bluuebunny/crossref_metadata_2025_split huggingface dataset:
Seminal Plasma and Semen Amyloids Enhance Cytomegalovirus Infection in Cell Culture
Authors: Tang Qiyi , Roan Nadia R. , Yamamura Yasuhiro 
Published: September 2013

ABSTRACTAmong the modes of transmission available to the cytomegalovirus (CMV) is sexual transmission, primarily via semen. Both male-to-female (M-F) and male-to-male (M-M) sexual transmission significantly contribute toward the spread of CMV infections in the global population. Semen plays an important role in carrying the viral particle that invades the vaginal or rectal mucosa, thereby initiating viral replication. Both semen and seminal plasma (SP) can enhance HIV-1 infection in cell culture, and two amyloid fibrils, semen-derived enhancer of viral infection (SEVI) and amyloids derived from the semenogelins (SEM amyloids), have been identified as seminal factors sufficient to enhance HIV-1 infection (J. Munch et al., Cell131:1059–1071, 2007; N. R. Roan et al., Cell Host Microbe10:541–550, 2011; F. Arnold et al., J. Virol. 86:1244–1249, 2012). Whether SP, SEVI, or SEM amyloids can enhance other viral infections has not been extensively examined. In this study, we found that SP, SEVI, and SEM amyloids strongly enhance both human CMV (HCMV) and murine CMV infection in cell culture. SEVI and SEM amyloids increased infection rates by >10-fold, as determined by both flow cytometry and fluorescence microscopy. Viral replication was increased by 50- to 100-fold. Moreover, viral growth curve assays showed that SP, SEVI, and SEM amyloids sped up the kinetics of CMV replication such that the virus reached its replicative peak more quickly. Finally, we discovered that SEM amyloids and SEVI counteracted the effect of anti-gH in protecting against CMV infection. Collectively, the data suggest that semen enhances CMV infection through interactions between semen amyloid fibrils and viral particles, and these interactions may prevent HCMV from being neutralized by anti-gH antibody.
Human Astrocytic Cells Support Persistent Coxsackievirus B3 Infection
Authors: Zhang Xiaowei , Zheng Zhenhua , Shu Bo , Liu Xijuan , Zhang Zhenfeng , Liu Yan , Bai Bingke , Hu Qinxue , Mao Panyong , Wang Hanzhong 
Published: September 2013

ABSTRACT

Enteroviruses can frequently target the human central nervous system to induce a variety of neurological diseases. Although enteroviruses are highly cytolytic, emerging evidence has shown that these viruses can establish persistent infections both
in vivo
and
in vitro
. Here, we investigated the susceptibility of three human brain cell lines, CCF-STTG1, T98G, and SK-N-SH, to infection with three enterovirus serotypes: coxsackievirus B3 (CVB3), enterovirus 71, and coxsackievirus A9. Persistent infection was observed in CVB3-infected CCF-STTG1 cells, as evidenced by prolonged detection of infectious virions, viral RNA, and viral antigens. Of note, infected CCF-STTG1 cells expressed the nonfunctional canonical viral receptors coxsackievirus-adenovirus receptor and decay-accelerating factor, while removal of cell surface chondroitin sulfate from CCF-STTG1 cells inhibited the replication of CVB3, suggesting that receptor usage was one of the major limiting factors in CVB3 persistence. In addition, CVB3 curtailed the induction of beta interferon in infected CCF-STTG1 cells, which likely contributed to the initiation of persistence. Furthermore, proinflammatory chemokines and cytokines, such as vascular cell adhesion molecule 1, interleukin-8 (IL-8), and IL-6, were upregulated in CVB3-infected CCF-STTG1 cells and human progenitor-derived astrocytes. Our data together demonstrate the potential of CCF-STTG1 cells to be a novel cell model for studying CVB3-central nervous system interactions, providing the basis toward a better understanding of CVB3-induced chronic neuropathogenesis.
A MicroRNA Encoded by Autographa californica Nucleopolyhedrovirus Regulates Expression of Viral Gene ODV-E25
Authors: Zhu Mengxiao , Wang Jinwen , Deng Riqiang , Xiong Peiwen , Liang Hai , Wang Xunzhang 
Published: September 2013

ABSTRACT

Baculovirus-encoded microRNAs (miRNAs) have been described in
Bombyx mori
nucleopolyhedrovirus; however, most of their functions remain unclear. Here we report the identification and characterization of an miRNA encoded by
Autographa californica
nucleopolyhedrovirus. The identified miRNA, AcMNPV-miR-1, perfectly matched a segment in the coding sequence of the viral gene ODV-E25 and downregulated ODV-E25 mRNA expression, which likely resulted in a reduction of infectious budded virions and accelerated the formation of occlusion-derived virions.
Dynamic Viral Dissemination in Mice Infected with Yellow Fever Virus Strain 17D
Authors: Erickson Andrea K. , Pfeiffer Julie K. 
Published: September 2013

ABSTRACTArboviruses such as yellow fever virus (YFV) are transmitted between arthropod vectors and vertebrate hosts. While barriers limiting arbovirus population diversity have been observed in mosquitoes, whether barriers exist in vertebrate hosts is unclear. To investigate whether arboviruses encounter bottlenecks during dissemination in the vertebrate host, we infected immunocompetent mice and immune-deficient mice lacking alpha/beta interferon (IFN-α/β) receptors (IFNAR−/−mice) with a pool of genetically marked viruses to evaluate dissemination and host barriers. We used the live attenuated vaccine strain YFV-17D, which contains many mutations compared with virulent YFV. We found that intramuscularly injected immunocompetent mice did not develop disease and that viral dissemination was restricted. Conversely, 32% of intramuscularly injected IFNAR−/−mice developed disease. By following the genetically marked viruses over time, we found broad dissemination in IFNAR−/−mice followed by clearance. The patterns of viral dissemination were similar in mice that developed disease and mice that did not develop disease. Unlike our previous results with poliovirus, these results suggest that YFV-17D encounters no major barriers during dissemination within a vertebrate host in the absence of the type I IFN response.
Evaluation of Novel Acyclic Nucleoside Phosphonates against Human and Animal Gammaherpesviruses Revealed an Altered Metabolism of Cyclic Prodrugs upon Epstein-Barr Virus Reactivation in P3HR-1 Cells
Authors: Coen Natacha , Duraffour Sophie , Naesens Lieve , Krečmerová Marcela , Van den Oord Joost , Snoeck Robert , Andrei Graciela 
Published: September 2013

ABSTRACTAcyclic nucleoside phosphonates (ANPs), such as (S)-1-[(3-hydroxy-2-phosphonomethoxy)propyl)]cytosine (HPMPC), are an important group of broad-spectrum antiviral agents with activity against DNA viruses. In this report, we present thein vitropotencies of novel ANPs against gammaherpesviruses, including Kaposi's sarcoma-associated herpesvirus, Epstein-Barr virus (EBV), and three animal gammaherpesviruses. 1-(S)-[3-hydroxy-2-(phosphonomethoxy)propyl]-5-azacytosine (HPMP-5-azaC), (S)-9-[3-hydroxy-2-(phosphonomethoxy)propyl]-3-deazaadenine (3-deaza-HPMPA), and their cyclic derivatives have emerged as highly potent antigammaherpesvirus agents. Interestingly, cyclic prodrugs of ANPs exhibited reduced activities against EBV strain P3HR-1, but not against EBV strain Akata. Cell culture metabolism studies with HPMPC and cyclic HPMPC revealed that these differences were attributable to an altered drug metabolism in P3HR-1 cells after EBV reactivation and, more specifically, to a reduced hydrolysis of cyclic HPMPC by cyclic CMP phosphodiesterase. We did not correlate this effect with phosphodiesterase downregulation, or to functional mutations. Instead, altered cyclic AMP levels in P3HR-1 cells indicated a competitive inhibition of the phosphodiesterase by this cyclic nucleotide. Finally, both HPMPC and HPMP-5-azaC emerged as highly effective inhibitorsin vivothrough significant inhibition of murine gammaherpesvirus replication and dissemination. With the current need for potent antigammaherpesvirus agents, our findings underline the requirement of appropriate surrogate viruses for antiviral susceptibility testing and highlight HPMP-5-azaC as a promising compound for future clinical development.
Heading in football, long-term cognitive decline and dementia: evidence from screening retired professional footballers
Authors: Vann Jones Simon Andrew , Breakey Richard William , Evans Philip John 
Published: September 2013

BackgroundHeading impairs cognition in the short and medium-terms; however, little is known about the long-term consequences. This study aimed to investigate the hypothesis that chronic low-level head trauma is associated with persistent cognitive decline.MethodsAll members of Former Player Associations (FPAs) from four professional football clubs in the UK were contacted to participate in the study. Participants were required to complete a self-assessed test of cognition, the Test Your Memory questionnaire. Further information was collected from respondents in order to analyse the potential effect of a number of variables on cognition.Results10 of 92 respondents (10.87%) screened positive for possible mild cognitive impairment (MCI) or dementia. There was no association between low-risk and high-risk playing positions (HR = 0.40, p = 0.456) or length of playing career (HR = 1.051 95% CI 0.879 to 1.257, p = 0.586) and a positive screening result. Age was a risk factor (HR = 1.137 per additional year, 95% CI 1.030 to 1.255, p < 0.05), although this was not significantly different from the population prevalence across age groups.ConclusionsThese results suggest that once a player ends their playing career, their risk of harm falls in line with the population, suggesting either that changes are reversible or that heading may not be as harmful as commonly thought. Future longitudinal studies of large numbers of professional football players are needed to support the findings from this study.
Balloon augmented Onyx embolization utilizing a dual lumen balloon catheter: utility in the treatment of a variety of head and neck lesions
Authors: Spiotta Alejandro M , Miranpuri Amrendra S , Vargas Jan , Magarick Jordan , Turner Raymond D , Turk Aquilla S , Chaudry M Imran 
Published: September 2013

IntroductionEndovascular embolization for tumors and vascular malformations has emerged as an important preoperative adjunct prior to resection. We describe the advantages of utilizing a recently released dual lumen balloon catheter for ethylene vinyl alcohol copolymer, also known as Onyx (ev3, Irvine, California, USA), embolization for a variety of head and neck pathologies.MethodsA retrospective review of all cases utilizing the Scepter C balloon catheter (MicroVention Inc, Tustin, California, USA) for use in balloon augmented embolization was performed over a 4 month period from October 2012 to February 2013 at the Medical University of South Carolina, Charleston, South Carolina, USA. Charts and angiographic images were reviewed. Representative cases involving diverse pathologies are summarized and illustrate the observed advantages of balloon augmented Onyx embolization with a dual lumen balloon catheter.Case illustrationsBalloon augmented Onyx embolization utilizing a novel dual lumen balloon catheter was employed to treat both ruptured and unruptured arteriovenous malformations, intracranial dural arteriovenous fistulae, intracranial neoplasms, carotid body tumors, a thyroid mass, and an extracranial arteriovenous fistula.ConclusionsThe dual lumen balloon catheter has several advantages for use with Onyx embolization over older devices, including more efficient proximal plug formation and enhanced navigability for placement deep within the pedicles. The balloon augmented Onyx embolization technique represents a valuable tool to add to the armamentarium of the neurointerventionalist to address a variety of head and neck lesions.
Early results of the Axium MicroFX for Endovascular Repair of IntraCranial Aneurysm (AMERICA) study: a multicenter prospective observational registry
Authors: Fargen Kyle M , Blackburn Spiros , Carpenter Jeffrey S , Jabbour Pascal , Mack William J , Rai Ansaar T , Siddiqui Adnan H , Turner Raymond D , Mocco J 
Published: September 2013

BackgroundAxium MicroFX coils contain polymer (polyglycolic/polylactic acid, PGLA) microfilaments designed to significantly impact intra-aneurysmal flow and to encourage aneurysm thrombosis. To provide preliminary evaluation of the safety and suggested efficacy of the MicroFX design, we performed a multicenter prospective single-arm trial, AxiumMicroFX forEndovascularRepair ofIntraCranial Aneurysm study (AMERICA).MethodsAMERICA is a prospective multicenter 100 aneurysm observational study evaluating the safety and efficacy of Axium MicroFX PGLA coils. Enrollment was started in April 2010 and completed in October 2012.Results99 patients underwent treatment for 100 aneurysms at 13 centers. Mean age was 60.2 years, most were women (72%) and 18% of patients had previously undergone treatment for a separate aneurysm. 22% of patients underwent treatment after acute aneurysmal subarachnoid hemorrhage (SAH). Of these patients, all were Hunt and Hess grade 1–3. Pre-procedure modified Rankin score (mRS) was 0–2 in 92% of patients. The majority of aneurysms were anterior circulation (86%), with the most common aneurysm locations being the anterior communicating artery (23%) followed by the supraclinoid internal carotid artery and posterior communicating artery (18% each). The mean maximum diameter was 6.5 mm. Axium MicroFX coils could be placed in all but one treatment (99%). Raymond grade at conclusion of coiling was I (complete) in 52%, II (dog ear or residual neck) in 33% and III (residual aneurysm) in 15%. Discharge mRS was significantly worse in patients with SAH (62% mRS 0–2) compared with electively treated aneurysms (mRS 0–2 in 94%, p<001). Major events were uncommon (6% thromboembolic events, 3% intraoperative vessel or aneurysm rupture) and device-related adverse events (AE) were rare (2% of cases).ConclusionsThis prospective study of Axium MicroFX coils demonstrates excellent aneurysm occlusion rates. 52% of aneurysms were completely occluded post-procedure. Within the ruptured aneurysm group, post-procedure occlusion rates were 63.6%. Major AE rates were consistent with historical data.
Effects of high-amount–high-intensity exercise on in vivo platelet activation: Modulation by lipid peroxidation and AGE/RAGE axis
Authors: Santilli Francesca , Vazzana Natale , Iodice Pierpaolo , Lattanzio Stefano , Liani Rossella , Bellomo Rosa Grazia , Lessiani Gianfranco , Perego Francesca , Saggini Raoul , Davì Giovanni 
Published: September 2013

SummaryPhysical activity is associated with cardiovascular risk reduction, but the effects of exercise on platelet activation remain controversial. We investigated the effects of regular high-amount, high intensity aerobic exercise on in vivo thromboxane (TX)-dependent platelet activation and plasma levels of platelet-derived proteins, CD40L and P-selectin, and whether platelet variables changes may be related to changes in high-density lipoprotein (HDL) and in the extent of oxidative stress and oxidative stress-related inflammation, as reflected by urinary isoprostane excretion and endogenous soluble receptor for advanced glycation end-products (esRAGE), respectively. Urinary excretion of 11-dehydro-TXB2 and 8-iso-prostaglandin (PG)F2α and plasma levels of P-selectin, CD40L and esRAGE were measured before and after a eight-week standardised aerobic high-amount–high-intensity training program in 22 sedentary subjects with low-to-intermediate risk. Exercise training had a clear beneficial effect on HDL cholesterol (+10%, p=0.027) and triglyceride (-27%, p=0.008) concentration. In addition, a significant (p<0.0001) decrease in urinary 11-dehydro-TXB2 (26%), 8-iso-PGF2α (21 %), plasma P-selectin (27%), CD40L (35%) and a 61% increase in esRAGE were observed. Multiple regression analysis revealed that urinary 8-iso-PGF2α [beta=0.33, SEM=0.116, p=0.027] and esRAGE (beta=-0.30, SEM=31.3, p=0.046) were the only significant predictors of urinary 11-dehydro-TXB2 excretion rate over the training period. In conclusion, regular high-amount–high-intensity exercise training has broad beneficial effects on platelet activation markers, paralleled and possibly associated with changes in the lipoprotein profile and in markers of lipid peroxidation and AGE/RAGE axis. Our findings may help explaining why a similar amount of exercise exerts significant benefits in preventing cardiovascular events.
Sevoflurane Preconditioning Attenuates Myocardial Ischemia/Reperfusion Injury via Caveolin-3–Dependent Cyclooxygenase-2 Inhibition
Authors: Zhao Jianli , Wang Feng , Zhang Yanqing , Jiao Liyuan , Lau Wayne Bond , Wang Lili , Liu Baojiang , Gao Erhe , Koch Walter J. , Ma Xin-Liang , Wang Yajing 
Published: September 2013

Background—
The inhaled anesthetic sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (MI/R) injury via mechanisms involving AMP-activated protein kinase (AMPK) and caveolin-3 (Cav-3). However, the relative contributions of AMPK and Cav-3 to sevoflurane preconditioning (SF-PreCon)–mediated cardioprotection and their precise underlying mechanisms of action remain incompletely understood.

Methods and Results—

SF-PreCon (consisting of 3 cycles of 15-minute exposure to 2% sevoflurane before 30 minutes of MI) decreased MI/R injury in wild-type mice (caspase-3 activity, −29.1%; infarct size, −20.2%; and left ventricular end diastolic pressure, −33.8%). In cardiac-specific AMPKα2 dominant-negative overexpressing mice, the cardioprotective effect of SF-PreCon was largely retained (caspase-3 activity, −26.7%; infarct size, −16.7%; and left ventricular end-diastolic pressure, −25.9%;
P
<0.01). In contrast, SF-PreCon failed to significantly protect Cav-3 knockout mice against MI/R injury (
P
>0.05). SF-PreCon significantly decreased MI/R-induced superoxide generation in wild-type (−43.6%) and AMPK dominant-negative overexpressing mice (−35.5%;
P
<0.01) but not in Cav-3 knockout mice. SF-PreCon did not affect nicotinamide adenine dinucleotide phosphate oxidase expression but significantly inhibited cyclooxygenase-2 expression in wild-type (−38.7%) and AMPK dominant-negative overexpressing mice (−35.8%) but not in Cav-3 knockout mice.

Conclusions—
We demonstrate for the first time SF-PreCon mediates cardioprotection against MI/R injury via caveolin-3–dependent cyclooxygenase-2 inhibition and antioxidative effects.
Late Repair of Ischemic Mitral Regurgitation Does Not Prevent Left Ventricular Remodeling
Authors: Beaudoin Jonathan , Levine Robert A. , Guerrero J. Luis , Yosefy Chaim , Sullivan Suzanne , Abedat Susan , Handschumacher Mark D. , Szymanski Catherine , Gilon Dan , Palmeri Nicholas O. , Vlahakes Gus J. , Hajjar Roger J. , Beeri Ronen 
Published: September 2013

Background—
Ischemic mitral regurgitation (MR) is a frequent complication of myocardial infarction associated with left ventricular (LV) dilatation and dysfunction, which doubles mortality. At the molecular level, moderate ischemic MR is characterized by a biphasic response, with initial compensatory rise in prohypertrophic and antiapoptotic signals, followed by their exhaustion. We have shown that early MR repair 30 days after myocardial infarction is associated with LV reverse remodeling. It is not known whether MR repair performed after the exhaustion of compensatory mechanisms is also beneficial. We hypothesized that late repair will not result in LV reverse remodeling.

Methods and Results—

Twelve sheep underwent distal left anterior descending coronary artery ligation to create apical myocardial infarction and implantation of an LV-to-left atrium shunt to create standardized moderate volume overload. At 90 days, animals were randomized to shunt closure (late repair) versus sham (no repair). LV remodeling was assessed by 3-dimensional echocardiography, d
P
/d
t
, preload-recruitable stroke work, and myocardial biopsies. At 90 days, animals had moderate volume overload, LV dilatation, and reduced ejection fraction (all
P
<0.01 versus baseline,
P
=NS between groups). Shunt closure at 90 days corrected the volume overload (regurgitant fraction 6±5% versus 27±16% for late repair versus sham,
P
<0.01) but was not associated with changes in LV volumes (end-diastolic volume 106±15 versus 110±22 mL; end-systolic volume 35±6 versus 36±6 mL) or increases in preload-recruitable stroke work (41±7 versus 39±13 mL mm Hg) or d
P
/d
t
(803±210 versus 732±194 mm Hg/s) at 135 days (all
P
=NS). Activated Akt, central in the hypertrophic process, and signal transducer and activator of transcription 3 (STAT3), a critical node in the hypertrophic stimulus by cytokines, were equally depressed in both groups.

Conclusions—
Late correction of moderate volume overload after myocardial infarction did not improve LV volume or contractility. Upregulation of prohypertrophic intracellular pathways was not observed. This contrasts with previously reported study in which early repair (30 days) reversed LV remodeling. This suggests a window of opportunity to repair ischemic MR after which no beneficial effect on LV is observed, despite successful repair.
Ethanol Promotes Arteriogenesis and Restores Perfusion to Chronically Ischemic Myocardium
Authors: Lassaletta Antonio D. , Elmadhun Nassrene Y. , Liu Yuhong , Feng Jun , Burgess Thomas A. , Karlson Nicholas W. , Laham Roger J. , Sellke Frank W. 
Published: September 2013

Background—
Moderate alcohol consumption is known to be cardioprotective compared with either heavy drinking or complete abstinence. We assessed the hypothesis that ethanol supplementation would improve myocardial function in the setting of chronic ischemia.

Methods and Results—

Sixteen male Yorkshire swine underwent placement of an ameroid constrictor into the left circumflex artery to induce chronic myocardial ischemia. Postoperatively, animals were supplemented with either 90 mL of ethanol (EtOH) daily (50%/V, EtOH) or 80 g of sucrose of equal caloric value (SUC), serving as controls. Seven weeks after ameroid placement, arteriolar density (1.74±0.210% versus 3.11±0.368% area of arterioles per low-powered field in sucrose (SUC) versus EtOH;
P
=0.004), myocardial perfusion (ratio of blood flow to the at-risk myocardium compared with the normal ventricle during demand pacing was 0.585±0.107 versus 1.08±0.138 for SUC versus EtOH;
P
=0.014), and microvascular reactivity were significantly increased in ethanol-treated animals compared with controls in the at-risk myocardium. Analysis of vascular endothelial growth factor and NOTCH pathway signaling suggested proneovascular and proliferative activity in the ischemic area. The average peak blood alcohol level in the treatment group was 40±4 mg/dL, consistent with levels of moderate drinking in humans.

Conclusions—
Ethanol supplementation increased arteriolar density and significantly improved myocardial perfusion and endothelium-dependent vasorelaxation in chronically ischemic myocardium. These findings suggest that, at moderate doses, ethanol directly promotes vasculogenesis and improves microvascular function, resulting in significant improvements in myocardial perfusion in the setting of chronic ischemia.