bluuebunny/crossref_metadata_2025_split huggingface dataset:
An Impaired Renal Function: A Predictor of Ventricular Arrhythmias and Mortality in Patients with Nonischemic Cardiomyopathy and Heart Failure
Authors: KREUZ JENS , HORLBECK FRITZ , HOYER FELIX , MELLERT FRITZ , FIMMERS ROLF , LICKFETT LARS , NICKENIG GEORG , SCHWAB JOERG O. 
Published: March 2011

Background: This study investigated the overall mortality and the incidence of ventricular tachyarrhythmia (VT) in 99 patients with nonischemic cardiomyopathy (NICM) and with an implantable cardioverter defibrillator (ICD) suffering from heart failure.
Methods: We performed a stepwise regression model to identify independent risk factors for the occurrence of ventricular arrhythmias. Using a Cox regression model, independent risk factors for total mortality were evaluated and, subsequently, a Kaplan‐Meier analysis was applied. The primary endpoint of this study was the identification of independent predictors of overall mortality and the incidence of malignant arrhythmias.
Results: One hundred twenty‐five VT (≥310 ms), 51 fast VT (between 310 ms and 240 ms), and 48 episodes of ventricular fibrillation (≤240 ms) were documented in 32 patients. Independent predictors of arrhythmias detected and treated by the ICD included female gender (odds ratio [OR] 3.4), lack of statin therapy (OR 3.5), and increased serum creatinine (OR 3.7). The Kaplan‐Meier analysis showed no difference in survival between participants with or without VT. Total mortality was predicted by increased age (OR 2.3) and an impaired renal function (OR 1.9), independently.
Conclusions: In this cohort of NICM patients with heart failure, female gender, lack of statin therapy, and increased creatinine represented independent risk factors for the incidence of malignant arrhythmias. Furthermore, renal insufficiency and age favored total mortality. Considering these results, impaired renal function might represent a valuable noninvasive tool to identify NICM patients who, despite ICD implantation, have the highest risk of mortality and therefore require a particularly thorough follow‐up. (PACE 2011; 34:894–899)
Mechanism of Complex Fractionated Electrograms Recorded During Atrial Fibrillation in a Canine Model
Authors: GERSTENFELD EDWARD P. , LAVI NIMROD , BAZAN VICTOR , GOJRATY SATTAR , KIM STEVEN J , MICHELE JOHN 
Published: March 2011

Background: Complex fractionated atrial electrograms (CFEs) have been described as a target during atrial fibrillation (AF) ablation; however, the mechanism leading to CFEs is poorly understood. We used noncontact mapping in a canine model of AF to determine the activation patterns in areas of CFEs.
Methods: Sustained AF was induced in 10 canines with 10–12 weeks of atrial tachy‐pacing at 440 ppm. A roving mapping catheter and noncontact multielectrode array (MEA) were deployed in the left atrium (LA). NavX software was used to construct a contact bipolar CFE LA map. The MEA was then used to reconstruct wavefront propagation in proximity to CFE regions. Wavefront propagation was assessed during three separate recording segments for each site.
Results: There were 34 CFE regions identified (3.4/dog) and 102 noncontact CFE regional activation sequences studied. The CFE regions were stereotypically located at the junctions of (1) the left pulmonary vein (PV)/posterior LA, (2) right inferior PV/posterior LA, (3) right superior PV/anterior LA, and (4) the LA roof. The majority (47%) of CFE recordings were characterized by wavefront collision, usually between circulating LA wavefronts and entry/exit from the PVs. Thirty‐eight (38%) CFE recordings were noted to be the central functional barrier of a reentrant wavefront. Ablation through CFE regions due to reentry led to AF termination and noninducibility in 3/5 animals.
Conclusions: In this pacing‐induced AF model, common causes of CFEs include: (1) wavefront collision, (2) conduction through channels of functional block, (3) reentry. The vast majority of these CFE regions were caused by wavefront collision rather than true “drivers” of AF. (PACE 2011; 34:844–857)
Chromosomal variability of human mesenchymal stem cells cultured under hypoxic conditions
Authors: Ueyama Hanae , Horibe Tomohisa , Hinotsu Shiro , Tanaka Tomoaki , Inoue Takeomi , Urushihara Hisashi , Kitagawa Akira , Kawakami Koji 
Published: March 2011

AbstractBone marrow derived human mesenchymal stem cells (hMSCs) have attracted great interest from both bench and clinical researchers because of their pluripotency and ease of expansion ex vivo. However, these cells do finally reach a senescent stage and lose their multipotent potential. Proliferation of these cells is limited up to the time of their senescence, which limits their supply, and they may accumulate chromosomal changes through ex vivo culturing. The safe, rapid expansion of hMSCs is critical for their clinical application. Chromosomal aberration is known as one of the hallmarks of human cancer, and therefore it is important to understand the chromosomal stability and variability of ex vivo expanded hMSCs before they are used widely in clinical applications. In this study, we examined the effects of culturing under ambient (20%) or physiologic (5%) O2 concentrations on the rate of cell proliferation and on the spontaneous transformation of hMSCs in primary culture and after expansion, because it has been reported that culturing under hypoxic conditions accelerates the propagation of hMSCs. Bone marrow samples were collected from 40 patients involved in clinical research. We found that hypoxic conditions promote cell proliferation more favourably than normoxic conditions. Chromosomal aberrations, including structural instability or aneuploidy, were detected in significantly earlier passages under hypoxic conditions than under normoxic culture conditions, suggesting that amplification of hMSCs in a low‐oxygen environment facilitated chromosomal instability. Furthermore, smoothed hazard‐function modelling of chromosomal aberrations showed increased hazard after the fourth passage under both sets of culture conditions, and showed a tendency to increase the detection rate of primary karyotypic abnormalities among donors aged 60 years and over. In conclusion, we propose that the continuous monitoring of hMSCs will be required before they are used in therapeutic applications in the clinic, especially when cells are cultured under hypoxic conditions.
Apoptosis related protein‐1 triggers melanoma cell death via interaction with the juxtamembrane region of p75 neurotrophin receptor
Authors: Selimovic Denis , Sprenger Achim , Hannig Matthias , Haïkel Youssef , Hassan Mohamed 
Published: March 2011

AbstractAlthough chemotherapeutic drugs could theoretically target all metastatic sites, current treatments do not provide complementary therapeutics. Therefore, the development of an alternative approach replacing the traditional therapy is urgently needed. To assess the killing efficiency of the functionally identified apoptosis‐related protein (APR)‐1 in melanoma cells, we established a system for the regulated expression of APR‐1. The induction of APR‐1 expression caused apoptosis of melanoma cells via the interaction with the juxtamembrane region of p75 neurotrophin receptor (p75NTR), and possible also via the competition with tumour necrosis factor receptor‐associated factor‐6 (TRAF6) and the catalytic receptor of neurotrophin (Trk) for the same p75NTR interacting site. The accumulation of APR‐1 in melanoma cells may block the physical association of p75NRT with TRAF6 and/or Trk, leading to the disruption of both NF‐κB and extracellular signal‐regulated kinase (ERK) pathways. Also, accumulation of APR‐1 protein enhanced the activity of both c‐Jun‐N‐terminal kinase (JNK) and p38 pathways. However, the analysis of APR‐1‐modulated pathways demonstrated the involvement of apoptosis‐regulating kinase 1‐JNK/p38 pathway in the induction of Bax expression leading to both mitochondrial dysregulation [as demonstrated by the loss of mitochondrial membrane potential, the release of both cytochrome c and apoptosis‐inducing factor into cytoplasm, and cleavage of caspase‐9, caspase‐3 and poly (ADP‐ribose) polymerase (PARP)] and endoplasmic reticulum stress as demonstrated by the increase of intracellular Ca2+ release. Thus, besides the analysis of its pro‐apoptotic function, our data provide insight into the molecular mechanism of APR‐1‐induced apoptosis of melanoma cells.
Progesterone enhances vascular endothelial cell migration via activation of focal adhesion kinase
Authors: Zheng Shuhui , Huang Jinghe , Zhou Kewen , Xiang Qiuling , Zhang Yaxing , Tan Zhi , Simoncini Tommaso , Fu Xiaodong , Wang Tinghuai 
Published: March 2011

AbstractThe mechanisms of progesterone on endothelial cell motility are poorly investigated. Previously we showed that progesterone stimulated endothelial cell migration via the activation of actin‐binding protein moesin, leading to actin cytoskeleton remodelling and the formation of cell membrane structures required for cell movement. In this study, we investigated the effects of progesterone on the formation of focal adhesion complexes, which provide anchoring sites for cell movement. In cultured human umbilical endothelial cells, progesterone enhanced focal adhesion kinase (FAK) phosphorylation at Tyr397 in a dose‐ and time‐dependent manner. Several signalling inhibitors interfered with progesterone‐induced FAK activation, including progesterone receptor (PR) antagonist ORG 31710, specific c‐Src kinase inhibitor PP2, phosphatidylinosital‐3 kinase (PI3K) inhibitor wortmannin as well as ρ‐associated kinase (ROCK‐2) inhibitor Y27632. It suggested that PR, c‐Src, PI3K and ROCK‐2 are implicated in this action. In line with this, we found that progesterone rapidly promoted c‐Src/PI3K/Akt activity, which activated the small GTPase RhoA/ρ‐associated kinase (ROCK‐2) complex, resulting in FAK phosphorylation. In the presence of progesterone, endothelial cells displayed enhanced horizontal migration, which was reversed by small interfering RNAs abrogating FAK expression. In conclusion, progesterone promotes endothelial cell movement via the rapid regulation of FAK. These findings provide new information on the biological actions of progesterone on human endothelial cells that are relevant for vascular function.
High‐molecular weight Aβ oligomers and protofibrils are the predominant Aβ species in the native soluble protein fraction of the AD brain
Authors: Upadhaya Ajeet Rijal , Lungrin Irina , Yamaguchi Haruyasu , Fändrich Marcus , Thal Dietmar Rudolf 
Published: March 2011

AbstractAlzheimer’s disease (AD) is characterized by the aggregation and deposition of amyloid β protein (Aβ) in the brain. Soluble Aβ oligomers are thought to be toxic. To investigate the predominant species of Aβ protein that may play a role in AD pathogenesis, we performed biochemical analysis of AD and control brains. Sucrose buffer‐soluble brain lysates were characterized in native form using blue native (BN)‐PAGE and also in denatured form using SDS‐PAGE followed by Western blot analysis. BN‐PAGE analysis revealed a high‐molecular weight smear (>1000 kD) of Aβ42‐positive material in the AD brain, whereas low‐molecular weight and monomeric Aβ species were not detected. SDS‐PAGE analysis, on the other hand, allowed the detection of prominent Aβ monomer and dimer bands in AD cases but not in controls. Immunoelectron microscopy of immunoprecipitated oligomers and protofibrils/fibrils showed spherical and protofibrillar Aβ‐positive material, thereby confirming the presence of high‐molecular weight Aβ (hiMWAβ) aggregates in the AD brain. In vitro analysis of synthetic Aβ40‐ and Aβ42 preparations revealed Aβ fibrils, protofibrils, and hiMWAβ oligomers that were detectable at the electron microscopic level and after BN‐PAGE. Further, BN‐PAGE analysis exhibited a monomer band and less prominent low‐molecular weight Aβ (loMWAβ) oligomers. In contrast, SDS‐PAGE showed large amounts of loMWAβ but no hiMWAβ40 and strikingly reduced levels of hiMWAβ42. These results indicate that hiMWAβ aggregates, particularly Aβ42 species, are most prevalent in the soluble fraction of the AD brain. Thus, soluble hiMWAβ aggregates may play an important role in the pathogenesis of AD either independently or as a reservoir for release of loMWAβ oligomers.
Cerebral correlates of psychotic syndromes in neurodegenerative diseases
Authors: Jellinger Kurt A. 
Published: March 2011

Abstract

Introduction

Old age and Alzheimer’s disease

Lewy body diseases

Psychosis has been recognized as a common feature in neurodegenerative diseases and a core feature of dementia that worsens most clinical courses. It includes hallucinations, delusions including paranoia, aggressive behaviour, apathy and other psychotic phenomena that occur in a wide range of degenerative disorders including Alzheimer’s disease, synucleinopathies (Parkinson’s disease, dementia with Lewy bodies), Huntington’s disease, frontotemporal degenerations, motoneuron and prion diseases. Many of these psychiatric manifestations may be early expressions of cognitive impairment, but often there is a dissociation between psychotic/behavioural symptoms and the rather linear decline in cognitive function, suggesting independent pathophysiological mechanisms. Strictly neuropathological explanations are likely to be insufficient to explain them, and a large group of heterogeneous factors (environmental, neurochemical changes, genetic factors, etc.) may influence their pathogenesis. Clinico‐pathological evaluation of behavioural and psychotic symptoms (PS) in the setting of neurodegenerative and dementing disorders presents a significant challenge for modern neurosciences. Recognition and understanding of these manifestations may lead to the development of more effective preventive and therapeutic options that can serve to delay long‐term progression of these devastating disorders and improve the patients’ quality of life. A better understanding of the pathophysiology and distinctive pathological features underlying the development of PS in neurodegenerative diseases may provide important insights into psychotic processes in general.
Reliability of the vertical magnification factor on panoramic radiographs: clinical implications for posterior mandibular implants
Authors: Vazquez Lydia , Nizam Al Din Yassin , Christoph Belser Urs , Combescure Christophe , Bernard Jean‐Pierre 
Published: March 2011

AbstractObjectives: Panoramic radiographs allow evaluation of the available bone height for implant treatment planning while imparting a low radiation dose. As panoramic radiography produces image distortion, reference objects are required to determine the exact magnification. This study aims to estimate a panoramic unit's vertical magnification factor (MF) by measuring the length of dental implants used as radiopaque reference objects on postoperative panoramic radiographs. We compared our findings to the vertical MF listed by the panoramic unit manufacturer, and studied the reproducibility and accuracy of our measuring method by analyzing the inter‐ and intraobserver agreements.Material and methods: Using a digital calliper, we measured the length of 32 implants on 17 postoperative panoramic radiographs taken with a Scanora® unit. The implants were 10mm‐long standard Straumann® implants placed in the posterior segments of mandibles. The MF was calculated by dividing the implant's radiological length by the implant's real length.Results: The mean calculated vertical MF was 1.27 ± 0.01 (1.245–1.295) and was lower than the manufacturer's MF (1.3). The vertical MF was 1.28 ± 0.01 in the premolar and 1.27 ± 0.01 in the molar regions. There was an excellent intraobserver reliability (0.96 for observer 1; 0.93 for observer 2) and a good interobserver reliability (0.85 at measurement session 1; 0.8 at measurement session 2)Conclusions: The observed reliability of the MF confirms that a panoramic radiograph can be used for preoperative implant length evaluation in the posterior mandibular segments. MF stability should be verified with other panoramic units. In clinical practice, using the implant length as a reference object on postoperative panoramic radiographs is a simple and effective evaluation method to estimate a panoramic unit's MF.To cite this article:
Vazquez L, Nizam Al Din Y, Belser UC, Combescure C, Bernard J‐P. Reliability of the vertical magnification factor on panoramic radiographs: clinical implications for posterior mandibular implants. Clin. Oral Impl. Res. xx, 2011; 000–000. doi: 10.1111/j.1600‐0501.2010.02131.x
Point‐of‐care oral‐based diagnostics
Authors: Hart RW , Mauk MG , Liu C , Qiu X , Thompson JA , Chen D , Malamud D , Abrams WR , Bau HH 
Published: March 2011

Oral Diseases (2011) 17, 745–752Many of the target molecules that reside in blood are also present in oral fluids, albeit at lower concentrations. Oral fluids are, however, relatively easy and safe to collect without the need for specialized equipment and training. Thus, oral fluids provide convenient samples for medical diagnostics. Recent advances in lab‐on‐a‐chip technologies have made minute, fully integrated diagnostic systems practical for an assortment of point‐of‐care tests. Such systems can perform either immunoassays or molecular diagnostics outside centralized laboratories within time periods ranging from minutes to an hour. The article briefly reviews recent advances in devices for point‐of‐care testing with a focus on work that has been carried out by the authors as part of a NIH program.
Three‐dimensional tomographic mapping related to primary stability and structural miniscrew characteristics
Authors: Silvestrini Biavati A , Tecco S , Migliorati M , Festa F , Marzo G , Gherlone E , Tetè S 
Published: March 2011

To cite this article:
Silvestrini Biavati A, Tecco S, Migliorati M, Festa F, Marzo G, Gherlone E, Tetè S:  Three‐dimensional tomographic mapping related to primary stability and structural miniscrew characteristics  Orthod Craniofac Res 2011;14:88–99Structured AbstractAuthors –  Silvestrini Biavati A, Tecco S, Migliorati M, Festa F, Marzo G, Gherlone E, Tetè SObjectives –  To evaluate the maxilla, mandible, and cortical plates on computerized tomographic (CT) scans to achieve accurate three‐dimensional bone thickness measurements.Setting and Sample Population –  We selected the CT scans of 25 subjects (among 102), aged 18–58 years (10 men, 15 women), with nearly complete dentition.Material and Methods –  We performed interradicular and bucco‐lingual (including cortical plate thickness) measurements in dental areas distal to the canines in both alveolar arches, at three levels (5, 8, and 11 mm) from the alveolar ridge.Results –  The mean thicknesses of the cortical plates in the maxilla were 1.10 mm buccally and 1.27 mm on the palatal side (p < 0.05). In the mandible, cortical plates were 2.23 mm buccally and 2.02 mm lingually. Mandibular buccal and lingual cortical plates became thicker distally in the second and third molar areas. There was considerable variation in cortical thickness (from 0.25 to 5.50 mm).Based on interradicular distances, only 13% of measured sites in the maxilla were suitable for miniscrew insertion (≥3.3 mm), but 63% of sites were suitable in the mandible.Conclusion –  This study showed considerable individual variation in bone thickness. Our data suggested that the palatal/lingual side may provide greater primary stability for miniscrews. The palatal area, between the second upper bicuspid and the first molar, appeared to be the most suitable area for tapered 7‐ to 9‐mm miniscrews, starting at 1.5–2 mm from the alveolar crest.
Copying medical summaries on deceased infants to bereaved parents
Authors: Clarke Paul , Booth David 
Published: March 2011

AbstractAim:  When an infant dies following neonatal intensive care, a detailed medical summary about the infant’s life and death is sent to the general practitioner (GP). Our practice is to send an exact copy of this summary to the parents also. We evaluated the opinions of bereaved parents and their GPs on this practice.Methods:  We carried out a postal questionnaire survey of bereaved parents who had been sent a copy of our medical summary on their deceased infant and their GPs. Parents were asked to rate the summary for its helpfulness, their understanding of it and how distressing it was to receive. We concurrently surveyed via e‐mail all paediatricians in our region to ask whether they routinely copied letters to bereaved parents.Results:  Only 3 of 32 (9%) paediatricians routinely copied summaries to bereaved parents. Thirteen of 21 (62%) parents responded: all but one found the copied summary very helpful, most did not find it especially distressing and most reported a fair understanding of it despite its detailed medical content. Almost all their GPs supported copying the summaries to parents.Conclusion:  Most bereaved parents welcome an exact copy of the detailed medical summary that provides a complete record of their baby’s clinical course, brief life and terminal events.
Role of angiotensin‐converting enzyme gene polymorphism in persistent pulmonary hypertension of the newborn
Authors: De Jesus Lilia C , Kazzi S Nadya J , Dahmer Mary K , Chen Xinguang , Quasney Michael W 
Published: March 2011

AbstractAim:  To evaluate the association of angiotensin‐converting enzyme (ACE) gene polymorphism with risk/severity of persistent pulmonary hypertension of the newborn (PPHN) among at risk infants.Methods:  Infants ≥34 weeks with respiratory distress at birth were recruited. PPHN was diagnosed clinically and by cardiac echocardiogram. Control group consisted of infants with respiratory distress who did not develop PPHN. ACE genotyping (DD, II, DI genotypes) and serum ACE levels were determined.Results:  A total of 120 infants were included (PPHN = 44; control = 76). Frequency of ACE DD genotype was not different between the two groups of infants (25% versus 33%). Among PPHN infants, severity of illness did not differ between genotypes. Mean (SD) serum ACE levels [15 (9) versus 24 (13) versus 29 (14) U/L] were positively associated with the number of D alleles and inversely associated with infants’ gestational age (GA) and level of cardiovascular support.Conclusion:  Angiotensin‐converting enzyme gene polymorphism did not impact the risk or severity of PPHN among infants ≥34 weeks GA.
Methaemoglobinaemia with G6PD deficiency: rare cause of persistently low saturations in neonates
Authors: Titheradge Hannah , Nolan Katie , Sivakumar Shanmugasundaram , Bandi Srinivas 
Published: March 2011

AbstractWe report a very rare case of methaemoglobinaemia associated with glucose 6 phosphate dehydrogenase (G6PD) deficiency, complicating a respiratory illness in a preterm neonate. This neonate had consistently low saturation readings despite being ventilated at moderately high pressures in 100% oxygen. An arterial blood gas confirmed a high methaemoglobin level and a high pO2, inconsistent with the saturations. In addition, the bilirubin increased to exchange levels and was difficult to control with quadruple phototherapy. A double volume exchange transfusion was performed, which reduced both bilirubin and methaemoglobin. The pulse oximetry then started to correlate well with pO2. G6PD deficiency was confirmed.Conclusion:  Paediatricians should remember that methaemoglobinaemia is a rare but important cause of persistently low saturations, and exchange transfusion is a reliable treatment for this condition.