bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dexmedetomidine provides neuroprotection: impact on ketamine‐induced neuroapoptosis in the developing rat brain
Authors: DUAN X. , LI Y. , ZHOU C. , HUANG L. , DONG Z. 
Published: July 2014

BackgroundKetamine and dexmedetomidine are increasingly used in combination in pediatric patients. This study examined the hypothesis that dexmedetomidine attenuated ketamine‐induced neurotoxicity.MethodsNeonatal rats were randomly divided into four groups (n = 10, male 5, female 5). Group S + S received an equal volume of normal saline intraperitoneally and subcutaneously at an interval of 5 min. Group K + S received an intraperitoneal injection of 75 mg/kg ketamine followed by subcutaneous injection of normal saline 5 min later. Group S + D were given subcutaneously 25 μg/kg dexmedetomidine 5 min after injection of normal saline. Group K + D received a subcutaneous injection of 25 μg/kg dexmedetomidine 5 min after ketamine injection. The above drugs were given once daily for 3 days. Neuronal apoptosis in the CA1 region and the dentate gyrus of rats was examined by transferase dUTP nick end labeling (TUNEL) assays. Learning and memory abilities of 2‐month old rats were examined by Morris water maze test. The results were analyzed by analysis of variance.ResultsThe percentage of TUNEL‐positive cells in group K + S (CA1, 49.0 ± 9.46 and dentate gyrus, 49.4 ± 5.41) was markedly higher than that in group K + D (CA1, 37.2 ± 5.54 and dentate gyrus, 35.2 ± 5.06) (F = 5.49, P < 0.05 and F = 13.51, P < 0.001, respectively). Group K + S took significantly longer time and swimming distance to find the hidden platform on the fourth and fifth training days than group K + D (P < 0.05). Moreover, group K + D spent considerably more time in the target quadrant than group K + S (P < 0.05). Dexmedetomidine alone caused a small but statistically insignificant increase in neuronal apoptosis of the CA1 region and the dentate gyrus of neonatal rats compared with normal saline.ConclusionIn conclusion, ketamine caused neuroapoptosis and impaired brain functions in the developing rat brain which can be effectively attenuated by dexmedetomidine. Dexmedetomidine alone was not neurotoxic to the developing brain.
Short general anaesthesia induces prolonged changes in gene expression in the mouse hippocampus
Authors: PEKNY T. , ANDERSSON D. , WILHELMSSON U. , PEKNA M. , PEKNY M. 
Published: July 2014

BackgroundThe long‐term molecular changes in the central nervous system constitute an important aspect of general anaesthesia, but little is known about to what extent these molecular changes are affected by anaesthesia duration. The aim of the present study was to evaluate the effects of short duration (20 min) general anaesthesia with isoflurane or avertin on the expression of 20 selected genes in the mouse hippocampus at 1 and 4 days after anaesthesia.MethodsNine to eleven‐weeks‐old male mice received one of the following treatments: 20 min of avertin‐induced anaesthesia (n = 11), 20 min of isoflurane‐induced anaesthesia (n = 10) and no anaesthesia (n = 5). One and four days after anaesthesia, gene expression in the hippocampus was determined with reverse transcription quantitative real‐time polymerase chain reaction.ResultsWe found that anaesthesia led to the upregulation of six genes: Hspd1 (heat shock protein 1), Plat (tissue plasminogen activator) and Npr3 (natriuretic peptide receptor 3) were upregulated only 1 day after anaesthesia, whereas Thbs4 (thrombospondin 4) was upregulated only 4 days after anaesthesia. Syp (synaptophysin) and Mgst1 (microsomal glutathione S‐transferase 1) were upregulated at both time points. Hspd1, Mgst1 and Syp expression was increased regardless of the anaesthetic used, Npr3 and Plat were increased only in mice exposed to avertin, and Thbs4 was upregulated only after isoflurane‐induced anaesthesia.ConclusionsThis study shows that some of the effects of short general anaesthesia on gene expression in the mouse hippocampus persist for at least 4 days.
Hormone replacement therapy enhances IGF‐1 signaling in skeletal muscle by diminishing miR‐182 and miR‐223 expressions: a study on postmenopausal monozygotic twin pairs
Authors: Olivieri Fabiola , Ahtiainen Maarit , Lazzarini Raffaella , Pöllänen Eija , Capri Miriam , Lorenzi Maria , Fulgenzi Gianluca , Albertini Maria C. , Salvioli Stefano , Alen Markku J. , Kujala Urho M. , Borghetti Giulia , Babini Lucia , Kaprio Jaakko , Sipilä Sarianna , Franceschi Claudio , Kovanen Vuokko , Procopio Antonio D. 
Published: July 2014

SummaryMiRNAs are fine‐tuning modifiers of skeletal muscle regulation, but knowledge of their hormonal control is lacking. We used a co‐twin case–control study design, that is, monozygotic postmenopausal twin pairs discordant for estrogen‐based hormone replacement therapy (HRT) to explore estrogen‐dependent skeletal muscle regulation via miRNAs. MiRNA profiles were determined from vastus lateralis muscle of nine healthy 54–62‐years‐old monozygotic female twin pairs discordant for HRT (median 7 years). MCF‐7 cells, human myoblast cultures and mouse muscle experiments were used to confirm estrogen's causal role on the expression of specific miRNAs, their target mRNAs and proteins and finally the activation of related signaling pathway. Of the 230 miRNAs expressed at detectable levels in muscle samples, qPCR confirmed significantly lower miR‐182, miR‐223 and miR‐142‐3p expressions in HRT using than in their nonusing co‐twins. Insulin/IGF‐1 signaling emerged one common pathway targeted by these miRNAs. IGF‐1R and FOXO3A mRNA and protein were more abundantly expressed in muscle samples of HRT users than nonusers. In vitro assays confirmed effective targeting of miR‐182 and miR‐223 on IGF‐1R and FOXO3A mRNA as well as a dose‐dependent miR‐182 and miR‐223 down‐regulations concomitantly with up‐regulation of FOXO3A and IGF‐1R expression. Novel finding is the postmenopausal HRT‐reduced miRs‐182, miR‐223 and miR‐142‐3p expression in female skeletal muscle. The observed miRNA‐mediated enhancement of the target genes' IGF‐1R and FOXO3A expression as well as the activation of insulin/IGF‐1 pathway signaling via phosphorylation of AKT and mTOR is an important mechanism for positive estrogen impact on skeletal muscle of postmenopausal women.
The replicometer is broken: telomeres activate cellular senescence in response to genotoxic stresses
Authors: Suram Anitha , Herbig Utz 
Published: July 2014

SummaryTelomeres, the ends of our linear chromosomes, can function as ‘replicometers’, capable of counting cell division cycles as they progressively erode with every round of DNA replication. Once they are critically short, telomeres become dysfunctional and consequently activate a proliferative arrest called replicative senescence. For many years, telomeres were thought to be autonomous structures, largely isolated from cell intrinsic and extrinsic signals, whose function is to prevent limitless cellular proliferation, a characteristic of most cancer cells. It is becoming increasingly evident, however, that telomeres not only count cell divisions, but also function as sensors of genotoxic stresses to stop cell cycle progression prematurely and long before cells would have entered replicative senescence. This stable growth arrest, triggered by dysfunctional telomeres that are not necessarily critically short, likely evolved as a tumor‐suppressing mechanism as it prevents proliferation of cells that are at risk for acquiring potentially hazardous and transforming mutations both in vitro and in vivo. Here, we review studies supporting the concept that telomeres are important cellular structures whose function not only is to count cell divisions, but also to act as molecular switches that can rapidly stop cell cycle progression permanently in response to a variety of stresses, including oncogenic signals.
SIRT1‐mediated epigenetic downregulation of plasminogen activator inhibitor‐1 prevents vascular endothelial replicative senescence
Authors: Wan Yan‐Zhen , Gao Peng , Zhou Shuang , Zhang Zhu‐Qin , Hao De‐Long , Lian Li‐Shan , Li Yong‐Jun , Chen Hou‐Zao , Liu De‐Pei 
Published: July 2014

SummaryThe inactivation of plasminogen activator inhibitor‐1 (PAI‐1) has been shown to exert beneficial effects in age‐related vascular diseases. Limited information is available on the molecular mechanisms regarding the negatively regulated expression of PAI‐1 in the vascular system. In this study, we observed an inverse correlation between SIRT1, a class III histone deacetylase, and PAI‐1 expression in human atherosclerotic plaques and the aortas of old mice, suggesting that internal negative regulation exists between SIRT1 and PAI‐1. SIRT1 overexpression reversed the increased PAI‐1 expression in senescent human umbilical vein endothelial cells (HUVECs) and aortas of old mice, accompanied by decreased SA‐β‐gal activity in vitro and improved endothelial function and reduced arterial stiffness in vivo. Moreover, the SIRT1‐mediated inhibition of PAI‐1 expression exerted an antisenescence effect in HUVECs. Furthermore, we demonstrated that SIRT1 is able to bind to the PAI‐1 promoter, resulting in a decrease in the acetylation of histone H4 lysine 16 (H4K16) on the PAI‐1 promoter region. Thus, our findings suggest that the SIRT1‐mediated epigenetic inhibition of PAI‐1 expression exerts a protective effect in vascular endothelial senescence.
College Law Enforcement and Security Department Responses to Alcohol‐Related Incidents: A National Study
Authors: Bernat Debra H. , Lenk Kathleen M. , Nelson Toben F. , Winters Ken C. , Toomey Traci L. 
Published: July 2014

BackgroundCampus police and security personnel are often the first to respond to alcohol‐related incidents on campus. The purpose of this study is to examine how campus law enforcement and security respond to alcohol‐related incidents, and how consequences and communication differ based on characteristics of the incident.MethodsDirectors of campus police/security from 343 colleges across the United States completed a survey regarding usual practice following serious, underage, and less serious alcohol incidents on and off campus.ResultsCampus law enforcement and security most commonly reported contacting campus officials. A minority reported issuing citations and referring students to the health center. Enforcement actions were more commonly reported for serious and underage incidents than for less serious incidents. Large (vs. small) colleges, public (vs. private) colleges, and those located in small (vs. large) towns more consistently reported taking actions against drinkers.ConclusionsUnderstanding how campus police and security respond to alcohol‐related incidents is essential for reducing alcohol‐related problems on college campuses.
The Effect of Energy Drinks on the Urge to Drink Alcohol in Young Adults
Authors: McKetin Rebecca , Coen Alice 
Published: July 2014

BackgroundRecently, Marczinski and colleagues (2013) showed that energy drinks combined with alcohol augment a person's desire to drink more alcohol relative to drinking alcohol alone. The current study replicates the findings of Marczinski and colleagues (2013) using a robust measure of alcohol craving.MethodsSeventy‐five participants aged 18 to 30 years were assigned to an alcohol only or alcohol+energy drink condition in a double‐blind randomized pre‐ versus posttest experiment. Participants received a cocktail containing either 60 ml of vodka and a Red Bull® Silver Edition energy drink (alcohol+energy drink condition) or 60 ml of vodka with a soda water vehicle (alcohol‐only condition); both cocktails contained 200 ml of fruit drink. The primary outcome measure was the Alcohol Urge Questionnaire taken at pretest and at 20 minutes (posttest). Other measures taken at posttest were the Biphasic Alcohol Effects Questionnaire, the Drug Effects Questionnaire, and breath alcohol concentration (BAC).ResultsThe alcohol+energy drink condition showed a greater pre‐ versus posttest increase in urge to drink alcohol compared with the alcohol‐only condition (B = 3.24, p = 0.021, d = 0.44). Participants in the alcohol+energy drink condition had significantly higher ratings on liking the cocktail and wanting to drink more of the cocktail, and lower BACs, than the alcohol‐only condition. When examined at specific BACs, the effect of the energy drink on the pre‐ to posttest increase in urge to drink was largest and only significant at BACs of 0.04–0.05 (cf. < 0.04 g/dl).There were no significant differences in stimulation, sedation, feeling the effects of the cocktail, or feeling high.ConclusionsCombining energy drinks with alcohol increased the urge to drink alcohol relative to drinking alcohol alone. More research is needed to understand what factors mediate this effect and whether it increases subsequent alcohol consumption.
The Assessment of Relationship between Fragmented QRS Complex and Left Ventricular Wall Motion Score Index in Patients with ST Elevation Myocardial Infarction Who Underwent Primary Percutaneous Coronary Intervention
Authors: Uslu Nevzat , Gul Mehmet , Cakmak Huseyin Altug , Atam Ali , Pusuroglu Hamdi , Satilmisoglu Hulusi , Akkaya Emre , Aksu Hale Unal , Kalkan Ali Kemal , Surgit Ozgur , Erturk Mehmet , Aksu Huseyin , Eksik Abdurrahman 
Published: July 2014

ObjectivesFragmented QRS (fQRS) has been found to be associated with high mortality and arrhythmic events in acute coronary syndromes. Regional systolic function using wall motion score index (WMSI) is an alternative to left ventricular ejection fraction (LVEF) for the assessment of left ventricular systolic function. The aim of this study was to investigate the relation between the presence of fQRS on admission electrocardiogram (ECG) and WMSI in ST elevation myocardial infarction (STEMI) underwent primary coronary intervention (PCI). The in‐hospital and long‐term prognostic significance of persistent fQRS was also evaluated.MethodsIn this retrospective study, 542 patients with a diagnose of STEMI underwent primary PCI were included. Study patients were divided into two groups according to the presence (n = 153) or absence (n = 389) of a fQRS on admission ECG.ResultsWMSI was found to be significantly higher in fQRS(+) group compared to the fQRS(–) group (P < 0.001). In multivariete analysis, WMSI was found to be an independent predictor of fQRS, and fQRS was inversely associated with LVEF. The in‐hospital reinfarction (P = 0.003), MACE (P = 0.024), intraaortic balloon pump use (P = 0.014), and advanced heart failure (P < 0.001) were found to be significantly more frequent in the fQRS(+) group. The presence of fQRS on admission was found to be associated with an increase in long‐term cardiovascular mortality (P = 0.028), and long‐term all‐cause mortality (P = 0.022).ConclusionWMSI was significantly related with the presence of the fQRS, which reflects the linking between impairment of regional left ventricular systolic function and the presence of severe myocardial injury in STEMI.
Computing Volume Potentials for Noninvasive Imaging of Cardiac Excitation
Authors: van der Graaf A.W. Maurits , Bhagirath Pranav , van Driel Vincent J.H.M. , Ramanna Hemanth , de Hooge Jacques , de Groot Natasja M.S. , Götte Marco J.W. 
Published: July 2014

BackgroundIn noninvasive imaging of cardiac excitation, the use of body surface potentials (BSP) rather than body volume potentials (BVP) has been favored due to enhanced computational efficiency and reduced modeling effort. Nowadays, increased computational power and the availability of open source software enable the calculation of BVP for clinical purposes. In order to illustrate the possible advantages of this approach, the explanatory power of BVP is investigated using a rectangular tank filled with an electrolytic conductor and a patient specific three dimensional model.MethodsMRI images of the tank and of a patient were obtained in three orthogonal directions using a turbo spin echo MRI sequence. MRI images were segmented in three dimensional using custom written software. Gmsh software was used for mesh generation. BVP were computed using a transfer matrix and FEniCS software.ResultsThe solution for 240,000 nodes, corresponding to a resolution of 5 mm throughout the thorax volume, was computed in 3 minutes. The tank experiment revealed that an increased electrode surface renders the position of the 4 V equipotential plane insensitive to mesh cell size and reduces simulated deviations. In the patient‐specific model, the impact of assigning a different conductivity to lung tissue on the distribution of volume potentials could be visualized.ConclusionGeneration of high quality volume meshes and computation of BVP with a resolution of 5 mm is feasible using generally available software and hardware. Estimation of BVP may lead to an improved understanding of the genesis of BSP and sources of local inaccuracies.
Subprime Housing Goes South: Constructing Securitized Mortgages for the Poor in Mexico
Authors: Soederberg Susanne 
Published: July 2014

AbstractMexico represents the largest market for residential mortgage‐backed securitization (RMBS) in Latin America. Despite its significance to questions of development, there has been no critical analysis on the social implications and power dimensions of RMBS with regard to low‐income housing in Mexico. This essay fills this gap by demystifying the technical and thus apolitical nature of RMBS as well as by explaining how and why state‐sponsored securitization schemes subsidize financial and construction interests in the name of expanding home ownership for the poor. In so doing, the analysis employs a historical materialist approach that, first, places RMBS within the contradictory nature of capital accumulation processes in Mexico and relations of class‐based power therein, and second, views RMBS as an integral feature of housing policy that is inextricably linked to the nerve centre of capital accumulation, namely: the credit system.
Three novel IGF1R mutations in microcephalic patients with prenatal and postnatal growth impairment
Authors: Juanes Matias , Guercio Gabriela , Marino Roxana , Berensztein Esperanza , Warman Diana Mónica , Ciaccio Marta , Gil Silvia , Bailez Marcela , Rivarola Marco A. , Belgorosky Alicia 
Published: July 2014

SummaryBackgroundIGF1R gene mutations have been associated with varying degrees of intrauterine and postnatal growth retardation, and microcephaly.ObjectiveTo identify and characterize IGF1R gene variations in a cohort of 28 Argentinean children suspected of having IGF‐1 insensitivity, who were selected on the basis of the association of pre/postnatal growth failure and microcephaly.MethodsThe coding sequence and flanking intronic regions of IGF1R gene were amplified and directly sequenced. Functional characterization was performed by two in vitro assays: 1) [Methyl‐3H] thymidine incorporation into DNA in fibroblast cell primary cultures from patients and controls treated with IGF‐1 for 16‐24 h. 2) PI3K/Akt pathway was evaluated with phospho‐Akt (Ser473) STAR ELISA Kit (Millipore) in fibroblast cultures from patients and controls stimulated with IGF‐1 for 10 min. Prepubertal clinical and GH‐IGF‐1 axis evaluation was followed up.ResultsWe identified three novel heterozygous missense mutations in three unrelated patients, de novo p.Arg1256Ser, de novo p.Asn359Tyr and p.Tyr865Cys. In control cells, proliferation assay showed that IGF‐1 significantly induced DNA synthesis at 20 h and Akt phosphorylation assay that it significantly stimulated phosphorylation after 10 min (P < 0·05 by anova and Bonferroni Tests). However, no significant increase was observed in any of the three patient fibroblasts in both functional studies. GH therapy growth response in two patients was inconsistent.ConclusionThese variations led to failure of the IGF1R function causing pre‐ and postnatal growth retardation and microcephaly. Microcephaly should be considered in the evaluation of SGA patients, because it seems to favour the frequency of detection of IGF1R mutations.
Clinical and Radiographic Evaluation of Marginal Bone Changes around Platform‐Switching Implants Placed in Crestal or Subcrestal Positions: A Randomized Controlled Clinical Trial
Authors: Kütan Esma , Bolukbasi Nilufer , Yildirim‐Ondur Esra , Ozdemir Tayfun 
Published: July 2014

AbstractBackgroundIt has been reported in many articles that marginal bone resorptions are prevented by platform‐switching design. However, what occurs when these implants are placed in the apical position is not completely known.PurposeThis report describes a randomized controlled clinical trial study that aims to test the hypothesis that less resorption will occur when platform‐switching implants are placed 1 mm below bone level.Materials and MethodsA total of 56 randomly selected implants were inserted bilaterally, either 1 mm below bone level (test group, 28 implants) or at bone level (control group, 28 implants) of the patients' posterior regions. Marginal bone resorptions were examined through periapical radiographies taken with the parallel technique at the time of crown cementation and the third, sixth, 12th, and 36th months after prosthetic loading. The modified plaque index, gingival index, bleeding on probing, and probing depths were used for follow‐up periodontal care of the implants.ResultsAfter 3 years, the mean radiographic vertical bone loss in the control group was significantly lower than in the test group (0.56 ± 0.35 mm and 1.21 ± 1.05 mm, respectively) (p < .01). In terms of periodontal indexes, there were no statistically significant differences between the two groups (p > .05). No peri‐implantitis or peri‐implant mucositis was observed around the test or control implants.ConclusionsMore marginal bone resorptions occurred after the third year of loading in implants placed 1 mm below bone level. However, the resorptions did not reach the implants thread. In the control group, the first bone implant contact was placed under the level of the first threads. Therefore, the present randomized clinical trial confirmed the hypothesis that placing platform‐switching implants 1 mm below bone level reduced marginal bone loss. It can be noted that to reduce resorption, platform‐switching implants should be placed below bone level.
Failure of total hip implants: metals and metal release in 52 cases
Authors: Jakobsen Stig S. , Lidén Carola , Søballe Kjeld , Johansen Jeanne D. , Menné Torkil , Lundgren Lennart , Bregnbak David , Møller Per , Jellesen Morten S. , Thyssen Jacob P. 
Published: July 2014

SummaryBackgroundThe pathogenesis of total joint replacement failure is multifactorial. One hypothesis suggests that corrosion and wear of alloys result in metal ion release, which may then cause sensitization and even implant failure, owing to the acquired immune reactivity.ObjectivesTo assess cobalt, nickel and chromium(VI) release from, and the metal composition of, failed metal‐on‐ethylene total hip replacements.Materials/methodsImplant components from 52 revision cases were evaluated with spot tests for free nickel, cobalt, and chromium (VI) ions. Implant composition was determined with X‐ray fluorescence spectroscopy, and information on the reason for revision and complications in relation to surgery was collected from the medical charts when possible (72%). For 10 implants, corrosion was further characterized with scanning electron microscopy.ResultsWe detected cobalt release from three of 38 removed femoral heads and from one of 24 femoral stems. Nickel release was detected from one of 24 femoral stems. No chromium(VI) release was detected.ConclusionsWe found that cobalt and nickel were released from some failed total hip arthroplasties, and corrosion was frequently observed. Metal ions and particles corroded from metal‐on‐polyethylene may play a role in the complex aetiopathology of implant failure.