Miracle-dz/UniFAR-FTUs huggingface dataset:
Loss reduction for phased-array demultiplexers using a double etch technique

Wavelength Division Multiplexing (WDM) is an effective technique to exploit the huge bandwidth of optical fibres. Key components in such WDM-systems are demultiplexers which spatially separate the different wavelength channels. Phased-array demultiplexers combine ease of fabrication and low insertion losses. Silica-based phased-array demultiplexers are realised with low losses from 2-3 dB [1,2]. InP-based demultiplexers show slightly higher on-chip losses of 4-6 dB [3,4]. In addition they have considerably higher fibre coupling losses (several dB’s), but the advantage of InP-based demultiplexers is that they can be integrated with active components. Earlier we reported a low-loss demultiplexer with reduced fibre coupling loss by applying deeply etched InGaAsP waveguides with a relatively large core and a low index contrast, which had an almost circular mode profile [5]. The component had 4-5 dB on-chip loss and fibre coupling loss of about 1 dB to a tapered fibre. In this article we report a method to further reduce the on-chip losses.
Differences in regulation of Ca2+-activated Cl- channels in colonic and parotid secretory cells.

We investigated the regulation of Ca2+-activated Cl- channels in cells from the human colonic cell line T84 and acinar cells from rat parotid glands. The participation of multifunctional Ca2+- and calmodulin-dependent protein kinase (CaM kinase) II in the activation of these channels was studied using selective inhibitors of calmodulin and CaM kinase II. Ca2+-dependent Cl- currents were recorded using the whole cell patch-clamp technique. Direct inhibition of CaM kinase II by 40 μM peptide 281-302 or by 10 μM KN-62, another CaM kinase inhibitor, did not block the Cl- current in parotid acinar cells, whereas in T84 cells KN-62 markedly inhibited the Ca2+-dependent Cl- current. We also used the calmodulin-binding domain peptide 290-309 (0.5 μM), which competitively inhibits the activation of CaM kinase II. This peptide reduced the Cl- current in T84 cells by ∼70% but was without effect on the channels in parotid acinar cells. We conclude that the Ca2+-dependent Cl- channels in T84 cells are activated by CaM kinase II but that the channels in parotid acinar cells must be regulated by a fundamentally different Ca2+-dependent mechanism that does not utilize CaM kinase II or any calmodulin-dependent process.
Smooth Muscle Cell–Mineralocorticoid Receptor as a Mediator of Cardiovascular Stiffness With Aging

Stiffening of the vasculature with aging is a strong predictor of adverse cardiovascular events, independent of all other risk factors including blood pressure, yet no therapies target this process. MRs (mineralocorticoid receptors) in smooth muscle cells (SMCs) have been implicated in the regulation of vascular fibrosis but have not been explored in vascular aging. Comparing SMC-MR–deleted male mice to MR-intact littermates at 3, 12, and 18 months of age, we demonstrated that aging-associated vascular stiffening and fibrosis are mitigated by MR deletion in SMCs. Progression of cardiac stiffness and fibrosis and the decline in exercise capacity with aging were also mitigated by MR deletion in SMC. Vascular gene expression profiling analysis revealed that MR deletion in SMC is associated with recruitment of a distinct antifibrotic vascular gene expression program with aging. Moreover, long-term pharmacological inhibition of MR in aged mice prevented the progression of vascular fibrosis and stiffness and induced a similar antifibrotic vascular gene program. Finally, in a small trial in elderly male humans, short-term MR antagonism produced an antifibrotic signature of circulating biomarkers similar to that observed in the vasculature of SMC-MR–deleted mice. These findings suggest that SMC-MR contributes to vascular stiffening with aging and is a potential therapeutic target to prevent the progression of aging-associated vascular fibrosis and stiffness.
Extracellular Vesicle Subtypes Released From Activated or Apoptotic T-Lymphocytes Carry a Specific and Stimulus-Dependent Protein Cargo

Extracellular vesicles (EVs) are released from nearly all mammalian cells and different EV populations have been described. Microvesicles represent large EVs (LEVs) released from the cellular surface, while exosomes are small EVs (SEVs) released from an intracellular compartment. As it is likely that different stimuli promote the release of distinct EV populations, we analyzed EVs from human lymphocytes considering the respective release stimuli (activation Vs. apoptosis induction). We could clearly separate two EV populations, namely SEVs (average diameter <200 nm) and LEVs (diameter range between 200 and 1000 nm). Morphology and size were analyzed by electron microscopy and nanoparticle tracking analysis. Apoptosis induction caused a massive release of LEVs, while activated T-cells released SEVs and LEVs in considerably lower amounts. The release of SEVs from apoptotic T-cells was comparable with LEV release from activated ones. LEVs contained signaling proteins and proteins of the actin-myosin cytoskeleton. SEVs carried cytoplasmic/endosomal proteins like the 70-kDa heat shock protein 70 (HSP70) or tumor susceptibility 101 (TSG101), microtubule-associated proteins, and ubiquitinated proteins. The protein expression profile of SEVs and LEVs changed substantially after the induction of apoptosis. After apoptosis induction, HSP70 and TSG101 (often used as exosome markers) were highly expressed within LEVs. Interestingly, in contrast to HSP70 and TSG101, gelsolin and eps15 homology domain-containing protein 3 (EHD3) turned out to be specific for SEVs irrespective of the stimulus causing the EV release. Finally, we detected several subunits of the proteasome (PSMB9, PSMB10) as well as the danger signal HMGB1 exclusively within apoptotic cell-released LEVs. Thus, we were able to identify new marker proteins that can be useful to discriminate between distinct LEV subpopulations. The mass spectrometry proteomics data are available via ProteomeXchange with identifier PXD009074.
IFN Regulatory Factor 2 Inhibits Expression of Glycolytic Genes and Lipopolysaccharide-Induced Proinflammatory Responses in Macrophages

Rapid initiation and timely resolution of inflammatory response in macrophages are synergistic events that are known to be equally critical to optimal host defense against pathogen infections. However, the regulation of these processes, in particular by a specific cellular metabolic program, has not been well understood. In this study, we found that IFN regulatory factor 2 (IRF2) underwent an early degradation in a proteasome-mediated pathway in LPS-treated mouse macrophages, followed by a later recovery of the expression via transactivation. We showed that IRF2 was anti-inflammatory in that knockdown of this protein promoted the production of LPS-induced proinflammatory mediators. Mechanistically, although IRF2 apparently did not target the proximal cytoplasmic signaling events upon LPS engagements, it inhibited HIF-1α–dependent expression of glycolytic genes and thereby cellular glycolysis, sequential events necessary for the IRF2 anti-inflammatory activity. We found that macrophages in endotoxin tolerant state demonstrated deficiency in LPS-augmented glycolysis, which was likely caused by failed downregulation of IRF2 and the ensuing upregulation of the glycolytic genes in these cells. In contrast to observations with LPS, knockdown of IRF2 decreased IL-4–induced macrophage alternative activation. The pro–IL-4 activity of IRF2 was dependent on KLF4, a key mediator of the alternative activation, which was transcriptionally induced by IRF2. In conclusion, our data suggest that IRF2 is an important regulator of the proinflammatory response in macrophages by controlling HIF-1α–dependent glycolytic gene expression and glycolysis. This study also indicates IRF2 as a novel therapeutic target to treat inflammatory disorders associated with dysregulations of macrophage activations.
The immediate and long-term effects of time perspective on Internet gaming disorder

Backgrounds and aims This study focuses on the role of time perspective (TP) in Internet gaming disorder (IGD). An inventory-based study on 377 massive multiplayer online role playing game players was conducted, followed by a 3-year-follow-up in which 48 active players from the original sample participated. We proposed that TP factors (negative TP and future positive TP) will influence either the current presence of IGD symptoms or the further development of IGD over time. In other words, the effect of TP is stable. Finally, game usage patterns were analyzed in the sense of changes in playing time and IGD symptoms in gamers after 3 years. Methods To access the variables, two scales were administered through online inventory, the Zimbardo Time Perspective Inventory-short, and Charlton and Danforths’ Core Addiction Scale, both in 2012 (N = 377) and 2015 (N = 48). The amount of time that gamers usually spent playing were obtained through self-reports. Results The study’s primary presumptions were confirmed. Both negative TP and future positive TP were confirmed as significant predictors of the presence of IGD symptoms, either immediately or in the following 3 years. Data on game usage showed a significant decrease in playing time and IGD symptoms between year 0 and year 3 of the study.
Exploring Reliability and Validity of the Deployment Risk and Resilience Inventory-2 Among a Nonclinical Sample of Discharged Soldiers Following Mandatory Military Service.

The Deployment Risk and Resilience Inventory (DRRI) is a widely used questionnaire assessing deployment-related risk and resilience factors among war veterans. Its successor, the DRRI-2, has only been validated and used among veterans deployed for overseas military missions, but because many countries still enforce compulsory military service, validating it among nonclinical samples of healthy discharged soldiers following mandatory service is also a necessity. In the current study, a sample of 101 discharged Israeli soldiers (39 males, 62 females; mean time since discharge 13.92, SD = 9.09 years) completed the DRRI-2. There were 52 participants who completed the questionnaire at a second time point (mean time between assessments 19.02, SD = 6.21 days). Both physical and mental health status were examined, as well as symptomatology of depression, anxiety, and posttraumatic stress disorder. Cronbach's αs for all latent variables in the inventory ranged from . 47 to . 95. The DRRI-2 risk factors were negatively associated with psychological functioning, whereas resilience factors were positively associated with better self-reported mental health. Test-retest reliability coefficients were generally high (Pearson correlations were .61 to .94, all p values < .01). Our study provides evidence for the reliability and validity of the DRRI-2 in assessing salient deployment experiences among a nonclinical sample following mandatory military service.
Vascular and hemodynamic effects of behavioral stress in borderline hypertensive and Wistar-Kyoto rats.

In borderline hypertensive rats (BHR), behavioral stress produces hypertension, which has been attributed to increases in sympathetic nervous system activity and peripheral changes in vascular structure. However, the mechanisms mediating development of stress-induced hypertension have not been well defined. Experiments were designed to determine hemodynamic effects and changes in small mesenteric artery (≈300 μm) vascular reactivity in response to 10 days of air-jet stress (2 h/day) in BHR and in Wistar-Kyoto (WKY) rats. The acute stress-induced increase in mean arterial pressure (AP) was impaired in WKY rats compared with BHR on day 1, and habituation developed to the increase in AP in BHR, but not WKY rats. Conversely, WKY rats adapted to the stress-induced tachycardia to a larger extent than BHR. The mechanisms mediating endothelium-dependent relaxation to acetylcholine (ACh) were altered in small mesenteric arteries isolated from WKY rats and BHR after 10 days of air-jet stress. Inhibition of nitric oxide synthase activity had a significantly larger inhibitory effect on ACh-induced relaxation in vessels from stressed compared with control BHR. Also, cyclooxygenase products contributed to ACh-induced relaxation of small mesenteric arteries from stressed WKY rats, but not control WKY rats. Endothelium-independent relaxation to nitroprusside was impaired in vessels from stressed WKY rats, but not stressed BHR. Finally, contraction to phenylephrine was impaired in vessels from stressed BHR, but not WKY rats. In conclusion, changes in vascular reactivity induced by air-jet stress appear to correlate with, and may contribute to, the differential hemodynamic adaptations to stress observed in WKY rats and BHR.
Directed self‐assembly of block copolymer‐based nanocomposites in thin films

Exploiting the full potential of metal and semiconductor nanoparticles for advanced nanotechnological applications requires their organization into predefined structures with high orientational control. Nanofabrication approaches that combine high resolution lithography and self-assembly afford the advantages of accurate placement, compositional diversity, and reduced production costs. This review concentrates on the creation of organized nanoparticle superstructures assisted by recent developments in the directed self-assembly of block copolymers, and delineates possible applications. Copyright © 2016 John Wiley & Sons, Ltd.
Evaluating worker-centered smart interventions on the shop floor

This paper presents the evaluation strategy and the first results we obtained when we used the FACTS4WORKERS evaluation framework. The purpose of the framework is to prove whether the project interventions achieve the expected results, which are: improving workers’ job satisfaction, increasing innovation and problem solving skills as well as enhancing productivity. Because of the diversity of the industrial partners and of the workplaces where the interventions are going to be implemented, the different languages, legal and cultural environments the framework was conceived as general as possible to be adapted to any particular case. We present here one example for using the framework, the first results of these measurements and the feedback the evaluation provides both for supporting the decisions about the interventions and about the framework itself.
Synthesizing High-Frequency Rules from Different Data Sources

Many large organizations have multiple data sources, such as different branches of an interstate company. While putting all data together from different sources might amass a huge database for centralized processing, mining association rules at different data sources and forwarding the rules (rather than the original raw data) to the centralized company headquarter provides a feasible way to deal with multiple data source problems. In the meanwhile, the association rules at each data source may be required for that data source in the first instance, so association analysis at each data source is also important and useful. However, the forwarded rules from different data sources may be too many for the centralized company headquarter to use. This paper presents a weighting model for synthesizing high-frequency association rules from different data sources. There are two reasons to focus on high-frequency rules. First, a centralized company headquarter is interested in high-frequency rules because they are supported by most of its branches for corporate profitability. Second, high-frequency rules have larger chances to become valid rules in the union of all data sources. In order to extract high-frequency rules efficiently, a procedure of rule selection is also constructed to enhance the weighting model by coping with low-frequency rules. Experimental results show that our proposed weighting model is efficient and effective.
Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality

Synchronization of brain activity fluctuations is believed to represent communication between spatially distant neural processes. These interareal functional interactions develop in the background of a complex network of axonal connections linking cortical and subcortical neurons, termed the human "structural connectome. " Theoretical considerations and experimental evidence support the view that the human brain can be modeled as a system operating at a critical point between ordered (subcritical) and disordered (supercritical) phases. Here, we explore the hypothesis that pathologies resulting from brain injury of different etiologies are related to this model of a critical brain. For this purpose, we investigate how damage to the integrity of the structural connectome impacts on the signatures of critical dynamics. Adopting a hybrid modeling approach combining an empirical weighted network of human structural connections with a conceptual model of critical dynamics, we show that lesions located at highly transited connections progressively displace the model toward the subcritical regime. The topological properties of the nodes and links are of less importance when considered independently of their weight in the network. We observe that damage to midline hubs such as the middle and posterior cingulate cortex is most crucial for the disruption of criticality in the model. However, a similar effect can be achieved by targeting less transited nodes and links whose connection weights add up to an equivalent amount. This implies that brain pathology does not necessarily arise due to insult targeted at well-connected areas and that intersubject variability could obscure lesions located at nonhub regions. Finally, we discuss the predictions of our model in the context of clinical studies of traumatic brain injury and neurodegenerative disorders.
Optical-Resolution Photoacoustic Microscopy for In Vivo Volumetric Microvascular Imaging in Intact Tissues

Photoacoustic tomography (PAT), a blooming biomedical imaging technique [1], combines optical absorption contrast and ultrasonic detection. It has broken through the imaging depth barrier of high-resolution pure optical imaging methods by using the diffusive photons and conserves the ultrasonic resolution. In addition, PAT also images targets within the ballistic and quasi-ballistic regime with micron or submicron optical resolution, which is achieved by the recently developed optical-resolution photoacoustic microscopy (OR–PAM) [2].
Atrophic Vaginitis in Breast Cancer Survivors: A Difficult Survivorship Issue

Management of breast cancer includes systematic therapies including chemotherapy and endocrine therapy can lead to a variety of symptoms that can impair the quality of life of many breast cancer survivors. Atrophic vaginitis, caused by decreased levels of circulating estrogen to urinary and vaginal receptors, is commonly experienced by this group. Chemotherapy induced ovarian failure and endocrine therapies including aromatase inhibitors and selective estrogen receptor modulators can trigger the onset of atrophic vaginitis or exacerbate existing symptoms. Symptoms of atrophic vaginitis include vaginal dryness, dyspareunia, and irritation of genital skin, pruritus, burning, vaginal discharge, and soreness. The diagnosis of atrophic vaginitis is confirmed through patient-reported symptoms and gynecological examination of external structures, introitus, and vaginal mucosa. Lifestyle modifications can be helpful but are usually insufficient to significantly improve symptoms. Non-hormonal vaginal therapies may provide additional relief by increasing vaginal moisture and fluid. Systemic estrogen therapy is contraindicated in breast cancer survivors. Continued investigations of various treatments for atrophic vaginitis are necessary. Local estrogen-based therapies, DHEA, testosterone, and pH-balanced gels continue to be evaluated in ongoing studies. Definitive results are needed pertaining to the safety of topical estrogens in breast cancer survivors.
Approximate minimum SER precoding for spatial multiplexing over Ricean channels

The approximate minimum average symbol error rate (SER) precoder is designed for spatial multiplexing (SM) system in Ricean channels. Based on long-term channel state information (CSI), a closed-form solution that combines eigen-beamforming (E-BF) and power allocation is presented for correlated Ricean channel. Moreover, a simple precoder only based on K-factor and line-of-sight (LOS) departure angle is derived for independent Ricean channel, which needs less feedback overhead and lower computational complexity. The simulation results confirm the effectiveness of these precoders.
Contamination sources, biofilm-forming ability and biocide resistance of Staphylococcus aureus in tilapia-processing facilities

The major contamination sources, biofilm-forming ability and biocide resistance of Staphylococcus aureus in tilapia-processing plants were evaluated. Twenty-five processing control points were analysed twice in two factories, including whole tilapias, frozen fillets, water and food-contact surfaces. No final product was contaminated with S. aureus. However, high concentrations of S. aureus carrying enterotoxin (se) genes were found in several processing points of both factories due to the application of inadequate hygienic and handling procedures, which generate a high risk of cross-contamination of the tilapia fillets with staphylococcal enterotoxins. Nine S. aureus strains were characterized by RAPD-PCR using primers AP-7, ERIC-2 and S. A wide diversity of se gene profiles was detected, most strains being multi-se-carriers. All S. aureus strains showed high biofilm-forming ability on stainless steel and polystyrene. Biofilm-forming ability was correlated with the presence of fliC H7 and the type of origin surface (metallic or plastic). A marked resistance of S. aureus to peracetic acid and sodium hypochlorite was also observed, required doses being higher than those recommended by manufacturers to be eradicated. Case-by-case approaches are thus recommended to determine the sources and degree of contamination present in each factory, which would allow applying precise responses that avoid, or at least reduce, the presence of bacterial pathogens and the emergence of antimicrobial resistance.
Regulation of connective tissue growth factor expression by prostaglandin E2.

Transforming growth factor-β (TGF-β) stimulates α1(I) collagen mRNA synthesis in human lung fibroblasts through a mechanism that is partially sensitive to cycloheximide and that may involve synthesis of connective tissue growth factor (CTGF). Northern blot analyses indicate that TGF-β stimulates time- and dose-dependent increases in CTGF mRNA. In TGF-β-stimulated fibroblasts, maximal levels of CTGF mRNA (3.7-fold above baseline) occur at 6 h. The TGF-β-stimulated increase in CTGF mRNA was not blocked by cycloheximide. Nuclear run-on analysis indicates that TGF-β increases the CTGF transcription rate. The TGF-β-stimulated increases in CTGF transcription and steady-state levels of CTGF mRNA are attenuated in prostaglandin E2(PGE2)-treated fibroblasts. PGE2 fails to attenuate luciferase activity induced by TGF-β in fibroblasts transfected with the TGF-β-responsive luciferase reporter construct p3TP-LUX. In amino acid-deprived fibroblasts, PGE2and insulin regulate α1(I) collagen mRNA levels without affecting CTGF mRNA levels. The data suggest that the regulation of α1(I) collagen mRNA levels by TGF-β and PGE2 may function through both CTGF-dependent and CTGF-independent mechanisms.