bluuebunny/crossref_metadata_2025_split huggingface dataset:
TQM across multiple countries:Convergence HypothesisversusNational Specificityarguments
Authors: Rungtusanatham M. , Forza C. , Koka B.R. , Salvador F. , Nie W. 
Published: December 2004

AbstractWe provide conceptual clarity and new empirical findings for the question of whether or not TQM is universal in its applicability. At the conceptual level, we reposition and reframe the “universality of TQM” question in light of two conflicting theoretical perspectives in the international business literature – one that supports the universal applicability of TQM (i.e., theConvergence Hypothesisargument) and another that questions the universal applicability of TQM (i.e., theNational Specificityargument). We do so to provide a stronger theoretical basis for the “universality of TQM” question and to motivate and initiate a “strong inference” epistemological approach [Platt, J.R., 1964. Strong inference. Science 146 (364), 347–353] to examine, at the empirical level, the applicability of TQM across multiple countries. For this empirical assessment, we compare both the adoption levels of the Deming‐based TQM constructs and the patterns of Deming‐based TQM relationships among German, Italian, Japanese, and USA plants, using secondary data from 143 plants in Round Two of the World‐Class Manufacturing project. After assessing measurement quality (i.e., reliability and validity) and measurement equivalence (i.e., translation, calibration, and metric), MANOVA analysis and regression analysis were deployed to derive relevant empirical results – empirical results that have implications not only for the question of whether or not TQM is universal in its applicability but also for the theoretical tension between theConvergence Hypothesisargument and theNational Specificityargument.
Molecular chain stretch is a multiaxial failure criterion for conventional and highly crosslinked UHMWPE
Authors: Bergström J. S. , Rimnac C. M. , Kurtz S. M. 
Published: December 2004

AbstractThe development of accurate theoretical failure, fatigue, and wear models for ultra‐high molecular weight polyethylene (UHMWPE) is an important step towards better understanding the micromechanisms of the surface damage that occur in load bearing orthopaedic components and improving the lifetime of joint arthoplasties. Previous attempts to analytically predict the clinically observed damage, wear, and fatigue failure modes have met with limited success due to the complicated interaction between microstructural deformations and continuum level stresses. In this work, we examined monotonic uniaxial and multiaxial loading to failure of UHMWPE using eight failure criteria (maximum principal stress, Mises stress, Tresca stress, hydrostatic stress, Coulomb stress, maximum principal strain, Mises strain, and chain stretch). The quality of the predictions of the different models was assessed by comparing uniaxial tension and small punch test data at different rates with the failure model predictions. The experimental data were obtained for two conventional (unirradiated and gamma radiation sterilized in nitrogen) and two highly crosslinked (150 kGy, remelted and annealed) UHMWPE materials. Of the different failures models examined, the chain stretch failure model was found to capture uniaxial and multiaxial failure data most accurately for all of the UHMWPE materials. In addition, the chain stretch failure criterion can readily be calculated for contemporary UHMWPE materials based on available uniaxial tension data. These results lay the foundation for future developments of damage and wear models capable of predicting multiaxial failure under cyclic loading conditions. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.
Contact pressures in the flexed hip joint during lateral trochanteric loading
Authors: Sparks Damon R. , Beason David P. , Etheridge Brandon S. , Alonso Jorge E. , Eberhardt Alan W. 
Published: December 2004

AbstractAcetabular fractures are an especially problematic outcome of motor vehicle side impacts. While fracture type has been correlated with impact direction and femoral orientation, actual contact pressures in the hip joint have not been quantified for lateral loading conditions. In the present study, we used pressure sensitive film to measure contact areas and pressures in seven hip joints from four cadavers under quasi‐static lateral loading through the greater trochanter. The aim was to quantify the interactions of the femoral head with the acetabulum associated with variations in femoral orientation. Three angles of hip flexion (80°, 90°, 100°) and hip abduction (−10°, 0°, 10°) were tested, producing nine test orientations for each joint. We observed that contact areas, pressures, and forces varied significantly with femoral orientation for the adducted hip. The principal locations of load transmission were in the anterior and posterior regions of the acetabulum. For the abducted femur, contact pressures were concentrated anteriorly, and with increased adduction, anterior contact pressures diminished while posterior and superior pressures increased. The movement of pressure sites was consistent with mechanisms of acetabular fractures described by Letournel and Judet and provides new data for validation of finite element models of the pelvis in side impact. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.
Growth and integration of neocartilage with native cartilage in vitro
Authors: Zhang Zijun , McCaffery J. Michael , Spencer Richard G. S. , Francomano Clair A. 
Published: December 2004

AbstractPoor integration of neocartilage with recipient has been a major obstacle to articular cartilage restoration. An in vitro study was designed to provide insights regarding the integration process. Cartilage explants and chondrocytes were harvested from the distal sternum of 16‐day‐old chick embryos. Four million chondrocytes and one 1 mm3 explant were centrifuged together in a 0.75 ml tube. In the constructs, consisting of cartilage explant and chondrocyte pellet, isolated chondrocytes attached to the surface of the explant at the beginning of the culture, followed by significant chondrocyte death at the interface between chondrocyte pellet and explant. Chondrocyte apoptosis was seen almost exclusively at this interface. Meanwhile, the interface was a zone with active extracellular matrix deposition as demonstrated by immunohistochemistry. By two weeks, the junction of neocartilage and native cartilage explant had formed an acellular zone with collagen fibrils orientated parallel with the surface of the cartilage explant. In conclusion, chondrocyte death leads to acellularity and fibril network reorganization at the neocartilage/explant interface, and impacts the quality of cartilage repair as abnormal matrix remodeling implies. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.
Endothelial dysfunction in patients with recent myocardial infarction and hyperhomocysteinaemia: effects of vitamin supplementation
Authors: CHIA Stanley , WILSON Robert , LUDLAM Christopher A. , WEBB David J. , FLAPAN Andrew D. , NEWBY David E. 
Published: December 2004

Hyperhomocysteinaemia is a prothrombotic condition that may cause oxidative endothelial injury and impair endogenous fibrinolysis. Vitamin supplementation enhances endothelial function in hyperhomocysteinaemic patients, but responses in patients with co-existing coronary artery disease have been variable. It is also unknown whether hyperhomocysteinaemia is associated with reduced fibrinolytic responses in patients with coronary artery disease. The study aims were to test the hypothesis that patients with recent myocardial infarction and hyperhomocysteinaemia have impaired endothelium-dependent vasomotion and fibrinolysis that is rectified by vitamin supplementation. From a cohort of 120 patients admitted with acute myocardial infarction, 18 patients were recruited from the upper (n=9) and lower (n=9) plasma homocysteine quartiles into a randomized double-blind placebo-controlled crossover trial. Following a 4-week course of placebo or folate/cyanocobalamin/pyridoxine supplements, FBF (forearm blood flow) was measured using venous occlusion plethysmography during intra-arterial substance P (4–16 pmol/min), acetylcholine (5–20 μg/min) and sodium nitroprusside (2–8 μg/min) infusions. All vasodilators caused dose-dependent increases in infused FBF (P&lt;0.05). Patients in the upper homocysteine quartile (16.8±2.9 compared with 7.9±0.7 μmol/l; P=0.003) had reduced vasodilatation to acetylcholine (P=0.01) and substance P (P&lt;0.05), but not sodium nitroprusside. There were no differences in substance P-induced tissue plasminogen activator release. Vitamin supplementation increased serum folate and vitamin B12 concentrations (P&lt;0.05), but did not significantly lower homocysteine, or affect FBF or fibrinolytic responses. In patients with recent myocardial infarction, hyperhomocysteinaemia is associated with impaired endothelium-dependent vasodilatation, but no alteration in the acute fibrinolytic capacity. This endothelial vasomotor dysfunction is unaltered by vitamin supplementation.
Effect of C-reactive protein on Fcγ receptor II in cultured bovine endothelial cells
Authors: ESCRIBANO-BURGOS Marta , LÓPEZ-FARRÉ Antonio , del MAR GONZÁLEZ María , MACAYA Carlos , GARCÍA-MÉNDEZ Antonio , MATEOS-CÁCERES Petra J. , ALONSO-ORGAZ Sergio , CARRASCO Carolina , RICO Luis A. , PORRES CUBERO Juan Carlos 
Published: December 2004

The major CRP (C-reactive protein) receptor on leucocytes has been identified as the low-affinity IgG receptor Fcγ receptor II (CD32). Our aim was to assess whether inflammation may modify the presence of the CD32 receptor in BAEC (bovine aortic endothelial cells). Confocal microscopy experiments showed a weak expression of the CD32 receptor in control BAEC that was slightly increased by 10 μg/ml CRP. Incubation of BAEC with TNF-α (tumour necrosis factor-α) did not modify the fluorescence signal of CD32. Addition of CRP to TNF-α-incubated BAEC enhanced the fluorescence signal of the CD32 receptors. The CD32 receptors showed a perinuclear cytoplasmic localization in BAEC. An alteration of the NO (nitric oxide)-dependent vasorelaxation has been defined as endothelial dysfunction. Endothelial dysfunction has been associated with the presence of superoxide anion and with a reduction in the expression of the eNOS (endothelial NO synthase). A concentration of CRP similar to that detected in patients with cardiovascular risk (10 μg/ml) failed to modify the generation of superoxide anion stimulated by TNF-α. Western blot experiments showed that TNF-α decreased the expression of the eNOS protein, which was partially protected by treatment with 10 μg/ml CRP. The protective effect of 10 μg/ml CRP on eNOS expression in TNF-α-incubated BAEC was prevented by an antibody against CD32 receptors. In conclusion, the present results suggest that, although CRP has been associated with inflammation, CRP may protect the expression of eNOS protein against pro-inflammatory mediators such as TNF-α.
Reshaping the way we view vitamin D signalling and the role of vitamin D in health
Authors: Fleet James C. , Hong Jie , Zhang Zhentao 
Published: December 2004

AbstractAlthough the biological requirement for vitamin D can be met by epidermal exposure to UV light, there are a number of conditions where this production does not occur or is not sufficient to meet biological needs. When this happens, vitamin D must be consumed and is a nutrient. However, two distinct observations have caused researchers to rethink certain dogma in vitamin D biology. First, it appears that in addition to the hormonally active form of 1,25 dihydroxyvitamin D (1,25(OH)2D), circulating levels of 25 hydroxyvitamin D have a critical importance for optimal human health. This and other data suggest that extra-renal production of 1,25(OH)2D contributes to Ca homeostasis and cancer prevention. Second, in addition to its role in the transcriptional activation of genes through the vitamin D receptor there is now compelling evidence that 1,25(OH)2D has a second molecular mode of action; the rapid activation of second-messenger and kinase pathways. The purpose of this second mode of action is only now being explored. The present review will discuss how these two areas are reshaping our understanding of vitamin D metabolism and action.
Functional Analysis ofAvr9/Cf-9 Rapidly ElicitedGenes Identifies a Protein Kinase, ACIK1, That Is Essential for Full Cf-9–Dependent Disease Resistance in Tomato
Authors: Rowland Owen , Ludwig Andrea A. , Merrick Catherine J. , Baillieul Fabienne , Tracy Frances E. , Durrant Wendy E. , Fritz-Laylin Lillian , Nekrasov Vladimir , Sjölander Kimmen , Yoshioka Hirofumi , Jones Jonathan D.G. 
Published: December 2004

AbstractTomato (Lycopersicon esculentum) Cf genes confer resistance to the fungal pathogen Cladosporium fulvum through recognition of secreted avirulence (Avr) peptides. Plant defense responses, including rapid alterations in gene expression, are immediately activated upon perception of the pathogen. Previously, we identified a collection of Avr9/Cf-9 rapidly (15 to 30 min) elicited (ACRE) genes from tobacco (Nicotiana tabacum). Many of the ACRE genes encode putative signaling components and thus may play pivotal roles in the initial development of the defense response. To assess the requirement of 42 of these genes in the hypersensitive response (HR) induced by Cf-9/Avr9 or by Cf-4/Avr4, we used virus-induced gene silencing (VIGS) in N. benthamiana. Three genes were identified that when silenced compromised the Cf-mediated HR. We further characterized one of these genes, which encodes a Ser/Thr protein kinase called Avr9/Cf-9 induced kinase 1 (ACIK1). ACIK1 mRNA was rapidly upregulated in tobacco and tomato upon elicitation by Avr9 and by wounding. Silencing of ACIK1 in tobacco resulted in a reduced HR that correlated with loss of ACIK1 transcript. Importantly, ACIK1 was found to be required for Cf-9/Avr9- and Cf-4/Avr4-mediated HRs but not for the HR or resistance mediated by other resistance/Avr systems, such as Pto/AvrPto, Rx/Potato virus X, or N/Tobacco mosaic virus. Moreover, VIGS of LeACIK1 in tomato decreased Cf-9–mediated resistance to C. fulvum, showing the importance of ACIK1 in disease resistance.
CRS1, a Chloroplast Group II Intron Splicing Factor, Promotes Intron Folding through Specific Interactions with Two Intron Domains
Authors: Ostersetzer Oren , Cooke Amy M. , Watkins Kenneth P. , Barkan Alice 
Published: December 2004

Abstract
Group II introns are ribozymes that catalyze a splicing reaction with the same chemical steps as spliceosome-mediated splicing. Many group II introns have lost the capacity to self-splice while acquiring compensatory interactions with host-derived protein cofactors. Degenerate group II introns are particularly abundant in the organellar genomes of plants, where their requirement for nuclear-encoded splicing factors provides a means for the integration of nuclear and organellar functions. We present a biochemical analysis of the interactions between a nuclear-encoded group II splicing factor and its chloroplast intron target. The maize (Zea mays) protein Chloroplast RNA Splicing 1 (CRS1) is required specifically for the splicing of the group II intron in the chloroplast atpF gene and belongs to a plant-specific protein family defined by a recently recognized RNA binding domain, the CRM domain. We show that CRS1's specificity for the atpF intron in vivo can be explained by CRS1's intrinsic RNA binding properties. CRS1 binds in vitro with high affinity and specificity to atpF intron RNA and does so through the recognition of elements in intron domains I and IV. These binding sites are not conserved in other group II introns, accounting for CRS1's intron specificity. In the absence of CRS1, the atpF intron has little uniform tertiary structure even at elevated [Mg2+]. CRS1 binding reorganizes the RNA, such that intron elements expected to be at the catalytic core become less accessible to solvent. We conclude that CRS1 promotes the folding of its group II intron target through tight and specific interactions with two peripheral intron segments.
Proliferation, apoptosis, and survivin expression in a spectrum of melanocytic nevi
Authors: Florell Scott R. , Bowen Anneli R. , Hanks Adrianne N. , Murphy Kelley J. , Grossman Douglas 
Published: December 2004

Background:  Apoptosis is important for maintenance of tissue homeostasis and often dysregulated in cutaneous neoplasms. The apoptosis inhibitor survivin is expressed in melanoma and non‐melanoma skin cancers and benign keratinocytic lesions. Its expression has not been studied in melanocytic nevi.Objective:  We determined the expression pattern of survivin in benign melanocytic nevi in comparison to markers of proliferation and apoptosis.Methods:  Six cases of each of the following melanocytic nevi were retrieved from a dermatopathology archive: compound dysplastic nevus, intradermal nevus, compound nevus, neurotized intradermal nevus, and Spitz nevus. Survivin expression was evaluated by in situ hybridization. Apoptotic and proliferation indices were calculated by counting immunoreactive cells in terminal deoxynucleotidyl transferase (TdT)‐mediated dUTP nick end labeling and proliferating cell nuclear antigen immunostained sections, respectively.Results:  All nevi, regardless of histologic type, expressed survivin. Compound melanocytic lesions expressed survivin in both epidermal and dermal compartments. The apoptotic rate was low for dysplastic, compound, and Spitz nevi, and apoptotic cells were not identified in any neurotized nevus. The proliferative index was highest for Spitz nevi, while all other nevi demonstrated rare positive cells.Conclusions:  Survivin is consistently expressed in benign melanocytic lesions, while apoptotic cells are rarely identified, suggesting the dysregulation of apoptotic pathways with the accumulation of cells in these neoplasms.
Cluster designation 5 staining of normal and non‐lymphoid neoplastic skin*
Authors: Bogner Paul N. , Su Lyndon D. , Fullen Douglas R. 
Published: December 2004

Background:  Immunohistochemical staining for cluster designation 5 (CD5) has been found to label a variety of non‐lymphoid tumors.Methods:  A variety of eccrine, apocrine, follicular, epithelial, and pagetoid lesions were selected and stained with an anti‐CD5 monoclonal antibody (Novocastra Labs, Newcastle upon Tyne, UK, clone 4C7) by immunohistochemistry. The intensity of positive cytoplasmic staining was graded semiquantitatively (1+ weak staining, 2+ strong staining). Additionally, the percentage of positive lesional cells was placed in one of four categories: >75%, 25–75%, 1–25%, and <1%.Results:  Within normal skin, CD5 labeled lymphocytes, apocrine glands, deep dermal eccrine glands, and smooth muscle (weak). The majority of benign and malignant apocrine lesions demonstrated strong focal (36%, n = 11)‐to‐diffuse (64%, n = 16) staining. In contrast, labeling of benign eccrine tumors was more focal, tending to localize around ducts (79%, n = 19). Microcystic adnexal carcinoma demonstrated focal staining of deeper ductal structures (71%, n = 7), whereas desmoplastic trichoepithelioma and basal cell carcinoma showed only rare positive cells. All cases of mammary (n = 7) and extramammary (n = 8) Paget's disease labeled diffusely for CD5. Pagetoid Bowen's disease (n = 6), intraepidermal sebaceous carcinoma (n = 3), nor melanoma in situ (n = 6) showed any CD5 staining.Conclusions:  Immunohistochemical staining for CD5 is extremely useful in the differential diagnosis of pagetoid epidermal lesions and will mark mammary and extramammary Paget's disease, but not pagetoid Bowen's disease, melanoma in situ, or sebaceous carcinoma.
Monkeypox virus: histologic, immunohistochemical and electron‐microscopic findings
Authors: Bayer‐Garner I. B. 
Published: December 2004

Background:  Human monkeypox, an emerging viral zoonosis first recognized in Africa, has recently emerged in the mid‐western US. Initially, it presents with skin eruptions and fevers with diaphoresis and rigors. Clinically, the skin lesions progress from papules to vesiculopustules to resolving eschars.Methods:  Three cutaneous biopsy specimens from two patients with polymerase chain reaction (PCR)‐proven monkeypox were available for review. The histologic, immunohistochemical and electron‐microscopic features were identified.Results:  The clinical progression of lesions is mirrored histologically with ballooning degeneration of basal keratinocytes and spongiosis of a mildly acanthotic epidermis progressing to full thickness necrosis of a markedly acanthotic epidermis containing few viable keratinocytes. A lichenoid‐mixed inflammatory cell infiltrate is present, which exhibits progressive exocytosis with the keratinocyte necrosis. Inflammation of the superficial and deep vascular plexes, eccrine units and follicles is also present. Viral cytopathic effect is manifest by multinucleated syncytial keratinocytes. Immunohistochemically, viral antigen is detected within keratinocytes of the lesional epidermis, follicular and eccrine epithelium and few dermal mononuclear cells. Electron microscopy reveals virions at various stages of assembly within the keratinocyte cytoplasm.Conclusions:  The histologic differential diagnosis includes herpes simplex virus, varicella and other pox viruses, such as smallpox. The first one may be differentiated histologically, immunohistochemically and electron microscopically. The last two may be differentiated using PCR assay for the monkeypox extracellular‐envelope virus protein gene.
m
-Xylene-Responsive
Pu
-
PnifH
Hybrid σ
54
Promoters That Overcome Physiological Control in
Pseudomonas putida
KT2442
Authors: Carmona Manuel , Fernández Silvia , Rodríguez María J. , de Lorenzo Víctor 
Published: December 2004

ABSTRACT

The sequences surrounding the −12/−24 motif of the
m-
xylene-responsive σ
54
promoter
Pu
of the
Pseudomonas putida
TOL plasmid pWW0 were replaced by various DNA segments of the same size recruited from
PnifH
σ
54
promoter variants known to have various degrees of efficacy and affinity for σ
54
-RNA polymerase (RNAP). In order to have an accurate comparison of the output in vivo of each of the hybrids, the resulting promoters were recombined at the same location of the chromosome of
P. putida
KT2442 with a tailored vector system. The promoters included the upstream activation sequence (UAS) for the cognate regulator of the TOL system (XylR) fused to the −12/−24 region of the wild-type
PnifH
and its higher σ
54
-RNAP affinity variants
PnifH049
and
PnifH319
. As a control, the downstream region of the
glnAp2
promoter (lacking integration host factor) was fused to the XylR UAS as well. When the induction patterns of the corresponding
lacZ
fusion strains were compared in vivo, we observed that promoters bearing the RNAP binding site of
PnifH049
and
PnifH319
were not silenced during exponential growth, as is distinctly the case for the wild-type
Pu
promoter or for the
Pu-PnifH
variant. Taken together, our results indicate that the promoter sequence(s) spanning the −12/−24 region of
Pu
dictates the coupling of promoter output to growth conditions.