Miracle-dz/UniFAR-FTUs huggingface dataset:
The effectiveness of mobile-health behaviour change interventions for cardiovascular disease self-management: A systematic review

Background Mobile wireless devices (mHealth) have been used to deliver cardiovascular disease self-management interventions to educate and support patients in making healthy lifestyle changes. This systematic review aimed to determine the effectiveness of mHealth interventions on behavioural lifestyle changes and medication adherence for cardiovascular disease self-management. Methods A comprehensive literature search was conducted from inception through to 3 March 2015 using MEDLINE, PubMed, PsycINFO, EMBASE and The Cochrane Library. Eligible studies used an experimental trial design to determine the effectiveness of an mHealth intervention to change lifestyle behaviours in any cardiovascular disease population. Data extracted included intervention and comparison group characteristics with a specific focus on the use of behaviour change techniques. Results Seven studies met our inclusion criteria and were included in the qualitative synthesis. All interventions were delivered in part by mobile phone text messaging. Three studies were effective at improving adherence to medication and two studies increased physical activity behaviour. No effects were observed on dietary behaviour or smoking cessation, measured in one study each. Simple text messaging interventions appeared to be most effective; however, no clear relationships were found between study findings and intervention dose, duration or behaviour change techniques targeted. Conclusions Our review found mHealth has the potential to change lifestyle behaviour. Results are still limited to a small number of trials, inconsistent outcome measures and ineffective reporting of intervention characteristics. Large scale, longitudinal studies are now warranted to gain a clear understanding of the effects of mHealth on behaviour change in the cardiovascular disease population.
Cardiovascular Risk Calculators: Understanding Differences and Realising Economic Implications

In recent years, the concept of "global cardiovascular risk assessment" has grown in interest for its role in primary prevention of cardiovascular diseases. Interventions for reducing the risk of relapse for persons with cardiovascular past history are well agreed-on. But for persons without such a history, the risk of a first attack varies greatly and this variability implies a range in the intensity of interventions. In several countries, guidelines for general practitioners have been diffused about pharmaceutical prescriptions in the different risk classes. In particular, in Italy, a governmental drug management commission has established that Statins, the most used cholesterol lowering medicines, can be refunded by the National Healthcare System only if they are prescribed to hyper-cholesterol patients with a global risk greater than 20%. The question is: how to calculate the risk? We performed a review of both the web and the literature and we found a lot of different "risk calculators". By means of a simulation study, we showed that these tools, when used for the same person, may lead to very different results. We estimated the economic impact of using one or another calculator.
Do you know your patient? Knowing individuals with dementia combined with evidence-based care promotes function and satisfaction in hospitalized older adults.

Do you know your patient? More than 20 years ago Dr. Afaf Meleis wrote about the importance of knowing your patient and the unique opportunity for nurses to use this knowledge to improve care (Schumacher, Jones, & Meleis, 1999). “Knowing your patient” can mean different things to different nurses depending on how you define knowing and where one practices. In this editorial, we present one practical case exemplar and evidence to support this approach.
Anaplastic lymphoma kinase inhibitors in elderly patients with advanced non-small cell lung cancer

ABSTRACT Introduction: Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths in the USA and worldwide. At diagnosis, half of the patients are over 70 years of age, and most present with advanced disease for which chemotherapy provides modest benefit with significant toxicity. Older patients often have more comorbidities than their younger counterparts and tend to be excluded from clinical trials. Areas covered: A small percentage (less than 7%) of patients with NSCLC have the anaplastic lymphoma kinase (ALK) rearrangement. Compared to the general NSCLC population, this clinically distinct group has a relatively younger median age of 51 years at diagnosis. As such, elderly patients with ALK-positive disease are both a minority within this group and are expected to be underrepresented in clinical trials. Expert commentary: Despite promising results in the general population, data about the efficacy and safety of ALK inhibitors in the elderly population remains scarce. In our review, we briefly discuss the current evidence of ALK inhibitors in the general population and we shed light on this subgroup of elderly patients with advanced ALK-positive disease.
A defucosylated anti‐CD317 antibody exhibited enhanced antibody‐dependent cellular cytotoxicity against primary myeloma cells in the presence of effectors from patients

The humanized monoclonal antibody (mAb) against CD317 antigen (anti‐HM1.24 antibody; AHM), which is highly expressed on multiple myeloma (MM), induces antibody‐dependent cellular cytotoxicity (ADCC). However, the antitumor activity of AHM in the clinical setting has not been clearly demonstrated. In this study, we produced defucosylated AHM and evaluated its potency for clinical application by performing autologous ADCC assays against primary MM cells from patients. Defucosylated AHM that was produced in rat myeloma YB2/0 cells expressing a low level of fucosyltransferase (FUT8) showed significant ADCC activity against three out of six primary MM cells in the presence of autologous PBMC, whereas conventional AHM did not. The results indicate that the potency of AHM to induce ADCC against primary MM cells was insufficient, but was significantly augmented by defucosylation. To generate more homogenous defucosylated monoclonal antibodies (mAb) for fermentation, we disrupted the GFT gene that encodes a GDP‐fucose transporter in a CHO/DXB11 cell line by sequential homologous recombination. Analysis of the N‐linked oligosaccharide in the defucosylated AHM produced by the established GFT(−/−)CHO cell line showed that a majority (93.4%) of the oligosaccharide was fucose free. The GFT(−/−) cells stably produced defucosylated mAb over passages. These results demonstrate that GTF(−/−)CHO‐produced defucosylated AHM (GFTKO‐AHM) will be a promising new therapeutic antibody against MM in the clinical setting. (Cancer Sci 2010)
Secret Sharing With Trusted Third Parties Using Piggy Bank Protocol

This paper presents a new scheme to distribute secret shares using two trusted third parties to increase security and eliminate the dependency on single trusted third party. This protocol for communication between a device and two trusted third parties uses the piggy bank cryptographic paradigm. We also present a protocol to give law enforcing agencies access to sensitive information present on a cell phone or a device using secret sharing scheme. The ideas for classical systems may also be applied to quantum schemes.
Depletion of chlorine into HCl ice in a protostellar core The CHESS spectral survey of OMC-2 FIR 4 ?

The freezeout of gas-phase species onto cold dust grains can drastically alter the chemistry and the heating-cooling balance of protostellar material. In contrast to well-known species such as carbon monoxide (CO), the freezeout of various carriers of elements with abundances $<10^{-5}$ has not yet been well studied. Our aim here is to study the depletion of chlorine in the protostellar core, OMC-2 FIR 4. We observed transitions of HCl and H2Cl+ towards OMC-2 FIR 4 using the Herschel Space Observatory and Caltech Submillimeter Observatory facilities. Our analysis makes use of state of the art chlorine gas-grain chemical models and newly calculated HCl-H$_{2}$ hyperfine collisional excitation rate coefficients. A narrow emission component in the HCl lines traces the extended envelope, and a broad one traces a more compact central region. The gas-phase HCl abundance in FIR 4 is 9e-11, a factor of only 0.001 that of volatile elemental chlorine. The H2Cl+ lines are detected in absorption and trace a tenuous foreground cloud, where we find no depletion of volatile chlorine. Gas-phase HCl is the tip of the chlorine iceberg in protostellar cores. Using a gas-grain chemical model, we show that the hydrogenation of atomic chlorine on grain surfaces in the dark cloud stage sequesters at least 90% of the volatile chlorine into HCl ice, where it remains in the protostellar stage. About 10% of chlorine is in gaseous atomic form. Gas-phase HCl is a minor, but diagnostically key reservoir, with an abundance of <1e-10 in most of the protostellar core. We find the 35Cl/37Cl ratio in OMC-2 FIR 4 to be 3.2\pm0.1, consistent with the solar system value.
Genetic Characterization of Mutants Resistant to the Antiauxin p-Chlorophenoxyisobutyric Acid Reveals That AAR3, a Gene Encoding a DCN1-Like Protein, Regulates Responses to the Synthetic Auxin 2,4-Dichlorophenoxyacetic Acid in Arabidopsis Roots1[C][W]

To isolate novel auxin-responsive mutants in Arabidopsis (Arabidopsis thaliana), we screened mutants for root growth resistance to a putative antiauxin, p-chlorophenoxyisobutyric acid (PCIB), which inhibits auxin action by interfering the upstream auxin-signaling events. Eleven PCIB-resistant mutants were obtained. Genetic mapping indicates that the mutations are located in at least five independent loci, including two known auxin-related loci, TRANSPORT INHIBITOR RESPONSE1 and Arabidopsis CULLIN1. antiauxin-resistant mutants (aars) aar3-1, aar4, and aar5 were also resistant to 2,4-dichlorophenoxyacetic acid as shown by a root growth assay. Positional cloning of aar3-1 revealed that the AAR3 gene encodes a protein with a domain of unknown function (DUF298), which has not previously been implicated in auxin signaling. The protein has a putative nuclear localization signal and shares homology with the DEFECTIVE IN CULLIN NEDDYLATION-1 protein through the DUF298 domain. The results also indicate that PCIB can facilitate the identification of factors involved in auxin or auxin-related signaling.
Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation

In this study, Pengelly et al. investigated the physiological role of Histone H2A monoubiquitylation (H2Aub), a key effector in transcriptional repression by PRC1. They generated Drosophila strains that lack H2Aub and found that repression of all canonical PRC1 target genes is maintained in the absence of H2Aub and that the mutant animals do not exhibit the phenotypes that are characteristic for mutants lacking Polycomb function. The findings suggest that the mechanism by which PRC1 represses gene transcription is independent of H2Aub.
Predictive Biomarkers and Personalized Medicine Impact of ABCB 1 Allelic Variants on QTc Interval Prolongation

Purpose: Although the ABCB1 (P-glycoprotein) drug transporter is a constituent of several blood–tissue barriers (i.e., blood–brain and blood–nerve), its participation in a putative blood–heart barrier has been poorly explored. ABCB1 could decrease the intracardiac concentrations of drugs that cause QT prolongation and cardiotoxicity. Experimental Design: ABCB1-related romidepsin transport kinetics were explored in LLC-PK1 cells transfected with different ABCB1 genetic variants. ABCB1 plasma and intracardiac concentrations were determined in Abcb1a/1b ( / ) mice and wild-type FVB controls. These same mice were used to evaluate romidepsin-induced heart rate-corrected QT interval (QTc) prolongation over time. Finally, a cohort of 83 individuals with available QTcB and ABCB1 genotyping data were used to compare allelic variation in ABCB1 versus QTc-prolongation phenotype. Results: Here, we show that mice lacking the ABCB1-type P-glycoprotein have higher intracardiac concentrations of a model ABCB1 substrate, romidepsin, that correspond to changes in QT prolongation from baseline (DQTc) over time. Consistent with this observation, we also show that patients carrying genetic variants that could raise ABCB1 expression in the cardiac endothelium have lower DQTc following a single dose of romidepsin. Conclusions: To our knowledge, this is the first evidence that Abcb1-type P-glycoprotein can limit intracardiac exposure to a drug that mediates QT prolongation and suggests that certain commonly inherited polymorphisms in ABCB1 may serve as markers for QT prolongation following the administration of ABCB1-substrate drugs. Clin Cancer Res; 17(4); 937–46. 2010 AACR.
Acid Profiles and pH of Carious Dentin in Active and Arrested Lesions

Organic acids in caries lesions play important roles in initiation and progress of dental caries. We investigated relationships between clinical types of dentin caries and acid profile or pH in the lesions. Caries lesions in dentin from 76 permanent teeth were classified into active, arrested, situated beneath a restoration, and unclassified types. The pH of carious dentin was distinctly lower than that of sound dentin (p < 0.001). Carious dentin with a high percentage of lactate had a lower pH than that with a high percentage of acetate and propionate (p < 0.001). Dentin from active lesions showed a mean pH of 4.9, and the dominant acid was lactate (mean percentage, 88.2). In contrast, carious dentin from arrested lesions showed a higher pH, 5.7, with acetate and propionate as the dominant acids (mean percentages of acetate and propionate, 64.0 and 18.2, respectively). The acid profile (mean percentages of acetate and propionate, 54.0 and 27.7, respectively) and pH (mean 5.8) of carious dentin sampled from lesions beneath a restoration were similar to those of dentin from arrested lesions. This study showed a clear relationship between clinical classification of dentin caries and acid profile and pH, suggesting that both factors are important in dentin caries etiology.
Van der Waals metal-semiconductor junction: Weak Fermi level pinning enables effective tuning of Schottky barrier

The Schottky barrier for carrier injection into 2D semiconductors can be effectively tuned by using 2D metals. Two-dimensional (2D) semiconductors have shown great potential for electronic and optoelectronic applications. However, their development is limited by a large Schottky barrier (SB) at the metal-semiconductor junction (MSJ), which is difficult to tune by using conventional metals because of the effect of strong Fermi level pinning (FLP). We show that this problem can be overcome by using 2D metals, which are bounded with 2D semiconductors through van der Waals (vdW) interactions. This success relies on a weak FLP at the vdW MSJ, which is attributed to the suppression of metal-induced gap states. Consequently, the SB becomes tunable and can vanish with proper 2D metals (for example, H-NbS2). This work not only offers new insights into the fundamental properties of heterojunctions but also uncovers the great potential of 2D metals for device applications.
Bactericidal effect of 5-azacytidine on Escherichia coli carrying EcoRII restriction-modification enzymes

5-Azacytidine was found to be bactericidal to Escherichia coli carrying plasmids specifying EcoRII restriction-modification systems, but not to the same strains lacking these plasmids. Of other base analogs tested, only 5(beta-D-ribofuranosyl)isocytidine had similar, although weaker, effects. Plasmids that had lost the EcoRII restriction-modification system did not confer sensitivity to 5-azacytidine. Mutants defective in the restriction function remained sensitive to the toxic effects of the drug; however, a mutant defective in the modification function lost most of the sensitivity to 5-azacytidine. For the bactericidal effect to be seen, the cells had to be growing; cells in the stationary phase of growth were not killed by the drug. The drug inhibited the methylase enzyme, and an inhibitor of the enzyme could be detected in vitro in extracts of cells that had been treated with 5-azacytidine. This nalidixic acid inhibited its formation. Coumermycin but not nalidixic acid antagonized the bactericidal effect of the drug; however, coumermycin was more effective in preventing the inhibition of the methylase by 5-azacytidine than was nalidixic acid.
L4-33K, an Adenovirus-encoded Alternative RNA Splicing Factor*>

Splicing of the adenovirus IIIa mRNA is subjected to a strict temporal regulation during virus infection such that efficient IIIa 3′ splice site usage is confined to the late phase of the infectious cycle. Here we show that the adenovirus L4-33K protein functions as a virus-encoded RNA splicing factor that preferentially activates splicing of transcripts with a weak 3′ splice site sequence context, a sequence configuration that is shared by many of the late adenovirus 3′ splice sites. Furthermore, we show that L4-33K activates IIIa splicing through the IIIa virus infection-dependent splicing enhancer element (3VDE). This element was previously shown to be the minimal element, both necessary and sufficient, for activation of IIIa splicing in the context of an adenovirus-infected cell. L4-33K stimulates an early step in spliceosome assembly and appears to be the only viral protein necessary to convert a nuclear extract prepared from uninfected HeLa cells to an extract with splicing properties very similar to a nuclear extract prepared from adenovirus late-infected cells. Collectively, our results suggest that L4-33K is the key viral protein required to activate the early to late switch in adenovirus major late L1 alternative splicing.
Approaches to DNA mutagenesis: an overview.

In the last several years, the use of double-stranded DNA templates together with thermostable-polymerase PCR has essentially replaced the use single-stranded DNA templates using the thermolabile polymerase for in vitro mutagenesis. Numerous PCR methods are now available, such as overlap-extension PCR, megaprimer PCR, and inverse PCR. All these PCR methods are reliable, effective, and convenient, although they are more prone to high rates of spontaneous error in mutant DNAs than are methods using thermolabile polymerases. Some improvements, such as the introduction of methylated templates, have been employed to minimize PCR errors. On the other hand, because of the introduction of many selection measures (e.g., restoration of antibiotic resistance, restoration of replication origin and unique site elimination), both double-stranded and single-stranded DNAs can now be used as templates for mutagenesis using thermolabile polymerase methods. For PCR methods, selection measures such as nested PCR has developed. All these selection measures have greatly improved the efficiency of mutagenesis by removing wild-type templates prior to transformation. Many efficient methods are available for both SDM and REM. Mutations can be introduce in vitro or in vivo, either by mutagenic primers or by erroneous DNA synthesis. Thus, choices largely depend on the experimental needs and resources of the investigator.
Functional implications of tissue factor localization to cell–cell contacts in myocardium

Recently published studies suggest that the procoagulant receptor protein tissue factor (TF) is involved in vitro in cell adhesion and migration, via an interaction of its cytoplasmic domain with cytoskeletal proteins. Interestingly, TF is abundantly expressed in myocardium, but not in skeletal muscle. To elucidate the possible roles of TF in the myocardium, this study examined the cellular distribution of TF in relation to cytoskeletal proteins, as well as its relative amounts in different segments of premature, mature, and pathologically altered cardiac muscle. In juvenile and adult hearts, TF was predominantly detectable in the transverse part of the intercalated discs, where it co‐localized with cytoskeletal proteins such as desmin and vinculin. The lowest amount of TF was observed in right atrial and the highest in left ventricular myocardium, which correlated with the number of contact sites of cardiomyocytes in these segments of the cardiac muscle. Lower levels of TF were present in structurally altered myocardium from patients with hypertension or ventricular hypertrophy. In addition, TF expression was decreased in human heart during sepsis and transiently decreased in rabbit heart in an endotoxaemia model, which indicates that a reduction in TF may contribute to cardiac failure in sepsis. The microtopography of TF at cardiomyocyte contact sites indicates that TF may play a structural role in the maintenance of cardiac muscle. Copyright © 2000 John Wiley & Sons, Ltd.
Identification and characterization of a bioactive lantibiotic produced by Staphylococcus warneri

Abstract Lantibiotics are a group of potent antibacterial agents that contain unusual amino acids, such as the thioether amino acids lanthionine and methyllanthionine, and the didehydroamino acids didehydroalanine and didehydro-aminobutyric acid. Here, we report on an antibacterial lantibiotic peptide named SWLP1 (Staphylococcus warneri lantibiotic peptide 1), which is secreted from Staphylococcus warneri (deposited with DSMZ, accession number DSM 16081). SWLP1 was purified from growth media. The purified peptide displays antibacterial activity against several species, including Staphylococcus epidermidis. The molecular mass of SWLP1 is 2998.9 Da as determined by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. The sequence and possible structure was elucidated by combining electrospray ionization mass spectrometry/mass spectrometry data of ethanethiol-treated and non-ethanethiol-treated tryptic fragments of the SWLP1. SWLP1 contains three thioether bridges, one didehydroalanine, and three didehydroaminobutyric acids. This peptide has the potential to be used in treatment of several Gram-positive bacterial infections.
Edinburgh Research Explorer Identification and cloning of a novel phosphatase expressed at high levels in differentiating growth plate chondrocytes

Growth plate chondrocytes progress through a proliferative phase before acquiring a terminally-differentiated phenotype. In this study we used Percoll density gradients to separate chick growth plate chondrocytes into populations of different maturational phenotype. By applying agarose gel differential display to these populations we cloned a cDNA encoding a novel 268 amino acid protein (3X11A). 3X11A contains two peptide motifs that are conserved in a recently identified superfamily of phosphotransferases. It is likely that 3X11A is a phosphatase, but its substrate specificity remains uncertain. 3X11A expression is upregulated 5-fold during chondrocyte terminal differentiation and its expression is approximately 100-fold higher in hypertrophic chondrocytes than in non-chondrogenic tissues. This suggests that 3X11A participates in a biochemical pathway that is particularly active in differentiating chondrocytes. (cid:223) 1999 Elsevier Science B.V. All rights reserved.