Miracle-dz/UniFAR-FTUs huggingface dataset:
Mortality and Renal Replacement Therapy after renal artery stenting for Atherosclerotic Renovascular Disease

Purpose— To identify the risk factors for progression to renal replacement therapy (RRT) and all-cause mortality in patients who underwent renal artery (RA) stent placement for atherosclerotic renal artery stenosis (RAS). Materials and Methods— A retrospective study was performed from June 1996 to June 2009 that identified 1052 patients that underwent RA stent placement. The glomerular filtration rate at the time of RA stent placement was estimated from the serum creatinine level and divided into renal disease stages 1–5. Univariate and multivariable Cox proportional hazards models were used to determine which factors were associated with each endpoint. Results— The times to progression to all-cause mortality and RRT were similar for chronic kidney (CKD) stages 1/2/3A and served as the reference group. In multivariable analysis, highgrade proteinuria (P<.001), higher CKD stage [stage 5 vs. 1-3A, (P<.001)], stage 4 vs. 1-3A, (P<. 001), stage 3B vs. 1-3A, (P=.02)] remained independently associated with increased risk of progression to RRT. Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEi/ ARB) use was associated with decreased risk of progression to RRT (P=0.03). Higher CKD stage [stage 5 vs. 1-3A, (P<.001), stage 4 vs. 1-3A (P=.004), carotid artery disease (P<.001), diabetes mellitus diabetes have an increased risk for all-cause mortality after renal artery stenting. ACEi/ARB use in this patient population has a decreased risk of progression to RRT and patients on statins have a decreased risk of all-cause mortality.
Utilization of D-3-Hydroxy13-'4Cjbutyrate for Lipogenesis in vivo in Lactating Rat Mammary Gland

Incorporation of D-3-hydroxy[3-'4C]butyrate into lipid in vivo suggests that lactating mammary gland is a major site of ketone-body utilization. The incorporation decreases in short-term insulin deficiency (2h) and on starvation (24h), but increases again on refeeding (2h). The activity of cytosolic acetoacetyl-CoA synthetase parallels the changes in nutritional state, but is not affected by short-term insulin deficiency. Ketone bodies may regulate rat mammary-gland metabolism and provide an alternative substrate for lipogenesis and energy Studies in vitro have that acetoacetate increases glucose lipogenesis, taken the gland lipid mammary
Primary Human Chondrocyte Extracellular Matrix Formation and Phenotype Maintenance using RGD-derivatized PEGDM Hydrogels Possessing a Continuous Gradient in Modulus

Efficient ex vivo methods for expanding primary human chondrocytes while maintaining phenotype is critical to advancing autologous cell sourcing efforts for tissue engineering applications. While there is significant activity in the literature, systematic approaches are necessary to determine and optimize the chemical and mechanical scaffold properties for hyaline cartilage generation using limited cell numbers. Functionalized hydrogels possessing continuous variations in physico-chemical properties are therefore an efficient three-dimensional platform for studying several properties simultaneously. Herein, we describe a polyethylene glycol dimethacrylate (PEGDM) hydrogel system possessing a gradient in modulus (~27,000 Pa to 3,800 Pa) containing a uniform concentration of arginine–glycine–aspartic acid peptide (RGD) to enhance cellular adhesion for the correlation of primary human osteoarthritic chondrocyte proliferation, phenotype maintenance, and ECM production to the hydrogel properties. Cell number and chondrogenic phenotype (CD14:CD90 ratios) were found to decline in regions with higher storage modulus (>13,100 Pa), while regions with lower storage modulus maintained cell number and phenotype. Over three weeks of culture, hydrogel regions possessing lower storage modulus experience an increase in ECM content (~200%) compared to regions with higher storage modulus. Variations in the amount and organization of cytoskeletal markers actin and vinculin were observed within the modulus gradient which are indicative of the differences in chondrogenic phenotype maintenance and ECM expression. Thus scaffold mechanical properties significantly impact on modulating human osteoarthritic chondrocyte behavior and tissue formation.
A point-of-purchase intervention featuring in-person supermarket education impacts healthy food purchases

Objective— This study tested the efficacy of a multicomponent supermarket point-of-purchase (POP) intervention featuring in-person nutrition education on the nutrient composition of food purchases. Design— The design was a randomized trial comparing the intervention to usual care (no treatment). Setting— A supermarket in a socioeconomically diverse region of Phoenix, Arizona. Participants— One-hundred fifty-three adult shoppers were recruited on-site. Intervention— The intervention consisted of brief shopping education by a nutrition educator and an explanation and promotion of a supermarket POP healthy shopping program that included posted shelf signs identifying healthy foods, sample shopping lists, tips, and signage. Main Outcome Measures— Outcomes included purchases of total, saturated, and trans fat (g/ 1000 kcals), and fruits, vegetables, and dark green and bright yellow vegetables (servings/1000 kcals) derived through nutritional analysis of participant shopping baskets. Analysis— Analysis of covariance compared the intervention and control groups on food purchasing patterns while adjusting for household income. Results— The intervention resulted in greater purchasing of fruit and green and yellow vegetables. No other group differences were observed. Conclusions and Implications— Long-term evaluations of supermarket interventions should be conducted to improve the evidence base, and to determine the potential for impact on food choices associated with decreased chronic disease. This pilot study a randomized to examine the impact of a POP healthy The
Valosin containing protein mutations in fronto-temporal lobar degeneration: Clinical presentation, pathology and pathogenesis

Inclusion body myopathy (IBM) associated with paget’s disease of the bone (PDB) and frontotemporal dementia (FTD) or IBMPFD , is a rare multisystem degenerative disorder due to mutations in valosin containing protein (VCP). VCP is a ubiquitously expressed protein that facilitates the degradation of proteins via the ubiquitin proteasome and autophagy pathways. Affected brain and muscle tissue in IBMPFD have ubiquitinated and TAR DNA binding protein-43 (TDP-43) inclusions. In skeletal muscle, this pathology is consistent with IBM. While in the CNS, IBMPFD is a frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-U) subtype. Recent studies suggest that IBMPFD mutations in VCP disrupt its function in protein degradation. This review will explore the clinical phenotype and pathology of IBMPFD with an emphasis on central nervous system degeneration. In addition, we will discuss the current understanding regarding VCP’s function in terminally differentiated tissue and how disease associated mutations result in both myo- and neurodegeneration. patients have muscle weakness, it is an isolated symptom in ~30% of patients. In contrast, 32% of patients clinically have FTD and 3% have FTD as an isolated phenotype This heterogeneity is seen with the same mutation and even within isolated families bearing the same mutation. One study identified an arginine to histidine missense mutation at residue 159 in VCP (VCP-R159H) in three unrelated families (7). 6/6 affected patients in one R159H family exhibited FTD without associated PDB or IBM. Whereas in another family, only one of 5 affected family members had FTD and 5/5 had PDB and weakness. This was not due to variations in family members ages since family 1’s (all FTD) ages ranged from 67 to 86 and family 3’s (PDB and IBM) ages ranged from 60–76 or clinical reporting since all patients had neuropsychological assessment associated with a clinical evaluation. Because of this heterogeneity, any evaluation of supposed FTD should ask about a family history of PDB and muscular weakness, specifically IBM.
Allosteric Modification, the Primary ATP Activation Mechanism of ANF-RGC

ANF-RGC is the prototype receptor membrane guanylate cyclase being both the receptor and the signal transducer of the most hypotensive hormones, ANF and BNP. It is a single transmembrane-spanning protein. After binding these hormones at the extracellular domain it at its intracellular domain signals activation of the C-terminal catalytic module and accelerates the production of its second messenger, cyclic GMP, which controls blood pressure, cardiac vasculature and fluid secretion. ATP is obligatory for the post-transmembrane dynamic events leading to ANF-RGC activation. It functions through the ATP regulated module, ARM (KHD) domain, of ANF-RGC. In the current over-a-decade-held-model “phosphorylation of the KHD is absolutely required for hormone-dependent activation of NPR-A” (Potter, L.R., and T. Hunter. 1998. Mol. Cell. Biol. 18: 2164–2172). The presented study challenges this concept. It demonstrates that, instead, ATP allosteric modification of ARM is the primary signaling step of ANF-GC activation. In this 2-step new dynamic model, ATP in the first step binds ARM. This triggers in it a chain of transduction events, which cause its allosteric modification. The modification partially activates (about 50%) ANF-RGC; and concomitantly also prepares the ARM for the second successive step. In this second step, ARM is phosphorylated and ANF-RGC achieves additional (~50%) full catalytic activation. The study defines a new paradigm of ANF-RGC signaling mechanism.
CLINICAL AND BIOLOGICAL RELEVANCE OF EZH2 IN TRIPLE NEGATIVE BREAST CANCER in the orthotopic MB-231 mouse model of breast carcinoma. Our results

The polycomb group protein, enhancer of zeste homolog 2 (EZH2), is a transcriptional repressor involved in cell cycle regulation and has been linked to aggressive breast cancer. We examined the clinical and biological significance of EZH2 expression in triple-negative breast cancers. Tissue microarrays were constructed with invasive breast cancer cases and stained with EZH2, cytokeratin 5/6, epidermal growth factor receptor 1(EGFR) and p53. The expression of these markers was correlated with clinicopathologic variables and patients’ outcome. Furthermore, in vivo EZH2 gene silencing was achieved using siRNA incorporated into chitosan nanoparticles. Out of 261 cases of invasive breast cancer, high expression of EZH2 was detected in 87 (33%) cases, and it was strongly associated with a triple-negative breast cancer phenotype ( P <.001) compared to all other non-triple negative breast cancers. Furthermore, high EZH2 was significantly associated with high histologic grade ( P =.01), estrogen receptor negativity ( P <.001), progesterone receptor negativity ( P <.001), EGFR positivity ( P =.04), and high p53 expression ( P <. 001). Survival analysis demonstrated that patients with high EZH2 had a poorer overall survival, compared to those with low EZH2 ( P =.03), and it retained its significance as an independent prognostic factor ( P =.02). In addition, EZH2 gene silencing resulted in significant reduction in tumor growth ( P <.01)
LITERACIES, SKILLS AND COMPETENCES DEVELOPMENT BY DIGITAL STORIES

The article revises texts in English and in Portuguese about the production of digital stories for the educational context. The objective is to reflect upon the necessary characteristics for the development of experiences with audio-visual stories. The methodology used in this study is based on a bibliographical research. The results of the study indicate that the capacity to build coherent audio-visual narratives, as well as the ability to edit images and sounds, are demanded of the people involved in the educational context due to the insertion of multiple digital technologies in the daily life. Thus, it is argued that the experience with the production of digital stories in the classroom or outside the classroom may enhance the digital literacy of the students.
Phenanthriplatin Acts as a Covalent Topoisomerase II Poison

Drugs capable of trapping topoisomerase II (Top2), an essential enzyme that cleaves double-stranded DNA in order to remove naturally occurring knots and tangles, can serve as potent anticancer agents. The monofunctional platinum anticancer agent phenanthriplatin, cis-[Pt(NH 3 ) 2 (phenanthridine)Cl](NO 3 ), is shown here to act as a Top2 poison in addition to its known modes of action as a DNA and RNA polymerase inhibitor. Its potency therefore combines diverse modes of action by which phenanthriplatin can kill cancer cells. Covalent DNA-platinum lesions implicated in Top2 poisoning are distinctive from those generated by known topoisomerase poisons, which typically exert their action by intercalation at the topoisomerase cleavage site.
AHP Topsis para la selección de proveedores considerando el riesgo asociado a la calidad

El problema de selección de proveedores es un problema complejo que integra muchos atributos, muchos de los cuales se encuentran en conflicto o es difícil de medir. En este artículo se presenta una metodología multicriterio para seleccionar proveedores que integra el riesgo asociado a la calidad, está basada en las técnicas AHP difuso y TOPSIS. Además, ha sido validado con los datos de un caso real para la selección de un proveedor de empaques en la fabricación de bombas hidráulicas. Palabras-Clave: Selección de proveedores, Riesgo en la Cadena de Suministro, AHP difuso, TOPSIS ABSTRACT:
Behavior-Environment System

In this paper, I attempt to describe the implications of dynamical approaches to science for research in the experimental study of behavior. I discuss the differences between classical and dynamical science, and focus on how dynamical science might see replication differently from classical science. Focusing on replication specifically, I present some problems that the classical approach has in dealing with dynamics and multiple causation. I ask about the status and meaning of "error" variance, and whether it may be a potent source of information. I show how a dynamical approach can handle the sort of control by past events that is hard for classical science to understand. These concerns require, I believe, an approach to variability that is quite different from the one most researchers currently employ. I suggest that some of these problems can be overcome by a notion of "behavioral state," which is a distillation of an organism's history.
Integrin b 6 Mediates Phospholipid and Collectin Homeostasis by Activation of Latent TGF- b 1

Surfactant lines the alveolar surface and prevents alveolar collapse. Derangements of surfactant cause respiratory failure and interstitial lung diseases. The collectins, surfactant proteins A and D, are also important in innate host defense. However, surfactant regulation in thepostnatallungispoorlyunderstood.Wefoundthattheepithelial integrin, a v b 6,regulatessurfactanthomeostasis invivo byactivating latent transforming growth factor (TGF)- b . Adult mice lacking the b -subunit of a v b 6 ( Itgb6 2 / 2 ) developed increased bronchoalveolar lavage phospholipids and surfactant proteins A and D, and demon- strated abnormal-appearing alveolar macrophages, reminiscent of the human disease pulmonary alveolar proteinosis. Using lung- speciﬁc expression of constitutively active TGF- b 1 in Itgb6 2 / 2 mice, we found that TGF- b 1 was sufﬁcient to normalize these abnormalities. Tgf b 1 -deﬁcient mice also demonstrated increased phospholi-pidsandsurfactant proteinsAandD,but micelackingthekeyTGF- b signaling molecule, SMAD3, did not. Therefore, integrin-mediated activation of latent TGF- b 1 regulates surfactant constituents independent of intracellular SMAD3. In vivo increases in surfactant proteinAandDwerenotassociatedwithincreasesinmRNAfortheseproteinsinalveolartissuefrom Itgb6 2 / 2 mice. On the other hand, isolated alveolar macrophages from Itgb6 2 / 2 mice were defectivein processing phospholipids in vitro , suggesting that reduced surfac-tantclearancecontributestoalteredsurfactanthomeostasisinthesemice in vivo . These ﬁndings show that a v b 6 and TGF- b 1 regulate homeostasis of phospholipids and collectins in adult mouse lungs and may have implications for anti-ﬁbrotic therapeutics that inhibit active TGF- b in the lung. implications for the treatment of ﬁbrotic lung diseases, such as idiopathic pulmonary ﬁbrosis, that target transforming growth factor- b in the lung. Our work also identiﬁes mediators that may have relevance to human disorders of surfactant dysregulation. Alveolar macrophages wild-type Itgb6 6 4.5 versus 96% 6 2.7 positively staining P 5 0.45). Taken together, these data suggest that the abnormal macrophage phenotype observed in Itgb6 2 / 2 mice is not due to a global disruption of macrophage maturation.
A COMPARISON OF THE COMPLEMENT, CONGLUTININ, AND NATURAL ANTI-SHEEP RED CELL ANTIBODY TITRES OF THE SERUM OF NEW BORN AND OLDER CALVES

The plasma of the newborn calf is known to be low in gamma globulin but this protein fraction increases rapidly after ingestion of colostrum during the first 24 to 36 hours of life (1-3). By means of electrophoretic analysis, Pierce demonstrated that certain of the proteins in the serum of the newborn calf had the mobilities of alphaand beta-globulins, the former fraction being composed largely of a protein differing from any present in adult cattle serum (4). At ten days, both gamma1and gamma2-globulin could be detected in the plasma, the former being higher; at 30 days, the amount of gamma2 exceeded that of gamma1, and a smaller globulin component, gamma3, had appeared. The albumin concentration was found to fluctuate with the changes in serum globulins (4). In other studies of the proteins of preand postcolostral calf serum, attention has been focused mainly on antibody globulins (5), these passively-acquired antibodies from the immune dam being believed to have an important function in temporarily protecting the young animal against the respective infections. "Natural" or "normal" antibodies may also be transferred passively in the colostrum, as is illustrated in the work of Kerr and Robertson (6) and Pierce (7). In studies of the agglutinins in cattle sera for the protozoan species Trichomonas foetus, Kerr and Robertson (6) found them to be of two kinds, one kind acquired as a result of infection with or injection of this protozoan, the other present in the serum of all adult cattle tested, including animals with no history of this infection. Both kinds were demonstrable in the colostrum of an immune cow. The natural agglutinins transmitted in the colostrum of the non-immune dam, disappeared from the calf's blood in two weeks to two months. Autogenous development of natural agglutinins
Characterisation of the substrate speciﬁcity of homogeneous vaccinia virus uracil-DNA glycosylase

The decision to stop smallpox vaccination and the loss of speciﬁc immunity in a large proportion of the population could jeopardise world health due to the possibility of a natural or provoked re-emergence of smallpox. Therefore, it is mandatory to improve the current capability to prevent or treat such infections. The DNA repair protein uracil-DNA glycosylase (UNG) is one of the viral enzymes important for poxvirus pathogenesis. Consequently, the inhibition of UNG could be a rational strategy for the treatment of infections with poxviruses. In order to develop inhibitor assays for UNG, as a ﬁrst step, we have characterised the recombinant vaccinia virus UNG (vUNG) and compared it with the human nuclear form (hUNG2) and catalytic fragment (hUNG) UNG. In contrast to hUNG2, vUNG is strongly inhibited in the presence of 7.5 mM MgCl 2 . We have shown that highly puriﬁed vUNG is not inhibited by a speciﬁc uracil-DNA glycosylase inhibitor. Interestingly, both viral and human enzymes preferentially excise uracil when it is opposite to cytosine. The present study provides the basis for the design of speciﬁc inhibitors for vUNG.
A REVIEW ON ELECTROMAGNETICS (EM) EXPOSURE MEASUREMENT TECHNIQUES FROM BASE STATION

EM exposure in the range of non-ionizing radiations (NIR) which falls in the radio frequency up to 3GHz is mainly sourced from mobile phone base stations, broadcast towers and radar facilities. This reviews based on previous researcher obtained results and methods in order to determine the best technique to measure the exposure. Moreover, the estimation of exposure levels by considering the specification of the antennas installed and area of the base stations itself was also reviewed. It was found that numerous study of NIR exposure level has been conducted in other countries, while Malaysia has become aware of the importance. Most of the studies used field meter to carry out the measurement, and the exposure level obtained were far lower than the limit recommended by World Health Organization (WHO).
Quantitative proteomics analysis of phosphorylated proteins in the hippocampus of Alzheimer disease subjects

Phosphorylation on tyrosine, threonine and serine residues represents one of the most important post-translational modifications and is a key regulator of cellular signaling of multiple biological processes that require a strict control by protein kinases and protein phosphatases. Abnormal protein phosphorylation has been associated with several human diseases including Alzheimer disease (AD). One of the characteristic hallmarks of AD is the presence of neurofibrillary tangles, composed of microtubule-associated, abnormally hyperphosphorylated tau protein. However, several others proteins showed altered phosphorylation levels in AD suggesting that deregulated phosphorylation may contribute to AD pathogenesis. Phosphoproteomics has recently gained attention as a valuable approach to analyze protein phosphorylation, both in a quantitave and a qualitative way. We used the fluorescent phosphospecific Pro-Q Diamond dye to identify proteins that showed alterations in their overall phosphorylation in the hippocampus of AD vs. control (CTR) subjects. Significant changes were found for 17 proteins involved in crucial neuronal process such as energy metabolism or signal transduction. These phosphoproteome data may provide new clues to better understand molecular pathways that are deregulated in the pathogenesis and progression