bluuebunny/crossref_metadata_2025_split huggingface dataset:
Systematic review and meta‐analysis of studies involving telehome monitoring‐based telenursing for patients with chronic obstructive pulmonary disease
Authors: Kamei Tomoko , Yamamoto Yuko , Kajii Fumiko , Nakayama Yuki , Kawakami Chiharu 
Published: October 2012

AbstractAimThis systematic review evaluated the effects of telehome monitoring‐based telenursing (THMTN) on health outcomes and use of healthcare services and compared them with the effects of conventional treatment in patients with severe and very severe chronic obstructive pulmonary disease (COPD).MethodsAn extensive published work search of several databases was performed in May and October 2011. Randomized controlled trials and non‐randomized controlled clinical trials were evaluated. Parameters included hospitalization rate, number of visits to the emergency department, exacerbations, mean number of hospitalizations, mean duration of bed days of care, mortality, and health‐related quality of life by the duration of THMTN and COPD severity. A random effects model was applied. Risk ratio and mean difference were calculated. Heterogeneity was assessed using the I2 statistic.ResultsNine original articles involving 550 participants were identified in the meta‐analysis. THMTN decreased hospitalization rates, emergency department visits, exacerbations, mean number of hospitalizations, and mean duration of bed days of care in severe and very severe COPD patients. Hospitalization rates and emergency department visits were comparable between patients undergoing THMTN of different durations. In addition, THMTN had no effect on mortality.ConclusionTHMTN significantly decreases the use of healthcare services; however, it does not affect mortality in severe and very severe COPD patients.
Fumagillin‐induced aseptic meningoencephalitis in a kidney transplant recipient with microsporidiosis
Authors: Audemard A. , Le Bellec M.L. , Carluer L. , Dargère S. , Verdon R. , Castrale C. , Lobbedez T. , Hurault de Ligny B. 
Published: October 2012

AbstractMicrosporidiosis is an opportunistic infection in organ transplant recipients and patients with other cellular immunodeficiency. Fumagillin is an effective treatment against Enterocytozoon bieneusi, one of the two main species causing the microsporidiosis involved in human diseases. We report the first case, to our knowledge, of a probable drug‐induced aseptic meningoencephalitis, after administration of fumagillin in a kidney transplant recipient with microsporidiosis.
Quantifying Ca2+ release and inactivation of Ca2+ release in fast‐ and slow‐twitch muscles
Authors: Barclay C. J. 
Published: October 2012

Key points
Calcium ions initiate muscle contraction and are an important determinant of the force and energy cost of contraction.
Existing estimates of the amount of calcium released into mammalian muscle cells are uncertain and existing descriptions of the effects of prior stimulation on calcium release are inconsistent.
Calcium release was quantified by measuring the amount of ATP used to pump Ca2+ back to its pre‐release storage site.
Calcium release was greater in fast‐ than slow‐twitch muscle, was reduced immediately following a stimulus and recovered with a time course that depended on muscle type and temperature.
Ca2+ release and inactivation in fast‐twitch muscle resembles that of amphibian muscle but that of slow‐twitch muscle is distinctive in exhibiting a slower and less temperature‐sensitive reversal.
Abstract  The aims of this study were to quantify the Ca2+ release underlying twitch contractions of mammalian fast‐ and slow‐twitch muscle and to comprehensively describe the transient inactivation of Ca2+ release following a stimulus. Experiments were performed using bundles of fibres from mouse extensor digitorum longus (EDL) and soleus muscles. Ca2+ release was quantified from the amount of ATP used to remove Ca2+ from the myoplasm following stimulation. ATP turnover by crossbridges was blocked pharmacologically (N‐benzyl‐p‐toluenesulphonamide for EDL, blebbistatin for soleus) and muscle heat production was used as an index of Ca2+ pump ATP turnover. At 20°C, Ca2+ release in response to a single stimulus was 34 and 84 μmol (kg muscle)−1 for soleus and EDL, respectively, and increased with temperature (30°C: soleus, 61 μmol kg−1; EDL, 168 μmol kg−1). Delivery of another stimulus within 100 ms of the first produced a smaller Ca2+ release. The maximum magnitude of the decrease in Ca2+ release was greater in EDL than soleus. Ca2+ release recovered with an exponential time course which was faster in EDL (mean time constant at 20°C, 32.1 ms) than soleus (65.6 ms) and faster at 30°C than at 20°C. The amounts of Ca2+ released and crossbridge cycles performed are consistent with a scheme in which Ca2+ binding to troponin‐C allowed an average of ∼1.7 crossbridge cycles in the two muscles.
Interaction of the Echinocandin Caspofungin with Amphotericin B or Voriconazole against Aspergillus Biofilms
In Vitro
Authors: Liu Weixia , Li Lijuan , Sun Yi , Chen Wei , Wan Zhe , Li Ruoyu , Liu Wei 
Published: October 2012

ABSTRACT

Aspergillus
biofilms were prepared from 22 strains of
Aspergillus
spp. via a 96-well plate-based method. Using a broth microdilution checkerboard technique with the XTT [2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] colorimetric assay, we demonstrated a synergistic antifungal activity against 18 of 22
Aspergillus
biofilm strains with a combination of caspofungin and amphotericin B and against 13 of 22 strains with a combination of caspofungin and voriconazole. We did not observe antagonism.
Exacerbation of Influenza Virus Infections in Mice by Intranasal Treatments and Implications for Evaluation of Antiviral Drugs
Authors: Smee Donald F. , von Itzstein Mark , Bhatt Beenu , Tarbet E. Bart 
Published: October 2012

ABSTRACT

Compounds lacking oral activity may be delivered intranasally to treat influenza virus infections in mice. However, intranasal treatments greatly enhance the virulence of such virus infections. This can be partially compensated for by giving reduced virus challenge doses. These can be 100- to 1,000-fold lower than infections without such treatment and still cause equivalent mortality. We found that intranasal liquid treatments facilitate virus production (probably through enhanced virus spread) and that lung pneumonia was delayed by only 2 days relative to a 1,000-fold higher virus challenge dose not accompanied by intranasal treatments. In one study, zanamivir was 90 to 100% effective at 10 mg/kg/day by oral, intraperitoneal, and intramuscular routes against influenza A/California/04/2009 (H1N1) virus in mice. However, the same compound administered intranasally at 20 mg/kg/day for 5 days gave no protection from death although the time to death was significantly delayed. A related compound, Neu5Ac2en (
N
-acetyl-2,3-dehydro-2-deoxyneuraminic acid), was ineffective at 100 mg/kg/day. Intranasal zanamivir and Neu5Ac2en were 70 to 100% protective against influenza A/NWS/33 (H1N1) virus infections at 0.1 to 10 and 30 to 100 mg/kg/day, respectively. Somewhat more difficult to treat was A/Victoria/3/75 virus that required 10 mg/kg/day of zanamivir to achieve full protection. These results illustrate that treatment of influenza virus infections by the intranasal route requires consideration of both virus challenge dose and virus strain in order to avoid compromising the effectiveness of a potentially useful antiviral agent. In addition, the intranasal treatments were shown to facilitate virus replication and promote lung pathology.
Enterotoxigenic Escherichia coli Prevents Host NF-κB Activation by Targeting IκBα Polyubiquitination
Authors: Wang Xiaogang , Hardwidge Philip R. 
Published: October 2012

ABSTRACTThe NF-κB pathway regulates innate immune responses to infection. NF-κB is activated after pathogen-associated molecular patterns are detected, leading to the induction of proinflammatory host responses. As a countermeasure, bacterial pathogens have evolved mechanisms to subvert NF-κB signaling. EnterotoxigenicEscherichia coli(ETEC) causes diarrheal disease and significant morbidity and mortality for humans in developing nations. The extent to which this important pathogen subverts innate immune responses by directly targeting the NF-κB pathway is an understudied topic. Here we report that ETEC secretes a heat-stable, proteinaceous factor that blocks NF-κB signaling normally induced by tumor necrosis factor (TNF), interleukin-1β, and flagellin. Pretreating intestinal epithelial cells with ETEC supernatant significantly blocked the degradation of the NF-κB inhibitor IκBα without affecting IκBα phosphorylation. Data from immunoprecipitation experiments suggest that the ETEC factor functions by preventing IκBα polyubiquitination. Inhibiting clathrin function blocked the activity of the secreted ETEC factor, suggesting that this yet-uncharacterized activity may utilize clathrin-dependent endocytosis to enter host cells. These data suggest that ETEC evades the host innate immune response by directly modulating NF-κB signaling.
GROUP EXTENSIONS OVER INFINITE WORDS
Authors: DIEKERT VOLKER , MYASNIKOV ALEXEI 
Published: October 2012

Non-Archimedean words have been introduced as a new type of infinite words which can be investigated through classical methods in combinatorics on words due to a length function. The length function, however, takes values in the additive group of polynomials ℤ[t] (and not, as traditionally, in ℕ), which yields various new properties. Non-Archimedean words allow to solve a number of interesting algorithmic problems in geometric and algorithmic group theory. There is also a connection to logic and the first-order theory in free groups (Tarski Problems). In the present paper we provide a general method to use infinite words over a discretely ordered abelian group as a tool to investigate certain group extensions for an arbitrary group G. The central object is a group E (A, G) which is defined in terms of a non-terminating, but confluent rewriting system. The groupG as well as some natural HNN-extensions of G embed into E (A, G) (and still "behave like" G), which makes it interesting to study its algorithmic properties. In order to show that every group G embeds into E (A, G) we combine methods from combinatorics on words, string rewriting and group theory.
Mixed speculative multithreaded execution models
Authors: Xekalakis Polychronis , Ioannou Nikolas , Cintra Marcelo 
Published: October 2012

The current trend toward multicore architectures has placed great pressure on programmers and compilers to generate thread-parallel programs. Improved execution performance can no longer be obtained via traditional single-thread instruction level parallelism (ILP), but, instead, via multithreaded execution. One notable technique that facilitates the extraction of parallel threads from sequential applications is thread-level speculation (TLS). This technique allows programmers/compilers to generate threads without checking for inter-thread data and control dependences, which are then transparently enforced by the hardware. Most prior work on TLS has concentrated on thread selection and mechanisms to efficiently support the main TLS operations, such as squashes, data versioning, and commits.
This article seeks to enhance TLS functionality by combining it with other speculative multithreaded execution models. The main idea is that TLS already requires extensive hardware support, which when slightly augmented can accommodate other speculative multithreaded techniques. Recognizing that for different applications, or even program phases, the application bottlenecks may be different, it is reasonable to assume that the more versatile a system is, the more efficiently it will be able to execute the given program.
Toward this direction, we first show that mixed execution models that combine TLS with Helper Threads (HT), RunAhead execution (RA) and MultiPath execution (MP) perform better than any of the models alone. Based on a simple model that we propose, we show that benefits come from being able to extract additional ILP without harming the TLP extracted by TLS. We then show that by combining all the execution models in a unified one that combines all these speculative multithreaded models, ILP can be further enhanced with only minimal additional cost in hardware.
Contrary Regulation of Bladder Cancer Cell Proliferation and Invasion by Dexamethasone-Mediated Glucocorticoid Receptor Signals
Authors: Zheng Yichun , Izumi Koji , Li Yi , Ishiguro Hitoshi , Miyamoto Hiroshi 
Published: October 2012

Abstract
In patients with advanced bladder cancer, glucocorticoids are frequently given to reduce acute toxicity, particularly hyperemesis, during chemotherapy, as well as to improve cachectic conditions. However, it remains unclear whether glucocorticoids directly affect the development and progression of bladder cancer through the glucocorticoid receptor pathway. Glucocorticoid receptor expression was first investigated in human bladder cancer lines and tissue microarrays. Then, the effects of dexamethasone on glucocorticoid receptor transcription, cell proliferation, apoptosis/cell cycle, and invasion were examined in bladder cancer lines. Finally, mouse xenograft models for bladder cancer were used to assess the efficacy of dexamethasone on tumor progression. All the cell lines and tissues examined were found to express glucocorticoid receptor. Dexamethasone increased glucocorticoid receptor–mediated reporter activity and cell proliferation, and inhibited apoptosis in the presence or absence of cisplatin. In contrast, dexamethasone suppressed cell invasion, the expression of its related genes [MMP-2/MMP-9, interleukin (IL)-6, VEGF], and the activity of MMP-2/MMP-9, and also induced mesenchymal-to-epithelial transition. In addition, dexamethasone increased IκBα protein levels and cytosolic accumulation of NF-κB. In xenograft-bearing mice, dexamethasone slightly augmented the growth of the inoculated tumors but completely prevented the development of bloody ascites, suggestive of peritoneal dissemination of tumor cells, and actual metastasis. In all these assays, dexamethasone effects were abolished by a glucocorticoid receptor antagonist or glucocorticoid receptor knockdown via RNA interference. Thus, glucocorticoid receptor activation resulted in promotion of cell proliferation via inhibiting apoptosis yet repression of cell invasion and metastasis. These results may provide a basis of developing improved chemotherapy regimens, including or excluding glucocorticoid receptor agonists/antagonists, for urothelial carcinoma. Mol Cancer Ther; 11(12); 2621–32. ©2012 AACR.
Mechanisms of Human Atrial Fibrillation Initiation
Authors: Krummen David E. , Bayer Jason D. , Ho Jeffrey , Ho Gordon , Smetak Miriam R. , Clopton Paul , Trayanova Natalia A. , Narayan Sanjiv M. 
Published: October 2012

Background—
Mechanisms of atrial fibrillation (AF) initiation are incompletely understood. We hypothesized that rate-dependent changes (restitution) in action potential duration (APD) and activation latency are central targets for clinical interventions that induce AF. We tested this hypothesis using clinical experiments and computer models.

Methods and Results—

In 50 patients (20 persistent, 23 paroxysmal AF, 7 controls), we used monophasic action potential catheters to define left atrial APD restitution, activation latency, and AF incidence from premature extrastimuli. Isoproterenol (n=14), adenosine (n=10), or rapid pacing (n=36) was then initiated to determine impact on these parameters. Compared with baseline in AF patients, isoproterenol and rapid pacing decreased activation latency (64±14 versus 31±13 versus 24±14 ms;
P
<0.05), steepened maximum APD restitution slope (0.8±0.7 versus 1.7±0.5 versus 1.1±0.5;
P
<0.05), and increased AF incidence (12% versus 64% versus 84%;
P
<0.05). Conversely, adenosine shortened APD (
P
<0.05), yet increased activation latency (86±27 ms;
P
=0.002) so that maximum APD restitution slope did not steepen (1.0±0.5;
P
=NS), and AF incidence was unchanged (10%;
P
=NS). In controls, no intervention steepened APD restitution or initiated AF. Computational modeling revealed that isoproterenol steepened APD restitution by increased L-type calcium current and decreased activation latency via enhanced rapid delayed potassium reactifier current inactivation, whereas rapid pacing steepened APD restitution via increased cardiac inward potassium rectifier current.

Conclusions—
Steep APD restitution is a common pathway for AF initiation by isoproterenol and tachycardia via reduced activation latency that enables engagement of steep APD restitution at rapid rates. Modeling suggests that AF initiation from each intervention uses distinct ionic mechanisms. This insight may help design interventions to prevent AF.
The signal transducers STAT5 and STAT3 control expression of Id2 and E2-2 during dendritic cell development
Authors: Li Haiyan S. , Yang Cliff Y. , Nallaparaju Kalyan C. , Zhang Huiyuan , Liu Yong-Jun , Goldrath Ananda W. , Watowich Stephanie S. 
Published: October 2012

Abstract
Cytokines and transcription factors play key roles in dendritic cell (DC) development, yet information about regulatory interactions between these signals remains limited. Here we show that the cytokines GM-CSF and Flt3L induce the transcriptional mediators Id2 and E2-2 and control DC lineage diversification by STAT–dependent pathways. We found that STAT5 is required for tissue CD103+ DC generation and plasmacytoid DC (pDC) suppression in steady state or response to GM-CSF. STAT5 stimulates GM-CSF–dependent expression of Id2, which controls CD103+ DC production and pDC inhibition. By contrast, pDCs, but not CD103+ DCs, are dependent on STAT3. Consistently, STAT3 stimulates Flt3L-responsive expression of the pDC regulator Tcf4 (E2-2). These data suggest that STATs contribute to DC development by controlling transcription factors involved in lineage differentiation.
Co-occurrence of resistance to different antibiotics among aquatic bacteria
Authors: Voolaid Veiko , Jõers Arvi , Kisand Veljo , Tenson Tanel 
Published: October 2012

Abstract

Background
Antibiotic resistance is not confined to pathogens, but is also widespread in various natural environments. In nature the microbes producing antibiotic compounds have been around for millions of years. Heavy use of antibiotics in medicine and veterinary practice may lead to the accumulation of resistance genes in microbial populations, followed by a rise in multiresistant bacteria.

Results
To test the extent of resistance among aquatic bacteria, we have collected 760 isolates resistant to at least one antibiotic. The phylogeny of the isolates covers a wide range of Proteobacteria, Actinobacteria and Bacteroidetes. In order to determine the extent of multiresistance, the isolates were tested on six antibiotics. As the growth rate of the different bacteria was highly variable, the classical medical resistance tests could not be used, and an alternative method considering the full growth curve was developed. In general, the overall resistances to different antibiotics could be explained by random, independent distribution. An exception to this was the resistances against tetracycline and chloramphenicol, which tended to occur in pairs.

Conclusions
We conclude that there is no massive spread of multiresistance determinants in the studied environment, although some specific cases can be found, awaiting for molecular characterization of the resistance mechanisms.
Risk factors for ischemic stroke; results from 9 years of follow-up in a population based cohort of Iran
Authors: Fahimfar Noushin , Khalili Davood , Mohebi Reza , Azizi Fereidoun , Hadaegh Farzad 
Published: October 2012

Abstract

Background
Data about the risk factors of stroke are sparse in the Middle East populations. We aimed to determine the potential risk factors and their population attributable fraction (PAF) for stroke in an Iranian population.

Methods
A cohort Study consisted of 1089 men and 1289 women, with mean (SD) ages of 61.1(7.6) and 59.0(6.7) years, respectively. Cox regression was implemented to estimate the hazard ratio (HR) of each risk factor for stroke events in a stepwise method. We calculated a multivariate adjusted population attributable fraction (PAF) for any risk factors remained in the model.

Results
During 9.3 years of follow-up, 69 events of stroke occurred with incidence rates of 4.5 (95% CI: 3.3-6.0) and 2.5 (1.7-3.6) in 1000 person-years for men and women respectively. Among potential risk factors, only age ≥ 65 years (HR: 2.03, CI: 1.24-3.31), male gender (HR: 2.00, CI: 1.16-3.43), hypertension (HR: 3.03, CI: 1.76-5.22), diabetes mellitus (HR: 2.18, CI: 1.34-3.56), and chronic kidney disease (CKD) (HR: 2.01, CI: 1.22-3.33), were independently associated with increased risk of stroke events in the total population. A paired homogeneity test showed that the hazard ratio of CKD did not differ from other independent risk factors. The PAFs were 29.7% and 25% for male gender and age ≥ 65 as non-modifiable and 48.6%, 29.1% and 22.0% for hypertension, CKD and diabetes as modifiable risk factors respectively.

Conclusion
Following this population based study of Iranians, we demonstrated that among modifiable risk factors, CKD as well as hypertension and diabetes are the strongest independent predictors of stroke.
Li-Fraumeni syndrome with simultaneous osteosarcoma and liver cancer: Increased expression of a CD44 variant isoform after chemotherapy
Authors: Yoshida Go J , Fuchimoto Yasushi , Osumi Tomoo , Shimada Hiroyuki , Hosaka Seiichi , Morioka Hideo , Mukai Makio , Masugi Yohei , Sakamoto Michiie , Kuroda Tatsuo 
Published: October 2012

Abstract

Background
Li-Fraumeni syndrome (LFS) is a hereditary cancer predisposition syndrome that is commonly associated with a germline mutation in the tumor suppressor gene p53. Loss of p53 results in increased expression of CD44, a cancer stem cell (CSC) marker, which is involved in the scavenging of reactive oxygen species (ROS). Here, we report a change in the expression of a CD44 variant isoform (CD44v8-10) in an 8-year-old female LFS patient with osteosarcoma and atypical liver cancer after chemotherapy.

Case presentation
The patient visited a clinic with a chief complaint of chronic pain in a bruise on her right knee. Magnetic resonance imaging (MRI) raised the possibility of a bone malignancy. Biochemical testing also revealed significantly elevated levels of AFP, which strongly suggested the existence of a primary malignancy in the liver. MRI imaging showed the simultaneous development of osteosarcoma and liver cancer, both of which were confirmed upon biopsy. Combined therapy with surgical resection after chemotherapy was successful in this patient. Regardless of the absence of a familial history of hereditary cancer, a germline mutation in p53 was identified (a missense mutation defined as c.722 C>T, p.Ser241Phe). To better understand the cancer progression and response to treatment, immunohistochemical (IHC) analysis of biopsy specimens obtained before and after chemotherapy was performed using a specific antibody against CD44v8-10.

Conclusion
This case demonstrates the ectopic up-regulation of CD44v8-10 in a biopsy sample obtained after cytotoxic chemotherapy, which confers high levels of oxidative stress on cancer cells. Because the alternative splicing of CD44 is tightly regulated epigenetically, it is possible that micro-environmental stress resulting from chemotherapy caused the ectopic induction of CD44v8-10 in vivo.