Miracle-dz/UniFAR-FTUs huggingface dataset:
An RNA Helicase, DDX1, Interacting with Poly(A) RNA and Heterogeneous Nuclear Ribonucleoprotein K*

Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is a multifunctional protein known to be involved in the regulation of transcription, translation, nuclear transport, and signal transduction. To systematically obtain insight into mechanisms of hnRNP K activities, we set out to identify protein factors that interact with hnRNP K by using glutathione S-transferase-hnRNP K affinity chromatography followed by liquid chromatography/mass spectrometry/mass spectrometry analysis. Several partner proteins in the K562 cell lysates were identified through this method. One of them is a DEAD box-containing putative RNA helicase, DDX1. In vitro binding and co-immunoprecipitation studies confirmed the protein-protein interaction between hnRNP K with DDX1, and the region spanning amino acids 1–276 of hnRNP K is apparently responsible for its physical interaction with DDX1. Interestingly, their interaction was disrupted by the addition of poly(C), poly(A), and poly(U) RNA substrates. We found that DDX1 was a homopolymeric poly(A) RNA-binding protein. On the other hand, the ATPase activity of the purified recombinant DDX1 protein was stimulated by these homopolymeric RNAs and yeast total RNA but not by DNA. Moreover, the immunoprecipitated DDX1 complex but not purified DDX1 can unwind double-stranded RNA having single-stranded poly(A) overhangs.
Starvation-induced Changes of Somatostatin, Glucagon, and Insulin Secretion from the Isolated Perfused Rat Pancreas

The effect of 16- and 48-h fasting on pancreatic somatostatin, insulin, and glucagon secretion was studied, using the isolated perfused rat pancreas. In the presence of 4.4 mM glucose, basal somatostatin and insulin concentrations in the perfusate were significantly lower in 48-h fasted rats than in fed animals, whereas basal glucagon secretion was significantly elevated in fasted rats. The infusion of 19 mM arginine significantly augmented secretion of somatostatin and glucagon and attenuated insulin secretion in 48-h fasted rats. It is concluded that fasting causes a decrease in basal pancreatic somatostatin secretion in vitro, although the response to arginine is rather exaggerated. Insulin and glucagon secretion also changed during the fasting. These results suggest that not only insulin and glucagon, but also somatostatin contribute to nutrient homeostasis.
Sex-specific, independent associations of insulin resistance with erythrocyte sedimentation rate in apparently healthy subjects

Summary Insulin resistance and erythrocyte sedimentation rate (ESR, a non-specific marker of inflammation) are known risk factors for cardiovascular disease. Although obesity is associated with increased ESR, it is unclear whether insulin resistance is associated with ESR in humans. The relationship between insulin resistance and ESR was studied in a cross-sectional, health-area based study of 140 (89 men and 51 women) apparently healthy Caucasians subjects. ESR, additional inflammatory markers [soluble tumor necrosis alpha receptors 1 and 2 (sTNFR1 and sTNFR2); C-reactive protein (CRP)], and insulin sensitivity ( S I, frequently sampled intravenous glucose tolerance test with minimal model analysis) were assessed in all subjects. An interaction with sex was documented in the relationship between ESR and both insulin resistance and obesity (p < 0.05), as log ESR correlated with log S I in men (r= –0.29, p = 0.009), but not in women (r= –0.14, p = 0.33), and correlated with body mass index (BMI) in women (r=0.49, p= < 0.0001), but not in men (r=0.15, p = 0.16). On multivariate analyses, these associations proved to be independent of known covariates, such as age, hematocrit, smoking and additional inflammatory markers in both men and women. In a replication study, variables independently associated with ESR were also insulin resistance (homeostasis model assessment) in men and obesity markers (either BMI or fat mass) in women. In conclusion, ESR is independently associated with either insulin resistance or obesity in a sex-specific manner. These findings contribute to explain the known relationship of this inflammatory marker with cardiovascular disease.
Microstructural analyses of the posterior cerebellar lobules in relapsing-onset multiple sclerosis and their implication in cognitive impairment

Background The posterior cerebellar lobules seem to be the anatomical substrate of cognitive cerebellar processes, but their microstructural alterations in multiple sclerosis (MS) remain unclear. Objectives To correlate diffusion metrics in lobules VI to VIIIb in persons with clinically isolated syndrome (PwCIS) and in cognitively impaired persons with MS (CIPwMS) with their cognitive performances. Methods Sixty-nine patients (37 PwCIS, 32 CIPwMS) and 36 matched healthy subjects (HS) underwent 3T magnetic resonance imaging, including 3D T1-weighted and diffusion tensor imaging (DTI). Fractional anisotropy (FA) and mean diffusivity (MD) were calculated within each lobule and in the cerebellar peduncles. We investigated the correlations between cognitive outcomes and the diffusion parameters of cerebellar sub-structures and performed multiple linear regression analysis to predict cognitive disability. Results FA was generally lower and MD was higher in the cerebellum and specifically in the vermis Crus II, lobules VIIb and VIIIb in CIPwMS compared with PwCIS and HS. In hierarchical regression analyses, 31% of the working memory z score variance was explained by FA in the left lobule VI and in the left superior peduncle. Working memory was also associated with MD in the vermis Crus II. FA in the left lobule VI and right VIIIa predicted part of the information processing speed (IPS) z scores. Conclusion DTI indicators of cerebellar microstructural damage were associated with cognitive deficits in MS. Our results suggested that cerebellar lobular alterations have an impact on attention, working memory and IPS.
Severity of ulcerative colitis is associated with a polymorphism at diamine oxidase gene but not at histamine N-methyltransferase gene.

AIM To analyse the role of two common polymorphisms in genes coding for histamine metabolising enzymes as it relates to the risk to develop ulcerative colitis (UC) and the clinical course of these patients. METHODS A cohort of 229 unrelated patients with UC recruited from a single centre and 261 healthy volunteers were analysed for the presence of Thr105Ile and His645Asp amino acid substitutions at histamine N-methyltransferase (HNMT) and diamine oxidase (ABP1) enzymes, respectively, by amplification-restriction procedures. All patients were phenotyped and followed up for at least 2 years (mean time 11 years). RESULTS There were no significant differences in the distribution of ABP1 alleles between ulcerative colitis patients and healthy individuals [OR (95% CI) for variant alleles=1.22 (0.91-1.61)]. However, mutated ABP1 alleles were present with higher frequency among the 58 patients that required immunosuppressive drugs [OR (95 % CI) for carriers of mutated alleles 2.41 (1.21-4.83; P=0.006)], with a significant gene-dose effect (P=0.0038). In agreement with the predominant role of ABP1 versus HNMT on local histamine metabolism in human bowel, the frequencies for carriers of HNMT genotypes or mutated alleles were similar among patients, regardless clinical evolution, and control individuals. CONCLUSION The His645Asp polymorphism of the histamine metabolising enzyme ABP1 is related to severity of ulcerative colitis.
L’institutionnalisation croissante du discours sur les «meilleures pratiques» de gouvernance en France:un état des lieux

(VF)Les « meilleures pratiques » de gouvernance font l’objet de plusieurs rapports officiels (rapports Vienot I, Vienot II et Bouton). Au-dela du discours tenu par les instances patronales qui en font la promotion, ces pratiques rentrent-elles dans les mœurs ? C’est-a-dire, les entreprises s’approprient-elles le discours des codes de gouvernance ? Nous tentons dans le present article d’apporter un debut de reponse a cette question pour le cas de la France. Pour ce faire, nous proposons de decrire la dynamique d’adoption declaree des «meilleures pratiques» de gouvernance par les entreprises francaises cotees. A defaut de verifier les pratiques effectives des entreprises, une telle etude des declarations permet d’apprecier la legitimite du discours sur la gouvernance, au-dela du cercle de ses premiers promoteurs. L’analyse des declarations des entreprises francaises cotees montre que le nombre d’entreprises declarant se conformer aux standards promus par les codes de gouvernance augmente de facon constante et couvre desormais la grande majorite des entreprises cotees. Le discours sur les «meilleures pratiques» de gouvernance a aujourd’hui atteint une legitimite telle que, meme des entreprises au capital relativement verrouille qui subissent peu la pression des investisseurs institutionnels anglo-saxons se sentent desormais obligees de se declarer conformes aux standards des codes de bonne conduite. Ceci semble indiquer un certain mimetisme dans l’adoption du discours standard sur la gouvernance qui, pourtant, n’est pas le seul possible, mais a initialement ete developpe en reference a un type d’entreprise bien particulier. (VA) Corporate governance “best practices” have been codified in several official reports (Vienot I, Vienot II and Bouton). But do they receive any attention from actors beyond the circle of their initial promoters? Do firms actually adopt the discourse? The present paper tries to answer this question for the case of France through an analysis of the annual declarations of listed companies concerning their governance practices. This analysis reveals the fact that the dominant discourse on corporate governance “best practice” has attained a degree of legitimacy such that even companies with a rather concentrated control structure feel compelled to state their conformity with the governance standards. This likely indicates a certain extent of mimetic behavior with respect to financial communication.
Vibration Control of a Flexible Beam With Output Constraint

In this paper, we present the vibration control design for a Euler-Bernoulli beam with the boundary output constraint. To prevent the constraint violation, a novel barrier Lyapunov function is employed for the control design and stability analysis. This paper represents an important step in extending the barrier Lyapunov function theory to distributed parameter systems. Model-based barrier control is proposed to suppress the vibration of a flexible Euler-Bernoulli beam under the boundary output constraint. Then, adaptive control is designed to handle the system parametric uncertainties. The vibration suppression is well achieved without violation of the constraint. Numerical simulations are provided to illustrate the performance of the control system.
Automatic characterization of sleep need dissipation dynamics using a single EEG signal

In the two-process model of sleep regulation, slow-wave activity (SWA, i.e. the EEG power in the 0.5-4 Hz frequency band) is considered a direct indicator of sleep need. SWA builds up during non-rapid eye movement (NREM) sleep, declines before the onset of rapid-eye-movement (REM) sleep, remains low during REM and the level of increase in successive NREM episodes gets progressively lower. Sleep need dissipates with a speed that is proportional to SWA and can be characterized in terms of the initial sleep need, and the decay rate. The goal in this paper is to automatically characterize sleep need from a single EEG signal acquired at a frontal location. To achieve this, a highly specific and reasonably sensitive NREM detection algorithm is proposed that leverages the concept of a single-class Kernel-based classifier. Using automatic NREM detection, we propose a method to estimate the decay rate and the initial sleep need. This method was tested on experimental data from 8 subjects who recorded EEG during three nights at home. We found that on average the estimates of the decay rate and the initial sleep need have higher values when automatic NREM detection was used as compared to manual NREM annotation. However, the average variability of these estimates across multiple nights of the same subject was lower when the automatic NREM detection classifier was used. While this method slightly over estimates the sleep need parameters, the reduced variability across subjects makes it more effective for within subject statistical comparisons of a given sleep intervention.
Late Reversal of Cerebral Perfusion and Water Diffusion after Transient Focal Ischemia in Rats

Region-specific cerebral blood flow (CBF) and the apparent diffusion coefficient (ADC) of tissue water in the rat brain were quantified by high-field magnetic resonance imaging at 9.4 T in the rat suture occlusion model. Cerebral blood flow and ADC were compared during the short- (4.5 hours) and long-term (up to 6 days) reperfusion after 80 minutes of transient middle cerebral artery occlusion, and correlated with the histology analysis. On occlusion, average CBF fell from ∼100 to less than 50 mL 100 g−1 min−1 in the cortex, and to less than 20 mL 100 g−1 min−1 in the caudate putamen (CP). Corresponding ADC values decreased from (6.98 ± 0.82) × 10−4 to (5.49 ± 0.54) × 10−4 mm2/s in the cortex, and from (7.16 ± 0.58) × 10−4 to (4.86 ± 0.62) × 10−4 mm2/s in the CP. On average, CBF recovered to ∼50% of baseline in the first 24 hours of reperfusion. After 2 to 4 days, a strong hyperperfusion in the ipsilateral cortex and CP, up to ∼300 mL 100 g−1 min−1, was observed. The ADC ratio in the ipsilateral and contralateral CP was also inverted in the late reperfusion period. Histology revealed more severe tissue damage at the late stage of reperfusion than at 4.5 hours. Significant reversal of CBF and ADC during the late reperfusion period may reflect the impairment of autoregulation in the ischemic regions. Vascular factors may play an important role in the infarct development after 80-minute focal ischemia.
Studies of lipoxygenases in the epithelium of cultured bovine cornea using an air interface model.

Epithelial lipoxygenases of bovine cornea were investigated in organ culture models. Subcellular fractions of the epithelium were incubated with(14)C-labelled arachidonate and the metabolites were analysed. Bovine corneal epithelial cells contain 15-lipoxygenase type 2 and 12-lipoxygenases of the leukocyte and the platelet types. The 15-lipoxygenase activity was prominent in the cytosolic fraction. Twelve- and 15-lipoxygenases occurred in the microsomal fraction, where the 15-lipoxygenase activity appeared to be favoured by low protein levels. The lipoxygenase activities strongly declined within 24 hr when the cornea was covered with cell culture medium, but were maintained with high activity in an air interface organ culture model for at least 72 hr. Cultured corneas were studied in pairs in the air interface model under influence of inflammatory stimuli. The epithelial 15- and 12-lipoxygenase activities were only slightly augmented by treatment with 12-O-tetradecanoyl-phorbol-13-acetate (10 microM, 8-72 hr), and remained unchanged after treatment with lipopolysaccharide (1-100 microgram ml(-1), 8-72 hr) or UV irradiation (301 nm, 0.17 J cm(-2); 8-24 hr). In some experiments, 5-lipoxygenase activity was detectable, as judged from liquid chromatography-mass spectrometry and chiral chromatography. Reverse transcription-polymerase chain reaction and Northern blot analysis were therefore used to identify mRNA of 5-lipoxygenase and related enzymes in bovine epithelium. 5-Lipoxygenase was detected as an amplicon of 695 bp, which had 91% nucleotide sequence identity with human 5-lipoxygenase and by Northern blot as a 3.0 kb mRNA. Leukotriene A(4)hydrolase was detected with the same techniques. The amino acid sequence of a 612 bp fragment was 90% identical with human leukotriene A(4)hydrolase and the size of the mRNA was 2.7 kb. The two enzymes were also detected in human corneal epithelium by reverse transcription-polymerase chain reaction.
Proposal of a Redundant Drive Wire Mechanism for producing motions with high acceleration and high precision

A new wire mechanism called Redundant Drive Wire Mechanism (RDWM) is proposed. The purpose of this paper is to build up the theory of a RDWM with fast motion and fine motion. First, the basic concepts of the proposed mechanism is presented. Second, the vector closure condition for the proposed mechanism is developed. Next, we present the basic equations, propose the basic structure of RDWM with the Internal DOF module, Double Actuation Modules and Precision Modules together with the properties of the mechanism. Finally, we conduct the simulation to show the validity of the RDWM.
Biosynthesis of Poly(3-Hydroxyalkanoic Acid) Copolymer from CO(inf2) in Pseudomonas acidophila through Introduction of the DNA Fragment Responsible for Chemolithoautotrophic Growth of Alcaligenes hydrogenophilus

Pseudomonas acidophila is a bacterial strain producing a poly(3-hydroxyalkanoic acid) (PHA) copolymer from low-molecular-weight organic compounds such as formate and acetate. The genes responsible for PHA production were cloned in cosmid pIK7 containing a 14.8-kb HindIII fragment of P. acidophila DNA. With the aim of developing a means of producing a PHA copolymer from CO(inf2), cosmid pIK7 was introduced into a polymer-negative mutant of the chemolithoautotrophic bacterium Alcaligenes eutrophus PHB(sup-)4. However, the recombinant strain produced a homopolymer of 3-hydroxybutyric acid (polyhydroxybutyric acid) from CO(inf2). Since it was thought that the composition of the accumulated polymer might depend not on the PHA biosynthetic genes but on the metabolism of the host strain, a recombinant plasmid, pFUS, containing the genes for chemolithoautotrophic growth of the hydrogen-oxidizing bacterium A. hydrogenophilus was introduced into P. acidophila by conjugation. The recombinant plasmid pFUS was stably maintained in P. acidophila in the absence of chemolithoautotrophic or antibiotic selection. This pFUS-harboring strain possessed the ability to grow under a gas mixture of H(inf2), O(inf2), and CO(inf2) in a mineral salts medium, and PHA copolymer accumulation was confirmed by nuclear magnetic resonance spectral analysis. A gas chromatogram obtained by gas chromatography-mass spectrometry showed the composition of the polymer to be 52.8% 3-hydroxybutyrate, 41.1% 3-hydroxyoctanoate, and 6.1% 3-hydroxydecanoate. This is the first report of the production of a PHA copolymer from CO(inf2) as sole carbon source.
Menin, a gene product responsible for multiple endocrine neoplasia type 1, interacts with the putative tumor metastasis suppressor nm23.

Although the gene responsible for multiple endocrine neoplasia type 1 (MEN1) has been identified, the function of its gene product, menin, is unknown. To examine the biological role of the MEN1 gene, we searched for associated proteins with a yeast two-hybrid system using the MEN1 cDNA fragment as bait. On screening a rat fetal brain embryonic day 17 library, in which a high level of MEN1 expression was detected, we identified a putative tumor metastasis suppressor nm23/nucleoside diphosphate (NDP) kinase as an associated protein. This finding was confirmed by in vitro interaction assays based on glutathione S-transferase pull down experiments. The association required almost the entire menin protein, and several missense MEN1 mutations reported in MEN1 patients caused a loss of the binding activity for nm23. This result suggests that this interaction may play important roles in the biological functions of the menin protein, including tumor suppressor activity.
Ribosomal Protein S6, a Target of Rapamycin, Is Involved in the Regulation of rRNA Genes by Possible Epigenetic Changes in Arabidopsis *

Background: Ribosomal protein S6 has been known to be a key downstream effector of the TOR signaling pathway. Results: We demonstrated that ribosomal protein interacts with a histone deacetylase and binds to rRNA gene promoter. Conclusion: The TOR signaling controls rRNA synthesis via interaction of RPS6 to rRNA genes. Significance: This study links the environmental signals via TOR kinase to control growth of an organism by regulating ribosome biogenesis. The target of rapamycin (TOR) kinase pathway regulates various biological processes, including translation, synthesis of ribosomal proteins, and transcription of rRNA. The ribosomal protein S6 (RPS6) is one of the well known downstream components of the TOR pathway. Ribosomal proteins have been known to have diverse functions in regulating cellular metabolism as well as protein synthesis. So far, however, little is known about other possible role(s) of RPS6 in plants, besides being a component of the 40 S ribosomal subunit and acting as a target of TOR. Here, we report that RPS6 may have a novel function via interaction with histone deacetylase 2B (AtHD2B) that belongs to the plant-specific histone deacetylase HD2 family. RPS6 and AtHD2B were localized to the nucleolus. Co-expression of RPS6 and AtHD2B caused a change in the location of both RPS6 and AtHD2B to one or several nucleolar spots. ChIP analysis suggests that RPS6 directly interacts with the rRNA gene promoter. Protoplasts overexpressing both AtHD2B and RPS6 exhibited down-regulation of pre-18 S rRNA synthesis with a concomitant decrease in transcription of some of the ribosomal proteins, suggesting their direct role in ribosome biogenesis and plant development. This is consistent with the mutation in rps6b that results in reduction in 18 S rRNA transcription and decreased root growth. We propose that the interaction between RPS6 and AtHD2B brings about a change in the chromatin structure of rDNA and thus plays an important role in linking TOR signaling to rDNA transcription and ribosome biogenesis in plants.
Association of HLA-DPB1*0301 With IDDM in Mexican-Americans

Susceptibility to IDDM has been associated with specific alleles at the HLA class II loci in a variety of human populations. Previous studies among Mexican-Americans, a group ancestrally derived from Native Americans and Hispanic whites, showed that the DR4 haplotypes (DRB1*0405-DQB1*0302 and DRB1*0402-DQB1*0302) and the DR3 haplotype (DRB1*0301-DQB1*0201) were increased among patients and suggested a role for both DR and DQ alleles in susceptibility and resistance. Based on the analysis of 42 Mexican-American IDDM families and ethnically matched control subjects by polymerase chain reaction/sequence-specific oligonucleotide probe typing, we report an association of IDDM with the DPB1 allele, *0301 (relative risk = 6.6; P = 0.0012) in this population. The analysis of linkage disequilibrium patterns in this population indicates that the observed increased frequency in DPB1*0301 among patients cannot be attributed simply to linkage disequilibrium with high-risk DR-DQ haplotypes. These data suggest that in addition to alleles at the DRB1 and DQB1 loci, polymorphism at the DPB1 locus may also influence IDDM risk.