Miracle-dz/UniFAR-FTUs huggingface dataset:
Hepatitis A in workers exposed to sewage: a systematic review

OBJECTIVES To assess whether the scientific literature supports the hypothesis that workers exposed to sewage are at higher risk of hepatitis A (HA). METHODS All original papers reporting epidemiological studies published in English, French, or German which reported on the risk of HA infection in workers exposed to sewage were eligible. They were identified by several methods and each original paper was assessed independently with a checklist by two people. Studies were classified according to the strength of their design. Non-eligible studies were also examined to assess the impact of publication bias. If the risk estimates diverged widely, causes for heterogeneity were assessed. A distinction was made between seroprevalence studies based on subclinical HA (defined only by the presence of anti-HA antibodies) and clinical HA. RESULTS 17 eligible studies were identified. No indication of an increased risk of clinical HA could be found. For seroprevalence the studies with the strongest design suggested a slightly increased risk of subclinical HA with an odds ratio (OR) <2.5. Heterogeneity was considerable and precluded a meta-analysis. Considering non-eligible studies would still decrease the OR. CONCLUSIONS The systematic review does not confirm an increased risk of clinical HA in workers exposed to sewage. An increased risk of subclinical HA cannot be excluded but the association between seropositivity and exposure to sewage was not strong and became still weaker if publication bias was taken into account.
The influence of different diets on metabolism and atherosclerosis processes—A porcine model: Blood serum, urine and tissues 1H NMR metabolomics targeted analysis

The global epidemic of cardiovascular diseases leads to increased morbidity and mortality caused mainly by myocardial infarction and stroke. Atherosclerosis is the major pathological process behind this epidemic. We designed a novel model of atherosclerosis in swine. Briefly, the first group (11 pigs) received normal pig feed (balanced diet group—BDG) for 12 months, the second group (9 pigs) was fed a Western high-calorie diet (unbalanced diet group—UDG) for 12 months, the third group (8 pigs) received a Western type high-calorie diet for 9 months later replaced by a normal diet for 3 months (regression group—RG). Clinical measurements included zoometric data, arterial blood pressure, heart rate and ultrasonographic evaluation of femoral arteries. Then, the animals were sacrificed and the blood serum, urine and skeletal muscle tissue were collected and 1H NMR based metabolomics studies with the application of fingerprinting PLS-DA and univariate analysis were done. Our results have shown that the molecular disturbances might overlap with other diseases such as onset of diabetes, sleep apnea and other obesity accompanied diseases. Moreover, we revealed that once initiated, molecular changes did not return to homeostatic equilibrium, at least for the duration of this experiment.
Antiprotozoal and Antimycobacterial Activities of Pure Compounds from Aristolochia elegans Rhizomes

We analyzed the antimycobacterial activity of the hexane extract of rhizomes from Aristolochia elegans. Some compounds of this extract were purified and tested against a group of drug-resistant Mycobacterium tuberculosis strains. We also evaluated their antiprotozoal activities. The hexane extract was active against M. tuberculosis H37Rv at a MIC = 100 μg mL−1; the pure compounds eupomatenoid-1, fargesin, and (8R,8′R,9R)-cubebin were active against M. tuberculosis H37Rv (MIC = 50 μg mL−1), while fargesin presented activity against three monoresistant strains of M. tuberculosis H37Rv and a MDR clinical isolate of M. tuberculosis (MIC < 50 μg mL−1). Both the extract and eupomatenoid-1 were very active against E. histolytica and G. lamblia (IC50 < 0.624 μg mL−1); in contrast, fargesin and (8R,8′R,9R)-cubebin were moderately active (IC50 < 275 μg mL−1). In this context, two compounds responsible for the antimycobacterial presented by A. elegans are fargesin and cubebin, although others may exert this activity also. In addition to the antimycobacterial activity, the hexane extract has important activity against E. histolytica and G. lamblia, and eupomatenoid-1 is one of the compounds responsible for the antiparasite activity.
Infantile Pompe Disease: Clinical and Genetic Characteristics With an Experience of Enzyme Replacement Therapy

Pompe disease is an autosomal recessive disorder caused by lysosomal acid α-glucosidase deficiency. Infantile-onset Pompe disease presents with cardiomyopathy and hypotonia, leading to premature death. This article describes 7 infantile Pompe disease cases and provides their molecular bases and clinical outcomes after enzyme replacement therapy for the first time in Korea. Molecular genetic analyses revealed the presence of 9 different mutations, including 5 novel mutations (c.2171C>A, c.2774C>T, c.1582_3de12, c.1261_1263Tms, and c.1322_1326+9de114). The most common mutation in these 7 patients was c.1316T>A (28%). Four patients received intravenous recombinant human acid α-glucosidase therapy for 2 years, on average, without significant side effects during the treatment course. They all exhibited increased muscle power, with considerable improvement in cardiac function. Pompe disease is heterogeneous regarding both clinical features and molecular characteristics. Early identification of Pompe disease is very important, considering that enzyme replacement therapy is a safe and effective treatment for early-onset patients.
Regulation of FGF1 Gene Promoter through Transcription Factor RFX1

Fibroblast growth factor 1 (FGF1) has been suggested to have an important role in cell growth, proliferation, and neurogenesis. Human FGF1 gene 1B promoter (−540 to +31)-driven green fluorescence (F1BGFP) has been shown to monitor endogenous FGF1 expression. F1BGFP could also be used to isolate neural stem/progenitor cells from embryonic, neonatal, and adult mouse brains or to isolate glioblastoma stem cells (GBM-SCs) from human glioblastoma tissues. Here, we present evidence that transcription factor RFX1 could bind the 18-bp cis-elements (−484 to −467) of the F1B promoter, modulate F1BGFP expression and endogenous FGF1 expression, and further regulate the maintenance of GBM-SCs. These observations were substantiated by using yeast one-hybrid assay, electrophoretic mobility shift assay, chromatin immunoprecipitation assay, gain- and loss-of-function assays, and neurosphere assays. Overexpression of RFX1 was shown to down-regulate FGF-1B mRNA expression and neurosphere formation in human glioblastoma cells, whereas RNA interference knockdown of RFX1 demonstrated the opposite effects. Our findings provide insight into FGF1 gene regulation and suggest that the roles of FGF1 and RFX1 in the maintenance of GBM-SCs. RFX1 may negatively regulate the self-renewal of GBM-SCs through modulating FGF-1B and FGF1 expression levels by binding the 18-bp cis-elements of the F1B promoter.
Effects of perinatal exposure to PCBs and dioxins on play behavior in Dutch children at school age.

Polychlorinated biphenyls (PCBs) and dioxins are known as neurotoxic compounds that may modulate sex steroid hormones. Steroid hormones play a mediating role in brain development and may influence behaviors that show sex differences, such as childhood play behavior. In this study we evaluated the effects of perinatal exposure to environmental levels of PCBs and dioxins on childhood play behavior and whether the effects showed sex differences. As part of the follow-up to the Dutch PCB/dioxin study at school age, we used the Pre-School Activity Inventory (PSAI) to assess play behavior in the Rotterdam cohort (n = 207). The PSAI assesses masculine or feminine play behavior scored on three subscales: masculine, feminine, and composite. Prenatal exposure to PCBs was defined as the sum of PCB 118, 138, 153, and 180 in maternal and cord plasma and breast milk. For breast milk we measured additional PCBs as well as 17 dioxins. Respondents returned 160 questionnaires (age 7.5 years +/- 0.4). Effects of prenatal exposure to PCBs, measured in maternal and cord plasma, on the masculine and composite scales were different for boys and girls (p <.05). In boys, higher prenatal PCB levels were related with less masculinized play, assessed by the masculine scale (p(maternal) =. 042; p(cord) =. 001) and composite scale (p(cord) =. 011), whereas in girls higher PCB levels were associated with more masculinized play, assessed by the composite scale (p(PCBmilk) =. 028). Higher prenatal dioxin levels were associated with more feminized play in boys as well as girls, assessed by the feminine scale (p =.048). These effects suggest prenatal steroid hormone imbalances caused by prenatal exposure to environmental levels of PCBs, dioxins, and other related organochlorine compounds.
Sleep Deprivation Biases the Neural Mechanisms Underlying Economic Preferences

A single night of sleep deprivation (SD) evoked a strategy shift during risky decision making such that healthy human volunteers moved from defending against losses to seeking increased gains. This change in economic preferences was correlated with the magnitude of an SD-driven increase in ventromedial prefrontal activation as well as by an SD-driven decrease in anterior insula activation during decision making. Analogous changes were observed during receipt of reward outcomes: elevated activation to gains in ventromedial prefrontal cortex and ventral striatum, but attenuated anterior insula activation following losses. Finally, the observed shift in economic preferences was not correlated with change in psychomotor vigilance. These results suggest that a night of total sleep deprivation affects the neural mechanisms underlying economic preferences independent of its effects on vigilant attention.
The Efferent System or Olivocochlear Function Bundle – Fine Regulator and Protector of Hearing Perception

The efferent system of the ear possesses several distinct functions, in particular noise protection, mediation of selective attention and improvement of signal to noise ratio. It also supports adaptation and frequency selectivity by modification of the micromechanical properties of outer hair cells. There are many differences in anatomy and physiology between the medial and lateral olivocochlear system suggesting that they are functionally separate systems. The efferent system is affected by inner ear stressors, e.g. noise, ototoxic drugs, and might play a key role in tinnitus generation and maintenance. The anatomy, physiology and its realtionships to inner ear pathologies are discussed in this review article.
Lower limb vasodilatory capacity is not reduced in patients with moderate COPD

We compared exercise capacity (peak O2 uptake; V̇O2peak) and lower limb vasodilatory capacity in 9 patients with moderate COPD (FEV1 52.7 ± 7.6% predicted) and 9 age-matched healthy control subjects. V̇O2peak was measured via open circuit spirometry during incremental cycling. Calf blood flow (CBF) measurements were obtained at rest and after 5 minutes of ischemia using venous occlusion plethysmography. While V̇O2peak was significantly lower in the COPD patients (15.8 ± 3.5 mL·kg−1·min−1) compared with the control group (25.2 ± 3.5 mL·kg−1·min−1), there were no significant differences between groups in peak CBF or peak calf conductance measured 7 seconds post-ischemia. V̇O2peak was significantly correlated with peak CBF and peak conductance in the control group, whereas no significant relationship was found between these variables in the COPD group. However, the rate of decay in blood flow following ischemia was significantly slower (p < 0.05) for the COPD group (−0.036 ± 0.005 mL·100 mL−1·min−1·s−1) when compared with controls (−0.048 ± 0.015 mL·100 mL−1·min−1·s−1). The results suggest that the lower peak exercise capacity in patients with moderate COPD is not related to a loss in leg vasodilatory capacity.
Cerebral amyloid angiopathy and cognitive outcomes in community-based older persons

Objective: We tested the hypothesis that cerebral amyloid angiopathy (CAA) is related to Alzheimer disease (AD) dementia and decline in multiple cognitive systems in old age, independent of AD plaque and tangle pathology and other common age-related neuropathologies. Methods: Participants (n = 1,113) came from 2 longitudinal clinical-pathologic studies of aging, the Rush Memory and Aging Project and the Religious Orders Study. All underwent annual clinical evaluations including detailed cognitive testing for a mean of 7.1 years before death. Clinical diagnoses of AD were established after reviewing all clinical data, blinded to neuropathologic information. Neuropathologic examinations provided measures of CAA, AD pathology, macroscopic infarcts, microinfarcts, and neocortical Lewy bodies. The association of CAA with AD dementia was examined using logistic regression models, and its association with cognitive decline was examined using linear mixed models. Results: CAA was common, present in 78.9% of participants, and moderately related to AD pathology (ρ = 0.401, p < 0.0001). In analyses adjusted for plaques, tangles, and other common age-related neuropathologies, CAA was associated with an increased odds of AD dementia (odds ratio = 1.237, 95% confidence interval 1.082–1.414) and an increased rate of decline in global cognition, perceptual speed, episodic memory, and semantic memory. The associations of CAA with cognitive outcomes were not driven by the presence of capillary involvement. Conclusions: CAA is an important determinant of AD dementia and decline in multiple cognitive systems in old age.
Possible Role for TNF-α in Early Embryopathy Associated With Maternal Diabetes in the Rat

Tumor necrosis factor (TNF) bioactivity was assessed in culture media conditioned with uterine cells collected from control or diabetic rats on days 5 and 8 of pregnancy. On both days, diabetic uterine cells released significantly more biologically active TNF than did control cells, and this activity was significantly decreased by the addition of anti-TNF-α antibodies but not by the addition of normal IgG when WEHI 164 cells were used as a target. When uterine tissues from day 5 or day 8 pregnant diabetic rats were tested by Northern blot analysis, TNF-α mRNAs were twofold more abundant than in control samples, but the difference was not statistically significant (P = 0.086 and 0.100, respectively). Immunohistochemical analysis of diabetic day 5 uterine sections revealed that most of the TNF-α synthesis occurs in the epithelium lining the uterine lumen. Finally, the growth of day-5 embryos in culture medium conditioned with day-5 diabetic uterine cells was significantly reduced when compared with that of embryos in medium conditioned with control cells. Embryonic development was markedly improved when anti-TNF-α antibodies were added to the diabetic-cell conditioned medium. Our data support the hypothesis that TNF-α may be implicated in the developmental deficiencies observed in preimplantation embryos from pregnant diabetic rats.
Stacked Conditional Generative Adversarial Networks for Jointly Learning Shadow Detection and Shadow Removal

Understanding shadows from a single image consists of two types of task in previous studies, containing shadow detection and shadow removal. In this paper, we present a multi-task perspective, which is not embraced by any existing work, to jointly learn both detection and removal in an end-to-end fashion that aims at enjoying the mutually improved benefits from each other. Our framework is based on a novel STacked Conditional Generative Adversarial Network (ST-CGAN), which is composed of two stacked CGANs, each with a generator and a discriminator. Specifically, a shadow image is fed into the first generator which produces a shadow detection mask. That shadow image, concatenated with its predicted mask, goes through the second generator in order to recover its shadow-free image consequently. In addition, the two corresponding discriminators are very likely to model higher level relationships and global scene characteristics for the detected shadow region and reconstruction via removing shadows, respectively. More importantly, for multi-task learning, our design of stacked paradigm provides a novel view which is notably different from the commonly used one as the multi-branch version. To fully evaluate the performance of our proposed framework, we construct the first large-scale benchmark with 1870 image triplets (shadow image, shadow mask image, and shadow-free image) under 135 scenes. Extensive experimental results consistently show the advantages of STC-GAN over several representative state-of-the-art methods on two large-scale publicly available datasets and our newly released one.
Critical Role of Reactive Oxygen Species and Mitochondrial Membrane Potential in Korean Mistletoe Lectin-Induced Apoptosis in Human Hepatocarcinoma Cells

Viscum album L. coloratum agglutinin (VCA), isolated from Korean mistletoe, is a strong inducer of apoptosis in a variety of tumor cells; however, the underlying molecular mechanisms responsible are not clear. Here, we show that VCA induces apoptotic killing, as demonstrated by DNA fragmentation, Hoechst 33258 staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and flow cytometry analysis in hepatocarcinoma Hep3B cells. VCA treatment results in a significant increase in reactive oxygen species (ROS) and loss of mitochondrial membrane potential (Δψm). Furthermore, treatment with the antioxidant N-acetyl-l-cysteine reduces ROS induction by VCA, preventing apoptosis in Hep3B cells, indicating that oxidative stress is involved in VCA-mediated cell death. Our results also show rapid changes in mitochondrial transition permeability, Bax translocation, cytochrome c release, caspase-3 activity, and poly(ADP-ribose) polymerase degradation in Hep3B cells occurring in VCA-induced apoptosis. There is much evidence that implicates c-Jun NH2-terminal kinase (JNK) activation with apoptosis in a variety of cellular and animal models. In this study, we show that VCA induces JNK phosphorylation, which is abolished with pretreatment with a JNK inhibitor. Moreover, Hep3B cells overexpressing JNK1 or stress-activated protein kinase kinase (SEK1) seem to be more susceptible to cell death from ROS and loss of Δψm induced by VCA, whereas expression of dominant-negative JNK1 or SEK1 in Hep3B cells do not. These data suggest that JNK phosphorylation may be a major regulator involved in VCA-induced apoptosis. Together, these results suggest that VCA induces apoptosis by inducing ROS production and a loss of Δψm, in which JNK phosphorylation plays a critical role in these events.
Design and implementation of a real-time wireless sensor/actuator communication system

For industrial automation applications using production machines and robotic installations, truly wireless systems offer advantages in terms of cost and flexibility. Requirements on power supply and real time communication for such applications are highly demanding, and cannot be satisfied with today's off-the-shelf systems. A novel factory communication system, called WISA (wireless interface for sensors and actuators), has thus been developed which provides both wireless communication and wireless power supply. The power supply is based on magnetic coupling while real time wireless communication uses a new TDMA protocol combined with frequency hopping. The TDMA protocol uses optimized parameters for reliable and low delay transmission for a high number of active nodes. The frequency hopping sequences are optimized to mitigate effects of multi-path propagation, interference from other systems operating in the 2.4 GHz ISM band, and self-interference. The new design re-uses existing RF transceivers. The paper explains design concepts of the WISA communication system, and describes practical experience gained with its deployment in industrial environments
Approximation properties of fuzzy systems generated by the min inference

This paper discusses the approximation properties of fuzzy systems generated by the min inference. Firstly, the paper analyzes the properties of fuzzy basis functions (FBFs); Then based on the properties of FBPs, several basic approximation properties concerning approximation mechanisms, uniform approximation bounds, uniform convergency, and universal approximation are obtained. Further, the similarity and difference between the fuzzy systems generated by the product inference and by the min inference are discussed.
Multiple Functions of Glutamate Uptake via Meningococcal GltT-GltM l-Glutamate ABC Transporter in Neisseria meningitidis Internalization into Human Brain Microvascular Endothelial Cells

ABSTRACT We previously reported that Neisseria meningitidis internalization into human brain microvasocular endothelial cells (HBMEC) was triggered by the influx of extracellular l-glutamate via the GltT-GltM l-glutamate ABC transporter, but the underlying mechanism remained unclear. We found that the ΔgltT ΔgltM invasion defect in assay medium (AM) was alleviated in AM without 10% fetal bovine serum (FBS) [AM(−S)]. The alleviation disappeared again in AM(−S) supplemented with 500 μM glutamate. Glutamate uptake by the ΔgltT ΔgltM mutant was less efficient than that by the wild-type strain, but only upon HBMEC infection. We also observed that both GltT-GltM-dependent invasion and accumulation of ezrin, a key membrane-cytoskeleton linker, were more pronounced when N. meningitidis formed larger colonies on HBMEC under physiological glutamate conditions. These results suggested that GltT-GltM-dependent meningococcal internalization into HBMEC might be induced by the reduced environmental glutamate concentration upon infection. Furthermore, we found that the amount of glutathione within the ΔgltT ΔgltM mutant was much lower than that within the wild-type N. meningitidis strain only upon HBMEC infection and was correlated with intracellular survival. Considering that the l-glutamate obtained via GltT-GltM is utilized as a nutrient in host cells, l-glutamate uptake via GltT-GltM plays multiple roles in N. meningitidis internalization into HBMEC.
GENE DOPING IN SPORT – PERSPECTIVES AND RISKS

In the past few years considerable progress regarding the knowledge of the human genome map has been achieved. As a result, attempts to use gene therapy in patients’ management are more and more often undertaken. The aim of gene therapy is to replace defective genes in vivo and/or to promote the long-term endogenous synthesis of deficient protein. In vitro studies improve the production of human recombinant proteins, such as insulin (INS), growth hormone (GH), insulin-like growth factor-1 (IGF-1) and erythropoietin (EPO), which could have therapeutic application. Unfortunately, genetic methods developed for therapeutic purposes are increasingly being used in competitive sports. Some new substances (e.g., antibodies against myostatin or myostatin blockers) might be used in gene doping in athletes. The use of these substances may cause an increase of body weight and muscle mass and a significant improvement of muscle strength. Although it is proven that uncontrolled manipulation of genetic material and/or the introduction of recombinant proteins may be associated with health risks, athletes are increasingly turning to banned gene doping. At the same time, anti-doping research is undertaken in many laboratories around the world to try to develop and refine ever newer techniques for gene doping detection in sport. Thanks to the World Anti-Doping Agency (WADA) and other sports organizations there is a hope for real protection of athletes from adverse health effects of gene doping, which at the same time gives a chance to sustain the idea of fair play in sport.