bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of implant/abutment joint designs on abutment screw loosening in a dental implant system
Authors: Kitagawa Tsuyoshi , Tanimoto Yasuhiro , Odaki Misako , Nemoto Kimiya , Aida Masahiro 
Published: July 2005

AbstractThe objective of this study was to investigate the influence of implant/abutment joint designs on abutment screw loosening in a dental implant system, using nonlinear dynamic analysis of the finite element method (FEM). This finite element simulation study used two dental implant systems: the Ankylos implant system (Degusa Dental, Hanau, German) with a taper joint (taper joint‐type model), and the Bränemark implant system (Nobel Biocare, Gothenburg, Sweden) with an external hex joint (external hex joint‐type model). The nonlinear dynamic analysis was performed using three‐dimensional finite element analysis. In comparing the movement of the taper type‐joint model and external hex type‐joint model, it was found that the external hex type‐joint model had greater movement than the taper type‐joint model. The external hex joint‐type model showed rotation movement, whereas the movement of the taper joint‐type model showed no rotation. It was concluded that the nonlinear dynamic analysis used in this study clearly demonstrated the differences in rotation of components in dental implant systems with taper or external hex joints. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2005
The medium‐term results of treatment with hydroxyapatite implants
Authors: Shibuya Kazuyuki , Kurosawa Hisashi , Takeuchi Hiroyasu , Niwa Shigeo 
Published: July 2005

AbstractAlthough the short‐term results of implants with synthetic hydroxyapatite (HA), a bioactive material, have been favorable, few reports have been published concerning medium‐term outcomes for this therapy. The authors recently analyzed data supplied by 37 medical facilities nationwide concerning the outcomes of synthetic HA implants [Bonfil® (BF); Mitsubishi Materials Corporation, Tokyo] in 138 patients followed up for at least 5 years after treatment. When the data were analyzed, the patients were divided into two groups: the disease site‐filling group (62 cases where bone defects created by disease were filled with synthetic HA) and the donor site‐filling group (76 cases where bone defects created by bone donation were filled with synthetic HA). In the disease site‐filling group, synthetic HA was used in combination with autologous bone or autogenous bone marrow donated from the same patient in 77% of cases. In the donor site‐filling group, only synthetic HA was used in most cases. The average follow‐up period after implantation was 7.9 years in the disease site‐filling group and 9.1 years in the donor site‐filling group. Therapy was rated radiographically as “very effective” or “effective” in 81% of patients in the disease site‐filling group and in 89% of patients in the donor site‐filling group. The therapy was not rated as “ineffective” in any case from either group. These results suggest that synthetic HA may serve as a very useful substitute for cancellous bone if used carefully, with its initial strength taken into account. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2005
Clinical versus statistical prediction: The contribution of Paul E. Meehl
Authors: Grove William M. 
Published: July 2005

AbstractThe background of Paul E. Meehl's work on clinical versus statistical prediction is reviewed, with detailed analyses of his arguments. Meehl's four main contributions were the following: (a) he put the question, of whether clinical or statistical combinations of psychological data yielded better predictions, at center stage in applied psychology; (b) he convincingly argued, against an array of objections, that clinical versus statistical prediction was a real (not concocted) problem needing thorough study; (c) he meticulously and even‐handedly dissected the logic of clinical inference from theoretical and probabilistic standpoints; and (c) he reviewed the studies available in 1954 and thereafter, which tested the validity of clinical versus statistical predictions. His early conclusion that the literature strongly favors statistical prediction has stood up extremely well, and his conceptual analyses of the prediction problem (especially his defense of applying aggregate‐based probability statements to individual cases) have not been significantly improved since 1954. © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1233–1243, 2005.
The ethical implications of Paul Meehl's work on comparing clinical versus actuarial prediction methods
Authors: Dawes Robyn M. 
Published: July 2005

AbstractPaul E. Meehl's work comparing statistical versus actuarial prediction—and the large body of research that followed by others on the same topic—was mainly theoretical and empirical. Meehl also suggested that this work led to a “practical” conclusion, which was quite strong. The author argues that, in addition, it leads to an ethical conclusion, equally strong. Whether the scientific findings are combined with an overarching ethical principle that the best predictions possible should be made for clients, or whether these findings are framed as delineating what can be done for clients—and that clinicians ought not to attempt to do what they cannot—the conclusion is the same. Whenever statistical prediction rules (SPR's) are available for making a relevant prediction, they should be used in preference to intuition. Any modification of these rules should be systematic and subject to the same type of evaluation originally used to assess the SPR's themselves. It is even possible to develop near‐optimal rules in new situations. Providing service that assumes that clinicians “can do better” simply based on self‐confidence or plausibility in the absence of evidence that they can actually do so is simply unethical. © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1245–1255, 2005.
In praise of clinical judgment: Meehl's forgotten legacy
Authors: Westen Drew , Weinberger Joel 
Published: July 2005

AbstractAlthough Paul E. Meehl demonstrated the limits of informal aggregation of data and prognostication by presumed experts, he remained convinced that clinical experience confers expertise of some kind. The authors explore this forgotten side of Meehl's legacy by reconsidering the validity of clinical judgment in its natural context, everyday clinical work. Three domains central to clinical practice are examined: diagnosis, interpretation of meaning, and intervention. It is argued that a more sanguine picture of clinical expertise emerges when the focus shifts from prediction at high levels of inference to (a) judgments at a moderate level of inference, (b) contexts for which clinical training and experience are likely to confer expertise, and (c) conditions that optimize the expression of that expertise (e.g., use of instruments designed for expert observers). The authors conclude by examining domains in which clinical judgment could prove useful in knowledge generation (e.g., hypothesis generation, identification of falsifying instances, item development). © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1257–1276, 2005.
Production of ellagic acid from degradation of valonea tannins by Aspergillus niger and Candida utilis
Authors: Shi Bi , He Qiang , Yao Kai , Huang Wen , Li Qing 
Published: July 2005

AbstractTwo fungal strains, effective in converting valonea (Quercus aegilops) tannins into ellagic acid (EA), were isolated from soil contaminated by valonea tannins, and were tentatively identified as Aspergillus niger and Candida utilis. Properties of EA accumulation by the two isolates from valonea tannins' fermentation were studied. Both the strains preferred sucrose to glucose as the additional carbon and energy source. The most suitable concentrations of valonea tannins in fermentation media for EA accumulation by A niger and C utilis were 5.0 and 9.0 g dm−3 with EA yields of 12.1 and 8.9% (w/w), respectively. The optimal temperature for the two strains was 28 °C, while the preferred pH values of the fermentation media were 4.5–5.0 for A niger and 4.8–5.2 for C utilis. The tannin tolerances of A niger and C utilis were adapted to 20 and 25 g dm−3 by gradually increasing the concentrations of valonea tannins in the culture media. The adapted strain of A niger was able to completely degrade 20 g dm−3 valonea tannins with an EA yield of 14.3% in 9 days. Meanwhile, the adapted strain of C utilis decreased the valonea tannins' level from 25 to 9.1 g dm−3 with an EA yield of 11.48%. The degradation ability of A niger came from tannase whose activity in the medium was 63 U cm−3 at the ninth day of fermentation, and that of C utilis was due to both tannase and polyphenol oxidase (PPO) whose activities were 32 U cm−3 and 29 U cm−3 at the ninth day. The coculture of both the adapted strains could completely degrade 25 g dm−3 valonea tannins in only 7 days with a remarkably increased EA yield (21%). The activities of tannase and PPO of the coculture at the seventh day were 66 U cm−3 and 47 U cm−3 respectively, which proved the synergistic effect of the two enzymes on valonea tannins' degradation and EA accumulation. Copyright © 2005 Society of Chemical Industry
Exploration of peptide motifs for potent non‐viral gene delivery highly selective for dividing cells
Authors: Parker Alan L. , Collins Louise , Zhang Xiaohong , Fabre John W. 
Published: July 2005

AbstractBackgroundThe immunogenicity of viral DNA vectors is an important problem for gene therapy. The use of peptide motifs for gene delivery would largely overcome this problem, and provide a simple, safe and powerful approach for non‐viral gene therapy.MethodsWe explored the functional properties of two motifs: the (Lys)16 motif (for binding and condensing DNA, and probably also nuclear translocation of plasmids) and the fusogenic peptide motif of influenza virus (for acid‐dependent endocytic escape of peptide/DNA particles). The physical properties and gene delivery efficiencies of (Lys)16‐containing peptides in combination with free fusogenic peptide were evaluated, and compared with a single composite peptide incorporating both moieties. Post‐mitotic corneal endothelial cells and growth‐arrested HeLa were included, so as not to neglect the question of nuclear translocation of plasmids.ResultsThe fusogenic moiety in the composite peptide was able to adopt an alpha‐helical configuration unhindered by the (Lys)16 moiety, and retained acid‐dependent fusogenic properties. The composite peptide gave remarkably high levels of gene delivery to dividing cell lines. However, in marked contrast to (Lys)16/DNA complexes plus free fusogenic peptide, the composite peptide was completely ineffective for gene delivery to post‐mitotic and growth‐arrested cells.ConclusionsAttachment of the fusogenic peptide to (Lys)16 appears to block (Lys)16‐mediated nuclear translocation of plasmid, but not fusogenic peptide mediated endocytic escape. This strengthens the experimental basis for (Lys)16‐mediated nuclear translocation of plasmids, and provides a single peptide with potent gene delivery properties, restricted to dividing cells. This property is potentially useful in experimental biology and clinical medicine. Copyright © 2005 John Wiley & Sons, Ltd.
New designer drug 2,5‐dimethoxy‐4‐ethylthio‐β‐phenethylamine (2C‐T‐2): studies on its metabolism and toxicological detection in rat urine using gas chromatography/mass spectrometry
Authors: Theobald Denis S. , Staack Roland F. , Puetz Michael , Maurer Hans H. 
Published: July 2005

AbstractStudies are described on the metabolism and the toxicological analysis of the phenethylamine‐derived designer drug 2,5‐dimethoxy‐4‐ethylthio‐β‐phenethylamine (2C‐T‐2) in rat urine using gas chromatography/mass spectrometry (GC/MS) after enzymatic cleavage of conjugates, liquid‐liquid extraction and derivatization. The structures of 14 metabolites were assigned tentatively by detailed interpretation of their mass spectra. Identification of these metabolites indicated that 2C‐T‐2 was metabolized by sulfoxidation followed by N‐acetylation and either hydroxylation of the S‐ethyl side chain or demethylation of one methoxy group, O‐demethylation of the parent compound followed by N‐acetylation and sulfoxidation, deamination followed by reduction to the corresponding alcohol followed by partial glucuronidation and/or sulfation or by oxidation to the corresponding acid followed either by partial glucuronidation or by degradation to the corresponding benzoic acid derivative followed by partial glucuronidation. Furthermore, 2C‐T‐2 was metabolized by N‐acetylation of the parent compound followed either by O‐demethylation and sulfoxidation or by S‐dealkylation, S‐methylation and sulfoxidation. The authors' systematic toxicological analysis (STA) procedure using full‐scan GC/MS after acid hydrolysis, liquid‐liquid extraction microwave‐assisted acetylation allowed the detection of an intake of a dose of 2C‐T‐2 in rat urine, which corresponds to a common drug users' dose. Assuming similar metabolism, the described STA procedure should be suitable for proof of an intake of 2C‐T‐2 in human urine. Copyright © 2005 John Wiley & Sons, Ltd.
Evidence for macrophage‐mediated myelin disruption in an animal model for Charcot‐Marie‐Tooth neuropathy type 1A
Authors: Kobsar Igor , Hasenpusch‐Theil Kerstin , Wessig Carsten , Müller Hans Werner , Martini Rudolf 
Published: July 2005

AbstractCharcot‐Marie‐Tooth neuropathy type 1A (CMT1A) is the most common inherited neuropathy in humans and is mostly caused by a 1.5‐Mb tandem duplication of chromosome 17 comprising the gene for the peripheral myelin protein 22‐kDa (PMP22). Although there are numerous studies on the functional role of PMP22, the mechanisms of myelin degeneration under PMP22‐overexpression conditions have not yet been fully understood. We have shown previously that in mouse mutants hetero‐ or homozygously deficient for two other myelin components, P0 and Cx32, respectively, immune cells contribute to the demyelinating neuropathy. To test this possibility for PMP22 overexpression, we investigated a putative mouse model for CMT1A, i.e., the mouse strain C61 mildly overexpressing human PMP22 in peripheral nerves. Electron microscopic and electrophysiologic investigations revealed that this mouse strain develops pathologic features similar to those found in CMT1A patients. A novel finding, however, was the upregulation of CD8‐ and F4/80‐positive lymphocytes and macrophages, respectively, in peripheral nerves. The observation that macrophages enter endoneurial tubes of the mutants and obviously phagocytose morphologically normal myelin strongly suggests that the myelin degeneration is mediated at least partially by these phagocytic cells. By gene array technology and quantitative RT‐PCR of peripheral nerve homogenates from PMP22 mutants, monocyte chemoattractant protein‐1 (MCP‐1; ccl2) could be identified as a putative factor to attract or activate macrophages that attack myelin sheaths in this model of CMT1A. © 2005 Wiley‐Liss, Inc.
Changes in the amounts of chondroitin sulfate proteoglycans in rat brain after neonatal hypoxia‐ischemia
Authors: Matsui Fumiko , Kakizawa Hiroko , Nishizuka Masako , Hirano Kanako , Shuo Takuya , Ida Michiru , Tokita Yoshihito , Aono Sachiko , Keino Hiroomi , Oohira Atsuhiko 
Published: July 2005

AbstractChondroitin sulfate proteoglycans have been shown to participate in the pathogenesis of neuronal damages in the injured adult central nervous system (CNS). Upregulated expression of chondroitin sulfate proteoglycans has been reported around the injured sites and depletion of these chondroitin sulfate proteoglycans brings about increased axonal regeneration in the injured adult CNS. To examine if chondroitin sulfate proteoglycans are also involved in the pathologic process of hypoxia‐ischemia in the neonatal brain, expressions of three chondroitin sulfate proteoglycans, neurocan, phosphacan, and neuroglycan C, were examined in rat brains after neonatal hypoxia‐ischemia. Hypoxic‐ischemic rats were produced by ligating the right carotid artery of 7‐day‐old rats, followed by 8% oxygen exposure. Western blot analysis revealed that in contrast to injured adult CNS, the amount of neurocan was reduced 24 hr after hypoxia in the neonatal hypoxic‐ischemic cerebral hemisphere. The amounts of phosphacan and neuroglycan C were also reduced significantly 24 hr after hypoxia at the right injured cortex compared to those at the left cortex. Surprisingly, the immunohistologic staining for phosphacan was conversely intensified both at 24 hr and 8 days after hypoxia at the infarcted area. In addition, the habenula and fascicules retroflexus in the right cerebral hemisphere degenerated and became intensely immunostained with the anti‐phosphacan antibody shortly after hypoxia. Hypoxic‐ischemic insult may unmask phosphacan epitopes at the injured sites, resulting in intensified immunostaining. Because intensified immunostaining for neurocan and neuroglycan C was not observed, unmasking seems to be specific to phosphacan among these three chondroitin sulfate proteoglycans. © 2005 Wiley‐Liss, Inc.
A systematic review of prevalence studies of dementia in Parkinson's disease
Authors: Aarsland Dag , Zaccai Julia , Brayne Carol 
Published: July 2005

AbstractSubstantial variation in the prevalence of dementia in Parkinson's disease (PDD) has been reported. The aim of this study was to review systematically and critically previous studies of the prevalence of PDD using PubMed to search the literature. Studies focusing on PD and PDD, as well as those examining on the epidemiology of dementia subtypes, were included. Predefined inclusion and exclusion criteria were used and the quality of the studies included was rated. Articles were included if: (1) the proportion of PDD among patients with either PD or dementia was reported in an original study; (2) patients had been subjected to prospective clinical examination; and (3) strategies to include all subjects with either PD or dementia within the community or hospital clinics within a geographical area were employed. Twelve studies of the prevalence of PD or PDD (1,767 patients included) and 24 prevalence studies of dementia subtypes (4,711 patients included) met the inclusion criteria. In the PD/PDD studies, the proportion (mean and 95% confidence interval) with PDD in PD was 24.5% (17.4–31.5). There were significant methodological variations between studies and in the four studies that matched the quality criteria most closely, the rate of PDD was 31.1% (20.1–42.1). The prevalence of PDD was estimated as 0.5% in subjects 65 years or older. The percentage of PDD among those with dementia was 3.6% (3.1–4.1), with an estimated prevalence of PDD of 0.2% in subjects aged 65 years or older. Despite methodological variation, this systematic review suggests that 24 to 31% of PD patients have dementia, and that 3 to 4% of the dementia in the population would be due to PDD. The estimated prevalence of PDD in the general population aged 65 years and over is 0.2 to 0.5%. © 2005 Movement Disorder Society
Morphogens in motion: Growth control of the neural tube
Authors: Cayuso Jordi , Martí Elisa 
Published: July 2005

AbstractThe entire vertebrate nervous system develops from a simple epithelial sheet, the neural plate which, along development, acquires the large number and wide variety of neuronal cell types required for the construction of a functional mature nervous system. These include processes of growth and pattern formation of the neural tube that are achieved through complicated and tightly regulated genetic interactions. Pattern formation, particularly in the vertebrate central nervous system, is one of the best examples of a morphogen‐type of function. Cell cycle progression, however, is generally accepted to be dependent on cell‐intrinsic factors. Recent studies have demonstrated that proliferation of neural precursors is also somehow controlled by secreted signaling molecules, well‐known by their role as morphogens, such as fibroblast growth factor (FGF), vertebrate orthologs of the Drosophila wingless (Wnt), hedgehog (Hh), and transforming growth factor β (TGF‐β) families, that in turn regulate the activity of factors controlling cell cycle progression. In this review we will summarize the experimental data that support the idea that classical morphogens can be reused to regulate proliferation of neural precursors. © 2005 Wiley Periodicals, Inc. J Neurobiol 64: 376–387, 2005
Protective role of heat shock protein 27 in gastric mucosal injury
Authors: Ebert Matthias PA , Schäfer Claus , Chen Jie , Hoffmann Juliane , Gu Ping , Kubisch Constanze , Carl‐McGrath Stacy , Treiber Gerhard , Malfertheiner Peter , Röcken Christoph 
Published: July 2005

AbstractHeat shock protein 27 (HSP27) mediates cytoprotective effects through its function as a molecular chaperone and through the phosphorylation‐dependent stabilization of actin filaments. The role of HSP27 in gastric ulcer formation and healing is, however, unknown. The expression of HSP27 was studied in human gastric tissue specimens obtained from patients with gastric ulcers and from healthy Helicobacter pylori‐negative individuals, who received low‐dose aspirin, rofecoxib, and the combination in a prospective study. The susceptibility of the gastric mucosa to indomethacin‐induced lesions was further studied in transgenic mice overexpressing human HSP27 (TghuHSP27) and compared with wild‐type mice (Wt). The expression of HSP27, COX‐1, and COX‐2 was investigated in TghuHSP27 mice and Wt mice by immunohistochemistry and western blot analysis. While no specific changes in HSP27 expression were found following exposure of healthy human gastric mucosa to oral administration of aspirin or refocoxib, chronic gastric ulcers showed strong HSP27 expression at the ulcer base and margins. Here it was expressed by granulation tissue and regenerating surface epithelium. In TghuHSP27 mice, overexpression of HSP27 led to a significant decrease of indomethacin‐induced erosions and ulcers compared with Wt mice. COX‐1 and COX‐2 levels did not change. HSP27 is involved in chronic gastric ulcer repair mechanisms in humans, while overexpression of human HSP27 in gastric epithelial cells in mice reduces the susceptibility to non‐steroidal anti‐inflammatory drug (NSAID)‐induced gastric ulceration. This indicates that HSP27 expression is critical for mucosal protection in the stomach. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.