Miracle-dz/UniFAR-FTUs huggingface dataset:
H ∞ predictive control of networked control systems

This article is concerned with the problem of H ∞ predictive control of networked control system with random network delay. A new control scheme termed networked predictive control is proposed. This scheme mainly consists of the control prediction generator and network delay compensator. While designing the predictor, the control input to the actuator may be different due to networked induced time-delay and data dropout, and two cases are considered depending on the way that the observer obtains the plant control input u t . The necessary and sufficient conditions are given for the closed-loop networked predictive control system to be stochastically stable for different u t and random network delays in controller to actuator channel (CAC) and sensor to controller channel (SCC). A simulation study shows the effectiveness of the proposed scheme.
International Labor Union Policy and Growth with Creative Destruction

A multi-economy Schumpeterian growth model is constructed. Economies are interdependent through technology transfer. Households can stay as workers or become researchers at some cost. Workers are employed in production and researchers in R&D. Workers are unionized and union power depends on the government's protection. The main findings are as follows. If international technological dependence increases, then workers' wages, the growth rate, and the level of welfare fall. The international coordination of labor union policy raises workers' wages and promotes growth and welfare.
Impact of water supply and sanitation assistance on human welfare in rural Pakistan

The paper examines impact of two water supply and sanitation projects in rural Pakistan in improving access to water supply and sanitation and on health, education, and labour supply based on a household survey of 1300 project and 1300 comparison households. The impact was estimated using treatment effects based on a control-function approach. Overall findings show that the projects improved households’ access to water supply, reduced drudgery associated with fetching water and improved attendance of high-school-age girls in schools. However, the projects had no significant impact on the incidence and intensity of diarrhoea and on increasing labour force participation and hours available for work.
AVPR2 variants and mutations in nephrogenic diabetes insipidus: Review and missense mutation significance

Almost 90% of nephrogenic diabetes insipidus (NDI) is due to mutations in the arginine‐vasopressin receptor 2 gene (AVPR2). We retrospectively examined all the published mutations/variants in AVPR2. We planned to perform a comprehensive review of all the AVPR2 mutations/variants and to test whether any amino acid change causing a missense mutation is significantly more or less common than others. We performed a Medline search and collected detailed information regarding all AVPR2 mutations and variants. We performed a frequency comparison between mutated and wild‐type amino acids and codons. We predicted the mutation effect or reported it based on published in vitro studies. We also reported the ethnicity of each mutation/variant carrier. In summary, we identified 211 AVPR2 mutations which cause NDI in 326 families and 21 variants which do not cause NDI in 71 NDI families. We described 15 different types of mutations including missense, frameshift, inframe deletion, deletion, insertion, nonsense, duplication, splicing and combined mutations. The missense mutations represent the 55.83% of all the NDI published families. Arginine and tyrosine are significantly (P = 4.07E−08 and P = 3.27E−04, respectively) the AVPR2 most commonly mutated amino acids. Alanine and glutamate are significantly (P = 0.009 and P = 0.019, respectively) the least mutated AVPR2 amino acids. The spectrum of mutations varies from rare gene variants or polymorphisms not causing NDI to rare mutations causing NDI, among which arginine and tyrosine are the most common missense. The AVPR2 mutations are spread world‐wide. Our study may serve as an updated review, comprehensive of all AVPR2 variants and specific gene locations. J. Cell. Physiol. 217: 605–617, 2008. © 2008 Wiley‐Liss, Inc.
High Mobility Group Box-1 (HMGB1) Participates in the Pathogenesis of Alcoholic Liver Disease (ALD)*

Background: HMGB1 is a proinflammatory cytokine produced in response to tissue injury, but its role in ALD is unknown. Results: HMGB1 increases; translocates; and undergoes acetylation, phosphorylation, and oxidation in ALD. HMGB1 ablation in hepatocytes protects against steatosis and injury in ALD. Conclusion: HMGB1 plays a key role in ALD. Significance: Dissecting how the increase in HMGB1 causes hepatotoxicity is key for understanding the pathogenesis of ALD. Growing clinical and experimental evidence suggests that sterile inflammation contributes to alcoholic liver disease (ALD). High mobility group box-1 (HMGB1) is highly induced during liver injury; however, a link between this alarmin and ALD has not been established. Thus, the aim of this work was to determine whether HMGB1 contributes to the pathogenesis of ALD. Liver biopsies from patients with ALD showed a robust increase in HMGB1 expression and translocation, which correlated with disease stage, compared with healthy explants. Similar findings were observed in chronic ethanol-fed wild-type (WT) mice. Using primary cell culture, we validated the ability of hepatocytes from ethanol-fed mice to secrete a large amount of HMGB1. Secretion was time- and dose-dependent and responsive to prooxidants and antioxidants. Selective ablation of Hmgb1 in hepatocytes protected mice from alcohol-induced liver injury due to increased carnitine palmitoyltransferase-1, phosphorylated 5′AMP-activated protein kinase-α, and phosphorylated peroxisome proliferator-activated receptor-α expression along with elevated LDL plus VLDL export. Native and post-translationally modified HMGB1 were detected in humans and mice with ALD. In liver and serum from control mice and in serum from healthy volunteers, the lysine residues within the peptides containing nuclear localization signals (NLSs) 1 and 2 were non-acetylated, and all cysteine residues were reduced. However, in livers from ethanol-fed mice, in addition to all thiol/non-acetylated isoforms of HMGB1, we observed acetylated NLS1 and NLS2, a unique phosphorylation site in serine 35, and an increase in oxidation of HMGB1 to the disulfide isoform. In serum from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, disulfide-bonded non-acetylated HMGB1, and HMGB1 phosphorylated in serine 35. Hepatocytes appeared to be a major source of these HMGB1 isoforms. Thus, hepatocyte HMGB1 participates in the pathogenesis of ALD and undergoes post-translational modifications (PTMs) that could condition its toxic effects.
The Molecular Chaperone TRiC/CCT Binds to the Trp-Asp 40 (WD40) Repeat Protein WDR68 and Promotes Its Folding, Protein Kinase DYRK1A Binding, and Nuclear Accumulation*

Background: Trp-Asp (WD) repeat protein 68 (WDR68) is a binding partner of dual specificity tyrosine phosphorylation-regulated protein kinase (DYRK1A), a kinase partly responsible for aspects of Down syndrome. Results: The molecular chaperone T-complex protein 1 (TCP1) ring complex/chaperonin-containing TCP1 (TRiC/CCT) binds to WDR68 and modulates its structure, DYRK1A-binding, and cellular localization. Conclusion: TRiC/CCT is essential for correct folding and function of WDR68. Significance: TRiC/CCT may have a general role in forming the functional WD40 repeat seven-bladed β-propeller structure. Trp-Asp (WD) repeat protein 68 (WDR68) is an evolutionarily conserved WD40 repeat protein that binds to several proteins, including dual specificity tyrosine phosphorylation-regulated protein kinase (DYRK1A), MAPK/ERK kinase kinase 1 (MEKK1), and Cullin4-damage-specific DNA-binding protein 1 (CUL4-DDB1). WDR68 affects multiple and diverse physiological functions, such as controlling anthocyanin synthesis in plants, tissue growth in insects, and craniofacial development in vertebrates. However, the biochemical basis and the regulatory mechanism of WDR68 activity remain largely unknown. To better understand the cellular function of WDR68, here we have isolated and identified cellular WDR68 binding partners using a phosphoproteomic approach. More than 200 cellular proteins with wide varieties of biochemical functions were identified as WDR68-binding protein candidates. Eight T-complex protein 1 (TCP1) subunits comprising the molecular chaperone TCP1 ring complex/chaperonin-containing TCP1 (TRiC/CCT) were identified as major WDR68-binding proteins, and phosphorylation sites in both WDR68 and TRiC/CCT were identified. Co-immunoprecipitation experiments confirmed the binding between TRiC/CCT and WDR68. Computer-aided structural analysis suggested that WDR68 forms a seven-bladed β-propeller ring. Experiments with a series of deletion mutants in combination with the structural modeling showed that three of the seven β-propeller blades of WDR68 are essential and sufficient for TRiC/CCT binding. Knockdown of cellular TRiC/CCT by siRNA caused an abnormal WDR68 structure and led to reduction of its DYRK1A-binding activity. Concomitantly, nuclear accumulation of WDR68 was suppressed by the knockdown of TRiC/CCT, and WDR68 formed cellular aggregates when overexpressed in the TRiC/CCT-deficient cells. Altogether, our results demonstrate that the molecular chaperone TRiC/CCT is essential for correct protein folding, DYRK1A binding, and nuclear accumulation of WDR68.
Linkage of a mild late-onset phenotype of Fuchs corneal dystrophy to a novel locus at 5q33.1-q35.2.

PURPOSE To identify the disease locus associated with autosomal dominant Fuchs corneal dystrophy (FCD) in a large family and to compare the progression of severity in families mapped to the FCD1 and FCD2 loci. METHODS Seventeen individuals in a large family were examined by slit lamp biomicroscopy. Blood samples were collected, DNA was extracted, and a genome-wide scan was performed with a microarray SNP chip. After initial generation of a genome-wide, two-point LOD score, linkage was confirmed and the critical interval was established by genotyping of short tandem repeat (STR) microsatellite markers. RESULTS A genome-wide linkage scan localized the disease interval to the long arm of chromosome 5, with a maximum two-point parametric LOD score of 3.41. Haplotype analyses refined the critical interval to 5q33.1-q35.2, spanning a 27-Mb (29-cM) region. Clinical examination of affected individuals in this family revealed an early onset of FCD at approximately age 40, after which progression of the disease was significantly attenuated compared to the FCD1- and FCD2-linked families. CONCLUSIONS Late-onset FCD is linked to a novel locus on 5q33.1-q35.2 and is associated with a milder severity in age at onset and rate of progression than the FCD1 and FCD2 loci. Correlation of individual genotypes with unique rates of disease progression will provide important tools for disease management, as well as for identifying the underlying genetic lesion, offer insight into the pathomechanism of FCD.
Effectiveness of the training program for workers at construction sites of the high-speed railway line between Torino and Novara: impact on injury rates.

BACKGROUND There are very few published studies evaluating the impact of safety and health training on injury outcomes in the construction industry. The aim of this study was to assess the impact of the training program on injury rates at a major railway construction project. METHODS The population consisted of 2,795 workers involved in a safety training program at the construction sites of the high-speed railway line Torino-Novara. Two types of analyses were carried out in order to assess the effectiveness of the training program in reducing the number of injuries: (i) a pre-post analysis, which took into account the fact that workers were enrolled at different times and the training intervention did not occur at the same time for all subjects; (ii) an interrupted time-series model, which corrected for the time trend and considered the autocorrelation between individual observations. RESULTS Twenty-nine percent of workers who spent at least 1 day at the construction sites attended at least one training module. Pre-post analysis: At the end of the training program, the incidence of occupational injuries had fallen by 16% after the basic training module and by 25% following the specific modules. Time-series model: Training led to a 6% reduction in injury rates, which was not statistically significant. CONCLUSIONS The training program that was implemented had a moderately positive impact on the health of workers. Further studies are being conducted to obtain a more complete assessment of the actual effectiveness of the program in reducing the incidence of injuries.
Evaluation of bile reflux in nuclear imaging using optical flow with fluid mechanics

The Cholescintigraphy scan, also known as Diisopropyl Iminodiacetic Acid(DISIDA) is a nuclear imaging procedure to evaluate the function of the gallbladder. DISIDA images are used to estimate the bile flow situation. Because bile is flowing fluid, so we based on the fluid mechanics to model that the stomach connects with the gall bladder in several typical of bile reflux status or no bile reflux, then simulate the bile flow situation by our assumption model. In dynamic image analysis, optical flow techniques are widely used to track object borders as well as evaluate the object motion field. After that we apply optical flow to the sequences of 2-D DISIDA images to quantify bile flow is presented. The method utilizes couples of consecutive frames to compute, for each pixel, the 2-D apparent velocity vector which characterizes the interframe motion. According to this vector with every couples of frames, and therefore we can initially realize the afflux of bile reflux. Finally, we compare the optical flow result with the hydromechanics model, and hope to find the standard to estimate the degree of accuracy and reliability.
Rise and fall of pandemic Vibrio parahaemolyticus serotype O3:K6 in southern Chile.

Seafood consumption-related diarrhoea increased drastically in Chile when the pandemic strain of Vibrio parahaemolyticus serotype O3:K6 reached Region de Los Lagos, where most of Chile's seafood is produced. Outbreaks peaked in 2005 with 3725 clinical cases in this region and gradually decreased to fewer than 10 cases in 2010 and 2011. We show here that the pandemic strain concurrently vanished from mussels; we also report further environmental data. Integration of the 2010/2011 data with those obtained since 2004 suggests that after its arrival in southern Chile, the pandemic strain grew in mussels, likely facilitated by a minor rise in surface seawater temperature and by warming of the mussels in the intertidal region due to frequent sunny days. However, since these environmental parameters probably equally affected the pandemic strain and more than 30 V. parahaemolyticus DNA restriction clusters that inhabit local shellfish, a selective effect of bacteriophages is proposed. Lytic bacteriophage VP93 may have favoured the growth of the pandemic strain versus similar phage-sensitive strains, as shown here in a particular case. However, the pandemic strain's decline may have been promoted by temperate phage VP58.5, which kills the pandemic strain and increases the UV sensitivity of lysogenized phage-resistant cells.
Functional Implications of the Human T-Lymphotropic Virus Type 1 Transmembrane Glycoprotein Helical Hairpin Structure

ABSTRACT Retrovirus entry into cells follows receptor binding by the surface-exposed envelope glycoprotein (Env) subunit (SU), which triggers the membrane fusion activity of the transmembrane (TM) protein. TM protein fragments expressed in the absence of SU adopt helical hairpin structures comprising a central coiled coil, a region of chain reversal containing a disulfide-bonded loop, and a C-terminal segment that packs onto the exterior of the coiled coil in an antiparallel manner. Here we used in vitro mutagenesis to test the functional role of structural elements observed in a model helical hairpin, gp21 of human T-lymphotropic virus type 1. Membrane fusion activity requires the stabilization of the N and C termini of the central coiled coil by a hydrophobic N cap and a small hydrophobic core, respectively. A conserved Gly-Gly hinge motif preceding the disulfide-bonded loop, a salt bridge that stabilizes the chain reversal region, and interactions between the C-terminal segment and the coiled coil are also critical for fusion activity. Our data support a model whereby the chain reversal region transmits a conformational signal from receptor-bound SU to induce the fusion-activated helical hairpin conformation of the TM protein.
Barriers to commercialisation from the 'four knowledge bases' perspective: a study of innovation in the software development sector

Barriers in commercialising software innovations are studied from the perspective of four knowledge bases in product innovation: technology knowledge base, end-user knowledge base, brand knowledge base and business-logic knowledge base. Hypotheses are formulated based on case studies of publicly-funded innovation development projects in Finnish Information and Communication Technology (ICT) companies. The 'perfect technology syndrome' and diversification arising from any product innovation are put forward as important barriers of commercialisation.
The Benefits of Bagging for Forecast Models of Realized Volatility

This article shows that bagging can improve the forecast accuracy of time series models for realized volatility. We consider 23 stocks from the Dow Jones Industrial Average over the sample period 1995 to 2005 and employ two different forecast models, a log-linear specification in the spirit of the heterogeneous autoregressive model and a nonlinear specification with logistic transitions. Both forecast model types benefit from bagging, in particular in the 1990s part of our sample. The log-linear specification shows larger improvements than the nonlinear model. Bagging the log-linear model yields the highest forecast accuracy on our sample.
Structure-Function Relationships in the Neuropeptide S Receptor

Neuropeptide S (NPS) and its receptor (NPSR) are thought to have a role in asthma pathogenesis; a number of single nucleotide polymorphisms within NPSR have been shown to be associated with an increased prevalance of asthma. One such single nucleotide polymorphism leads to the missense mutation N107I, which results in an increase in the potency of NPS for NPSR. To gain insight into structure-function relationships within NPS and NPSR, we first carried out a limited structural characterization of NPS and subjected the peptide to extensive mutagenesis studies. Our results show that the NH2-terminal third of NPS, in particular residues Phe-2, Arg-3, Asn-4, and Val-6, are necessary and sufficient for activation of NPSR. Furthermore, part of a nascent helix within the peptide, spanning residues 5 through 13, acts as a regulatory region that inhibits receptor activation. Notably, this inhibition is absent in the asthma-linked N107I variant of NPSR, suggesting that residue 107 interacts with the aforementioned regulatory region of NPS. Whereas this interaction may be at the root of the increase in potency associated with the N107I variant, we show here that the mutation also causes an increase in cell-surface expression of the mutant receptor, leading to a concomitant increase in the maximal efficacy (Emax) of NPS. Our results identify the key residues of NPS involved in NPSR activation and suggest a molecular basis for the functional effects of the N107I mutation and for its putative pathophysiological link with asthma.
Thyrotropin Modulates Interferon-γ-Mediated Intercellular Adhesion Molecule-1 Gene Expression by Inhibiting Janus Kinase-1 and Signal Transducer and Activator of Transcription-1 Activation in Thyroid Cells.

TSH is known as an important hormone that plays the major role not only in the maintenance of normal physiology but also in the regulation of immunomodulatory gene expression in thyrocytes. The adhesion molecule intercellular adhesion molecule-1 (ICAM-1) was identified as one of the proteins that are abnormally expressed in the thyroid gland during autoimmune thyroid diseases. In this study we found that TSH inhibits interferon-gamma (IFNgamma)-mediated expression of the ICAM-1 gene, and we investigated the involved mechanisms in rat FRTL-5 thyroid cells. After exposure to IFNgamma, ICAM-1 expression is positively regulated at the level of transcription. This effect occurs via the IFNgamma-activated site (GAS) element in the ICAM-1 promoter as a consequence of the activation of STAT1 (signal transducer and activator of transcription-1), but not of STAT3. On the other hand, after exposure to TSH plus IFNgamma, ICAM-1 transcription is negatively modulated. We found that this inhibitory effect of TSH also occurs via the GAS element. Electrophoretic mobility shift assays confirmed that the IFNgamma-induced DNA-binding activities of STAT1 were reduced by TSH. Furthermore, our results showed that the inhibitory effect of TSH on IFNgamma signaling is caused by inhibition of tyrosine phosphorylation on STAT1, Janus kinase-1 (Jak1), and IFNgamma receptor a, but not Jak2. In conclusion, we have identified a novel mechanism in which TSH modulates the IFNgamma-mediated Jak/STAT signaling pathway through the inhibition of Jak1 and STAT1.
Private Equity, Buy-Outs and Insolvency Risk

Private Equity restructuring of companies using debt finance has been criticised for increasing financial distress and bankruptcy in the corporate sector and this was especially so in the aftermath of the financial crisis. We build a unique data set comprising the population of over eight million company year observations and 153,000 instances of insolvency covering the period 1995-2010 and encompassing the recessionary cycle. We examine the whole spectrum of buyout ownership types (pre and post buyout) in comparison with the private and public corporate population and over time. We provide direct evidence relating to whether buyouts and buy-ins, private equity backed or not, are more or less likely to fail in terms of entering formal insolvency proceedings than other firms and how this varies over the economic cycle. Controlling for size, age, sector and macro-economic conditions (base hazard) we find that private-equity backed buyouts are no more prone to insolvency than the non-buyout population and pre-buyout credit risk. Conditioning on company performance and operational characteristics we show that PE-backed companies do not carry more insolvency risk than other (distressed) companies and other buyout types. We find that leverage does not distinguish buyouts that fail from those that survive.
Note: Modification of the Gay-Berne potential for improved accuracy and speed.

A modification of the Gay-Berne (GB) potential is proposed which is about 10% to 20% more speed efficient and statistically more accurate in reproducing the energy of interaction of two linear Lennard-Jones tetratomics when averaged over all orientations. For the special cases of end-to-end and side-by-side configurations, the new potential is equivalent to the GB one. A simple generalization to dissimilar particles of D∞h symmetry is presented but does not retain the superior agreement with respect to its GB counterpart, except at close range.