Miracle-dz/UniFAR-FTUs huggingface dataset:
Macrophage therapy for murine liver fibrosis recruits host effector cells improving fibrosis, regeneration, and function

Clinical studies of bone marrow (BM) cell therapy for liver cirrhosis are under way but the mechanisms of benefit remain undefined. Cells of the monocyte‐macrophage lineage have key roles in the development and resolution of liver fibrosis. Therefore, we tested the therapeutic effects of these cells on murine liver fibrosis. Advanced liver fibrosis was induced in female mice by chronic administration of carbon tetrachloride. Unmanipulated, syngeneic macrophages, their specific BM precursors, or unfractionated BM cells were delivered during liver injury. Mediators of inflammation, fibrosis, and regeneration were measured. Donor cells were tracked by sex‐mismatch and green fluorescent protein expression. BM‐derived macrophage (BMM) delivery resulted in early chemokine up‐regulation with hepatic recruitment of endogenous macrophages and neutrophils. These cells delivered matrix metalloproteinases‐13 and ‐9, respectively, into the hepatic scar. The effector cell infiltrate was accompanied by increased levels of the antiinflammatory cytokine interleukin 10. A reduction in hepatic myofibroblasts was followed by reduced fibrosis detected 4 weeks after macrophage infusion. Serum albumin levels were elevated at this time. Up‐ regulation of the liver progenitor cell mitogen tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) preceded expansion of the progenitor cell compartment. Increased expression of colony stimulating factor‐1, insulin‐like growth factor‐1, and vascular endothelial growth factor also followed BMM delivery. In contrast to the effects of differentiated macrophages, liver fibrosis was not significantly altered by the application of macrophage precursors and was exacerbated by whole BM. Conclusion: Macrophage cell therapy improves clinically relevant parameters in experimental chronic liver injury. Paracrine signaling to endogenous cells amplifies the effect. The benefits from this single, defined cell type suggest clinical potential. (HEPATOLOGY 2011;)
Secretion of extracellular proteins by enterohemorrhagic Escherichia coli via a putative type III secretion system

Enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) infections result in attaching and effacing lesions on intestinal epithelial cells. Secretion of extracellular proteins via a type III secretion apparatus is necessary for the formation of attaching and effacing lesions by EPEC. We now show that EHEC also secretes polypeptides via a putative type III secretion system. The secreted EHEC proteins are recognized by rabbit antiserum raised against the proteins secreted from EPEC and by human serum from a patient infected with an EHEC O157:H7 strain.
Compact-Reconstruction WENO Methods for Compressible Flows

This project develops a program that solves the Euler equations of compressible flow in two dimensions using a Compact-Reconstruction Weighted Essentially NonOscillatory (CRWENO) scheme, modified to apply to grids with unequal spacing. The code will operate in parallel to reconstruct quantities along cell lines of a fixed Cartesian grid, and will be validated against several standard compressible flow problems.
Football Player's Performance and Market Value

A lot of money is involved with the transfers of top players in the big European football leagues. For various reasons, obtaining a good economic valuation of football players throughout the year is valuable, in other words, not just when a player has just transferred. Furthermore, it is relevant to consider how the market value of a player relates to the performance of that player. Both these factors again depend on the various parameters of the player, that might be gleaned from various public sources on the web. In this paper, we demonstrate how market value and performance of La Liga (the Spanish League) players can be modeled using extensive public data sources.
Characterization of Biochemical and Functional Effects of Antiplatelet Drugs as a Key to Their Clinical Development

Currently available antiplatelet drugs have been largely developed using Bom’s platelet aggregation technique (1) to characterize the dose-response relationship inpreclinical as well as in phase I/II studies. One notable exception is perhaps the development of low-dose aspirin during the last 10-15 years, largely based on biochemical end-points related to platelet arachidonate metabolism (2). Platelet aggregation in response to various agonists (e.g., ADP, collagen, arachidonate) added in vitro is a measure of “capacity”, which indicates what platelets can do when challenged by rather intense stimuli in a closed artificial system. The relevance of this capacity index to the actual occurrence of platelet activation in vivo is still unknown. Measurement of the plasma levels of platelet-derived products (e.g., thromboxane B2, platelet factor 4 or /3-thromboglobulin) might be inaccurate due to platelet activation ex vivo during blood sampling. Similar problems probably affect measurements of platelet-related antigens using flow cytometry. None of these analytical procedures can unequivocally establish the signal (generated in v/v0)-to-noise (generated ex vivo) ratio for the detection of platelet activation in health or disease. Measurement of TXB2 production during whole blood clotting is also a capacity index related to virtually maximal conversion of platelet arachidonic acid through the prostaglandin (PG)H-synthase pathway in response to endogenously formed thrombin (3). An alternative to these methods is the measurement of urinary excretion of major enzymatic metabolites of TXB2 which is thougt to be a reliable index of platelet function in vivo, following the demonstration that: (a) ll-dehydro-TXB2 and 2,3,-dinor-TXB2 are excreted at low rates under physiological circumstances (4) (thus, low background “noise” unaffected by sampling-related artifacts); (b) their excretion increases linearly with increased rates of entry of TXB2 into the systemic circulation (4,5); and (c) they are largely derived from platelet TXA2 biosynthesis in vivo (6). Moreover, studies of throm­ boxane metabolite excretion are directly relevant to an impor­ tant mechanism of amplification of platelet response to a variety of agonists as well as to the mechanism of action of aspirin in inhibiting platelet function.
Schizophrenia: developmental disturbance of brain and mind?

Schizophrenia is the most severe of the mental illnesses and affects approximately 0.8% of the population in Western societies. Postmortem and neuroimaging studies show that patients with schizophrenia have slightly larger cerebral ventricles than normal and a decrease in cortical volume, most markedly in the left temporal lobe. These changes are present at diagnosis and appear to show little change over extended periods of follow‐up. Associated findings such as lack of normal cerebral asymmetry and cytoarchitectonic changes suggestive of impaired migration of cortical neurons implicate aberrant neurodevelopment. Schizophrenics also show an excess of pregnancy and birth complications, and an association with prenatal exposure to maternal influenza. These and reports of abnormal psychological development in pre‐schizophrenic children add further support to the theory that the disorder has neurodevelopmental origins.
Combining deblurring and denoising for handheld HDR imaging in low light conditions

This paper proposes a probability formulation that unifies both single-image deblurring and multi-image denoising using variational inference. Based on this formulation, a new algorithm for deblurring a noisy and blurry image pair is presented. Besides, we provide also an approach that combines existing optical flow and image denoising techniques for High Dynamic Range imaging.
Crystal-face dependence of surface melting.

Ion-shadowing and -blocking experiments on a cylindrical single crystal of Pb reveal a strongly orientation-dependent disordering (melting) of the surface with increasing temperature. The thickness of the disordered surface layer is found to diverge logarithmically as the bulk melting point is approached. The process of disordering is shown to be driven by an orientation-dependent difference in free energy between the surface in its ordered and liquid states.
Tales of regeneration in zebrafish

Complex tissue regeneration involves exquisitely coordinated proliferation and patterning of adult cells after severe injury or amputation. Certain lower vertebrates such as urodele amphibians and teleost fish have a greater capacity for regeneration than mammals. However, little is known about molecular mechanisms of regeneration, and cellular mechanisms are incompletely defined. To address this deficiency, we and others have focused on the zebrafish model system. Several helpful tools and reagents are available for use with zebrafish, including the potential for genetic approaches to regeneration. Recent studies have shed light on the remarkable ability of zebrafish to regenerate fins. Developmental Dynamics 226:202–210, 2003. © 2003 Wiley‐Liss, Inc.
Treatment of radial artery graft spasm after coronary artery bypass grafting

Spasm of radial artery (RA) used as a conduit for CABG (coronary artery bypass graft) surgery is a rare phenomenon. Our experience with surgical treatment of RA spasm is reported. The patient with triple vessels disease was scheduled for elective CABG surgery. Both radial and mammary arteries were used to create four distal anastomoses. Seven hours after the patient was admitted to intensive care unit his condition started to deteriorate, severe ischemia and low cardiac output syndrome developed. Resternotomy was performed and intraortic balloon was inserted through the ascending aorta (patient had severe peripheral artery disease). During reexploration both RA‘s conduits were found spastic. Nitroglycerin and papaverin solutions were injected into the adjacent tissues of radial arteries. Following this treatment RA became dilated, ST segment on ECG came to normal. RA spasm can occur in rare cases despite prophylactic antispastic measures. However, early diagnosis and initiation of appropriate treatment might
Tropical Atlantic climate and ecosystem regime shifts during the Paleocene–Eocene Thermal Maximum

Abstract. The Paleocene–Eocene Thermal Maximum (PETM, 56 Ma) was a phase of rapid global warming associated with massive carbon input into the ocean–atmosphere system from a 13C-depleted reservoir. Many midlatitude and high-latitude sections have been studied and document changes in salinity, hydrology and sedimentation, deoxygenation, biotic overturning, and migrations, but detailed records from tropical regions are lacking. Here, we study the PETM at Ocean Drilling Program (ODP) Site 959 in the equatorial Atlantic using a range of organic and inorganic proxies and couple these with dinoflagellate cyst (dinocyst) assemblage analysis. The PETM at Site 959 was previously found to be marked by a ∼ 3.8 ‰ negative carbon isotope excursion (CIE) and a ∼ 4 °C surface ocean warming from the uppermost Paleocene to peak PETM, of which ∼ 1 °C occurs before the onset of the CIE. We record upper Paleocene dinocyst assemblages that are similar to PETM assemblages as found in extratropical regions, confirming poleward migrations of ecosystems during the PETM. The early stages of the PETM are marked by a typical acme of the tropical genus Apectodinium, which reaches abundances of up to 95 %. Subsequently, dinocyst abundances diminish greatly, as do carbonate and pyritized silicate microfossils. The combined paleoenvironmental information from Site 959 and a close-by shelf site in Nigeria implies the general absence of eukaryotic surface-dwelling microplankton during peak PETM warmth in the eastern equatorial Atlantic, most likely caused by heat stress. We hypothesize, based on a literature survey, that heat stress might have reduced calcification in more tropical regions, potentially contributing to reduced deep sea carbonate accumulation rates, and, by buffering acidification, also to biological carbonate compensation of the injected carbon during the PETM. Crucially, abundant organic benthic foraminiferal linings imply sustained export production, likely driven by prokaryotes. In sharp contrast, the recovery of the CIE yields rapid (≪ 10 kyr) fluctuations in the abundance of several dinocyst groups, suggesting extreme ecosystem and environmental variability.
An assessment of different optimization strategies for location tracking with an Android application on a smartphone

This paper presents a study of the efficacy of different optimization strategies for location tracking on an Android App that is run on a smartphone. The basic algorithm determines the most probable path of the user within a WiFi network by comparing raw RSSI measurements at each location with values in a fingerprint database. The investigated optimization strategies include: accounting for previous locations, increasing the number of WiFi scans per location, applying an advanced averaging technique, exploiting accelerometer data, shifting the frequency band from 2.4 to 5 GHz, and changing the position of the smartphone with respect to the body. It is shown that especially the accelerometer data allow enhancing the location estimation significantly. By combining different techniques, an average accuracy better than 2 m can be achieved.
Phospholipase Cγ2 Is Critical for Dectin-1-mediated Ca2+ Flux and Cytokine Production in Dendritic Cells*

Dectin-1 is a C-type lectin that recognizes β-glucan in the cell walls of fungi and plays an important role in anti-fungal immunity. It signals via tyrosine kinase Syk and adaptor protein Card9 to activate NF-κB leading to proinflammatory cytokine production in dendritic cells (DCs). Other than this, not much else is known of the mechanism of Dectin-1 signaling. We demonstrate here that stimulation of DCs with zymosan triggers an intracellular Ca2+ flux that can be attenuated by a blocking anti-Dectin-1 antibody or by pre-treatment of cells with the phospholipase C (PLC) γ-inhibitor U73122, suggesting that Dectin-1 signals via a PLCγ pathway to induce Ca2+ flux in DCs. Interestingly, treatment of DCs with particulate curdlan, which specifically engages Dectin-1, results in the phosphorylation of both PLCγ1 and PLCγ2. However, we show that PLCγ2 is the critical enzyme for Dectin-1 signaling in DCs. PLCγ2-deficient DCs have drastic impairment of Ca2+ signaling and are defective in their secretion of interleukin 2 (IL-2), IL-6, IL-10, IL-12, IL-23, and tumor necrosis factor α. PLCγ2-deficient DCs also exhibit impaired activation of ERK and JNK MAPKs and AP-1 and NFAT transcription factors in response to Dectin-1 stimulation. In addition, PLCγ2-deficient DCs are also impaired in their activation of NF-κB upon Dectin-1 engagement due to defective assembly of the Card9-Bcl10-Malt1 complex and impaired IKKα/β activation and IκBα degradation. Thus, our data indicate that pattern recognition receptors such as Dectin-1 could elicit Ca2+ signaling and that PLCγ2 is a critical player in the Dectin-1 signal transduction pathway.
Water saving traits co-map with a major terminal drought tolerance 12 quantitative trait loci in pearl millet ( Pennisetum glaucum ( L . ) R . Br . ) 13 14

Low transpiration rates under fully irrigated conditions decrease plant water use 66 at vegetative stage and then increase the water availability during grain filling and then 67 the terminal drought tolerance in pearl millet. 113 recombinant inbred lines developed 68 from a cross between H77/833-2 and PRLT2/89-33 (terminal drought sensitive × tolerant 69 genotype) were evaluated to map transpiration rate (Tr, a proxy for canopy conductance), 70 organs weight, leaf area and thickness and study their interactions. Transpiration rate was 71 increased by two H77/833-2 and two PRLT2/89-33 alleles on linkage group (LG) 2, 72 whose importance depended on the vapor pressure deficit. The two H77/833-2 and one 73 PRLT2/89-33 alleles co-mapped to a previously identified major terminal drought 74
Graft-Versus-Host Disease (GVHD) An Evidence-Based Management Guidelines.

Hematopoietic stem cell transplantation (SCT) provides effective therapy for patients with lymphohematopoietic, immunologic, metabolic and other disorders. Current estimates of annual numbers of allogeneic SCT are 12.000 to 15.000 worldwide, with continuing growth rate of 10 to 20% per year. Transplant-related mortality at one year after HLA-identical sibling transplants is about 30%. A major impediment to successful allogeneic-SCT or donor lymphocyte infusion (DLI) is the graft-versus-host disease (GVHD) mediated by immunologically competent cells, mainly T-lymphocytes, in the grafted blood or marrow. The resultant GVHD is a complex clinical syndrome, which involves the graft-versus-host reaction, as well as the infectious complications related to the compromised host immunity secondary to treatment of GVHD and/or GVHD per se. Although improvements have been made in the prevention of GVHD, these advances have not resulted in a concomittant improvement in the treatment of this condition, particularly of the severe form of GVHD that accounts for as much as 50% of the cases. Allo-SCT is used in increasingly older patients, in whom the risk for GVHD is greater. The use of unrelated donors and related but nonhuman leukocyte antigen (HLA)-identical donors is expanding. Acute and chronic GVHD are larger problems, both in incidence and in severity, in recipients of alternative-donor SCT. The use of DLI to treat relapsed disease or to achieve full donor chimerism after nonmyeloablative transplantation has resulted in the development of GVHD in a substantial number of these patients. Finally, many studies including a recent meta-analysis have clearly shown that patients receiving allogeneic peripheral blood stem cell transplants have a much higher incidence of chronic GVHD than comparable patients receiving marrow grafts.
Switching between the two action modes of the dual‐affinity nitrate transporter CHL1 by phosphorylation

To counteract fluctuating nutrient environments, plants have evolved high‐ and low‐affinity uptake systems. These two systems were traditionally thought to be genetically distinct, but, recently, two Arabidopsis transporters, AtKUP1 and CHL1, were shown to have dual affinities. However, little is known about how a dual‐affinity transporter works and the advantages of having a dual‐affinity transporter. This study demonstrates that, in the case of CHL1, switching between the two modes of action is regulated by phosphorylation at threonine residue 101; when phosphorylated, CHL1 functions as a high‐affinity nitrate transporter, whereas, when dephosphorylated, it functions as a low‐affinity nitrate transporter. This regulatory mechanism allows plants to change rapidly between high‐ and low‐affinity nitrate uptake, which may be critical when competing for limited nitrogen. These results demonstrate yet another regulatory role of phosphorylation in plant physiology.
Hemodynamic Effects of Peritoneal Dialysis

It is well recognized that dialysis patients display hugely elevated rates of cardiac mortality (1). It is also becoming appreciated that this rate of cardiovascular (CV) attrition is not driven by the same variety of risk factors or pathophysiological processes that are important in the general population (2). Classical complicated atherosclerotic disease appears not to be the predominant mode of death in either hemodialysis (HD) or peritoneal dialysis (PD) patients. This increase in CV mortality is driven by a combination of sudden cardiac death and heart failure. Intradialytic hemodynamic change is becoming increasingly appreciated as being of crucial importance in the development of the observed patterns of CV morbidity and mortality in HD patients. Patients receiving dialysis are particularly susceptible to myocardial ischemia through a variety of mechanisms involving myocardial small vessel changes, coronary atheroma, defective vasoregulation, and reduced peripheral arterial compliance (3). Hemodialysis is capable of inducing subclinical myocardial ischemia and this phenomenon is primarily related to ultrafiltration and hemodynamic instability. We have demonstrated that such perturbations result in highly significant changes in global and segmental myocardial blood flow consistent with the development of myocardial ischemia. The phenomenon of dialysis-induced cardiac injury is common, and around two thirds of prevalent HD patients display dialysisinduced myocardial ischemia. This is associated with increased rate of cardiac arrhythmias, development of reduced systolic cardiac function, and markedly increased mortality (4). Dialysis-induced myocardial stunning is abrogated by appropriate modification of the dialysis treatment to avoid relative hypotension (5,6) and to reduce the ultrafiltration burden. Further work has shown a dose–response relationship between the abrogation of myocardial stunning and the degrees of fluid removal and hemodynamic stress (7). These findings have been confirmed in cross-sectional studies of a variety of quotidian HD schedules (8). In contrast to HD, PD has until recently been considered to exert little, if any, signif icant hemodynamic effects. In many centers, PD has come to be regarded as the therapy of choice to manage the severely cardiovascularly compromised patient. However, in the past few years it has become increasingly appreciated that PD is also capable of exerting short-term effects on CV performance. As with HD, PD also appears to modulate these effects through a number of mechanisms. This article aims to review the studies relating to the effects of intraperitoneal fluid instillation, glucose-/non-glucose-containing fluids, fluid biocompatibility, and PD modality on short-term hemodynamic responses. Furthermore, it will consider what impact longer-term exposure to glucosecontaining fluids might have to systemic CV structural changes and how these changes might relate to increased propensity to demand ischemia in critical vascular beds.
Procedure for measuring radiation efficiency in downlink band for active mobile phones in a reverberation chamber

In this paper, we present a procedure for testing the performance of mobile phone antennas in receive mode by means of measurements in a reverberation chamber. The procedure is based on the reported received power of the phone internal power meter, i.e. no extra cable needs to be connected to the antenna under test and thus the uncertainty due to this can be avoided. In the reverberation chamber, the mobile phone is tested in a uniform multipath environment and with the possibility to easily include a head phantom in the setup to simulate the influence of a user.