Miracle-dz/UniFAR-FTUs huggingface dataset:
RECOVERY AND TESTING OF RAP BINDERS FROM RECYCLED ASPHALT PAVEMENTS

Extraction and recovery of asphalt cement from mixtures is a routine task in most asphalt laboratories. Characterization of extracted asphalt binder and aggregate is important for design, quality control, performance prediction and research purposes. Different methods, equipment and solvents for extraction of asphalt binders have significant effects on the properties of the extracted asphalt binder and aggregate. Under NCHRP 9-12, Incorporation of Reclaimed Asphalt Pavement in the Superpave System, a study was conducted to review the variables in extraction and recovery methods. One objective of this study was to evaluate different extraction and recovery methods and determine the best use for the NCHRP 9-12 study. The second objective was to determine if additional aging of recoverable binders is necessary when conducting mix designs in the laboratory. The experimental matrix developed included two different extraction procedures, two recovery methods and three different solvents. Properties of extracted aggregates and asphalt binders from two different Reclaimed Asphalt Pavements (RAP) were studied. The results demonstrate significant variability on properties of extracted asphalt binder with different solvents, extraction and recovery methods. However, the extracted RAP aggregate gradation was not significantly different with different methods and solvents. The aging of the recovered binders demonstrated insignificant changes for the blending of RAP binders.
Intravenous Immunoglobulins Modulate Neutrophil Activation and Vascular Injury Through Fc&ggr;RIII and SHP-1

Rationale: Intravascular neutrophil recruitment and activation are key pathogenic factors that contribute to vascular injury. Intravenous immunoglobulin (IVIG) has been shown to have a beneficial effect in systemic inflammatory disorders; however, the mechanisms underlying IVIG's inhibitory effect on neutrophil recruitment and activation are not understood. Objective: We studied the mechanisms by which IVIG exerts protection from neutrophil-mediated acute vascular injury. Methods and Results: We examined neutrophil behavior in response to IVIG in vivo, using real-time intravital microscopy. We found that an antibody that blocks both Fc&ggr;RIII and its inhibitory receptor counterpart, Fc&ggr;RIIB, abrogated the inhibitory effect of IVIG on leukocyte recruitment and heterotypic red blood cell (RBC) interactions with adherent leukocytes in wild-type mice. In the context of sickle cell disease, the blockade of both Fc&ggr;RIIB and III abrogated the protective effect of IVIG on acute vaso-occlusive crisis caused by neutrophil recruitment and activation. Analysis of Fc&ggr;RIIB- and Fc&ggr;RIII-deficient mice revealed the predominant expression of Fc&ggr;RIII on circulating neutrophils. Fc&ggr;RIII mediated IVIG-triggered inhibition of leukocyte recruitment, circulating RBC capture, and enhanced Mac-1 activity, whereas Fc&ggr;RIIB was dispensable. In addition, Fc&ggr;RIII-induced IVIG anti-inflammatory activity in neutrophils was mediated by recruitment of Src homology 2 (SH2)-containing tyrosine phosphatase-1 (SHP-1). Indeed, the protective effect of IVIG on leukocyte recruitment and activation was abrogated in SHP-1-mutant mice. Conclusions: Fc&ggr;RIII, a classic activating receptor, has an unexpected inhibitory role on neutrophil adhesion and activation via recruitment of SHP-1 in response to IVIG. Our results identify SHP-1 as a therapeutic target in neutrophil-mediated vascular injury.
Linking renal hypoxia and oxidative stress in chronic kidney disease: Based on clinical subjects and animal models.

This study aims to explore the relationships between renal function, hypoxia, and oxidative stress in chronic kidney disease (CKD). Seventy-six non-dialysis patients with CKD stages 1-5 and eight healthy subjects were included in the clinical research. They were divided into three groups: healthy subjects, CKD stages 1-3, and CKD stages 4-5. In the animal study, 16 rat models of CKD were established through 5/6 renal ablation/infarction (A/I) surgery, and 8 normal rats were split into 3 groups: Sham, CKD, and losartan groups. Blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI) was used to measure cortical and medullary T2* values (COT2* and MET2*) in all subjects and rats to evaluate renal oxygenation. Biochemical indicators were used to assess renal function and antioxidant capacity. Furthermore, the effects of losartan on renal fibrosis, hypoxia, and oxidative stress were examined using immunoblotting, colorimetric, and fluorometric assays. The results demonstrated significant positive associations between COT2* and MET2* with estimated glomerular filtration rate (eGFR). Patients with CKD stages 4-5 showed significantly lower serum superoxide dismutase (SOD) levels, which also had positive correlations with eGFR, COT2*, and MET2*. Furthermore, losartan treatment resulted in improved renal function and fibrosis, leading to increased levels of COT2*, MET2*, and SOD levels in 5/6 A/I rats. This was accompanied by reduced levels of hypoxia-inducible factor-1 alpha (HIF-1α) and malondialdehyde. Furthermore, losartan restored the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), and suppressed the expression of Kelch-like ECH-associated protein 1 (Keap1) in 5/6 A/I kidneys. The study indicates that decline in renal oxygenation and antioxidant capacity is associated with the severity of renal failure in CKD. Losartan can potentially alleviate renal hypoxia and oxidative stress in the treatment of CKD via Keap1-Nrf2/HO-1 pathway.
Blockade of brain stem gap junctions increases phrenic burst frequency and reduces phrenic burst synchronization in adult rat.

Recent investigations have examined the influence of gap junctional communication on generation and modulation of respiratory rhythm and inspiratory motoneuron synchronization in vitro using transverse medullary slice and en bloc brain stem-spinal cord preparations obtained from neonatal (1-5 days postnatal) mice. Gap junction proteins, however, have been identified in both neurons and glia in brain stem regions implicated in respiratory control in both neonatal and adult rodents. Here, we used an in vitro arterially perfused rat preparation to examine the role of gap junctional communication on generation and modulation of respiratory rhythm and inspiratory motoneuron synchronization in adult rodents. We recorded rhythmic inspiratory motor activity from one or both phrenic nerves before and during pharmacological blockade (i.e., uncoupling) of brain stem gap junctions using carbenoxolone (100 microM), 18alpha-glycyrrhetinic acid (25-100 microM), 18beta-glycyrrhetinic acid (25-100 microM), octanol (200-300 microM), or heptanol (200 microM). During perfusion with a gap junction uncoupling agent, we observed an increase in the frequency of phrenic bursts (~95% above baseline frequency; P < 0.001) and a decrease in peak amplitude of integrated phrenic nerve discharge (P < 0.001). The increase in frequency of phrenic bursts resulted from a decrease in both T(I) (P < 0.01) and T(E) (P < 0.01). In addition, the pattern of phrenic nerve discharge shifted from an augmenting discharge pattern to a "bell-shaped" or square-wave discharge pattern in most experiments. Spectral analyses using a fast Fourier transform (FFT) algorithm revealed a reduction in the peak power of both the 40- to 50-Hz peak (corresponding to the MFO) and 90- to 110-Hz peak (corresponding to the HFO) although spurious higher frequency activity (> or =130 Hz) was observed, suggesting an overall loss or reduction in inspiratory-phase synchronization. Although additional experiments are required to identify the specific brain stem regions and cell types (i.e., neurons, glia) mediating the observed modulations in phrenic motor output, these findings suggest that gap junction communication modulates generation of respiratory rhythm and inspiratory motoneuron synchronization in adult rodents in vitro.
Effect of Different Extraction Methods on the Quality and Stability of Coconut Oil

Aims: This study was conducted in order to assess the effect of different extraction methods on the physicochemical properties of coconut oil. Study Design: Coconut harvesting, cleaning, oil extraction, quality analysis. Place and Duration of Study: General Science Laboratory, School of Agriculture and Natural Resources, Catholic University Institute of Buea, South-West Region, Cameroon, from January 2018 to June 2018. Methodology: Oil samples were extracted from coconuts through five different methods, the traditional method 1 (Boiling and grilling for 2 hours), the traditional method 2 (cooling and grilling for 18 min), the maceration method (Hexane extraction), oven drying + pressing (Pressing 1) and finally sun drying + Pressing (Pressing 2). The obtained oils were then characterised by Original Research Article Djikeng et al.; AFSJ, 4(1): 1-8, 2018; Article no.AFSJ. 43263 2 determining their Peroxide, Thiobarbituric acid, Iodine, Acid values and oxidative stability (Rancimat method). Results: Results showed that the traditional method 1 significantly (p<0.05) alter the quality of coconut oil. The best extraction methods were hexane extraction, pressing methods 1 and 2, as they preserve better the quality of coconut oil and have the highest induction and stability times. Among these, hexane extraction and pressing method 1 were the best. Conclusion: The maceration and pressing methods are the best techniques for coconut oil extraction, as they preserve better its quality.
Atrx promotes heterochromatin formation at retrotransposons

More than 50% of mammalian genomes consist of retrotransposon sequences. Silencing of retrotransposons by heterochromatin is essential to ensure genomic stability and transcriptional integrity. Here, we identified a short sequence element in intracisternal A particle (IAP) retrotransposons that is sufficient to trigger heterochromatin formation. We used this sequence in a genome‐wide shRNA screen and identified the chromatin remodeler Atrx as a novel regulator of IAP silencing. Atrx binds to IAP elements and is necessary for efficient heterochromatin formation. In addition, Atrx facilitates a robust and largely inaccessible heterochromatin structure as Atrx knockout cells display increased chromatin accessibility at retrotransposons and non‐repetitive heterochromatic loci. In summary, we demonstrate a direct role of Atrx in the establishment and robust maintenance of heterochromatin.
The retail revolution and food-price mismeasurement

If a product sells for $3 this week at the local supermarket and $2 next week, what is the "real" price? What if that same product has a different price at a different store? Thanks to scanner technology, food prices differ a lot these days because they can be changed quickly and easily. How do our official statistics take these price movements into account? Not too well, according to Leonard Nakamura. In this article, he describes the retail revolution of recent years and how it has led to mismeasurement of food prices
The Effect of Low-Dose Marine n-3 Fatty Acids on Plasma Levels of sCD36 in Overweight Subjects: A Randomized, Double-Blind, Placebo-Controlled Trial

CD36 is a scavenger receptor involved in lipid uptake and inflammation. Recently, non-cell-bound CD36 (sCD36) was identified in plasma and suggested to be a marker of lipid accumulation in the vessel wall. Marine n-3 polyunsaturated fatty acids (PUFA) may have cardioprotective effects. This study evaluated the effect of marine n-3 PUFA on sCD36 levels in overweight subjects. Fifty overweight subjects were randomized to 1.1 g of n-3 PUFA or 2 g of olive oil daily for six weeks. Neutrophils were isolated at baseline and after six weeks of treatment while an adipose tissue biopsy was obtained at baseline. The content of n-3 PUFA in adipose tissue and neutrophils was analyzed by gas chromatography, while plasma levels of sCD36 were determined using an enzyme-linked immunosorbent assay (ELISA). After six weeks of supplement plasma sCD36 did not differ between supplements (P = 0.18). There was no significant correlation between plasma sCD36 levels and n-3 PUFA in neutrophils at baseline (r = −0.02, P = 0.88), after six weeks supplement (r = −0.03, P = 0.85) or in adipose tissue (r = 0.14, P = 0.34). This study therefore does not provide evidence for a cardioprotective effect of n-3 PUFA acting through a CD36-dependent mechanism.
K-ras and Dpc4 mutations in chronic pancreatitis: case series.

AIM To assess whether alterations in the K-ras, p53, and DPC4 genes are present in pancreatitis, a potential precancerous condition that can progress to pancreatic adenocarcinoma. To investigate the alterations occurring at hot spots of K-ras (exon 1), p53 (exons 5 and 7), and DPC4 (exons 8, 10 and 11). METHODS In 10 patients with acute and 22 with chronic pancreatitis, without pancreatic intraepithelial neoplasia (PanIN), DNA was isolated from paraffin embedded tissue samples. The extracted DNA was analyzed by polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP) analysis, single-strand conformation polymorphism (SSCP) analysis, and DNA sequencing. RESULTS In acute pancreatitis samples no mutations were found in any of the investigated genes. In 7 out of 22 samples of chronic pancreatitis nucleotide substitution at exon 1 of K-ras (five at codon 12 and two at codon 13) were found. No mutations in p53 (exons 5 and 7) were detected. Two samples had nucleotide substitutions at exons 8 and 11 of DPC4, introducing STOP signal and change in the amino acid sequence, respectively. One chronic pancreatitis sample displayed simultaneous mutations in K-ras (exon 1, codon 12) and DPC4 (exon 8, codon 358). CONCLUSION Mutations of K-ras and Dpc4 genes can accumulate already in non-malignant, inflammatory pancreatic tissue, suggesting its applicability in monitoring of further destruction of pancreatic tissue and progression into malignancy.
Palliative radiotherapy and chemotherapy instead of surgery in symptomatic rectal cancer with synchronous unresectable metastases: long-term results of a phase II study

Dobromira Tyc-Szczepaniak, Lucjan Wyrwicz, Katarzyna Wi sniowska, Wojciech Michalski, Lucyna Pietrzak and Krzysztof Bujko Department of Radiotherapy, Maria Skłodowska-Curie Memorial Cancer Centre, Warsaw, Poland; Clinical Oncology Division of Department of Gastrointestinal Oncology, Maria Skłodowska-Curie Memorial Cancer Centre, Warsaw, Poland; Department of Clinical Trials and Biostatistics Unit, Maria Skłodowska-Curie Memorial Cancer Centre, Warsaw, Poland
Prokaryotic Expression, Purification and Immunogenicity in Rabbits of the Small Antigen of Hepatitis Delta Virus

Hepatitis delta virus (HDV) is a viroid-like blood-borne human pathogen that accompanies hepatitis B virus infection in 5% patients. HDV has been studied for four decades; however, the knowledge on its life-cycle and pathogenesis is still sparse. The studies are hampered by the absence of the commercially-available HDV-specific antibodies. Here, we describe a set of reproducible methods for the expression in E. coli of His-tagged small antigen of HDV (S-HDAg), its purification, and production of polyclonal anti-S-HDAg antibodies in rabbits. S-HDAg was cloned into a commercial vector guiding expression of the recombinant proteins with the C-terminal His-tag. We optimized S-HDAg protein purification procedure circumventing a low affinity of the His-tagged S-HDAg to the Ni-nitrilotriacetyl agarose (Ni-NTA-agarose) resin. Optimization allowed us to obtain S-HDAg with >90% purity. S-HDAg was used to immunize Shinchilla grey rabbits which received 80 μg of S-HDAg in two subcutaneous primes in the complete, followed by four 40 μg boosts in incomplete Freunds adjuvant. Rabbits were bled two weeks post each boost. Antibody titers determined by indirect ELISA exceeded 107. Anti-S-HDAg antibodies detected the antigen on Western blots in the amounts of up-to 100 pg. They were also successfully used to characterize the expression of S-HDAg in the eukaryotic cells by immunofluorescent staining/confocal microscopy.
The Goblet Cell Protein Clca1 (Alias mClca3 or Gob-5) Is Not Required for Intestinal Mucus Synthesis, Structure and Barrier Function in Naive or DSS-Challenged Mice

The secreted, goblet cell-derived protein Clca1 (chloride channel regulator, calcium-activated-1) has been linked to diseases with mucus overproduction, including asthma and cystic fibrosis. In the intestine Clca1 is found in the mucus with an abundance and expression pattern similar to Muc2, the major structural mucus component. We hypothesized that Clca1 is required for the synthesis, structure or barrier function of intestinal mucus and therefore compared wild type and Clca1-deficient mice under naive and at various time points of DSS (dextran sodium sulfate)-challenged conditions. The mucus phenotype in Clca1-deficient compared to wild type mice was systematically characterized by assessment of the mucus protein composition using proteomics, immunofluorescence and expression analysis of selected mucin genes on mRNA level. Mucus barrier integrity was assessed in-vivo by analysis of bacterial penetration into the mucus and translocation into sentinel organs combined analysis of the fecal microbiota and ex-vivo by assessment of mucus penetrability using beads. All of these assays revealed no relevant differences between wild type and Clca1-deficient mice under steady state or DSS-challenged conditions in mouse colon. Clca1 is not required for mucus synthesis, structure and barrier function in the murine colon.
On the probabilistic characterization of drought events

Drought characterization is an important step in water resources systems planning and management. The assessment of extreme drought events may help decision makers to set effective drought mitigation tools. Drought events can be objectively identified by three main characteristics, namely: drought duration, accumulated deficit and drought intensity. In this paper the joint cumulative distribution functions (cdf's) of accumulated deficit and duration and of intensity and duration are derived as functions of the stochastic characteristics of the underlying variable, which is assumed to be either normal, lognormal, or gamma distributed. The derived cdf's are then applied to determine the return period of critical droughts by considering jointly two drought characteristics, e.g. droughts with accumulated deficit and duration greater than or equal to some fixed values. The methodology has been tested and applied using numerical simulations and records of annual precipitation series. The results of such applications show a good correspondence between the observed and the analytical results.
Nonlocal component of radiative flux perturbation

Radiative flux perturbation (RFP) is defined as the top‐of‐the‐atmosphere (TOA) radiative imbalance after the atmosphere‐land system adjusts fully to an external perturbation, and serves as a useful metric for quantifying climate forcing. This paper presents an effort to address the issue of whether a forcing imposed persistently over a specific region may alter the radiative balance elsewhere through atmospheric circulation, thus giving rise to a nonlocal component of RFP. We perturb the climate simulated with an atmospheric general circulation model (AGCM) solely by increasing the cloud droplet number concentration over the land, and observe widespread positive (warming) RFP over the ocean, along with the expected negative (cooling) RFP over the land. A detailed analysis suggests that the oceanic (or nonlocal) RFP is closely associated with a reduction in low cloud amount, which can be attributed primarily to the horizontal advection of drier land boundary layer air and to the oceanic boundary layer top entrainment of drier free troposphere air. By examining how the land surface and atmospheric energy balances are re‐established, we are able to identify the physical mechanisms behind the strong hydrological impact of a tropical land shortwave (SW) forcing (the multiplier effect). In contrast, the hydrological cycle is relatively insensitive to an extratropical forcing.
Effects of exercise training on cardiovascular adrenergic system

In heart failure (HF), exercise has been shown to modulate cardiac sympathetic hyperactivation which is one of the earliest features of neurohormonal derangement in this syndrome and correlates with adverse outcome. An important molecular alteration related to chronic sympathetic overstimulation in HF is represented by cardiac β-adrenergic receptor (β-AR) dysfunction. It has been demonstrated that exercise reverses β-AR dysfunction by restoring cardiac receptor membrane density and G-protein-dependent adenylyl cyclase activation. In particular, several evidence indicate that exercise reduces levels of cardiac G-protein coupled receptor kinase-2 (GRK2) which is known to be involved in both β1-AR and β2-AR dysregulation in HF. Similar alterations of β-AR system have been described also in the senescent heart. It has also been demonstrated that exercise training restores adrenal GRK2/α-2AR/catecholamine (CA) production axis. At vascular level, exercise shows a therapeutic effect on age-related impairment of vascular reactivity to adrenergic stimulation and restores β-AR-dependent vasodilatation by increasing vascular β-AR responsiveness and reducing endothelial GRK2 activity. Sympathetic nervous system overdrive is thought to account for >50% of all cases of hypertension and a lack of balance between parasympathetic and sympathetic modulation has been observed in hypertensive subjects. Non-pharmacological, lifestyle interventions have been associated with reductions in SNS overactivity and blood pressure in hypertension. Several evidence have highlighted the blood pressure lowering effects of aerobic endurance exercise in patients with hypertension and the significant reduction in sympathetic neural activity has been reported as one of the main mechanisms explaining the favorable effects of exercise on blood pressure control.
Landsat-5 Thematic Mapper Thermal Band Calibration Update

The Landsat-5 thematic mapper (TM) has been operational since 1984. For much of its life, the calibration of TM has been neglected, but recent efforts are attempting to monitor stability and absolute calibration. This letter focuses on the calibration of the TM thermal band from 1999 to the present. Initial studies in the first two years of the TM mission showed that the thermal band was calibrated within the error in the calibration process (plusmn 0.9 K at 300 K). The calibration was not rigorously monitored again until 1999. While the internal calibrator has behaved as expected, recent vicarious calibration results show a significant offset error of 0.092 W/m2 ldr sr ldr mum or about 0.68 K at 300 K. This offset error was corrected on April 2, 2007 within the U.S. processing system through the modification of a calibration coefficient for all data acquired on or after April 1, 1999. Users can correct their own Level-1 data processed prior to April 2, 2007, by adding 0.092 W/m2 ldr sr ldr mum to their radiance level products. The state of the calibration between 1985 and 1999 is unknown; no changes for data acquired in those years are being recommended here.