Miracle-dz/UniFAR-FTUs huggingface dataset:
TGF-beta(1) downregulates PTHrP in coronary endothelial cells.

Parathyroid hormone-related peptide (PTHrP) is expressed throughout the cardiovascular system including coronary endothelial cells. Factors involved in the regulation of cardiac PTHrP expression have not been examined before. This study investigates the influence of transforming growth factor (TGF)-beta(1)on ventricular PTHrP expression. Coronary endothelial cells were isolated from ventricles of adult rats and PTHrP protein expression in these cultures was analysed by immunoblotting. TGF-beta(1)caused a concentration-dependent reduction in PTHrP protein within 24 h. In transgenic mice over-expressing TGF-beta(1)ventricular PTHrP protein expression and release was reduced compared to non-transgenic littermates. Similar concerns hold for PTHrP mRNA content (RT-PCR). Since ventricular TGF-beta(1)expression increases under pathophysiological conditions like arterial hypertension, ventricular PTHrP expression was further determined in aging spontaneously hypertensive (SHR-SP) and normotensive rats. TGF- beta(1)expression was increased in SHR-SP and ventricular PTHrP mRNA expression was downregulated at the age of 10 months. PTHrP expression did not recover in elder SHR-SP in which TGF-beta(1)expression was normalized again. Finally, we investigated ventricular PTHrP expression in rats after banding of the ascending aorta which generates a pressure induced hypertrophy without an induction of TGF-beta(1)expression. In ventricles from these animals, PTHrP expression was transiently increased and normalized at day 3. In conclusion, PTHrP expression was reduced under all conditions in which coronary endothelial cells were exposed to TGF-beta(1). PTHrP expression does not correlate with cardiac hypertrophy. Since coronary endothelial cells represent the majority of PTHrP producing cells in the ventricle its downregulation by TGF- beta(1)seems to be relevant for the paracrine effects of PTHrP.
Design of a passive microwave sensor for the characterization of mobile engine oil

We are interested in this work to the design and more particularly the achievement of a passive and inexpensive microwave RFID sensor. This will be allowing us to control and to monitor the quality of the engine oil of a mobile. The sensor consists of a dipole placed inside the oil sump of the mobile. Knowing the variation of the relative permittivity of the engine oil, as a function of the distance travelled, we can detect when the latter is worn and when the emptying operation has to be carried out. The principle of this method consists in going back to the value of the relative permittivity of the engine oil from the variation of the resonant frequency of the dipole. This variation in frequency is directly related to the degradation of the engine oil. Analysis of the results of simulations and measurements showed a good sensitivity of the sensor, depending on the distance travelled.
Journal Writing and Learning Mathematics.

There has been a keen interest amongst researchers for some time in the ways language and learning mathematics interact. For useful reviews see Austin and Howson [1979], Bell, Costello, and Kuchemann [1985], and Ellerton and Clements [1991]. Much of the discussion has centered on the relation of language to concept formation. Stemming from this theme of language and mathematics there is a growing awareness of the importance of writing in mathematics [Kennedy, 1985; Bell and Bell, 1985; Withers, 1989; Turner, 1989]. The majority of reported work on writing to learn mathematics is focussed at a primary level. Exceptions to this focus are Bell and Bell [1985], Borasi and Rose [1989]. Bell and Bell [1985] is a study of the relation of writing to problem solving. They conclude their article with the following words:
The pH-Dependent Expression of the Urease Operon in Streptococcus salivarius Is Mediated by CodY

ABSTRACT Urease gene expression in Streptococcus salivarius 57.I, a strain of one of the major alkali producers in the mouth, is induced by acidic pH and excess amounts of carbohydrate. Expression is controlled primarily at the transcriptional level from a promoter, p ureI . Recent sequencing analysis revealed a CodY box located 2 bases 5′ to the −35 element of p ureI . Using continuous chemostat culture, transcription from p ureI was shown to be repressed by CodY, and at pH 7 the repression was more pronounced than that in cells grown at pH 5.5 under both 20 and 100 mM glucose. The direct binding of CodY to p ureI was demonstrated by electrophoretic mobility shift assay and chromatin immunoprecipitation (ChIP)–quantitative real-time PCR (qPCR). The result of ChIP-qPCR also confirmed that the regulation of CodY is indeed modulated by pH and the binding of CodY at neutral pH is further enhanced by a limited supply of glucose (20 mM). In the absence of CodY, the C-terminal domain of the RNA polymerase (RNAP) α subunit interacted with the AT tracks within the CodY box, indicating that CodY and RNAP compete for the same binding region. Such regulation could ensure optimal urease expression when the enzyme is most required, i.e., at an acidic growth pH with an excess amount of carbon nutrients.
Combinatorial Regulation of Photoreceptor Differentiation Factor, Neural Retina Leucine Zipper Gene Nrl, Revealed by in Vivo Promoter Analysis*

Development and homeostasis require stringent spatiotemporal control of gene expression patterns that are established, to a large extent, by combinatorial action of transcription regulatory proteins. The bZIP transcription factor NRL (neural retina leucine zipper) is critical for rod versus cone photoreceptor cell fate choice during retinal development and acts as a molecular switch to produce rods from postmitotic precursors. Loss of Nrl in mouse leads to a cone-only retina, whereas ectopic expression of Nrl in photoreceptor precursors generates rods. To decipher the transcriptional regulatory mechanisms upstream of Nrl, we identified putative cis-control elements in the Nrl promoter/enhancer region by examining cross-species sequence conservation. Using in vivo transfection of promoter-reporter constructs into the mouse retina, we show that a 0.9-kb sequence upstream of the Nrl transcription initiation site is sufficient to drive reporter gene expression in photoreceptors. We further define a 0.3-kb sequence including a proximal promoter (cluster A1) and an enhancer (cluster B) that can direct rod-specific expression in vivo. Electrophoretic mobility shift assays using mouse retinal nuclear extracts, in combination with specific antibodies, demonstrate the binding of retinoid-related orphan nuclear receptor β (RORβ), cone rod homeobox, orthodenticle homolog 2, and cyclic AMP response element-binding protein to predicted consensus elements within clusters A and B. Our studies demonstrate Nrl as a direct transcriptional target of RORβ and suggest that combinatorial action of multiple regulatory factors modulates the expression of Nrl in developing and mature retina.
A small‐molecule inhibitor of macrophage migration inhibitory factor for the treatment of inflammatory disease

Multiple sclerosis (MS) is a chronic, debilitating disease of the central nervous system (CNS) characterized by demyelination and axon loss. The proinflammatory cytokine macrophage migration inhibitory factor (MIF) has been shown to be elevated in the cerebrospinal fluid of patients during relapses. The purpose of this study was to evaluate a new small‐molecule inhibitor of MIF and its ability to reduce the severity of an animal model of MS, experimental autoimmune encephalomyelitis (EAE). We utilized 2 structurally related isoxazolines, which show in vitro inhibition of MIF tautomerase activity. We found that administration of an inhibitor of MIF to mice with established EAE immediately reduced the severity of clinical signs and expanded a population of regulatory T lymphocytes. We also noted that the inhibitor reduced relapses of disease in a relapsing/remitting model of EAE. An analysis of leukocyte migration into the brain revealed that administration of inhibitor reduced entry of these cells. No effects on inflammatory cytokine production or T‐cell activation in the periphery were noted. From these studies, we conclude that a small‐molecule inhibitor of MIF reduces the severity of EAE and prevents access of immune cells into the CNS, which could be of therapeutic relevance to MS.—Kithcart, A. P., Cox, G. M. , Sielecki, T. , Short, A. , Pruitt, J., Papenfuss, T. , Shawler, T. , Gienapp, I. , Satoskar, A. R. , Whitacre, C. C. A small‐molecule inhibitor of macrophage migration inhibitory factor for the treatment of inflammatory disease. FASEB J. 24, 4459–4466 (2010). www.fasebj. org
The Nature of Self-Regulatory Fatigue and “Ego Depletion”

Self-regulation requires overriding a dominant response and leads to temporary self-regulatory fatigue. Existing theories of the nature and causes of self-regulatory fatigue highlight physiological substrates such as glucose, or psychological processes such as motivation, but these explanations are incomplete on their own. Historically, theories of physical fatigue demonstrate a similar pattern of useful but incomplete explanations, as recent views of physical fatigue emphasize the roles of both physiological and psychological factors. In addition to accounting for multiple inputs, these newer views also explain how fatigue can occur even in the presence of sufficient resources. Examining these newer theories of physical fatigue can serve as a foundation on which to build a more comprehensive understanding of self-regulatory fatigue that integrates possible neurobiological underpinnings of physical and self-regulatory fatigue, and suggests the possible function of self-regulatory fatigue.
Changes of serum soluble receptor activator for nuclear factor-κB ligand after glucocorticoid therapy reflect regulation of its expression by osteoblasts.

CONTEXT Osteoporosis is a serious complication of systemic glucocorticoid therapy. The role of serum soluble receptor activator for nuclear factor-κB ligand (RANKL) in glucocorticoid-induced osteoporosis remains unclear. OBJECTIVE The objective of the study was to clarify the influence of serum soluble RANKL on the osteoprotegerin (OPG)/RANKL/receptor activator for nuclear factor-κB system in patients with systemic autoimmune diseases receiving glucocorticoid therapy. PATIENTS AND METHODS Sixty patients (40 women) with systemic autoimmune diseases who received initial glucocorticoid therapy with prednisolone (30-60 mg/d) plus bisphosphonate therapy were prospectively enrolled. Serum soluble RANKL and OPG levels were measured at 0, 1, 2, 3, and 4 wk after starting glucocorticoid therapy. The effects of dexamethasone on production of RANKL and OPG mRNA and protein by cultured normal human osteoblasts were evaluated by RT-PCR and ELISA, respectively. RESULTS The mean serum soluble RANKL level of the patients was unchanged by glucocorticoid therapy. Because the distribution of serum soluble RANKL was bimodal, the patients were stratified into two groups. Serum soluble RANKL decreased significantly in the higher soluble RANKL group (≥0.16 pmol/liter), whereas it increased significantly in the lower soluble RANKL group. The mean serum OPG level of the patients decreased significantly. Bone mineral density increased in the higher soluble RANKL group after starting glucocorticoid therapy, whereas it decreased in the lower soluble RANKL group. In cultures of unstimulated human osteoblasts, RANKL mRNA expression was increased and OPG mRNA was decreased by dexamethasone. Up-regulation of RANKL and OPG mRNA by IL-6 was suppressed by dexamethasone. CONCLUSION Serum soluble RANKL might be a useful marker of bone remodeling in patients with systemic autoimmune diseases receiving glucocorticoid therapy.
Image fusion using direction wavelet approach and performance evaluation of multiple source images

Image fusion is the approach to get one composite output image from number of variety of input images. We can fuse images which are out of focus, here images of different focal length are considered as input whereas output image is expected to be clear and visible. There are various types of sensors available today having wide variety of focal length and hence they generate images in which some objects are clear some are not. Again multi-sensor devices provide huge data to analyze and interpret. So we require some sort of mechanism to fuse all this data into single one. Therefore there is a basic requirement of certain image fusion algorithm which will perform the desired task and gives some accurate and reliable information about the scene. In the research work a method is developed to perform the fusion of multiple images to get a single image which is more informative, reliable and accurate. The proposed method is based on complex wavelet transform with the combination of direction wavelet decomposition method. The method is good at direction selectivity, also perfect reconstruction which is very important aspect for fusion of images. The final fused image is enhanced in such a way that it is useful for interpretation and analysis and assists to come up with certain decision about the scene.
STATCOM converters and control: A review

Static Synchronous compensator (STATCOM), a member of FACTS family has become a prominent device for reactive power compensation and dynamic performance improvement of the system. A voltage source converter (VSC) is at the heart of a STATCOM and has been realized by various topologies in literature. Its control can be divided into compensation and DC voltage balance. A review on converters for STATCOM and their control is presented along with the new emerging technologies in the system. One more attribute of STATCOM besides compensation is its use for improving system stability which is achieved through implementation of various control algorithms, switching techniques which have been reported in literature.
NEW SERVICE IN A COMMUNITY HOSPITAL: THE ROLE OF NURSING STAFF DEVELOPMENT

&NA; The purpose of this article is to describe strategies to assist nurses in staff development with planning and implementing a successful education program directed at preparing staff to provide a new patient service in a community hospital. The staff development instructor can play a crucial role in the successful implementation of a new service in a community hospital. This article focuses on the implementation of a cardiac surgery program in a community hospital.
Evaluation of brain function in severe human head trauma with multimodality evoked potentials. Part 2: Localization of brain dysfunction and correlation with posttraumatic neurological conditions.

is Electrophysiological investigations were undertaken in 51 comatose patients with severe head trauma to locate areas of brain dysfunction and to relate the loci of dysfunction to the patient's posttraumatic neurological condition. On the basis of evoked potential data, the presence of decortication or decerebration depended on cerebral hemispheric dysfunction. Brain-stem dysfunction, defined by evoked potentials, did not correlate with posturing. On the other hand, impaired oculocephalic responses and bilateral abnormal pupillary light responses were associated with brainstem dysfunction, while hemispheric dysfunction did not correlate with either: Duration of coma was dependent on hemispheric dysfunction. Brain-stem dysfunction was not significantly associated with prolonged coma. Furthermore, 80% of the head trauma patients who had Grade I or II multimodality evoked brain-injury potentials recorded in the acute period following head trauma (mean Day 3) became responsive within 30 days of their injury. Graded somatosensory brain injury potentials appeared to be a powerful prognostic tool as they significantly correlated with the patient's final outcome even when recorded early after injury. Abnormal multimodality evoked potentials recorded acutely consistently defined dysfunction of the visual, auditory, and motor systems in comatose patients, and were considerably more effective than the clinical neurological examination in diagnosing persisting focal deficits of these systems.
Receptivity to Protobacco Media and Its Impact on Cigarette Smoking Among Ethnic Minority Youth in California

Adolescents from different ethnic groups show different cigarette smoking prevalence rates, suggesting potential differences in receptivity to and influences from protobacco media. Understanding these differences will be helpful in tailoring smoking prevention and cessation programs for diverse adolescent populations in the United States. Data from cross-sectional surveys of 20,332 randomly sampled California boys and girls, 12-17 years of age, were analyzed. Results indicate that receptivity to protobacco media was lower among African Americans, Asian Americans, and Hispanics than among White youth. There was a consistent dose-response relationship between receptivity to protobacco media and 30-day cigarette smoking across ethnic groups. Having a cigarette brand preference was associated with the highest risk for cigarette smoking, having a favorite tobacco ad showed the lowest risk, while having received or being willing to use tobacco promotional items was associated with a moderate risk. After controlling for 13 covariates, the odds ratio for receptivity to protobacco media and 30-day cigarette smoking was significant for Whites (RR = 1.38, p < 0.01) and Hispanics (RR = 1.46, p < 0.01), but not for African American (RR = 1.05, p > 0.05) and Asian American (RR = 1.17, p > 0.05) youth. African American, Asian American, and Hispanic adolescents have a lower level of receptivity to protobacco media than do Whites. The association between media receptivity and 30-day cigarette smoking exists for all four ethnic groups without controlling for other smoking predictor variables, but only for Hispanics and Whites when other variables are controlled. Protecting adolescents from protobacco advertising influences is an important element in tobacco control among ethnic minority youth.
Measuring Factor Exposures: Uses and Abuses

A growing number of investors have come to view their portfolios (especially equity portfolios) as a collection of exposures to risk factors. The most prevalent and widely harvested of these risk factors is the market (equity risk premium), but there are also others, such as value and momentum (style premiums). Measuring exposures to these factors can be a challenge: Investors need to understand how factors are constructed and implemented in their portfolios, and they need to know how statistical analysis may be best applied. Without the proper model, rewards for factor exposures may be misconstrued as alpha, and investors may be misinformed about the risks their portfolios truly face. This article should serve as a practical guide for investors looking to measure portfolio factor exposures. The authors discuss some of the pitfalls associated with regression analysis and how factor design can matter a lot more than expected. Ultimately, investors with a clear understanding of the risk sources in an existing portfolio, and the risk exposures of other portfolios under consideration, may have an edge in building better-diversified portfolios.
Targeting senescent cholangiocytes and activated fibroblasts with B‐cell lymphoma‐extra large inhibitors ameliorates fibrosis in multidrug resistance 2 gene knockout (Mdr2−/−) mice

Cholangiocyte senescence has been linked to primary sclerosing cholangitis (PSC). Persistent secretion of growth factors by senescent cholangiocytes leads to the activation of stromal fibroblasts (ASFs), which are drivers of fibrosis. The activated phenotype of ASFs is characterized by an increased sensitivity to apoptotic stimuli. Here, we examined the mechanisms of apoptotic priming in ASFs and explored a combined targeting strategy to deplete senescent cholangiocytes and ASFs from fibrotic tissue to ameliorate liver fibrosis. Using a coculture system, we determined that senescent cholangiocytes promoted quiescent mesenchymal cell activation in a platelet‐derived growth factor (PDGF)‐dependent manner. We also identified B‐cell lymphoma‐extra large (Bcl‐xL) as a key survival factor in PDGF‐activated human and mouse fibroblasts. Bcl‐xL was also up‐regulated in senescent cholangiocytes. In vitro, inhibition of Bcl‐xL by the small molecule Bcl‐2 homology domain 3 mimetic, A‐1331852, or Bcl‐xL‐specific small interfering RNA induced apoptosis in PDGF‐activated fibroblasts, but not in quiescent fibroblasts. Likewise, inhibition of Bcl‐xL reduced the survival and increased apoptosis of senescent cholangiocytes, compared to nonsenescent cells. Treatment of multidrug resistance 2 gene knockout (Mdr2−/−) mice with A‐1331852 resulted in an 80% decrease in senescent cholangiocytes, a reduction of fibrosis‐inducing growth factors and cytokines, decrease of α‐smooth muscle actin–positive ASFs, and finally in a significant reduction of liver fibrosis. Conclusion: Bcl‐xL is a key survival factor in ASFs as well as in senescent cholangiocytes. Treatment with the Bcl‐xL‐specific inhibitor, A‐1331852, reduces liver fibrosis, possibly by a dual effect on activated fibroblasts and senescent cholangiocytes. This mechanism represents an attractive therapeutic strategy in biliary fibrosis. (Hepatology 2018;67:247‐259).
In Vitro Antiviral Activity and Resistance Profile of the Next-Generation Hepatitis C Virus NS3/4A Protease Inhibitor Glecaprevir

ABSTRACT Glecaprevir (formerly ABT-493) is a novel hepatitis C virus (HCV) NS3/4A protease inhibitor (PI) with pangenotypic activity. It inhibited the enzymatic activity of purified NS3/4A proteases from HCV genotypes 1 to 6 in vitro (half-maximal [50%] inhibitory concentration = 3.5 to 11.3 nM) and the replication of stable HCV subgenomic replicons containing proteases from genotypes 1 to 6 (50% effective concentration [EC50] = 0.21 to 4.6 nM). Glecaprevir had a median EC50 of 0.30 nM (range, 0.05 to 3.8 nM) for HCV replicons containing proteases from 40 samples from patients infected with HCV genotypes 1 to 5. Importantly, glecaprevir was active against the protease from genotype 3, the most-difficult-to-treat HCV genotype, in both enzymatic and replicon assays demonstrating comparable activity against the other HCV genotypes. In drug-resistant colony selection studies, glecaprevir generally selected substitutions at NS3 amino acid position A156 in replicons containing proteases from genotypes 1a, 1b, 2a, 2b, 3a, and 4a and substitutions at position D/Q168 in replicons containing proteases from genotypes 3a, 5a, and 6a. Although the substitutions A156T and A156V in NS3 of genotype 1 reduced susceptibility to glecaprevir, replicons with these substitutions demonstrated a low replication efficiency in vitro. Glecaprevir is active against HCV with most of the common NS3 amino acid substitutions that are associated with reduced susceptibility to other currently approved HCV PIs, including those at positions 155 and 168. Combination of glecaprevir with HCV inhibitors with other mechanisms of action resulted in additive or synergistic antiviral activity. In summary, glecaprevir is a next-generation HCV PI with potent pangenotypic activity and a high barrier to the development of resistance.
Modern methods of speech synthesis

We have examined various aspects of how to produce synthetic speech. There are numerous applications for such synthetic speech, mostly when starting from a textual input, i.e., TTS. Given the large amount of text in databases and the public's need to access information efficiently, synthetic speech is a natural way to obtain information. A major application of the future will be speech-to-speech translation, in which a person speaking in one language will be able to converse automatically with someone using another language: ASR would transcribe the original speech to a textual form in language A, then an automatic text translator would map that text to language B, and finally a TTS system for this second language would generate the output speech.