bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Clinical Experience With Celt ACD®: A Femoral Arterial Puncture Closure Device
Authors: JAN AFTAB , CREAN PETER , BULLESFELD LUTZ , COLEMAN JAMES , GRUBE EBERHARD , MULVIHILL NIALL 
Published: August 2013

AbstractIntroductionThis prospective nonrandomized study compared the safety and efficacy of a novel arterial closure device (ACD) in common femoral artery procedures to that of the FDA submitted historical manual pressure control group, who underwent either a diagnostic angiogram (DA) or a percutaneous coronary intervention (PCI) procedure.Methods and ResultsA total of 55 patients were enrolled in this study of the novel ACD. Of the 55 patients, 39 were enrolled in the DA group and 16 were enrolled in the PCI group. Six patients were excluded. A device was deployed in 49 patients. Time to hemostasis (TTH), time to ambulation (TTA), device function, and device‐related vascular complications were measured. In the device group, the TTH for the combined DA and PCI patients was 32 seconds (0.54 ± 0.93 minutes), significantly lower when compared with 16.0 ± 12.2 minutes (P < 0.0001) for the control group. Overall major vascular complication rate did not differ significantly, device group (1/49) and the historical control group (1/217). TTA in the combined PCI and DA device group was 226.4 ± 231.9 at the German site (site ambulation policy). In the Irish site, the average TTA in the PCI group was 187 minutes (n = 8) and 85 minutes (n = 14) in the DA group.ConclusionThe Celt ACD® device is safe, effective, and significantly decreases the TTH compared to manual pressure and has a low vascular complications rate. The device may be effective in early ambulation and discharge of patients postcoronary intervention procedures.
Simvastatin Decreases Stent‐Induced In‐Stent Restenosis Rate Via Downregulating the Expression of PCNA and Upregulating that of p27kip1
Authors: GAO CHUANYU , XU WENKE , XIAO WENTAO , YU JIE , LI MUWEI 
Published: August 2013

AbstractBackgroundThe inhibition of the proliferation and migration of vascular smooth muscle cells (VSMC) is one cholesterol‐independent effect of statins that could lower the rate of in‐stent restenosis (ISR), even if the exact mechanism remains unclear. The aim of this study was to explore the exact inhibitory mechanisms of simvastatin on ISR in vivo.MethodsForty‐five rabbits were randomized into 3 feeding groups of equal size (n = 15): normal rabbit chow (normal group), a high‐cholesterol diet (control group), and a simvastatin‐enriched high‐cholesterol diet (simvastatin group). Balloon de‐endothelialization was first performed in the control and simvastatin groups after 3 days, followed by stent deployment at week 14. All rabbits were killed at week 18, and the histological changes of the ISR segments were observed. The expressions of cyclin‐dependent kinase inhibitor p27 (p27kip1), proliferating cell nuclear antigen (PCNA), and α‐smooth muscle (α‐SM) actin were measured.ResultsIn the simvastatin group compared to the control group, the neointimal thickness, neointimal area, and degree of stenosis decreased, while the residual lumen area increased significantly (P < 0.05). Moreover, the expression of α‐SM actin in the control group decreased by 55.4% compared to the normal group, while it increased by 29.7% with respect to the simvastatin group (P < 0.05). Finally, the expression of p27kip1 increased, while that of PCNA decreased significantly in the simvastatin group compared to the control group (P < 0.05).ConclusionsSimvastatin may inhibit VSMC phenotype modulation and proliferation by downregulating the expression of PCNA and upregulating that of p27kip1.
Maternal Uterine Vascular Remodeling During Pregnancy
Authors: Osol George , Moore Lorna G. 
Published: August 2013

AbstractRemodeling of the maternal uterine vasculature during pregnancy is a unique cardiovascular process that occurs in the adult and results in significant structural and functional changes in large and small arteries and veins, and in the creation of the placenta—a new fetomaternal vascular organ. This expansive, hypertrophic process results in increases in both lumen circumference and length, and is effected through a combination of tissue and cellular hypertrophy, endothelial and vascular smooth muscle hyperplasia, and matrix remodeling. This review summarizes what is currently known about the time course and extent of the remodeling process, and how local vs. systemic factors influence its genesis. The main focus is on upstream maternal vessels rather than spiral artery changes, although the latter are considered from the overall hemodynamic perspective. We also consider some of the underlying mechanisms and provide a hypothetical scenario that integrates our current knowledge. Abrogation of this adaptive vascular process is associated with several human gestational pathologies such as preeclampsia and intrauterine growth restriction (IUGR), which not only raise the risk of infant mortality and morbidity but are also a significant source of maternal mortality and susceptibility to cardiovascular and other diseases for both mother and neonate later in life.
Cooperative and allosterically controlled nucleotide binding regulates the DNA binding activity of NrdR
Authors: McKethan Brandon L. , Spiro Stephen 
Published: August 2013

SummaryRibonucleotide reductases (RNRs) are required for the synthesis of deoxyribonucleoside triphosphates (dNTPs) from ribonucleotides. In Escherichia coli, regulation of RNR expression is co‐ordinated with the cell cycle, and involves several regulatory proteins. One of these, NrdR, has recently been shown to regulate all three nrd operons that encode RNR isoenzymes. Repression by NrdR is believed to be stimulated by elevated dNTPs, although there is no direct evidence for this model. Here, we sought to elucidate the mechanism by which NrdR regulates nrd expression according to the abundance of (d)NTPs. We determined that ATP and dATP bind to NrdR in a negatively cooperative fashion, such that neither can fully occupy the protein. Both nucleotides also appear to act as positive heterotropic effectors, since the binding of one stimulates binding of the other. Nucleotide binding stimulates self‐association of NrdR, with tri‐ and diphosphates stimulating oligomerization more effectively than monophosphates. As‐prepared NrdR contains (deoxy)nucleoside monophosphates, diphosphates and triphosphates, and its DNA binding activity is inhibited by triphosphates and diphosphates but not by monophosphates. We propose a model in which NrdR selectively binds (deoxy)nucleoside triphosphates, which are hydrolysed to their monophosphate counterparts in order to regulate DNA binding.
Tonsillectomy ameliorates histological damage of recurrent immunoglobulin A nephropathy after kidney transplantation
Authors: Hotta Kiyohiko , Fukasawa Yuichiro , Akimoto Mayuko , Tanabe Tatsu , Sasaki Hajime , Fukuzawa Nobuyuki , Seki Toshimori , Togashi Masaki , Harada Hiroshi 
Published: August 2013

AbstractAimRecurrence of immunoglobulin A (IgA) nephropathy (IgAN) after renal transplantation is important as a cause of graft failure under improving rejection control. However, no specific therapy for recurrent IgAN is currently available. In this study, we evaluated the histological efficacy of tonsillectomy for allograft IgAN.MethodsFifteen kidney recipients (male 9, female 6, mean age 40.9 ± 9.3 years), who received a diagnosis of IgA nephropathy by allograft biopsy, were enrolled in this study. Tonsillectomy was performed 44.1 ± 27.1 months after the kidney transplantation. All patients underwent a repeat graft biopsy at 23.8 ± 15.8 months after tonsillectomy.ResultsSix patients had microhematuria before tonsillectomy. At 12 months after treatment, the microhematuria disappeared in five of these patients and one patient had mild hematuria. Three patients had severe proteinuria (more than 1.0 g/gCr) before tonsillectomy and improved after treatment. On histological analysis, four patients had acute lesions including cellular or fibrocellular crescents. The acute lesions disappeared after these treatments in all patients. Eleven patients had chronic lesions including global sclerosis, segmental sclerosis and fibrous crescents. The chronic lesion was ameliorated in six patients, unchanged in three and deteriorated in two patients.ConclusionsTonsillectomy improves not only clinical findings but also ameliorates histological damage caused by recurrent IgAN after kidney transplantation. Tonsillectomy is a novel and effective treatment for recurrent IgAN.
Mucosal microfolds augment mixing at the wall of the distal ileum of the brushtail possum
Authors: Lentle R. G. , Janssen P. W. M. , DeLoubens C. , Lim Y. F. , Hulls C. , Chambers P. 
Published: August 2013

AbstractBackgroundRecent work suggests that mixing in the small intestine takes place in central luminal and peripheral compartments. However, while movements of villi have been described, the mechanisms by which peripheral mixing are engendered remain unclear.MethodsWe examined the disposition and movement of mucosa and associated villi during contractions of the everted terminal ileum of the brushtail possum. We then simulated the effect of these movements on peripheral mixing.Key ResultsCompression of the intestinal mucosa by phasic longitudinal or radial contractions created short‐lived microfolds, which were of similar scale to the attached villi. The packing density of the villous tips increased in the concavities and decreased on the crests of these microfolds. Simulations showed that these caused liquid digesta to be expelled from, or drawn into, intervillous spaces, significantly augmenting peripheral, but not bulk, luminal mixing.Conclusions & InferencesWe describe a mechanism by which peripheral mixing may be engendered by mucosal microfolds without requiring the coordinated contraction of individual villi or groups of villi.
Comparative transcriptomics as a tool for the identification of root branching genes in maize
Authors: Jansen Leentje , Hollunder Jens , Roberts Ianto , Forestan Cristian , Fonteyne Philippe , Van Quickenborne Charlotte , Zhen Rui‐Guang , McKersie Bryan , Parizot Boris , Beeckman Tom 
Published: August 2013

SummaryThe root system is fundamental for plant development, is crucial for overall plant growth and is recently being recognized as the key for future crop productivity improvement. A major determinant of root system architecture is the initiation of lateral roots. While knowledge of the genetic and molecular mechanisms regulating lateral root initiation has mainly been achieved in the dicotyledonous plant Arabidopsis thaliana, only scarce data are available for major crop species, generally monocotyledonous plants. The existence of both similarities and differences at the morphological and anatomical level between plant species from both clades raises the question whether regulation of lateral root initiation may or may not be conserved through evolution. Here, we performed a targeted genome‐wide transcriptome analysis during lateral root initiation both in primary and in adventitious roots of Zea mays and found evidence for the existence of common transcriptional regulation. Further, based on a comparative analysis with Arabidopsis transcriptome data, a core of genes putatively conserved across angiosperms could be identified. Therefore, it is plausible that common regulatory mechanisms for lateral root initiation are at play in maize and Arabidopsis, a finding that might encourage the extrapolation of knowledge obtained in Arabidopsis to crop species at the level of root system architecture.
Why do we need to use a zero reference? Reference influences on the ERPs of audiovisual effects
Authors: Tian Yin , Yao Dezhong 
Published: August 2013

AbstractUsing ERPs in the audiovisual stimulus, the current study is the first to investigate the influence of the reference on experimental effects (between two conditions). Three references, the average reference (AR), the mean mastoid (MM), and a new infinity zero reference (IR), were comparatively investigated via ERPs, statistical parametric scalp mappings (SPSM), and LORETA. Specifically, for the N1 (170–190 ms), the SPSM results showed an anterior distribution for MM, a posterior distribution for IR, and both anterior and posterior distributions for AR. However, the circumstantial evidence provided by LORETA is consistent with SPSM of IR. These results indicated that the newly developed IR could provide increased accuracy; thus, we recommend IR for future ERP studies.
Corneal collagen cross‐linking as treatment for infectious and noninfectious corneal melting in cats and dogs: results of a prospective, nonrandomized, controlled trial
Authors: Pot Simon A. , Gallhöfer Nicolin S. , Matheis Franziska L. , Voelter‐Ratson Katrin , Hafezi Farhad , Spiess Bernhard M. 
Published: August 2013

AbstractObjectiveUV‐A/Riboflavin cross‐linking of corneal collagen fibers (CXL) is a highly promising therapy for corneal melting in humans. A prospective interventional, nonrandomized, controlled study was conducted to compare the stabilizing effect of CXL treatment on melting keratitis in dogs and cats and the complication rate of CXL to those of standardized intensive medical treatment.ProceduresForty‐nine eyes with melting keratitis were included in the study between October 2009 and October 2012. All eyes were treated according to the same medical treatment protocol. Nineteen eyes were CXL‐treated, and 30 eyes were not. Follow‐up included slit‐lamp examination, fluorescein staining, ulcer size measurement, stromal stability evaluation, photographic documentation, and documentation of complications.ResultsFive of 19 eyes in the CXL group and 9/30 eyes in the control group required rescue stabilization due to continued melting. Seven of the nine control group corneas stabilized after rescue CXL treatment. At initial presentation, the ulcers in the canine CXL group were significantly deeper and larger than in the control group. Ulcer deepening during follow‐up was more pronounced in the canine control group than in the canine CXL group. CXL treatment‐related complications were not observed.ConclusionsBased on the similar failure rates in the control and CXL treatment groups despite the poorer initial situation in the CXL group, the tendency for the ulcers in the control group to deepen and the stabilization of all corneas receiving CXL rescue treatment, we believe that CXL has its place as an adjunctive therapy for melting keratitis in veterinary ophthalmology.
Occurrence of Cyclic di-GMP-Modulating Output Domains in Cyanobacteria: an Illuminating Perspective
Authors: Agostoni Marco , Koestler Benjamin J. , Waters Christopher M. , Williams Barry L. , Montgomery Beronda L. 
Published: August 2013

ABSTRACT

Microorganisms use a variety of metabolites to respond to external stimuli, including second messengers that amplify primary signals and elicit biochemical changes in a cell. Levels of the second messenger cyclic dimeric GMP (c-di-GMP) are regulated by a variety of environmental stimuli and play a critical role in regulating cellular processes such as biofilm formation and cellular motility. Cyclic di-GMP signaling systems have been largely characterized in pathogenic bacteria; however, proteins that can impact the synthesis or degradation of c-di-GMP are prominent in cyanobacterial species and yet remain largely underexplored. In cyanobacteria, many putative c-di-GMP synthesis or degradation domains are found in genes that also harbor light-responsive signal input domains, suggesting that light is an important signal for altering c-di-GMP homeostasis. Indeed, c-di-GMP-associated domains are often the second most common output domain in photoreceptors—outnumbered only by a histidine kinase output domain. Cyanobacteria differ from other bacteria regarding the number and types of photoreceptor domains associated with c-di-GMP domains. Due to the widespread distribution of c-di-GMP domains in cyanobacteria, we investigated the evolutionary origin of a subset of genes. Phylogenetic analyses showed that c-di-GMP signaling systems were present early in cyanobacteria and c-di-GMP genes were both vertically and horizontally inherited during their evolution. Finally, we compared intracellular levels of c-di-GMP in two cyanobacterial species under different light qualities, confirming that light is an important factor for regulating this second messenger
in vivo
.

IMPORTANCE
This study shows that many proteins containing cyclic dimeric GMP (c-di-GMP)-regulatory domains in cyanobacteria are associated with photoreceptor domains. Although the functional roles of c-di-GMP domain-containing proteins in cyanobacteria are only beginning to emerge, the abundance of these multidomain proteins in cyanobacteria that occupy diverse habitats ranging from freshwater to marine to soil environments suggests an important role for the regulation of c-di-GMP in these organisms. Indeed, we showed that light distinctly regulates c-di-GMP levels in
Fremyella diplosiphon
and Synechocystis sp. strain PCC6803. Our findings are consistent with the occurrence of c-di-GMP domains based on evolutionary origin and as an adaptation to specific habitat characteristics. Phylogenetic analyses of these domains clearly separate two distinctive clades, one composed of domains belonging predominantly to cyanobacteria and the other belonging to a mix of cyanobacteria and other bacteria. We further demonstrate that in cyanobacteria the acquisition of c-di-GMP signaling domains occurred both vertically and horizontally.
Old Cryptococcus neoformans Cells Contribute to Virulence in Chronic Cryptococcosis
Authors: Bouklas Tejas , Pechuan Ximo , Goldman David L. , Edelman Batya , Bergman Aviv , Fries Bettina C. 
Published: August 2013

ABSTRACT

Does cell age matter in virulence? The emergence of persister cells during chronic infections is critical for persistence of infection, but little is known how this occurs. Here, we demonstrate for the first time that the replicative age of the fungal pathogen
Cryptococcus neoformans
contributes to persistence during chronic meningoencephalitis. Generationally older
C. neoformans
cells are more resistant to hydrogen peroxide stress, macrophage intracellular killing, and antifungal agents. Older cells accumulate in both experimental rat infection and in human cryptococcosis. Mathematical modeling supports the concept that the presence of older
C. neoformans
cells emerges from
in vivo
selection pressures. We propose that advanced replicative aging is a new unanticipated virulence trait that emerges during chronic fungal infection and facilitates persistence. Therapeutic interventions that target old cells could help in the clearance of chronic infections.

IMPORTANCE
Our findings that the generational age of
Cryptococcus neoformans
cells matters in pathogenesis introduces a novel concept to eukaryotic pathogenesis research. We propose that emerging properties of aging
C. neoformans
cells and possibly also other fungal pathogens contribute to persistence and virulence. Whereas the replicative life span of strains may not matter for virulence
per se
, age-related resilience and thus the generational age of individual
C. neoformans
cells within a pathogen population could greatly affect persistence of the pathogen population and therefore impact outcome.
Severe Acute Respiratory Syndrome Coronavirus Nonstructural Proteins 3, 4, and 6 Induce Double-Membrane Vesicles
Authors: Angelini Megan M. , Akhlaghpour Marzieh , Neuman Benjamin W. , Buchmeier Michael J. 
Published: August 2013

ABSTRACT
Coronaviruses (CoV), like other positive-stranded RNA viruses, redirect and rearrange host cell membranes for use as part of the viral genome replication and transcription machinery. Specifically, coronaviruses induce the formation of double-membrane vesicles in infected cells. Although these double-membrane vesicles have been well characterized, the mechanism behind their formation remains unclear, including which viral proteins are responsible. Here, we use transfection of plasmid constructs encoding full-length versions of the three transmembrane-containing nonstructural proteins (nsps) of the severe acute respiratory syndrome (SARS) coronavirus to examine the ability of each to induce double-membrane vesicles in tissue culture. nsp3 has membrane disordering and proliferation ability, both in its full-length form and in a C-terminal-truncated form. nsp3 and nsp4 working together have the ability to pair membranes. nsp6 has membrane proliferation ability as well, inducing perinuclear vesicles localized around the microtubule organizing center. Together, nsp3, nsp4, and nsp6 have the ability to induce double-membrane vesicles that are similar to those observed in SARS coronavirus-infected cells. This activity appears to require the full-length form of nsp3 for action, as double-membrane vesicles were not seen in cells coexpressing the C-terminal truncation nsp3 with nsp4 and nsp6.

IMPORTANCE
Although the majority of infections caused by coronaviruses in humans are relatively mild, the SARS outbreak of 2002 to 2003 and the emergence of the human coronavirus Middle Eastern respiratory syndrome (MERS-CoV) in 2012 highlight the ability of these viruses to cause severe pathology and fatality. Insight into the molecular biology of how coronaviruses take over the host cell is critical for a full understanding of any known and possible future outbreaks caused by these viruses. Additionally, since membrane rearrangement is a tactic used by all known positive-sense single-stranded RNA viruses, this work adds to that body of knowledge and may prove beneficial in the development of future therapies not only for human coronavirus infections but for other pathogens as well.
Endogenous testosterone level and testosterone supplementation therapy in chronic obstructive pulmonary disease (COPD): a systematic review and meta-analysis
Authors: Atlantis Evan , Fahey Paul , Cochrane Belinda , Wittert Gary , Smith Sheree 
Published: August 2013

ObjectiveLow testosterone level may be a reversible risk factor for functional disability and deterioration in patients with chronic obstructive pulmonary disease (COPD). We sought to systematically assess the endogenous testosterone levels and effect of testosterone therapy on exercise capacity and health-related quality of life (HRQoL) outcomes in COPD patients, as well as to inform guidelines and practice.DesignSystematic review and meta-analysis.Data sourcesWe searched PubMed, Scopus, Cochrane Library, CINAHL, Health Source Nursing and PsychINFO and the reference lists of retrieved articles published before May 2012.Inclusion criteriaObservational studies on endogenous testosterone levels in people with chronic lung disease compared with controls, or randomised controlled trials (RCTs) on testosterone therapy for exercise capacity and/or HRQoL outcomes in COPD patients were eligible.Data extraction and analysisData on the mean difference in endogenous total testosterone (TT) values, and the mean difference in exercise capacity and HRQoL values were extracted and pooled using random effects meta-analysis.ResultsNine observational studies in 2918 men with COPD reported consistently lower levels of TT compared with controls (weighted mean difference was –3.21 nmol/L (95% CI −5.18 to −1.23)). Six RCTs in 287 participants yielded five studies on peak muscle strength and peak cardiorespiratory fitness outcomes (peak oxygen uptake (VO2) and workload) and three studies on HRQoL outcomes. Testosterone therapies significantly improved peak muscle strength (standardised mean difference (SMD) was 0.31 (95% CI 0.05 to 0.56)) and peak workload (SMD was 0.27 (95% CI 0.01 to 0.52)) compared with control conditions (all but one used placebo), but not peak VO2(SMD was 0.21 (95% CI −0.15 to 0.56)) or HRQoL (SMD was –0.03 (95% CI −0.32 to 0.25)).ConclusionsMen with COPD have clinically relevant lower than normal TT levels. Insufficient evidence from short-term studies in predominately male COPD patients suggests that testosterone therapy improves exercise capacity outcomes, namely peak muscle strength and peak workload.