bluuebunny/crossref_metadata_2025_split huggingface dataset:
Minimally invasive removal of lumbar intradural extramedullary lesions using the interlaminar approach
Authors: Zhu Yong-Jian , Ying Guang-Yu , Chen Ai-Qin , Wang Lin-Lin , Yu Dan-Feng , Zhu Liang-Liang , Ren Yu-Cheng , Wang Chen , Wu Peng-Cheng , Yao Ying , Shen Fang , Zhang Jian-Min 
Published: August 2015

OBJECT
Posterior midline laminectomy or hemilaminectomy has been successfully applied as the standard microsurgical technique for the treatment of spinal intradural pathologies. However, the associated risks of postoperative spinal instability increase the need for subsequent fusion surgery to prevent potential long-term spinal deformity. Continuous efforts have been made to minimize injuries to the surrounding tissue resulting from surgical manipulations. The authors report here their experiences with a novel minimally invasive surgical approach, namely the interlaminar approach, for the treatment of lumbar intraspinal tumors.

METHODS
A retrospective review was conducted of patients at the Second Affiliated Hospital of Zhejiang University School of Medicine who underwent minimally invasive resection of lumbar intradural-extramedullary tumors. By using an operative microscope, in addition to an endoscope when necessary, the authors were able to treat all patients with a unilateral, paramedian, bone-sparing interlaminar technique. Data including preoperative neurological status, tumor location, size, pathological diagnosis, extension of resections, intraoperative blood loss, length of hospital stay, and clinical outcomes were obtained through clinical and radiological examinations.

RESULTS
Eighteen patients diagnosed with lumbar intradural-extramedullary tumors were treated from October 2013 to March 2015 by this interlaminar technique. A microscope was used in 15 cases, and the remaining 3 cases were treated using a microscope as well as an endoscope. There were 14 schwannomas, 2 ependymomas, 1 epidermoid cyst, and 1 enterogenous cyst. Postoperative radiological follow-up revealed complete removal of all the lesions and no signs of bone defects in the lamina. At clinical follow-up, 14 of the 18 patients had less pain, and patients' motor/sensory functions improved or remained normal in all cases except 1.

CONClUSIONS
When meeting certain selection criteria, intradural-extramedullary lumbar tumors, especially schwannomas, can be completely and safely resected through a less-invasive interlaminar approach using a microscope, or a microscope in addition to an endoscope when necessary. This approach was advantageous because it caused even less bone destruction, resulting in better postoperative spinal stability, no need for facetectomy and fusion, and quicker functional recovery for the patients. Individualized surgical planning according to preoperative radiological findings is key to a successful microsurgical resection of these lesions through the interlaminar space.
Comparison of minimally invasive transspinous and open approaches for thoracolumbar intradural-extramedullary spinal tumors
Authors: Raygor Kunal P. , Than Khoi D. , Chou Dean , Mummaneni Praveen V. 
Published: August 2015

OBJECT
Spinal tumor resection has historically been performed via open approaches, although minimally invasive approaches have recently been found to be effective in small cohort series. The authors compare surgical characteristics and clinical outcomes of surgery in patients undergoing mini-open and open approaches for intradural-extramedullary tumor resection.

METHODS
The authors retrospectively reviewed 65 consecutive intradural-extramedullary tumor resections performed at their institution from 2007 to 2014. Patients with cervical tumors or pathology demonstrating neurofibroma were excluded (n = 14). The nonparametric Mann-Whitney U-test and Pearson chi-square test were used to compare continuous and categorical variables, respectively. Statistical analyses were performed using SPSS, with significance set at p < 0.05.

RESULTS
Fifty-one thoracolumbar intradural-extramedullary tumor resections were included; 25 were performed via the minimally invasive transspinous approach. There were no statistically significant differences in age, sex, body mass index, preoperative American Spinal Injury Association (ASIA) score, preoperative symptom duration, American Society of Anesthesiologists (ASA) physical status class, tumor size, or tumor location. There was no statistically significant difference between groups with respect to the duration of the operation or extent of resection, but the mean estimated blood loss was significantly lower in the minimally invasive surgery (MIS) cohort (142 vs 320 ml, p < 0.05). In each group, the 2 most common tumor pathologies were schwannoma and meningioma. There were no statistically significant differences in length of hospitalization, ASIA score improvement, complication rate, or recurrence rate. The mean duration of follow-up was 2 years for the MIS group and 1.6 years for the open surgery group.

CONCLUSIONS
This is one of the largest comparisons of minimally invasive and open approaches to the resection of thoracolumbar intradural-extramedullary tumors. With well-matched cohorts, the minimally invasive transspinous approach appears to be as safe and effective as the open technique, with the advantage of significantly reduced intraoperative blood loss.
Synthesis and biological evaluation of 6H-1-benzopyrano[4,3-b]quinolin-6-one derivatives as inhibitors of colon cancer cell growth
Authors: Li Tie-Ling , Guo Hai-Feng , Li Fu-Juan , Sun Zhi-Guo , Zhang Heng-Chun 
Published: August 2015

<p class="Abstract">A convenient synthesis of 6H-1-benzopyrano[4,3-b]quinolin-6-one derivatives was reported using 4-chloro-2-oxo-2H-chromene-3-carbaldehyde with different aromatic amines using silica sulfuric acid. The compounds were tested for their anticancer activity against colon (HCT-116 and S1-MI-80), prostate (PC3 and DU-145), breast (MCF-7 and MDAMB-231) cancer cells. These com-pounds showed more selectivity and potent cytotoxic activity against colon cancer cells. 3c was tested against five other colon cancer cell lines (HT-29, HCT-15, LS-180, LS-174, and LoVo), which had similar cytotoxicity and selectivity. 3c did not induce PXR-regulated ABCB1 or ABCG2 transporters. In fact, 3c induced cytotoxicity in HEK293 cells over expressing ABCB1 or ABCG2 to the same extent as in normal HEK293 cells. It was cytotoxic approximately 3- and 5-fold to resistant colon carcinoma S1-MI-80 cells. 3c also produced concentration-dependent changes in HCT-116 colon cancer cells, in mitochondrial membrane potential, leading to apoptosis, and sub-micromolar concentrations caused chromosomal DNA fragmentation. </p><p> </p>
Utility of Select Plasma MicroRNA for Disease and Cardiovascular Risk Assessment in Patients with Rheumatoid Arthritis
Authors: Ormseth Michelle J. , Solus Joseph F. , Vickers Kasey C. , Oeser Annette M. , Raggi Paolo , Stein C. Michael 
Published: August 2015

Objective.MicroRNA (miRNA) are small noncoding RNA that posttranscriptionally regulate gene expression and serve as potential mediators and markers of disease. Recently, plasma miR-24-3p and miR-125a-5p concentrations were shown to be elevated in rheumatoid arthritis (RA) and useful for RA diagnosis. We assessed the utility of 7 candidate plasma miRNA, selected for biological relevance, for RA diagnosis and use as markers of disease activity and subclinical atherosclerosis in RA.Methods.The cross-sectional study included 168 patients with RA and 91 control subjects of similar age, race, and sex. Plasma concentrations of miR-15a-5p, miR-24-3p, miR-26a-5p, miR-125a-5p, miR-146a-5p, miR-155-5p, and miR-223-3p were measured by quantitative PCR. Utility of plasma miRNA concentrations for RA diagnosis was assessed by area under the receiver-operating characteristic curve (AUROC). Associations between plasma miRNA concentrations and RA disease activity and coronary artery calcium score were assessed by Spearman correlations.Results.Plasma concentrations of miR-15a-5p, miR-24-3p, miR-26a-5p, miR-125a-5p, miR-146a-5p, miR-155-5p, and miR-223-3p were significantly increased in patients with RA. The highest AUROC for diagnosis of RA (AUROC = 0.725) was found in miR-24-3p, including among rheumatoid factor–negative patients (AUROC = 0.772). Among all patients with RA, the combination of miR-24-3p, miR-26a-5p, and miR-125a-5p improved the model modestly (AUROC = 0.747). One miRNA, miR-155-5p, was weakly inversely associated with swollen joint count (p = 0.024), but no other miRNA were associated with disease activity or coronary artery calcium score.Conclusion.The combination of miR-24-3p, miR-26a-5p, and miR-125a-5p had the strongest diagnostic accuracy for RA. Candidate miRNA had little or no association with RA disease activity or subclinical atherosclerosis.
Compassion Satisfaction and Compassion Fatigue Among Critical Care Nurses
Authors: Sacco Tara L. , Ciurzynski Susan M. , Harvey Megan Elizabeth , Ingersoll Gail L. 
Published: August 2015

BACKGROUNDAlthough critical care nurses gain satisfaction from providing compassionate care to patients and patients’ families, the nurses are also at risk for fatigue. The balance between satisfaction and fatigue is considered professional quality of life.OBJECTIVESTo establish the prevalence of compassion satisfaction and compassion fatigue in adult, pediatric, and neonatal critical care nurses and to describe potential contributing demographic, unit, and organizational characteristics.METHODSIn a cross-sectional design, nurses were surveyed by using a demographic questionnaire and the Professional Quality of Life Scale to measure levels of compassion fatigue and compassion satisfaction.RESULTSNurses (n = 221) reported significant differences in compassion satisfaction and compassion fatigue on the basis of sex, age, educational level, unit, acuity, change in nursing management, and major systems change.CONCLUSIONSUnderstanding the elements of professional quality of life can have a positive effect on work environment. The relationship between professional quality of life and the standards for a healthy work environment requires further investigation. Once this relationship is fully understood, interventions to improve this balance can be developed and tested.
The Src-Family Kinases Hck and Fgr Regulate Early Lipopolysaccharide-Induced Myeloid Cell Recruitment into the Lung and Their Ability To Secrete Chemokines
Authors: Mazzi Paola , Caveggion Elena , Lapinet-Vera Josè A. , Lowell Clifford A. , Berton Giorgio 
Published: August 2015

Abstract
Myeloid leukocyte recruitment into the lung in response to environmental cues represents a key factor for the induction of lung damage. We report that Hck- and Fgr-deficient mice show a profound impairment in early recruitment of neutrophils and monocytes in response to bacterial LPS. The reduction in interstitial and airway neutrophil recruitment was not due to a cell-intrinsic migratory defect, because Hck- and Fgr-deficient neutrophils were attracted to the airways by the chemokine CXCL2 as wild type cells. However, early accumulation of chemokines and TNF-α in the airways was reduced in hck−/−fgr−/− mice. Considering that chemokine and TNF-α release into the airways was neutrophil independent, as suggested by a comparison between control and neutrophil-depleted mice, we examined LPS-induced chemokine secretion by neutrophils and macrophages in wild type and mutant cells. Notably, mutant neutrophils displayed a marked deficit in their capability to release the chemokines CXCL1, CXCL2, CCL3, and CCL4 and TNF-α in response to LPS. However, intracellular accumulation of these chemokines and TNF-α, as well as secretion of a wide array of cytokines, including IL-1α, IL-1β, IL-6, and IL-10, by hck−/−fgr−/− neutrophils was normal. Intriguingly, secretion of CXCL1, CXCL2, CCL2, CCL3, CCL4, RANTES, and TNF-α, but not IL-1α, IL-1β, IL-6, IL-10, and GM-CSF, was also markedly reduced in bone marrow–derived macrophages. Consistently, the Src kinase inhibitors PP2 and dasatinib reduced chemokine secretion by neutrophils and bone marrow–derived macrophages. These findings identify Src kinases as a critical regulator of chemokine secretion in myeloid leukocytes during lung inflammation.
Id3 Controls Cell Death of 2B4+ Virus-Specific CD8+ T Cells in Chronic Viral Infection
Authors: Menner Alexandra J. , Rauch Katharina S. , Aichele Peter , Pircher Hanspeter , Schachtrup Christian , Schachtrup Kristina 
Published: August 2015

Abstract
Sustained Ag persistence in chronic infection results in a deregulated CD8+ T cell response that is characterized by T cell exhaustion and cell death of Ag-specific CD8+ T cells. Yet, the underlying transcriptional mechanisms regulating CD8+ T cell exhaustion and cell death are poorly defined. Using the experimental mouse model of lymphocytic choriomeningitis virus infection, we demonstrate that the transcriptional regulator Id3 controls cell death of virus-specific CD8+ T cells in chronic infection. By comparing acute and chronic infection, we showed that Id3− virus-specific CD8+ T cells were less abundant, whereas the absolute numbers of Id3+ virus-specific CD8+ T cells were equal in chronic and acute infection. Phenotypically, Id3− and Id3+ cells most prominently differed with regard to expression of the surface receptor 2B4; although Id3− cells were 2B4+, almost all Id3+ cells lacked expression of 2B4. Lineage-tracing experiments showed that cells initially expressing Id3 differentiated into Id3−2B4+ cells; in turn, these cells were terminally differentiated and highly susceptible to cell death under conditions of persisting Ag. Enforced Id3 expression specifically increased the persistence of 2B4+ virus-specific CD8+ T cells by decreasing susceptibility to Fas/Fas ligand–mediated cell death. Thus, our findings reveal that the transcriptional regulator Id3 promotes the survival of virus-specific CD8+ T cells in chronic infection and suggest that targeting Id3 might be beneficial for preventing cell death of CD8+ T cells in chronic infection or for promoting cell death of uncontrolled, hyperactive CD8+ T cells to prevent immunopathology.
Cholesterol Modification of p40-Specific Small Interfering RNA Enables Therapeutic Targeting of Dendritic Cells
Authors: Brück Jürgen , Pascolo Steve , Fuchs Kerstin , Kellerer Christina , Glocova Ivana , Geisel Julia , Dengler Katja , Yazdi Amir S. , Röcken Martin , Ghoreschi Kamran 
Published: August 2015

Abstract
Small interfering RNA (siRNA)–based therapies allow targeted correction of molecular defects in distinct cell populations. Although efficient in multiple cell populations, dendritic cells (DCs) seem to resist siRNA delivery. Using fluorescence labeling and radiolabeling, we show that cholesterol modification enables siRNA uptake by DCs in vitro and in vivo. Delivery of cholesterol-modified p40 siRNA selectively abolished p40 transcription and suppressed TLR-triggered p40 production by DCs. During immunization with peptide in CFA, cholesterol-modified p40 siRNA generated p40-deficient, IL-10–producing DCs that prevented IL-17/Th17 and IFN-γ/Th1 responses. Only cholesterol-modified p40-siRNA established protective immunity against experimental autoimmune encephalomyelitis and suppressed IFN-γ and IL-17 expression by CNS-infiltrating mononuclear cells without inducing regulatory T cells. Because cholesterol-modified siRNA can thus modify selected DC functions in vivo, it is intriguing for targeted immune therapy of allergic, autoimmune, or neoplastic diseases.
B Lymphocyte–Specific Loss of Ric-8A Results in a Gα Protein Deficit and Severe Humoral Immunodeficiency
Authors: Boularan Cedric , Hwang Il-Young , Kamenyeva Olena , Park Chung , Harrison Kathleen , Huang Zhen , Kehrl John H. 
Published: August 2015

Abstract
Resistance to inhibitors of cholinesterase 8A (Ric-8A) is a highly evolutionarily conserved cytosolic protein initially identified in Caenorhabditis elegans, where it was assigned a regulatory role in asymmetric cell divisions. It functions as a guanine nucleotide exchange factor for Gαi, Gαq, and Gα12/13 and as a molecular chaperone required for the initial association of nascent Gα subunits with cellular membranes in embryonic stem cell lines. To test its role in hematopoiesis and B lymphocytes specifically, we generated ric8fl/flvav1-cre and ric8fl/flmb1-cre mice. The major hematopoietic cell lineages developed in the ric8fl/flvav1-cre mice, notwithstanding severe reduction in Gαi2/3, Gαq, and Gα13 proteins. B lymphocyte–specific loss of Ric-8A did not compromise bone marrow B lymphopoiesis, but splenic marginal zone B cell development failed, and B cells underpopulated lymphoid organs. The ric8fl/flmb1-cre B cells exhibited poor responses to chemokines, abnormal trafficking, improper in situ positioning, and loss of polarity components during B cell differentiation. The ric8fl/flmb1-cre mice had a severely disrupted lymphoid architecture and poor primary and secondary Ab responses. In B lymphocytes, Ric-8A is essential for normal Gα protein levels and is required for B cell differentiation, trafficking, and Ab responses.
Role of SHIP1 in Invariant NKT Cell Development and Functions
Authors: Anderson Courtney K. , Salter Alexander I. , Toussaint Leon E. , Reilly Emma C. , Fugère Céline , Srivastava Neetu , Kerr William G. , Brossay Laurent 
Published: August 2015

Abstract
SHIP1 is a 5′-inositol phosphatase known to negatively regulate the signaling product of the PI3K pathway, phosphatidylinositol (3–5)-trisphosphate. SHIP1 is recruited to a large number of inhibitory receptors expressed on invariant NK (iNKT) cells. We hypothesized that SHIP1 deletion would have major effects on iNKT cell development by altering the thresholds for positive and negative selection. Germline SHIP1 deletion has been shown to affect T cells as well as other immune cell populations. However, the role of SHIP1 on T cell function has been controversial, and its participation on iNKT cell development and function has not been examined. We evaluated the consequences of SHIP1 deletion on iNKT cells using germline-deficient mice, chimeric mice, and conditionally deficient mice. We found that T cell and iNKT cell development are impaired in germline-deficient animals. However, this phenotype can be rescued by extrinsic expression of SHIP1. In contrast, SHIP1 is required cell autonomously for optimal iNKT cell cytokine secretion. This suggests that SHIP1 calibrates the threshold of iNKT cell reactivity. These data further our understanding of how iNKT cell activation is regulated and provide insights into the biology of this unique cell lineage.
Proteolytic Cleavage of AMPKα and Intracellular MMP9 Expression Are Both Required for TLR4-Mediated mTORC1 Activation and HIF-1α Expression in Leukocytes
Authors: Zhang Zhiyong , Amorosa Louis F. , Coyle Susette M. , Macor Marie A. , Lubitz Sara E. , Carson Jeffrey L. , Birnbaum Morris J. , Lee Leonard Y. , Haimovich Beatrice 
Published: August 2015

Abstract
LPS-induced TLR4 activation alters cellular bioenergetics and triggers proteolytic cleavage of AMPKα and HIF-1α expression in leukocytes. In human leukocytes, and more specifically neutrophils, AMPKα cleavage yields 55- and 35-kDa protein fragments. In this study, we address the mechanism by which AMPKα is cleaved and its relevance to human health. Our data indicate that AMPKα cleavage is linked to MMP9 expression and that both are required for mammalian target of rapamycin complex-1 and S6K1 activation and HIF-1α expression in LPS-stimulated human and mice leukocytes. Three key observations support this conclusion. First, no changes in AMPKα and TLR4 signaling intermediates (mammalian target of rapamycin complex-1/S6 kinase 1/HIF-1α) were detected in LPS-stimulated MMP9-deficient mice leukocytes. Second, rMMP9 cleaved human AMPKα ex vivo, producing degradation products similar in size to those detected following LPS stimulation. Third, MMP9 inhibitors prevented AMPKα degradation and HIF-1α expression in LPS-activated human leukocytes, whereas AMPK activators blocked MMP9 and HIF-1α expression. Significantly, AMPKα degradation, MMP9, and TLR4 signaling intermediates were all detected in leukocytes from patients with type 2 diabetes mellitus and patients following cardiopulmonary bypass surgery. Plasma from these two patient cohorts induced AMPKα cleavage and TLR4 signaling intermediates in healthy donor leukocytes and either a TLR4 inhibitor or polymyxin prevented these outcomes. Detection of AMPKα degradation, MMP9 expression, and TLR4 signaling intermediates described in this study in leukocytes, the most readily available human cells for clinical investigation, may provide a powerful tool for further exploring the role of TLR4 signaling in human diseases and lead to identification of new, context-specific therapeutic modalities for precision medicine.
Parafibromin Is a Component of IFN-γ–Triggered Signaling Pathways That Facilitates JAK1/2-Mediated Tyrosine Phosphorylation of STAT1
Authors: Wei Jin , Lian Huan , Zhong Bo , Shu Hong-Bing 
Published: August 2015

Abstract
IFN-γ (also known as type II IFN) is a cytokine that is critically involved in antiviral and immunomodulatory effects. IFN-γ activates JAK1 and JAK2, which lead to the phosphorylation and activation of the transcription factor STAT1. Whether and how additional molecules are involved in the process are not fully clear. In this study, we identified parafibromin as an important component of the IFN-γ–triggered signaling pathways. Overexpression of parafibromin promoted IFN-γ–triggered phosphorylation of STAT1 at Tyr701, subsequent expression of downstream genes, and cellular antiviral response, whereas knockdown of parafibromin had opposite effects. Parafibromin interacted with JAK1/2, promoted the interactions of JAK1–JAK2 and JAK1/2–STAT1, and promoted tyrosine phosphorylation of STAT1 by JAKs after IFN-γ stimulation. Our results reveal a previously uncharacterized role of parafibromin in mediating IFN-γ–triggered signaling and cellular effects.
Post-Holocaust Representations of Poland in Israeli Literature
Authors: Ronen Shoshana 
Published: August 2015

Abstract
The article discusses different images of Poland in post-Holocaust Hebrew literature. These texts portray journeys to Poland as a means of constructing a self-identity. Poland is a perfect place for such a search. It is the soil on which many Jews lived for centuries and where a large portion of the Jewish people was exterminated in World War II. Poland is, on the one hand, the place of origin and, on the other hand, the place where an entire civilization came to an end. The article distinguishes two main waves in journeys to Poland in Israeli literature. The first wave was the first encounter with Communist or Postcommunist Poland as it awakened to a new world. This wave was composed primarily of “second-generation” writers who were trying to construct their own identity and memory from the remnants of the destroyed Jewish world. For them, the journey to Poland was first and foremost a journey to the valley of death. The second wave was of Israeli writers who traveled to the same “void” as their predecessors, but they were fascinated by the memory of the absent Jews, which was constructed by Poles. They are distant from themselves, and they have a sense of irony as they observe the Polish reality around them. This Poland is different, democratic, and modern. The second-wave writers are not afraid to enter into a dialogue and interaction with Poles and they treat them as subjects, not as symbols of the “other”; but for first-wave writers, Poles were merely in the background, not partners for dialogue. However, in both waves the goal of the journey is to construct an identity by finding a link to the past that will establish a continuity: a continuity that offers the consolation of a complete story and therefore closure.