bluuebunny/crossref_metadata_2025_split huggingface dataset:
Open Bankart Repair versus Arthroscopic Repair with Transglenoid Sutures or Bioabsorbable Tacks for Recurrent Anterior Instability of the Shoulder
Authors: Freedman Kevin B. , Smith Adam P. , Romeo Anthony A. , Cole Brian J. , Bach Bernard R. 
Published: July 2004

Background In published comparative studies, it remains unknown if arthroscopic techniques for performing Bankart repair for anterior shoulder instability equal the success of open repair. Hypothesis The current literature supports a lower rate of recurrent instability after open Bankart repair compared to arthro-scopic repair with bioabsorbable tacks or transglenoid sutures. Study Design Meta-analysis. Methods A Medline search identified all randomized controlled trials or cohort studies that directly compared open repair to arthroscopic techniques of Bankart repair for traumatic, unilateral, recurrent anterior instability. Data collected from each study included patient demographics, surgical technique, rehabilitation, outcome, and complications. Results Six studies met all inclusion criteria. There were 172 patients in the arthroscopic group (90 patients with transglenoid sutures, 77 patients with arthroscopic tacks, and 5 patients with suture anchors) and 156 patients in the open group. The groups were similar in demographic characteristics. When comparing the arthroscopic to the open group, there was a significantly higher rate of recurrent dislocation (12.6% vs 3.4%; P = .01) and total recurrence (recurrent dislocation or subluxation) (20.3% vs 10.3%; P = .01). In addition, there was a higher proportion of patients with an excellent or good postoperative Rowe score in the open group (88%) than in the arthroscopic group (71%) (P = .01). Conclusions Arthroscopic Bankart repair using transglenoid sutures or bioabsorbable tacks results in a higher rate of recurrence of instability compared to open techniques. Studies comparing open repair to newer arthroscopic techniques using suture anchor fixation and capsular plication are necessary.
Consultation, Community and Empowerment
Authors: Mclaughlin Hugh , Brown Denise , Young Alys M. 
Published: July 2004

• Summary: This article offers a critical examination of the conceptual basis of service user involvement through the analysis of a practice example derived from the Deaf community. The Deaf community is located both socio-culturally and historically. • Findings: One authority’s attempts to consult with their own Deaf community is used as the lens to examine the issues, dilemmas and contradictions inherent in consultation and how consultation can be seen as a mechanism both for social control and for empowerment. • Applications: The authors identify some of the lessons for practice and argue against the uncritical acceptance of consultation. They identify preconditions for consultation to be beneficial both for the Deaf community and for those wishing to consult with that community.
Using Standardized Measures to Prioritize Services for Children and Families in Need
Authors: Buchanan Ann , Ritchie Charlotte 
Published: July 2004

• Summary: This article reports the findings of a small study on families in receipt of social services’ support (Buchanan et al., 2001b), which was commissioned in the UK by Barnardo’s and Wiltshire County Council. Children’s well-being was assessed using the Strengths and Difficulties Questionnaire (SDQ) and parental well-being was assessed using the General Health Questionnaire (GHQ). • Findings: The study showed high levels of both parental and child distress. Parents with high levels of distress often found it harder to access social services than those with lower levels. • Application: This study suggests that using standardized measures of well-being for both parents and children may help in prioritizing service provision. There was also evidence to indicate that both policy makers and practitioners should ensure that choice and availability of services are user led.
Well-Being among Minority Students
Authors: Ben-Ari Adital , Gil Sharon 
Published: July 2004

• Summary: The present study explores the relationship between perceived social support and well-being among students in the two main populations living in Israel: Jews and Arabs. More specifically, it compares the well-being of Israeli Jewish students and Palestinian students and examines the role of social support in their well-being. The sample comprised 207 undergraduate students in the schools of social work and nursing at one of the major universities in Israel, where more than half of the Palestinian students are enrolled. Three instruments were used: Psychological distress was measured by both the Brief Symptoms Inventory Scale( BSI;Derogatis, 1979) and the Beck Depression Inventory ( BDI; Beck and Steer, 1987); perceived social support was assessed by the Multidimensional Scale of Perceived Social Support( MSPSS;Zimet et al., 1988). • Findings: Findings show that the Palestinian students are significantly more distressed than their Jewish counterparts, according to all measures of well-being. At the same time, their perceived social support is significantly higher than that of the Jewish students. • Applications: The significance of the findings is discussed within the frameworks of stress and social support theories, as well as the modernization process and the prevailing norms and values of Arab culture.
Peroxisome proliferator-activated receptor-γ and its ligands attenuate biologic functions of human natural killer cells
Authors: Zhang Xia , Rodriguez-Galán Maria Cecilia , Subleski Jeff J. , Ortaldo John R. , Hodge Deborah L. , Wang Ji-Ming , Shimozato Osamu , Reynolds Della A. , Young Howard A. 
Published: July 2004

AbstractInterferon-γ (IFN-γ) production and cytolytic activity are 2 major biologic functions of natural killer (NK) cells that are important for innate immunity. We demonstrate here that these functions are compromised in human NK cells treated with peroxisome proliferator-activated-γ (PPAR-γ) ligands via both PPAR-γ-dependent and -independent pathways due to variation in PPAR-γ expression. In PPAR-γ-null NK cells, 15-deoxy-Δ12,14 prostaglandin J2 (15d-PGJ2), a natural PPAR-γ ligand, reduces IFN-γ production that can be reversed by MG132 and/or chloroquine, and it inhibits cytolytic activity of NK cells through reduction of both conjugate formation and CD69 expression. In PPARγ-positive NK cells, PPAR-γ activation by 15d-PGJ2 and ciglitazone (a synthetic ligand) leads to reduction in both mRNA and protein levels of IFN-γ. Overexpression of PPAR-γ in PPAR-γ-null NK cells reduces IFN-γ gene expression. However, PPAR-γ expression and activation has no effect on NK cell cytolytic activity. In addition, 15d-PGJ2 but not ciglitazone reduces expression of CD69 in human NK cells, whereas CD44 expression is not affected. These results reveal novel pathways regulating NK cell biologic functions and provide a basis for the design of therapeutic agents that can regulate the function of NK cells within the innate immune response. (Blood. 2004;104:3276-3284)
Dual role of phagocytic NADPH oxidase in bacterial killing
Authors: Rada Balázs K. , Geiszt Miklós , Káldi Krisztina , Timár Csaba , Ligeti Erzsébet 
Published: July 2004

AbstractThe classical model of bacterial killing by phagocytic cells has been recently challenged by questioning the toxic effect of oxygen products and attributing the fundamental role to K+ ions in releasing antimicrobial proteins within the phagosome. In the present study we followed \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2}^{{\cdot}-}\) \end{document} production, changes of membrane potential, K+ efflux, and bacterial killing in the presence of increasing concentrations of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium. Efficiency of bacterial killing was assessed on the basis of bacterial survival measured by a new semiautomated method. Very low rates of \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2}^{{\cdot}-}\) \end{document} production were accompanied by significant membrane depolarization and K+ release and parallel improvement of bacterial killing. When \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2}^{{\cdot}-}\) \end{document} production exceeded 20% of its maximal capacity, no further change was detected in the membrane potential and only minimal further K+ efflux occurred, yet bacterial survival decreased parallel to the increase of \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2}^{{\cdot}-}\) \end{document} production. The presented results indicate that both electrophysiological changes (depolarization and consequent ion movements) and the chemical effect of reactive oxygen species play a significant role in the killing of certain pathogens. The observation that an increase of membrane depolarization can compensate for decreased \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2}^{{\cdot}-}\) \end{document} production may be important for potential therapeutic applications.
Protein kinase A mediates inhibition of the thrombin-induced platelet shape change by nitric oxide
Authors: Jensen Baard Olav , Selheim Frode , Døskeland Stein Ove , Gear Adrian R. L. , Holmsen Holm 
Published: July 2004

AbstractThe thrombin-induced platelet shape change was blocked by nitric oxide (NO), as revealed by scanning electron microscopy, light transmission, and resistive-particle volume determination. The inhibitory effect of NO was accompanied by an increase in levels of both cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) and phosphorylation of the vasodilator-stimulated phosphoprotein (VASP). However, the inhibition of the shape change was only mimicked by cAMP analogs (Sp-5,6-DClcBIMPS, 8-AHA-cAMP, and 8-CPT-cAMP) and not by cGMP analogs (8-Br-PET-cGMP, 8-Br-cGMP, and 8-pCPT-cGMP). The effect of NO on the thrombin-induced shape change was prevented by the protein kinase A (PKA) antagonists Rp-8-Br-cAMPS and Rp-cAMPS. The protein kinase G (PKG) antagonist Rp-8-CPT-cGMPS strongly inhibited PKG-mediated 46-kDa VASP Ser239 phosphorylation, but did not inhibit the thrombin-induced shape change or the PKA-mediated VASP Ser157 phosphorylation. Whereas an inhibitor of cyclic nucleotide phosphodiesterase (PDE) 3A (milrinone) mimicked the effect of NO, inhibitors of PDE2 (erythro-9-(2-hydroxy-3-nonyl)adenine) and PDE5 (dipyridamole) were poorly effective. We concluded that (1) NO was a potent and reversible inhibitor of the platelet shape change, (2) the shape change was reversible, (3) the inhibitory effect of NO was mediated through activation of PKA, (4) the onset of the NO effect coincided with VASP Ser157 phosphorylation, and (5) removal of NO and platelet shape change coincided with VASP Ser157 dephosphorylation. These findings are compatible with elevation of cGMP by NO in a compartment close to PDE3A, PKA, and VASP, leading to a local increase of cAMP able to block thrombin-induced shape change. (Blood. 2004;104:2775-2782)
Neuropsychologic changes from before transplantation to 1 year in patients receiving myeloablative allogeneic hematopoietic cell transplant
Authors: Syrjala Karen L. , Dikmen Sureyya , Langer Shelby L. , Roth-Roemer Sari , Abrams Janet R. 
Published: July 2004

AbstractResearch indicates that myeloablative hematopoietic cell transplantation (HCT) impairs neurocognitive function. However, prospective studies on long-term effects are lacking. This longitudinal study examined neurocognitive changes over the first year in 142 adult recipients of allogeneic HC transplants who received neuropsychologic testing before transplantation and again after 80 days and 1 year. Age-, sex-, and education-adjusted population-based standardized scores were used for normative comparisons. Performance on all tests declined from before transplantation to 80 days (P &lt; .05) and improved by 1 year (P &lt; .05), returning to pretransplantation levels on all tests except for grip strength and motor dexterity. Although verbal fluency and memory recovered by 1 year, both were below norms at all 3 testing times (P &lt; .01). Logistic regressions indicated that patients without chemotherapy, other than hydroxyurea, previous to HCT and patients not receiving chronic graft-versus-host disease (GVHD) medication at 1 year had lower risk of impaired function (P &lt; .05). In conclusion, HCT was associated with significant generalized decline in neurocognitive performance at 80 days, with subsequent recovery to pretransplantation levels by 1 year for most survivors, except on motor tasks. Results indicate that long-term cognitive decrements, as distinct from motor disabilities, infrequently derive directly from HCT. (Blood. 2004;104:3386-3392)
A requirement for Notch1 distinguishes 2 phases of definitive hematopoiesis during development
Authors: Hadland Brandon K. , Huppert Stacey S. , Kanungo Jyotshnabala , Xue Yingzi , Jiang Rulang , Gridley Thomas , Conlon Ronald A. , Cheng Alec M. , Kopan Raphael , Longmore Gregory D. 
Published: July 2004

AbstractNotch1 is known to play a critical role in regulating fates in numerous cell types, including those of the hematopoietic lineage. Multiple defects exhibited by Notch1-deficient embryos confound the determination of Notch1 function in early hematopoietic development in vivo. To overcome this limitation, we examined the developmental potential of Notch1–/– embryonic stem (ES) cells by in vitro differentiation and by in vivo chimera analysis. Notch1 was found to affect primitive erythropoiesis differentially during ES cell differentiation and in vivo, and this result reflected an important difference in the regulation of Notch1 expression during ES cell differentiation relative to the developing mouse embryo. Notch1 was dispensable for the onset of definitive hematopoiesis both in vitro and in vivo in that Notch1–/– definitive progenitors could be detected in differentiating ES cells as well as in the yolk sac and early fetal liver of chimeric mice. Despite the fact that Notch1–/– cells can give rise to multiple types of definitive progenitors in early development, Notch1–/– cells failed to contribute to long-term definitive hematopoiesis past the early fetal liver stage in the context of a wild-type environment in chimeric mice. Thus, Notch1 is required, in a cell-autonomous manner, for the establishment of long-term, definitive hematopoietic stem cells (HSCs).
STAT3 regulates NF-κB recruitment to the IL-12p40 promoter in dendritic cells
Authors: Hoentjen Frank , Sartor R. Balfour , Ozaki Michitaka , Jobin Christian 
Published: July 2004

AbstractInterleukin-10-deficient (IL-10-/-) mice develop an IL-12-mediated intestinal inflammation in the absence of endogenous IL-10. The molecular mechanisms of the dysregulated IL-12 responses in IL-10-/- mice are poorly understood. In this study, we investigated the role of nuclear factor-κ B (NF-κB) and signal transducers and activators of transcription 3 (STAT3) in lipopolysaccharide (LPS)-induced IL-12p40 gene expression in bone marrow derived-dendritic cells (BMDCs) isolated from wild-type (WT) and IL-10-/- mice. We report higher IL-12p40 mRNA accumulation and protein secretion in LPS-stimulated BMDCs isolated from IL-10-/- compared with WT mice. LPS-induced NF-κB signaling is similar in IL-10-/- and WT BMDCs as measured by IκBα phosphorylation and degradation, RelA phosphorylation and nuclear translocation, and NF-κB transcriptional activity, with no down-regulatory effects of exogenous IL-10. Chromatin immunoprecipitation demonstrated enhanced NF-κB (cRel, RelA) binding to the IL-12p40 promoter in IL-10-/- but not WT BMDCs. Interestingly, LPS induced STAT3 phosphorylation in WT but not IL-10-/- BMDCs, a process blocked by IL-10 receptor blocking antibody. Adenoviral gene delivery of a constitutively active STAT3 but not control green fluorescence protein (GFP) virus blocked LPS-induced IL-12p40 gene expression and cRel recruitment to the IL-12p40 promoter. In conclusion, dysregulated LPS-induced IL-12p40 gene expression in IL-10-/- mice is due to enhanced NF-κB recruitment to the IL-12p40 promoter in the absence of activated STAT3.
Iron chelators with high antiproliferative activity up-regulate the expression of a growth inhibitory and metastasis suppressor gene: a link between iron metabolism and proliferation
Authors: Le Nghia T.V. , Richardson Des R. 
Published: July 2004

AbstractIron (Fe) is critical for proliferation, but its precise role in cell cycle progression remains unclear. In this study, we examined the mechanisms involved by assessing the effects of Fe chelators on the expression of molecules that play key roles in this process. In initial studies, gene arrays were used to assess gene expression after incubating cells with 2 Fe chelators, namely, desferrioxamine (DFO) and 2-hydroxy-1-naphthylaldehyde isonicotinoyl hydrazone (311), or the DNA-damaging agent, actinomycin D. From the genes assessed, only the N-myc downstream-regulated gene 1 (Ndrg1) was specifically up-regulated by Fe chelation. Although the function of Ndrg1 is unclear, previous studies showed it markedly slows tumor growth and acts as a potent metastasis suppressor. Incubation of cells with chelators markedly increased Ndrg1 mRNA and protein expression, but this was not found with their Fe complexes or when the Fe-binding site had been inactivated. Increased Ndrg1 expression following Fe chelation was related to the permeability and antiproliferative activity of chelators and could be reversed by Fe repletion. Moreover, Ndrg1 up-regulation after chelation occurred at the transcriptional level and was mediated by hypoxia inducible factor-1α (HIF-1α)-dependent and -independent mechanisms. Our investigation suggests Ndrg1 is a novel link between Fe metabolism and the control of proliferation.
Multi-Institutional Trial of Preoperative Chemoradiotherapy in Patients With Potentially Resectable Gastric Carcinoma
Authors: Ajani J.A. , Mansfield P.F. , Janjan N. , Morris J. , Pisters P.W. , Lynch P.M. , Feig B. , Myerson R. , Nivers R. , Cohen D.S. , Gunderson L.L. 
Published: July 2004

Purpose In the West, curative (R0) resection is achieved in approximately 50% of patients with localized gastric carcinoma, and more than 60% die of cancer following an R0 resection. A multi-institutional study of preoperative chemoradiotherapy was done to assess the R0 resection rate, pathologic complete response (pathCR) rate, safety, and survival in patients with resectable gastric carcinoma. Patients and Methods Operable patients with localized gastric adenocarcinoma were eligible. Staging also included a laparoscopy and endoscopic ultrasonography (EUS). Patients received up to two 28-day cycles of induction chemotherapy of fluorouracil, leucovorin, and cisplatin, followed by 45 Gy of radiation plus concurrent fluorouracil. Patients were then staged and surgery was attempted. Results Thirty-four patients were registered at three institutions. One ineligible patient was excluded. Most patients had a promixal cancer and EUST3N1 designation. Twenty-eight (85%) of 33 patients underwent surgery. The R0 resection rate was 70% and pathCR rate was 30%. A pathologic partial response (< 10% residual carcinoma in the primary) occurred in eight patients (24%). EUS T plus N and postsurgery T plus N correlation showed significant downstaging (P = < .01). The median survival time for 33 patients was 33.7 months. Patients achieving a pathCR or pathPR had a significantly longer median survival time (63.9 months) than those achieving less than pathPR (12.6 months; P = .03). There were two treatment-related deaths. Conclusion Our data suggest that the three-step strategy of preoperative induction chemotherapy followed by chemoradiotherapy resulted in substantial pathologic response that resulted in durable survival time. This strategy is worthy of a direct comparison with postoperative adjuvant chemoradiotherapy.
Treatment of Metastatic Ewing's Sarcoma or Primitive Neuroectodermal Tumor of Bone: Evaluation of Combination Ifosfamide and Etoposide—A Children's Cancer Group and Pediatric Oncology Group Study
Authors: Miser James S. , Krailo Mark D. , Tarbell Nancy J. , Link Michael P. , Fryer Christopher J.H. , Pritchard Douglas J. , Gebhardt Mark C. , Dickman Paul S. , Perlman Elizabeth J. , Meyers Paul A. , Donaldson Sarah S. , Moore Sheila , Rausen Aaron R. , Vietti Teresa J. , Grier Holcolmbe E. 
Published: July 2004

Purpose One hundred twenty patients with metastatic Ewing's sarcoma or primitive neuroectodermal tumor (PNET) of bone were entered onto a randomized trial evaluating whether the addition of ifosfamide and etoposide to vincristine, doxorubicin, cyclophosphamide, and dactinomycin improved outcomes. Methods Thirty-two patients had metastases to lungs only, 12 patients had metastases to bone marrow or bones only, 64 patients had metastases in multiple sites, and five patients had metastases in other sites; seven patients could not be assessed precisely. Treatment comprised 9 weeks of chemotherapy before local control and 42 weeks of chemotherapy; thereafter, regimen A consisted of vincristine 2 mg/m2, cyclophosphamide 1,200 mg/m2, and either doxorubicin 75 mg/m2 or dactinomycin 1.25 mg/m2. Regimen B consisted of regimen A alternating every 3 weeks with ifosfamide 1,800 mg/m2/d for 5 days and etoposide 100 mg/m2/d for 5 days. Results Patients treated on regimen B did not have significantly better survival than those treated on regimen A. The event-free survival (EFS) and survival (S) at 8 years were 20% (SE, 5%) and 32% (SE, 6%), respectively, for those treated on regimen A and 20% (SE, 6%) and 29% (SE, 6%), respectively, for those treated on regimen B. Patients who had only lung metastases had EFS and S of 32% (SE, 8%) and 41% (SE, 9%), respectively, at 8 years. There were six toxic deaths (5%), four from cardiac toxicity and two from sepsis (four treated on regimen B and two treated on regimen A). Two had second malignant neoplasms. Conclusion Adding ifosfamide and etoposide to standard therapy does not improve outcomes of patients with Ewing's sarcoma or PNET of bone with metastases at diagnosis.