bluuebunny/crossref_metadata_2025_split huggingface dataset:
Beyond Evidence: The Complexity of Maternity Care
Authors: Enkin Murray W. , Glouberman Sholom , Groff Philip , Jadad Alejandro R. , Stern Anita 
Published: November 2006

Preface:  This paper has been gestating for a long time‐‐the sixty years that I have been associated with maternity care. It was conceived during an era of medical authoritarianism, born in a time of nascent childbirth education and family‐centered maternity care, matured in a period of enthusiastic (but not unquestioning) homage to evidence‐based obstetrics, and culminated in a reluctant but comforting acceptance of uncertainty. It has passed through stages of enthusiasm, of disillusionment, and of reevaluation. It is, to use an ancient word I only recently learned, a clinamen, a swerve, a point of intellectual revision. Others in the Clinamen Collaboration share the authorship of this paper with me. Murray Enkin
Long‐Term Survival in Patients Treated with Cardiac Resynchronization Therapy: A 3‐Year Follow‐Up Study from the InSync/InSync ICD Italian Registry
Authors: GASPARINI MAURIZIO , LUNATI MAURIZIO , SANTINI MASSIMO , TRITTO MASSIMO , CURNIS ANTONIO , BOCCHIARDO MARIO , VINCENTI ANTONIO , PISTIS GIANFRANCO , VALSECCHI SERGIO , DENARO ALESSANDRA ,   On Behalf of the INSYNC/INSYNC ICD ITALIAN Registry Investigators
Published: November 2006

Background: Studies reporting the long‐term survival of patients treated with cardiac resynchronization therapy (CRT) outside the realm of randomized controlled trials are still lacking. The aim of this study was to quantify the survival of patients treated with CRT in clinical practice and to investigate the long‐term effects of CRT on clinical status and echocardiographic parameters.
Methods: The study population consisted of 317 consecutive patients with implanted CRT devices from eight Italian University/Teaching Hospitals. The patients were enrolled in a national observational registry and had a minimum follow‐up of 2 years. A visit was performed in surviving patients and mortality data were obtained by hospital file review or direct telephone contact.
Results: During the study period, 83 (26%) patients died. The rate of all‐cause mortality was significantly higher in ischemic than nonischemic patients (14% vs 8%, P = 0.002). Multivariate analysis showed that ischemic etiology (HR 1.72, CI 1.06–2.79; P = 0.028) and New York Heart Association (NYHA) class IV (HR 2.87, CI 1.24–6.64; P = 0.014) were the strongest predictors of all‐cause mortality. The effects of CRT persisted at long‐term follow‐up (for at least 2 years) in terms of NYHA class improvement, increase of left ventricular ejection fraction, decrease of QRS duration (all P = 0.0001), and reduction of left ventricular end‐diastolic and end‐systolic diameters (P = 0.024 and P = 0.011, respectively).
Conclusions: During long‐term (3 years) follow‐up after CRT, total mortality rate was 10%/year. The outcome of ischemic patients was worse mainly due to a higher rate of death from progressive heart failure. Ischemic etiology along with NYHA class IV was identified as predictors of death. Benefits of CRT in terms of clinical function and echocardiographic parameters persisted at the time of long‐term follow‐up.
Improvement of Quality of Life by Means of Antitachy Pacing: From PainFREE to the ADVANCE‐D Trial
Authors: LUNATI MAURIZIO , DEFAYE PASCAL , MERMI JOHANN , GARCIA‐ALBEROLA ARCADI , MERINO JOSÉ L. , ARENAL ANGEL , CAPPATO RICCARDO , NAVARRO XAVIER , PASSARDI MICAELA , SANTINI MASSIMO 
Published: November 2006

Background: Implantable cardioverter‐defibrillators (ICD) can terminate ventricular tachyarrhythmias with shocks (painful) or antitachycardia pacing (painless). According to the results of the Pacing Fast VT Reduces Shock ThErapies Trials, antitachycardia pacing (ATP) can avoid painful shocks and also increase device longevity. The purpose of the ADVANCE‐D (Atp DeliVery for PAiNless ICD ThErapy) study is to determine the most appropriate ventricular tachycardia (VT) therapy, so as to optimize painless therapy for life‐threatening arrhythmias.
Methods and Results: The ADVANCE‐D is a prospective, multicenter, parallel, two‐arm randomized study designed to evaluate the efficacy of two different sequences of ATP therapies (burst 15 pulses, 88%, vs burst 8 pulses, 88%), during an episode of spontaneous arrhythmia classified as fast VT (FVT) in patients with a Class I or IIA indication for ICD implantation (single and dual chamber devices). The primary endpoint is to compare the efficacy of two ATP therapies for FVT episodes. The study will enroll a minimum of 900 patients within 2 years, followed‐up for 12 months. The investigation is expected to be completed in 2007.
Conclusions: The ADVANCE‐D trial is the first large randomized clinical investigation aimed to evaluate optimal programming and efficacy of ATP.
Primary Prevention of Sudden Cardiac Death: Can We Afford the Cost of Cardioverter‐Defibrillators? Data from the Search‐MI Registry‐Italian Sub‐study
Authors: BORIANI GIUSEPPE , BIFFI MAURO , RUSSO MAURIZIO , LUNATI MAURIZIO , BOTTO GIANLUCA , PROCLEMER ALESSANDRO , VERGARA GIUSEPPE , RAHUE WERNER , MARTIGNANI CRISTIAN , RICCI RENATO , SANTINI MASSIMO ,   On Behalf of the SEARCH MI Registry Italian Investigators
Published: November 2006

Background: Large randomized trials show that in appropriately selected patients with left ventricular dysfunction, implantable cardioverter‐defibrillators (ICDs) can improve overall survival at 2–5 years. Since direct implementation of the criteria used in the MADIT II and SCD‐HeFT will lead to a marked rise in ICD implants, there is a growing fear that increased use of ICDs may cause a dramatic burden to health care systems. The ICD has traditionally been seen as an expensive form of treatment, which is difficult to accept at the first look. This is mainly due to the nonlinear character of the ICD investment, characterized by high initial expenditure, followed by a deferred pay‐off in terms of clinical benefits. Cost‐effectiveness analysis may help provide a different perspective on the problem of ICD cost, as may estimation of the daily cost of ICD treatment, assuming a time horizon of 5–7 years—a particularly interesting subject for further registry studies.
Methods and Results: Based on real expenditure data from 2002 to 2005, as recorded in the Search‐MI Registry‐Italian Sub‐study of patients implanted on MADIT II indications, we estimated the daily costs associated with the device and leads. Over a 5–7 year time horizon, the average daily cost was estimated to be €4.60–€6.70. Translation of these figures into U.S. market conditions suggests a daily cost of around $7.90–$11.40.
Conclusions: These findings appear useful to help evaluate the affordability of ICD in comparison with other therapeutic options in a context of limited available economic resources.
Autosomal dominant retinitis pigmentosa in Norway: a 20‐year clinical follow‐up study with molecular genetic analysis. Two novel rhodopsin mutations: 1003delG and I179F
Authors: Grøndahl Jan , Riise Ruth , Heiberg Arvid , Leren Trond , Christoffersen Terje , Bragadottir Ragnheidur 
Published: November 2006

Abstract.Purpose:  To examine the clinical picture and molecular genetics of 12 Norwegian families with autosomal dominant retinitis pigmentosa (adRP) in order to achieve a genotype−phenotype correlation.Methods:  In addition to a clinical ophthalmological examination, fundus photography, dark adaptometry and electroretinography were performed. Four genes were analysed: rhodopsin (RHO); retinitis pigmentosa 1 (RP1); retinal degeneration slow/peripherin (RDS/peripherin), and inosine monophosphate dehydrogenase 1 (IMPDH1). Seven of the families had been examined about 20 years previously. A total of 63 patients or first‐degree relatives (aged 18–79 years) were examined.Results:  Mutations were found only in the RHO gene. Seven families were given a diagnosis of classical RP. Two of them had novel mutation 1003delG, and one family had the mutation V345M. Four families had pericentral retinal dystrophy (PRD), two families with the mutation A164V and one with novel mutation I179F. One family was given a diagnosis of central and pericentral retinal dystrophy (CPRD), a special type of cone/rod dystrophy, and no mutation was found.Conclusions:  Six of 12 families had an RHO mutation. The mutation V345M and the novel mutation 1003delG both caused classical RP, the former indicating the most unfavourable prognosis. Two of the families with PRD had the A164V mutation with a favourable prognosis, whereas the novel mutation I179F caused PRD with extremely variable expressivity.
Comparisons between Pascal dynamic contour tonometry, the TonoPen, and Goldmann applanation tonometry in patients with glaucoma
Authors: Salvetat Maria L. , Zeppieri Marco , Tosoni Claudia , Brusini Paolo 
Published: November 2006

Abstract.Purpose:  To compare intraocular pressure (IOP) measurements taken with Pascal dynamic contour tonometry (DCT), the TonoPen and the Goldmann applanation tonometry (GAT). The influence of central corneal thickness (CCT) on IOP measurements taken with Pascal DCT and the TonoPen was evaluated.Methods:  One eye in each of 101 consecutive patients with primary open‐angle glaucoma (POAG) underwent ultrasonic CCT measurement and IOP evaluation with GAT, Pascal DCT and the TonoPen in random order. The agreement between results from Pascal DCT and the TonoPen and those of GAT was assessed using the Bland−Altman method. The deviation of Pascal DCT and TonoPen readings from GAT values, corrected for CCT, was calculated and correlated to CCT using a linear regression model.Results:  The mean of the differences in IOP measurements was 3.2 ± 2.4 mmHg for Pascal DCT minus GAT readings and 0.5 ± 4.5 mmHg for TonoPen minus GAT readings. The 95% confidence interval of differences in IOP measurements was higher between TonoPen and GAT readings (− 6 to 7 mmHg) than between Pascal and GAT readings (0.1−6.8 mmHg). Pascal DCT significantly overestimated IOP compared with GAT, especially for higher IOP readings. Bland−Altman scatterplots showed reasonable inter‐method agreement between Pascal DCT and GAT measurements, and poor agreement between TonoPen and GAT measurements. The deviations of Pascal DCT and TonoPen readings from the corrected GAT values were both highly correlated with CCT values (linear regression analysis, p < 0.0001). The mean change in measured IOP for a 10‐µm increase in CCT was 0.48 mmHg for Pascal DCT and 0.74 mmHg for the TonoPen.Conclusions:  Agreement with GAT measurements was higher for Pascal DCT than for TonoPen readings; however, Pascal DCT significantly overestimated IOP values compared with GAT. Measurements of IOP obtained with both Pascal DCT and the TonoPen appeared to be influenced by CCT, and this influence appeared to be greater for the latter.
Evaluation of selective calculus removal by a fluorescence feedback‐controlled Er:YAG laser in vitro
Authors: Krause Felix , Braun Andreas , Brede Olivier , Eberhard Jörg , Frentzen Matthias , Jepsen Søren 
Published: November 2006

AbstractObjectives: To evaluate the removal of subgingival calculus and dental hard tissues depending on the threshold level of a fluorescence feedback‐controlled Er:YAG laser.Material and Methods: Twenty teeth with calculus on the root surface were treated with an Er:YAG laser. Laser settings were 140 mJ and 10 Hz. The initial fluorescence threshold level of 5 [U] was reduced at intervals of 1 [U] for every laser treatment. Areas of residual calculus (RC) were evaluated using a surface analysis software. Loss of dental hard tissues was assessed by histomorphometric analysis of undecalcified ground sections.Results: Using a threshold value of 5 [U], the median amount of RC was 11% (0–78%). By lowering the threshold levels, the amount of RC decreased [level 1 [U]: 0% (0–26%)]. The laser‐treated root surfaces revealed a statistically significant reduction of the cementum thickness [median: 80 μm (0–250)] compared with the non‐treated opposite side [median: 90 μm (30–250)] (p<0.05).Conclusion: The amount of RC following laser irradiation depends on the fluorescence threshold level for a feedback‐controlled Er:YAG laser. It might be suggested that this laser system may be used with a threshold level even lower than 5 [U] without removing a clinically relevant amount of root cementum.
Differential expression of periodontal ligament‐specific markers and osteogenic differentiation in human papilloma virus 16‐immortalized human gingival fibroblasts and periodontal ligament cells
Authors: Pi S.‐H. , Lee S.‐K. , Hwang Y.‐S. , Choi M.‐G. , Lee S.‐K. , Kim E.‐C. 
Published: November 2006

Background and Objective:  Periodontal ligament cells and gingival fibroblasts are important in the remodeling of periodontal tissue, but human papilloma virus (HPV)16‐immortalized cell lines derived from human periodontal ligament cells and gingival fibroblasts has not been characterized. The purpose of this study was to establish and differentially characterize the immortalized cell lines from gingival fibroblasts and periodontal ligament by HPV16 transfection.Material and Methods:  Cell growth, cell cycle analysis, western blot for cell cycle regulatory proteins and osteogenic differentiation markers, and reverse transcription–polymerase chain reaction for periodontal ligament‐specific markers were performed.Results:  Both immortalized cell lines (immortalized gingival fibroblasts and immortalized periodontal ligament cells) grew faster than primary cultured gingival fibroblasts or periodontal ligament cells. Immortalized gingival fibroblasts and immortalized periodontal ligament cells overexpressed proteins p16 and p21, and exhibited degradation of proteins pRb and p53, which normally cause cell cycle arrest in G2/M‐phase. Western blotting and reverse transcription–polymerase chain reaction for periodontal ligament‐specific and osteogenic differentiation marker studies demonstrated that a cell line, designated IPDL, mimicked periodontal ligament gene expression for alkaline phosphatase, osteonectin, osteopontin, bone sialoprotein, bone morphogenic protein‐2, periostin, S‐100A4 and PDLs17.Conclusion:  These results indicate that IPDL and immortalized gingival fibroblast cell lines consistently retain normal periodontal ligament and gingival fibroblast phenotypes, respectively, and periodontal ligament markers and osteogenic differentiation in IPDL are distinct from immortalized gingival fibroblast cells.
Enamel matrix derivative stimulates chondrogenic differentiation of ATDC5 cells
Authors: Narukawa M. , Suzuki N. , Takayama T. , Shoji T. , Otsuka K. , Ito K. 
Published: November 2006

Background and Objectives:  Although enamel matrix derivative can promote chondrogenic differentiation of pluripotent mesenchymal precursor cells, the molecular mechanism that underlies this phenomenon is unclear. The purpose of this study was to determine the effect of enamel matrix derivative on chondrogenic differentiation. ATDC5 cells, which undergo a reproducible multistep chondrogenic differentiation, were cultured with or without enamel matrix derivative for up to 35 d.Methods and Results:  Cell proliferation and alkaline phosphatase activity increased markedly in cells cultured in the presence of enamel matrix derivative, compared with cells cultured in its absence. Deposition of Alcian blue‐positive cartilage matrix and Alizarin red‐positive mineralized nodules also increased significantly upon treatment with enamel matrix derivative. Expression of mRNAs encoding cartilage extracellular matrix proteins (type II collagen, type X collagen and aggrecan) and chondrogenic‐related transcription factors (Sox9, Zfp60 and AJ18) were measured using the real‐time polymerase chain reaction. Type II collagen, type X collagen and aggrecan mRNA expression increased markedly with enamel matrix derivative treatment. Transcription of Sox9, an important transcription factor that mediates chondrogenic differentiation, also increased with enamel matrix derivative treatment. The KRAB/C2H2 zinc‐finger transcription factors, Zfp60 and AJ18, were transiently expressed in the prehypertrophic stage, and their expression increased with enamel matrix derivative treatment. In a western blot analysis with anti‐insulin‐like growth factor‐I and anti‐bone morphogenetic protein‐6 immunoglobulin, bands corresponding to ≈ 14, ≈ 18 and ≈ 60 kDa were found in enamel matrix derivative.Conclusion:  Our study provides clear evidence that enamel matrix derivative promotes chondrogenic differentiation of ATDC5 cells.
Differential platelet‐activating factor synthesis by monocytes and polymorphonuclear leukocytes from subjects with localized aggressive periodontitis
Authors: Shin C. R. , Moores J. , Best A. M. , Tew J. G. , Schenkein H. A. , Barbour S. E. 
Published: November 2006

Background and Objective:  Platelet‐activating factor is elevated in localized aggressive periodontitis. We previously demonstrated that the elevated level of platelet‐activating factor in localized aggressive periodontitis is at least partially attributable to low levels of platelet‐activating factor acetylhydrolase, the enzyme that catabolizes platelet‐activating factor. The objective of this study was to determine if platelet‐activating factor synthesis was also elevated in localized aggressive periodontitis. To test this, platelet‐activating factor synthesis was quantified in the monocytes and polymorphonuclear neutrophils of periodontally healthy patients and of subjects with localized aggressive periodontitis.Material and Methods:  Cells were labeled with [3H]acetate and treated with vehicle or stimulated with calcium ionophore A23187. Platelet‐activating factor was extracted and quantified by scintillation counting.Results:  For both subject groups, resting monocytes and polymorphonuclear neutrophils produced platelet‐activating factor, and calcium ionophore A23187 stimulated platelet‐activating factor production in both cell types. However, calcium ionophore A23187‐activated monocytes from subjects with localized aggressive periodontitis produced less platelet‐activating factor than did activated periodontally healthy monocytes (p < 0.0001), suggesting an aberrant calcium ionophore A23187 response in monocytes from subjects with localized aggressive periodontitis. Indeed, when the data were expressed as fold induction of platelet‐activating factor synthesis in response to calcium ionophore A23187, monocytes from subjects with localized aggressive periodontitis exhibited only a fourfold increase in platelet‐activating factor synthesis, whereas calcium ionophore A23187‐stimulated monocytes from periodontally healthy, chronic periodontitis and generalized aggressive periodontitis subjects produced ≈ 12 times more platelet‐activating factor than did resting monocytes. In contrast, both resting and activated localized aggressive periodontitis polymorphonuclear neutrophils synthesized more platelet‐activating factor than did periodontally healthy polymorphonuclear neutrophils.Conclusion:  These data suggest that high levels of platelet‐activating factor in subjects with localized aggressive periodontitis result from both increased synthesis and reduced catabolism. While localized aggressive periodontitis polymorphonuclear neutrophils contribute to increased platelet‐activating factor mass through synthesis, the contribution of monocytes is probably the result of reduced catabolism by platelet‐activating factor acetylhydrolase.
Smoking modulates interleukin‐6:interleukin‐10 and RANKL:osteoprotegerin ratios in the periodontal tissues
Authors: César‐Neto J. B. , Duarte P. M. , De Oliveira M. C. G. , Tambeli C. H. , Sallum E. A. , Nociti F. H. 
Published: November 2006

Background and Objective:  This study evaluated the effect of smoking on the gene expression of interleukin‐1α, ‐1ra, ‐6, ‐8 and ‐10, tumor necrosis factor‐α, matrix metalloproteinase (MMP)‐2 and ‐8, receptor activator of NF‐κB ligand (RANKL) and osteoprotegerin, in sites with periodontitis.Material and Methods:  Gingival biopsies were divided into three groups: the healthy group (periodontally healthy subjects; n = 10); the periodontitis group [subjects with severe chronic periodontitis who never smoked (probing depth ≥ 7 mm) (n = 25)]; and the smoking group (subjects diagnosed with severe chronic periodontitis who smoked ≥ 1 pack per day for at least 10 years; n = 25). Gene and protein expressions were analyzed by quantitative polymerase chain reaction and enzyme‐linked immunosorbent assay, respectively.Results:  Data analysis demonstrated that, except for MMP‐8 and osteoprotegerin, the levels of all factors were increased by inflammation (p < 0.001). The levels of interleukin‐1α, ‐1ra, ‐6 and ‐8, and RANKL, were higher in smokers with periodontitis compared with controls, whereas the levels of interleukin‐10, MMP‐8 and osteoprotegerin were lower (p < 0.001). Smoking lowered the levels of interleukin‐1α, ‐8, ‐10, tumor necrosis factor‐α, MMP‐8 and osteoprotegerin, and increased the levels of interleukin‐6 and ‐1ra in sites with a comparable type of periodontitis (p < 0.001).Conclusion:  In conclusion, smoking modulates gene expression in the periodontium, and the influence of smoking on periodontal disease may involve effects of interleukin‐6:interleukin‐10 and RANKL:osteoprotegerin ratios.
(‐)‐Epigallocatechin gallate induces apoptosis, via caspase activation, in osteoclasts differentiated from RAW 264.7 cells
Authors: Yun J.‐H. , Kim C.‐S. , Cho K.‐S. , Chai J.‐K. , Kim C.‐K. , Choi S.‐H. 
Published: November 2006

Background and Objective:  Alveolar bone resorption is a characteristic feature of periodontal diseases and involves removal of both the mineral and the organic constituents of the bone matrix, a process mainly carried out by multinucleated osteoclast cells. (‐)‐Epigallocatechin gallate, the main constituent of green tea polyphenols, has been reported to induce the apoptotic cell death of osteoclasts and to modulate caspase activation in various tumor cells. In the present study, we investigated the inhibitory effect of (‐)‐epigallocatechin gallate on osteoclast survival and examined if (‐)‐epigallocatechin gallate mediates osteoclast apoptosis via caspase activation.Material and Methods:  The effect of (‐)‐epigallocatechin gallate on osteoclast survival was examined by tartrate‐resistant acid phosphatase (TRAP) staining in osteoclasts differentiated from RAW 264.7 cells. In addition, we evaluated the apoptosis of osteoclasts by (‐)‐epigallocatechin gallate using a DNA‐fragmentation assay. Involvement of caspase in (‐)‐epigallocatechin gallate‐mediated osteoclast apoptosis was evaluated by treatment with a general caspase inhibitor, Z‐VAD‐FMK. Moreover, the effect of (‐)‐epigallocatechin gallate on the activation of caspase‐3 was assessed by a colorimetric activity assay and western blotting.Results:  (‐)‐Epigallocatechin gallate significantly inhibited, in a dose‐dependent manner, the survival of osteoclasts differentiated from RAW 264.7 cells and induced the apoptosis of osteoclasts. Treatment with (‐)‐epigallocatechin gallate resulted in DNA fragmentation and induced the activation of caspase‐3 in RAW 264.7 cell‐derived osteoclasts. Additional treatment with Z‐VAD‐FMK suppressed these effects of (‐)‐epigallocatechin gallate.Conclusion:  From these findings, we could suggest that (‐)‐epigallocatechin gallate might prevent alveolar bone resorption by inhibiting osteoclast survival through the caspase‐mediated apoptosis.