoattractant), and extracellular matrix modulators (tissue inhibitor of matrix metalloproteinase-1, matrix metalloproteinase-13), but STAT6-independent regulation of IL-4Rα, total lung collagen, collagen-1A1, -1A2 mRNA, and parenchymal collagen and α smooth muscle actin accumulation. Thus, overexpression of mOSM induces STAT6-dependent pulmonary eosinophilia, mucous/goblet cell hyperplasia, and airway hyperresponsiveness but STAT6-independent mechanisms of lung tissue extracellular matrix accumulation. These results also suggest that eosinophil or neutrophil accumulation in mouse lungs is not required for OSM-induced lung parenchymal collagen deposition and that OSM may have unique roles in the pathogenesis of allergic and fibrotic lung disease.
Modulation of Dendritic Cell Differentiation in the Bone Marrow Mediates Sustained Immunosuppression after Polymicrobial Sepsis
Authors: Pastille Eva , Didovic Sonja , Brauckmann Daniela , Rani Meenakshi , Agrawal Hemant , Schade F. Ulrich , Zhang Yang , Flohé Stefanie B. 
Published: December 2010

Abstract
Murine polymicrobial sepsis is associated with a sustained reduction of dendritic cell (DC) numbers in lymphoid organs and with a dysfunction of DC that is considered to mediate the chronic susceptibility of post-septic mice to secondary infections. We investigated whether polymicrobial sepsis triggered an altered de novo formation and/or differentiation of DC in the bone marrow. BrdU labeling experiments indicated that polymicrobial sepsis did not affect the formation of splenic DC. DC that differentiated from bone marrow (bone marrow-derived DC [BMDC]) of post-septic mice released enhanced levels of IL-10 but did not show an altered phenotype in comparison with BMDC from sham mice. Adoptive transfer experiments of BMDC into naive mice revealed that BMDC from post-septic mice impaired Th1 priming but not Th cell expansion and suppressed the innate immune defense mechanisms against Pseudomonas bacteria in the lung. Accordingly, BMDC from post-septic mice inhibited the release of IFN-γ from NK cells that are critical for the protection against Pseudomonas. Additionally, sepsis was associated with a loss of resident DC in the bone marrow. Depletion of resident DC from bone marrow of sham mice led to the differentiation of BMDC that were impaired in Th1 priming similar to BMDC from post-septic mice. Thus, in response to polymicrobial sepsis, DC precursor cells in the bone marrow developed into regulatory DC that impaired Th1 priming and NK cell activity and mediated immunosuppression. The absence of resident DC in the bone marrow after sepsis might have contributed to the modulation of DC differentiation.
STIM1-Directed Reorganization of Microtubules in Activated Mast Cells
Authors: Hájková Zuzana , Bugajev Viktor , Dráberová Eduarda , Vinopal Stanislav , Dráberová Lubica , Janáček Jiří , Dráber Petr , Dráber Pavel 
Published: December 2010

Abstract
Activation of mast cells by aggregation of the high-affinity IgE receptors (FcεRI) initiates signaling events leading to the release of inflammatory and allergic mediators stored in cytoplasmic granules. A key role in this process play changes in concentrations of intracellular Ca2+ controlled by store-operated Ca2+ entry (SOCE). Although microtubules are also involved in the process leading to degranulation, the molecular mechanisms that control microtubule rearrangement during activation are largely unknown. In this study, we report that activation of bone marrow-derived mast cells (BMMCs) induced by FcεRI aggregation or treatment with pervanadate or thapsigargin results in generation of protrusions containing microtubules (microtubule protrusions). Formation of these protrusions depended on the influx of extracellular Ca2+. Changes in cytosolic Ca2+concentration also affected microtubule plus-end dynamics detected by microtubule plus-end tracking protein EB1. Experiments with knockdown or reexpression of STIM1, the key regulator of SOCE, confirmed the important role of STIM1 in the formation of microtubule protrusions. Although STIM1 in activated cells formed puncta associated with microtubules in protrusions, relocation of STIM1 to a close proximity of cell membrane was independent of growing microtubules. In accordance with the inhibition of Ag-induced Ca2+ response and decreased formation of microtubule protrusions in BMMCs with reduced STIM1, the cells also exhibited impaired chemotactic response to Ag. We propose that rearrangement of microtubules in activated mast cells depends on STIM1-induced SOCE, and that Ca2+ plays an important role in the formation of microtubule protrusions in BMMCs.
Seasonal FluMist Vaccination Induces Cross-Reactive T Cell Immunity against H1N1 (2009) Influenza and Secondary Bacterial Infections
Authors: Sun Keer , Ye Jianqiang , Perez Daniel R. , Metzger Dennis W. 
Published: December 2010

Abstract
T cell epitopes have been found to be shared by circulating, seasonal influenza virus strains and the novel pandemic H1N1 influenza infection, but the ability of these common epitopes to provide cross-protection is unknown. We have now directly tested this by examining the ability of live seasonal influenza vaccine (FluMist) to mediate protection against swine-origin H1N1 influenza virus infection. Naive mice demonstrated considerable susceptibility to H1N1 Cal/04/09 infection, whereas FluMist-vaccinated mice had markedly decreased morbidity and mortality. In vivo depletion of CD4+ or CD8+ immune cells after vaccination indicated that protective immunity was primarily dependent upon FluMist-induced CD4+ cells but not CD8+ T cells. Passive protection studies revealed little role for serum or mucosal Abs in cross-protection. Although H1N1 influenza infection of naive mice induced intensive phagocyte recruitment, pulmonary innate defense against secondary pneumococcal infection was severely suppressed. This increased susceptibility to bacterial infection was correlated with augmented IFN-γ production produced during the recovery stage of H1N1 influenza infection, which was completely suppressed in mice previously immunized with FluMist. Furthermore, susceptibility to secondary bacterial infection was decreased in the absence of type II, but not type I, IFN signaling. Thus, seasonal FluMist treatment not only promoted resistance to pandemic H1N1 influenza infection but also restored innate immunity against complicating secondary bacterial infections.
Neutrophils Require SHP1 To Regulate IL-1β Production and Prevent Inflammatory Skin Disease
Authors: Croker Ben A. , Lewis Rowena S. , Babon Jeff J. , Mintern Justine D. , Jenne Dieter E. , Metcalf Donald , Zhang Jian-Guo , Cengia Louise H. , O’Donnell Joanne A. , Roberts Andrew W. 
Published: December 2010

Abstract
The regulation of neutrophil recruitment, activation, and disposal is pivotal for circumscribed inflammation. SHP1Y208N/Y208N mutant mice develop severe cutaneous inflammatory disease that is IL-1R dependent. Genetic reduction in neutrophil numbers and neutrophilic responses to infection is sufficient to prevent the spontaneous initiation of this disease. Neutrophils from SHP1Y208N/Y208N mice display increased pro–IL-1β production due to altered responses to MyD88-dependent and MyD88-independent signals. The IL-1R–dependent inflammatory disease in SHP1Y208N/Y208N mice develops independently of caspase 1 and proteinase 3 and neutrophil elastase. In response to Fas ligand, a caspase 1-independent inducer of IL-1β production, neutrophils from SHP1Y208N/Y208N mice produce elevated levels of IL-1β but display reduced caspase 3 and caspase 7 activation. In neutrophils deficient in SHP1, IL-1β induces high levels of pro–IL-1β suggesting the presence of a paracrine IL-1β loop. These data indicate that the neutrophil- and IL-1–dependent disease in SHP1Y208N/Y208N mice is a consequence of loss of negative regulation of TLR and IL-1R signaling.
Immune Complex-Mediated Cell Activation from Systemic Lupus Erythematosus and Rheumatoid Arthritis Patients Elaborate Different Requirements for IRAK1/4 Kinase Activity across Human Cell Types
Authors: Chiang Eugene Y. , Yu Xin , Grogan Jane L. 
Published: December 2010

Abstract
IL-1R–associated kinases (IRAKs) are important mediators of MyD88-dependent signaling by the TLR/IL-1R superfamily and facilitate inflammatory responses. IRAK4 and IRAK1 function as active kinases and as scaffolds for protein–protein interactions. We report that although IRAK1/4 kinase activity is essential for human plasmacytoid dendritic cell (pDC) activation, it is dispensable in B, T, dendritic, and monocytic cells, which is in contrast with an essential active kinase role in comparable mouse cell types. An IRAK1/4 kinase inhibitor abrogated TLR7/9-induced IFN-α responses in both mouse and human pDCs, but other human immune cell populations activated via TLR7/9 or IL-1R were refractory to IRAK4 kinase inhibition. Gene ablation experiments using small interfering RNA demonstrated an essential scaffolding role for IRAK1 and IRAK4 in MyD88-dependent signaling. Finally, we demonstrate that autoimmune patient (systemic lupus erythematosus and rheumatoid arthritis) serum activates both pDC and B cells, but IRAK1/4 kinase inhibition affects only the pDC response, underscoring the differential IRAK1/4 functional requirements in human immune cells. These data reveal important species differences and elaborate cell type requirements for IRAK1/4 kinase activity.
Antigen-Driven Patterns of TCR Bias Are Shared across Diverse Outcomes of Human Hepatitis C Virus Infection
Authors: Miles John J. , Thammanichanond Duangtawan , Moneer Sarah , Nivarthi Usha K. , Kjer-Nielsen Lars , Tracy Samantha L. , Aitken Campbell K. , Brennan Rebekah M. , Zeng Weiguang , Marquart Louise , Jackson David , Burrows Scott R. , Bowden David S. , Torresi Joseph , Hellard Margaret , Rossjohn Jamie , McCluskey James , Bharadwaj Mandvi 
Published: December 2010

Abstract
Hepatitis C virus (HCV) infection causes significant morbidity and mortality worldwide. T cells play a central role in HCV clearance; however, there is currently little understanding of whether the disease outcome in HCV infection is influenced by the choice of TCR repertoire. TCR repertoires used against two immunodominant HCV determinants—the highly polymorphic, HLA-B*0801 restricted 1395HSKKKCDEL1403 (HSK) and the comparatively conserved, HLA-A*0101–restricted, 1435ATDALMTGY1443 (ATD)—were analyzed in clearly defined cohorts of HLA-matched, HCV-infected individuals with persistent infection and HCV clearance. In comparison with ATD, TCR repertoire selected against HSK was more narrowly focused, supporting reports of mutational escape in this epitope, in persistent HCV infection. Notwithstanding the Ag-driven divergence, T cell repertoire selection against either Ag was comparable in subjects with diverse disease outcomes. Biased T cell repertoires were observed early in infection and were evident not only in persistently infected individuals but also in subjects with HCV clearance, suggesting that these are not exclusively characteristic of viral persistence. Comprehensive clonal analysis of Ag-specific T cells revealed widespread use of public TCRs displaying a high degree of predictability in TRBV/TRBJ gene usage, CDR3 length, and amino acid composition. These public TCRs were observed against both ATD and HSK and were shared across diverse disease outcomes. Collectively, these observations indicate that repertoire diversity rather than particular Vβ segments are better associated with HCV persistence/clearance in humans. Notably, many of the anti-HCV TCRs switched TRBV and TRBJ genes around a conserved, N nucleotide-encoded CDR3 core, revealing TCR sequence mosaicism as a potential host mechanism to combat this highly variant virus.