Miracle-dz/UniFAR-FTUs huggingface dataset:
Effects of different levels of ergot in concentrates on the growing and slaughtering performance of bulls and on carry-over into edible tissue

Abstract The aim of the present study was to examine long-term effects of low levels of ergot alkaloids on growing bulls. Natural grown ergot with a mean total alkaloid concentrations of 633 mg/kg, and ergotamine (25%), ergocristine (15%) and ergosine (13%) as the most prominent alkaloids, was used. In a dose-response study 38 Holstein Friesian bulls were fed with three different doses of this ergot (0, 0.45 and 2.25 g/kg concentrate corresponding to an average total alkaloid concentration of the daily ration of 0, 69 and 421 µg/kg DM) over a period of approximately 230 days. Live weight, feed intake and health condition were monitored over the entire test period. The bulls were slaughtered at a live weight of approximately 550 kg. Carcass composition and quality were recorded and samples of liver, muscle, kidneys, fat, bile, urine and blood were analysed for ergot alkaloids. Liver enzyme activities and total bilirubin were measured in the blood. Statistically, no significant differences were detectable between the three feeding groups. Mean live weight gain over all groups was 1.41 kg/d with a mean dry matter intake of 7.35 kg/d. No carry over into tissues could be proved out of the experiment. To derive a no-effect level for beef cattle further research including higher ergot doses will be necessary.
Bringing oversight review in line with online research

The purpose of an oversight structure or institution is to protect human subjects from research that would pose unacceptable dangers or deny human rights. Review boards provide an independent assessment of research proposals. This additional level of scrutiny is meant to provide an additional level of protection for human subjects. However, oversight of human subject research, as currently carried out in the bureaucratic, rule‐based, clinically‐biased American system, is too cumbersome with regard to online research. In addition, it is not conducive to the training of ethical Internet researchers. Internet research differs from traditional human subject research in many ways, and the oversight rules governing traditional research do not easily relate to the complexities of conducting research online. Online researchers do not oppose the foundational principles of non‐maleficence (avoiding harm) and autonomy, nor do they reject the ideals of informed consent and confidentiality, nevertheless, they face pra.
The Clinical Relevance of L26, a B‐Cell‐Specific Antibody, in Hodgkin's Disease

Although Reed-Sternberg cells and their variants (RS/V) in most cases of Hodgkin's disease (HD) lack lymphocyte-associated antigens, some cases of HD, particularly nodular lymphocyte-predominant HD (NLPHD), contain RS/V cells that appear to be of B-cell origin. This study was designed to test whether differences in clinical presentation and therapeutic response exist between patients with HD of various histologic types whose tumors contain RS/V cells that express antigens recognized by L26, an antibody directed against B lymphocytes, and those that do not. We studied 46 patients with stages I and II HD who were treated with radiotherapy alone between 1969 and 1986. Although the expression of L26 and the other antibodies was not predictive for relapse-free, cause-specific, or absolute survival, the labeling of the RS/V cells with L26, independent of histologic type, was significantly associated with peripheral lymph nodal presentation, male gender, and infradiaphragmatic presentation.
Putative Treponema pallidum cytadhesins share a common functional domain

Three putative Treponema pallidum ligands (P1, P2, and P3) that bind host fibronectin were characterized by peptide mapping. Papain digestion of each protein yielded a comigrating peptide of approximately 12,000 molecular weight. An antibody to this protein fragment inhibited T. pallidum host cytadherence, indicating that this peptide may be the functional domain of these treponemal adhesins.
CD36-Mediated Hematoma Absorption following Intracerebral Hemorrhage: Negative Regulation by TLR4 Signaling

Promoting hematoma absorption is a novel therapeutic strategy for intracerebral hemorrhage (ICH); however, the mechanism of hematoma absorption is unclear. The present study explored the function and potential mechanism of CD36 in hematoma absorption using in vitro and in vivo ICH models. Hematoma absorption in CD36-deficient ICH patients was examined. Compared with patients with normal CD36 expression, CD36-deficient ICH patients had slower hematoma adsorption and aggravated neurologic deficits. CD36 expression in perihematomal tissues in wild-type mice following ICH was increased, whereas the hematoma absorption in CD36−/− mice was decreased. CD36−/− mice also showed aggravated neurologic deficits and increased TNF-α and IL-1β expression levels. The phagocytic capacity of CD36−/− microglia for RBCs was also decreased. Additionally, the CD36 expression in the perihematoma area after ICH in TLR4−/− and MyD88−/− mice was significantly increased, and hematoma absorption was significantly promoted, which was significantly inhibited by an anti-CD36 Ab. In vitro, TNF-α and IL-1β significantly inhibited the microglia expression of CD36 and reduced the microglia phagocytosis of RBCs. Finally, the TLR4 inhibitor TAK-242 upregulated CD36 expression in microglia, promoted hematoma absorption, increased catalase expression, and decreased the H2O2 content. These results suggested that CD36 mediated hematoma absorption after ICH, and TLR4 signaling inhibited CD36 expression to slow hematoma absorption. TLR4 inhibition could promote hematoma absorption and significantly improve neurologic deficits following ICH.
Hepcidin and anemia of the critically ill patient: bench to bedside.

A NEMIA occurs frequently in critically ill patients, with 60–66% of them having anemia when admitted to the intensive care unit (ICU), and is associated with worse outcomes (such as increased length of stay and increased mortality). Anemia is only partially corrected during ICU stay because recent recommendations have led to a decrease in transfusion triggers. Today the prevalence of anemia in patients being discharged from the ICU is very high, being found in at least 75% of the patients upon final hemoglobin measurement. This common, and severe anemia at ICU discharge may also be prolonged after the ICU stay. The median time to recovery of anemia is 11 weeks. One observational study reports that more than half of such patients are still anemic at 6 months. Although the impact of anemia on rehabilitation after ICU discharge or quality of life has not been fully evaluated, it is well accepted that anemia is associated with worse outcomes for postoperative rehabilitation and for patients with chronic diseases such as cancer and thus should retain our interest at the bedside and in the research unit. Because blood transfusion is not an option for complete correction of this anemia, one may advocate the use of other treatments, such as erythropoiesis-stimulating agents (ESA) or iron. ESA efficacy has been studied in critically ill patients and has not proven to be indicated, at least according to the design of the studies. Iron is needed for erythropoiesis and thus may be indicated for the treatment of this anemia, but iron is also a toxic compound with the ability to induce oxidative stress or promote bacterial growth. A better understanding of iron metabolism regulation may help to define the place of iron in these indications. The recent discovery of hepcidin (i.e., the master regulator of iron metabolism) has shed new light on the regulation of iron homeostasis and has increased understanding of the physiopathology of anemia in complex clinical situations where several regulatory circuits interfere with iron metabolism, such as anemia of inflammation and anemia of critically ill patients. This article reviews the link between iron metabolism and anemia in critically ill patients and discusses therapeutic perspectives in this area.
Distinct nonrandom patterns of chromosomal deletions in giant-cell lesions of bone

Cytogenetic analyses were performed on a bone giant cell reparative granuloma (GCRG) and on three bone giant cell tumors (GCT). The present GCRG case is the second to be described cytogenetically. A modal chromosome number of 46 was observed in all samples. Clonal chromosome abnormalities were detected in all cases. The numerical alterations most frequently observed involved the loss of chromosomes 17 and 18. Among the structural anomalies observed, there was preferential involvement of chromosomes 6 and 10. Three GCT cases presented del(10)(p13) and two cases presented del(6)(q25) (1 GCRG and 1 GCT). These breakpoints mapped on 10p and 6q may harbour genes of importance in the development of bone giant cell tumors.
RED BLOOD CELL SIZE IN MULTIPLE SCLEROSIS

In 1959 Plum & Fog reported that the mean red blood cell diameter is increased in patients with multiple sclerosis. They found normal red cell diameters in a ‘variety of other diseases’ and concluded that a slight macrocytosis without anaemia is a feature of multiple sclerosis. This work has not been repeated even though its relevance cannot be questioned while the pathogenesis and aetiology of multiple sclerosis remain unknown. There is no evidence suggesting that plaque formation affects the red cell directly and it is equally possible that the change found by Plum and Fog reflects an important metabolic disturbance related to the pathogenesis of this disease. Furthermore, if this change occurred consistently, their observation would have diagnostic implications and might be useful in the genetic and epidemiological investigation of multiple sclerosis. For these reasons and because it has been suggested that abnormal platelet adhesion to glass, known to occur in a number of diseases including multiple sclerosis, reflects abnormal red cell behaviour, the following study was undertaken to confirm Plum and Fog’s observation and to determine the relation between the mean red cell diameter and the duration, severity and activity of the disease.
The FGF Family in Humans, Mice, and Zebrafish: Development, Physiology, and Pathophysiology

In vertebrates, various signaling pathways are activated in a highly coordinated manner to ensure proper development and morphogenesis. Secreted signaling molecules such as FGFs (Fibroblast growth factors), BMPs (Bone morphogenetic factors), WNTs (Wingless/int), and Hedgehogs play crucial roles in development and morphogenesis by acting over variable distances to influence intracellular signaling events in neighboring cells. FGFs are polypeptide growth factors with diverse biological functions. The human FGF family comprises twenty-two members. The mouse and zebrafish are widely used vertebrate models for studying gene function in vivo. The mouse and zebrafish FGF families comprise twenty-two and twenty-eight members, respectively. These FGFs can be classified as paracrine, endocrine, and intracrine FGFs by their mechanisms of action (Itoh & Ornitz, 2008). Paracrine FGFs (canonical FGFs) mediate biological responses by binding to and activating cell surface tyrosine kinase FGFRs. They act as local paracrine signaling molecules and function in multiple developmental processes including differentiation, cell proliferation, and migration (Itoh & Ornitz, 2008; Beenken & Mohammadi, 2009). Endocrine FGFs are thought to mediate biological responses in an FGFR-dependent manner. However, they function over long distances as endocrine hormones (Kharitonenkov, 2009; Itoh, 2010). In contrast, intracrine FGFs act as FGFR-independent intracellular molecules that regulate the function of voltage-gated sodium channels (Goldfarb et al., 2007; Laezza et al., 2009). Targeted mutagenesis of Fgf genes in mice has elucidated their functions in development and metabolism. Studies with zebrafish Fgf mutant and knockdown embryos also have revealed their functions in development. In addition, evidence for the involvement of FGF signaling in hereditary, paraneoplastic, and metabolic diseases has also accumulated. FGF signaling disorders contribute to pathological conditions. In this article, we provide a succinct review of the FGF family in humans, mice, and zebrafish and their developmental physiological and pathophysiological roles.
VISUALIZATION STUDY OF CATHODE FLOODING WITH DIFFERENT OPERATING CONDITIONS IN A PEM UNIT FUEL CELL

Visualization technique was used to better understand the water build-up phenomena on the cathode side of a proton exchange membrane (PEM) unit fuel cell. In this study, a transparent PEM unit fuel cell with an active area of 25 cm2 was designed and fabricated to allow for the visualization of cathode channel with fuel cell performance characteristics. Two-phase flow due to the electrochemical reaction of fuel cell was experimentally investigated. The images photographed by CCD camera with various cell temperatures (30–50°C) and different inlet humidification levels were presented in this study. Results indicated that the flooding on the cathode side first occurs near the exit of cathode flow channel. As the fuel cell operating temperature increases, it was found that water droplets tend to evaporate easily because of increased saturation vapor pressure and it can have an influence on lowering the flooding level. The approaches of this study can effectively contribute to the detailed researches on water transport phenomena including modeling water transport of an operating PEM fuel cell.Copyright © 2005 by ASME
BDNF Protein Measured by a Novel Enzyme Immunoassay in Normal Brain and after Seizure: Partial Disagreement with mRNA Levels

Messenger RNA for brain‐derived neurotrophic factor (BDNF) is distributed in many brain regions and regulated by excitatory neuronal activity. Despite numerous studies of BDNF mRNA, the distribution and regulation of BDNF protein are poorly understood because of the difficulty of its quantitative measurement. We have established a two‐site enzyme immunoassay that detects trace amounts of BDNF protein (>1 pg/assay) but not other neurotrophins or growth factors. The highest levels of BDNF in adult rat brain were found in the hippocampus, followed by the hypothalamus, neocortex, cerebellum, thalamus and striatum. This pattern is similar, but not identical, to the distribution of BDNF mRNA. A similar disparity between BDNF protein and mRNA levels was observed in their changes after hilus lesion‐induced limbic seizures. In limbic structures, BDNF concentrations remained elevated 4 days after seizure onset, whereas BDNF mRNA has been reported previously to return to basal levels within 46 h. The temporal and spatial differences between the dynamics of protein and mRNA levels suggest the importance of post‐translational and/or subcellular processes for BDNF production. The persistence of the increases in BDNF content was also reflected in its biological activity, e.g. peptidergic differentiation activity. After limbic seizures, neuropeptide Y content was most markedly and persistently elevated in the entorhinal/amygdaloid region, where the most sustained up‐regulation of BDNF protein was observed. These results suggest that the sustained increase of BDNF protein in these limbic structures is involved in prolonged post‐seizure phenomena, including peptidergic alterations.
Metabolic syndrome: A multifaceted risk factor for kidney stones

Abstract Kidney stones and metabolic syndrome (MetS) are common conditions in industrialized countries. There is growing evidence of associations between kidney stone disease and MetS or some of its components. The link between uric acid stones and MetS is well understood, but the link with calcium oxalate (CaOx) stones, the most common kidney stone composition, is more complex, and MetS is frequently overlooked as a risk factor for calcium nephrolithiasis. The physiopathological mechanisms of kidney stone disease in MetS are reviewed in this article. Uric acid stones are a consequence of the excessively acidic urine that results from insulin resistance. The pathophysiology of CaOx stones may include: increased excretion of lithogenesis promoters and decreased excretion of inhibitors; increased risk of Randall's plaque development; and inflammatory damage to renal epithelia by oxidative stress, as a consequence of the insulin-resistant milieu that characterizes MetS. The last mechanism contributes to the adhesion of CaOx crystals to subepithelial calcium deposits working as anchor sites where stones can grow. The predominant MetS features could determine the chemical composition of the stones in each patient. Kidney stones may be a renal manifestation of MetS and features of this syndrome should be looked for in patients with idiopathic nephrolithiasis.
Comparative effects of losartan and nifedipine therapy on exercise capacity, Doppler echocardiographic parameters and endothelin levels in patients with secondary pulmonary hypertension.

OBJECTIVE Pulmonary hypertension (PHT) is associated with high mortality and morbidity. Interest has increased in the use of drugs that, because of their neurohumoral inhibitory effects, inhibit the renin angiotensin system. In this study, we sought to examine whether losartan therapy is non-inferior to nifedipine in the treatment of secondary PHT. METHODS This prospective randomized study consisted of 63 patients (mean age, 63.7+/- 9.1 years) with PHT who underwent Doppler echocardiographic examination. A baseline 6-minute walk test (6MWT) and cardiopulmonary exercise test (CPET) were performed, and the endothelin-1 level of each patient was measured. Patients were assigned to two groups receiving treatment with nifedipine (n=30) and losartan (n=33). After 2 months of treatment, those measurements were repeated. The groups were compared with regard to effectiveness for the studied parameters using 2*2 factorial ANOVA design for repeated measurements. RESULTS When posttreatment values were compared with baseline values in both groups, the following statistically significant changes were noted: the mean values of both mean and systolic pulmonary artery pressures (PAPs) were reduced (p<0.05) on Doppler echocardiography; exercise duration, work rate, and end-tidal carbon dioxide pressure (PETCO2) were higher (p<0.05 for all); and the minute ventilation (VE) and ventilatory equivalents for carbon dioxide (VE/VCO2) were lower (p<0.05 for both) according to the results of a CPET. No statistically significant change was noted in the mean levels of serum endothelin-1. With regard to the results cited above, no statistically significant difference was detected between the losartan and nifedipine groups (p>0.05). CONCLUSION The findings of this study indicate that losartan is non-inferior to nifedipine for reducing PAP and improving exercise capacity. However, the short-term use of losartan or nifedipine had no statistically significant effect on endothelin-1 levels in patients with secondary PHT.
The Impact of Transparency on Foreign Direct Investment

Non-transparency is a term given in this paper to a set of government policies that increase the risk and uncertainty faced by economic actors foreign investors. This increase in risk and uncertainty stems from the presence of bribery and corruption, unstable economic policies, weak and poorly enforced property rights, and inefficient government institutions. Our empirical analysis shows that the degree of non-transparency is an important factor in a country's attractiveness to foreign investors. High levels of non-transparency can greatly retard the amount of foreign investment that a country might otherwise expect. The simulation exercise presented in the statistical part of this paper reveals that on average a country could expect 40 percent increase in FDI from a one point increase in their transparency ranking. Pari passu, non-transparent policies translate into lower levels of FDI and hence lower levels of welfare and efficiency in the host country's economy. A nation that takes steps to increase the degree of transparency in its policies and institutions could expect significant increases in the level of foreign investment into their country. This increased investment translates into more resources, which in turn increases social welfare and economic efficiency.
Histopathology of the Peripheral Vestibular System after Cochlear Implantation in the Human

Objectives: The objective of this study was to describe the histology of the peripheral vestibular system in temporal bones from patients who in life had undergone cochlear implantation and to correlate the findings with previous reports of vestibular dysfunction after cochlear implantation. This is the first quantitative report of the impact of implantation on the vestibular neuronal end organ. Methods: There were 19 temporal bones available for histologic study. Of these, 17 were suitable for the description of the morphology of the membranous labyrinth, 8 for counting Scarpa's ganglion cells, and 6 for measuring the densities of vestibular hair cells. The bones were fixed, cut, and stained according to previously published methods. Preferably, the implanted electrode was left in situ. Vestibular hair cells were counted with Nomarski's optics. Results: Differences in Scarpa's ganglion cell counts and hair cell densities between the implanted and nonimplanted sides were not statistically significant. In 59% of the implanted bones, the cochlea was hydropic, and in the majority of these bones the saccule was collapsed. Conclusion: Cochlear implantation does not cause deafferentation of the peripheral vestibular system. Cochlear hydrops accompanied by saccular collapse is common and may cause attacks of vertigo of delayed onset, similar to Ménière's syndrome as previously reported in several clinical series. Hydrops could be caused by obstruction of endolymphatic flow in the ductus reuniens or in the hook portion of the cochlea or by damage to the lateral cochlear wall caused by implantation.
Establishment Risks for Invasive Species

This article presents a quantitative methodology for evaluating the probability of invasive pest species establishing persistent populations. The estimation of pest establishment relies on data and information describing the biology and ecology of the pest and its interactions with potential host species and the regional environment. This information is developed using a model construct borrowed from theoretical population ecology. The methodology for estimating the probability of pest establishment is part of an overall framework that explores the implications of reductions in pest invasions on subsequent establishment. The risk reduction framework integrates the engineering aspects of different technologies for reducing pest entry, the biology and ecology of pest species, the suitability of potentially susceptible hosts, and the quality of available habitats. The methodology for estimating the risk of establishment is presented using an example pest, the Asian longhorned beetle (Anoplophora glabripennis), which has been introduced into the United States via solid wood packing materials (SWPM) used in international commerce. Uncertainties inherent to the estimation of model parameters that determine the risk of establishment are defined, quantified, and propagated through the population model. Advantages and limitations of the proposed methodology are discussed along with recommendations to make the approach more useful in the management of risks posed by the establishment of pest populations.